Test Set

Front 1

Aricept a) List five common side effects (from at least three different systems) of these medications.

Back 1

1. Gastrointestinal: Nx, vomiting???, DIA, ABDO Pn, ANOREXIA<br />2. neuropsychiatric : insomnia, fatigue, headaches, SZ<br />3. cardiovascular : hypertension, syncope, BRADY<br><br>nausea, diarrhea, insomnia, vomiting, muscle cramp, fatigue and anorexia.

Front 2

Aricept -- b) Name two relative contraindications.

Back 2

1. Sick sinus syndrome<br />2. gastro-intestinal bleeding<br><br>Cardiac Disease, Cardiac Conduction Disturbances, Chronic Obstructive Pulmonary Disease (COPD), Asthma, Severe Cardiac Arrhythmias and Sick Sinus Syndrome

Front 3

Aricept -- Name three areas that you would assess for improvement to see if treatment was<br>effective.

Back 3

1. Cognitive (memory, calculation)<br>2. Behavioral (agitation, aggressiveness)<br>3. Functional (ADL’s and IADL’s).

Front 4

TD - Definition

Back 4

orofacial (ie, buccolingual, masticatory) hyperkinesia <br /><br />Tardive dyskinesias (TDs) are involuntary movements of the tongue, lips, face, trunk, and extremities that occur in patients treated with long-term dopaminergic antagonist medications. <br /><br />Tardive dyskinesia is characterized by repetitive, involuntary, purposeless movements, such as grimacing, tongue protrusion, lip smacking, puckering and pursing of the lips, and rapid eye blinking. Rapid movements of the extremities may also occur. Impaired movements of the fingers may also appear. <br /><br />choreoathetoid movements<br />vermiform movements of the tongue<br />lateral movements of the jaw<br /><br />• abnormal, involuntary, irregular Choreathetoid movements of the head, limbs, and trunk<br />• a delayed effect (after six months) of antipsychotic treatment<br />• peri-oral movements most common<br />o darting, twisting, protruding movements of the tongue o chewing and lateral jaw movements<br />o lip puckering<br />o facial grimacing<br />• exacerbated by stress, and disappears during sleep<br />• not provoked by urges to move

Front 5

TD -- Describe how you would assess tardive dyskinesia, and name three factors you would look for.

Back 5

“Do you feel restless inside? Do you have the urge to move? Are you able to keep your feet still?”<br><br>Inner restlessness, need to move, akathisia<br><br>provocative distraction<br><br>Signs of tardive dyskinesia may include any of the following:<br /><br />Continuous and repetitive movements of the mouth, tongue, and jaw<br />Facial grimacing<br />Lip smacking<br />Puffing of the cheeks<br />Uncontrollable movements of the arms, legs, fingers, and toes<br />Swaying motions of the trunk or hips<br />Movements of the jaw usually consist of an up-and-down motion, as if a person is chewing. When the tongue is affected, it may protrude or move around in a twisting manner.<br /><br />1. Ask patient to remove shoes and socks.<br />2. Ask patient if there is anything in his/her mouth (eg, gum, candy); if there is, to remove it.<br />3. Ask patient about the currentcondition of his/her teeth. Ask patient if he/she wears dentures. Do teeth or dentures bother the patient now?<br />4. Ask patient whether he/she notices any movements in mouth, face, hands, or feet. If yes, ask to describe and to what extent they currentlybother patient or interfere with his/her activities.<br />5. Have patient sit in chair with hands on knees, legs slightly apart and feet flat on floor. (Look at entire body for movements while in this position.)<br />6. Ask patient to sit with hands hanging unsupported. If male, between legs, if female and wearing a dress, hanging over knees. (Observe hands and other body areas.)<br />7. Ask patient to open mouth. (Observe tongue at rest in mouth.) Do this twice.<br />8. Ask patient to protrude tongue. (Observe abnormalities of tongue movement.) Do this twice.<br />9. Ask patient to tap thumb, with each finger, as rapidly as possible for 10 to 15 seconds; separately with right hand, then with left hand. (Observe facial and leg movements.)<br />10. Flex and extend patient's left and right arms (one at a time). (Note any rigidity.)<br />11. Ask patient to stand up. (Observe in profile. Observe all body areas again, hips included.)<br />12. Ask patient to extend both arms outstretched in front with palms down. (Observe trunk, legs, and mouth.)<br />13. Have patient walk a few paces, turn and walk back to chair. (Observe hands and gait.) Do this twice.

Front 6

TD -- DDx

Back 6

Tourettes, tardive dystonia, akathisia, and myoclonus<br /><br />hyperthyroidism<br /><br />tremor, epilepsy, corticobasilar<br /><br />Hallervorden-Spatz disease<br /><br>huntington, wilson<br><br />• mannerisms and stereotypies<br />• Meige’s syndrome and other senile dyskinesias<br />• dental problems (ill fitting dentures)<br />• Sydenham’s chorea<br />• drug toxicity (e.g. levodopa)

Front 7

TD -- Epidemiology

Back 7

Epidemiology<br /><br />Tardive dyskinesia most commonly occurs in patients with psychiatric conditions who are treated with antipsychotic medications for many years. One study reported that within the first four years of using antipsychotic medications, 18.5 percent of young adults develop symptoms. Furthermore, 31 percent of those over 55 years of age develop tardive dyskinesia symptoms in the same time frame.[13] Other estimates suggest that it occurs in 15-30% of patients receiving treatment with antipsychotic neuroleptic medications for 3 months or longer.<br /><br />5% YR.<br><br>The elderly and female patients are more prone to develop tardive dyskinesia.[citation needed] Cigarette smokers also have a higher prevalence of tardive dyskinesia.[citation needed] This claim is disputed, however,

Front 8

mechanism of action of typical antipsychotic medications that is thought to mediate their efficacy in diminishing positive psychotic symptoms.

Back 8

antipsychotic medications reduce the positive symptoms of schizophrenia through the blockade of D2 dopamine receptors in the mesolimbic pathway

Front 9

List three major dopamine pathways in the brain. Identify the presumed functional role of each of the different pathways.

Back 9

• mesolimbic pathway: reward pathway (from ventral tegmental area to nucleus accumbens)<br>• mesocortical pathway: learning and memory, negative symptoms (from substantia nigra and<br>ventral tegmental area to amygdala, septal nuclei, anterior cortex, olfactory tubercle); there is a high density of 5-HT2a receptors in this pathway; the blockade of 5-HT2a by atypical antipsychotics reverses some of the effect of dopamine blockade in this pathway, which may be why the atypicals are somewhat effective in negative symptoms (normally, serotonin inhibits dopamine release; blockage of 5-HT2a therefore increases dopamine release)<br>• nigrostriatal pathway: movement (from substantia nigra to caudate and putamen); again, the blockade of 5-HT2a in this pathway counteracts the D2 blockade, leading to less EPS and tardive dyskinesia<br>• tuberoinfundibular pathway: prolactin elevation; normally dopamine inhibits prolactin increase – blockade of dopamine causes prolactin elevation; the reverse is true for serotonin

Front 10

Diagnostic criteria for NMS

Back 10

<br><br>F – Fever<br>A – Autonomic instability<br>L – Leukocytosis<br>T – Tremor<br>E – Elevated enzymes (elevated CPK)<br>R – Rigidity of muscles<br><br><br><br>• muscle rigidity and elevated temperature in response to neuroleptic treatment<br />• two of the following: MIDWEST CDC<br />o mutism<br />o incontinence<br />o diaphoresis<br />o white count (leukocytosis)<br />o elevated or labile blood pressure o shaking (tremor)<br />o tachycardia<br />o changes in level of consciousness o Dysphagia<br />o CPK elevated

Front 11

NMS -- associated clinical features

Back 11

Revised mnemonic for NMS: FALTER<br>F – Fever<br>A – Autonomic instability<br>L – Leukocytosis<br>T – Tremor<br>E – Elevated enzymes (elevated CPK)<br>R – Rigidity of muscles<br>Increased body temperature &gt;38°C (&gt;100.4°F), or<br>Confused or altered consciousness<br>Diaphoresis &quot;sweat shock&quot;<br>Rigid muscles<br>Autonomic imbalance<br><br><br>• note that NMS is less likely with low potency, anticholinergic antipsychotics<br />• usually develops within four weeks of starting an antipsychotic<br />• other laboratory abnormalities<br />o note: leukocytosis and elevated CPK are the only ones that are part of the criteria o renal failure: myoglobinuria and proteinuria, elevated BUN and creatinine<br />o liver failure: elevated transaminases<br />o electrolyte changes: low calcium, magnesium, phosphate<br />o acidosis<br />o dehydration

Front 12

NMS -- treatment

Back 12

• discontinue neuroleptic<br />• supportive (fluid, ice packs, monitors)<br />• dopamine agonist (bromocriptine, amantadine) or dantrolene<br><br>stop neuroleptic drugs and to treat the hyperthermia aggressively, such as with cooling blankets or ice packs to the axillae and groin. Many cases require intensive care and circulatory and ventilatory support. Medications such as dantrolene sodium and bromocriptine may be used.[21] Apomorphine may be used however its use is supported by little evidence.[3] Benzodiazepines may be used to control agitation. Highly elevated myoglobin can damage the kidneys, therefore aggressive hydration may be required. Volume resuscitation is paramount. Benzodiazepines, dantrolene, and dopaminergic agents are a few pharmaceutical families that can be used to treat various degrees of NMS.

Front 13

You are about to start a patient on an antidepressant. List five factors to consider in choosing an antidepressant. [COMBO-O]

Back 13

• previous trials of antidepressants<br />• drug interactions<br />• symptom profile<br />• patient preference<br />• cost

Front 14

Clozapine. List the two most serious adverse effects associated with the use of

Back 14

Agranulocytosis<br />• rate of 1to2%<br />• most common in the first six months, but can occur at any time<br />• risk factors: increasing age, female gender<br />Seizures<br />• dose dependent<br />• rates: 5% if &gt; 600mg, 3-4% if 300 to 600mg, 1-2% if &lt; 300mg<br />• myoclonus can be a precursor to seizures<br />• management: temporary stop, and then restart at 50% dose, gradually increasing; add<br />anticonvulsant (not carbamazepine, due to combined Agranulocytosis risk)

Front 15

Clozapine -- List the baseline<br />measures needed prior to use, and the guidelines for monitoring its use.

Back 15

Baseline measures and monitoring<br />• baseline: CBC, renal function, ECG, liver function<br />• monitoring: weekly WBC for six months, then biweekly<br />• react to either WBC or ANC – yellow if ANC 1.5 to 2 or WBC 2 to 3.5 (red if lower, green<br />if higher)<br />• for yellow: twice weekly CBC until return to green<br />• for red: stop Clozapine, monitor blood work and clinical signs for four weeks<br /><br />if WBC is 2.0 to 3.0 or ANC &lt; 1.5, do CBC daily until above 3.0, then twice weekly until above 3.5<br />if WBC &lt; 2 or ANC &lt; 1, then discontinue clozapine permanently, do daily CBC until WBC &gt; 3.5, notify clozapine registry<br />

Front 16

indications for the use of methylphenidate in patients with ADHD.

Back 16

Indications for methylphenidate in ADHD<br>• family or patient wishes a trial<br>• significant symptoms of hyperactivity, inattention, or both<br>• patient greater than age six (dextroamphetamine in patients greater than age three)

Front 17

Contra-indications for methylphenidate in ADHD

Back 17

• liver disease<br>• psychosis<br>• anorexia<br>• glaucoma<br>• tachyarrhythmia<br>• anxiety, tension, agitation

Front 18

5 Side effects of methylphenidate

Back 18

• insomnia<br>• headache<br>• gastrointestinal irritability<br>• anorexia (weight loss)<br>• tachycardia, hypertension

Front 19

ritalin dose, onset (reg and SR)

Back 19

dosing is 5 to 40mg daily (dosing for dextroamphetamine is half that)<br>• start at 5mg bid then reassess and increase if needed by 5mg every three days<br>• onset of effect is 30 to 60 minutes, duration of effect is 3 to 5 hours<br>• the SR formulation has a slightly slower onset of action, and a duration of nine hours<br>

Front 20

clinical indications for prescribing ECT

Back 20

Indications for ECT in depression<br>• psychotic depression<br>• refusal to eat (life threatening)<br>• acute suicidality or homicidality<br>• contraindication to pharmacotherapy (medically ill, pregnant)<br>• failure of medication trials<br>• patient preference<br>• note: after ECT treatment, the best maintenance is an antidepressant + lithium<br>Indications for ECT in mania<br>• patients whose manic behavior has produced dangerous levels of exhaustion<br>Indications for ECT in schizophrenia<br>• marked catatonia<br>• marked affective symptoms<br>• marked positive symptoms unresponsive to pharmacotherapy<br>Other indications for ECT<br>• catatonia<br>• obsessive compulsive disorder

Front 21

10 SSx serotonin syndrome

Back 21

Cognitive effects: headache, agitation, hypomania, mental confusion, hallucinations, coma<br /><br />Autonomic effects: shivering, sweating, hyperthermia, hypertension, tachycardia, nausea, diarrhea.<br /><br />Somatic effects: myoclonus (muscle twitching), hyperreflexia (manifested by clonus), tremor<br /><br /><br />• DR. MUST CHECK DEATH<br />• diarrhea<br />• rigidity<br />• myoclonus<br />• uncontrollable shivering<br />• sweating (diaph)<br />• tremor<br />• coma<br />• HYPER-reflexia<br />• e – death<br />• cardiovascular collapse<br />• k – confusion (delirium)<br />• disorientation<br />• e – status epilepticus<br />• ataxia •t<br />• HYPERthermia (fever)<br /><br />serotonin syndrome: mental status changes, agitation, myoclonus, hyperreflexia, hypertonicity, fever, diaphoresis, shivering, tremor, autonomic instability, death<br />lab findings: increased CK, 1. Recent addition or increase in a known serotonergic agent<br />2. Absence of other possible aetiologies (infection, substance abuse, withdrawal, etc.) 3. No recent addition or increase of a neuroleptic agent<br />4. At least three of the following symptoms:<br />Mental status changes (confusion, hypomania) Agitation<br />Myoclonus<br />Hyperreflexia<br />Diaphoresis Shivering Tremor Diarrhoea Incoordination Fever<br /><br />significant problem with Sternbach’s criteria is the inclusion of four criteria that relate to mental status, which weights the definition towards patients with an abnormal mental state. Sternbach’s criteria include confusion, hypomania, restlessness and ataxia (incoordination). Because only three are required to occur for the diagnosis of serotonin syndrome to be made, someone with an anticho- linergic delirium would meet the clinical criteria. Ataxia or incoordination is also a problematic feature, since serotonin toxicity does not appear to cause cerebellar features, and any patient who is agitated and confused may appear to be ataxic.<br /><br /><br />Hunter Serotonin Toxicity Criteria: Decision Rules<br />In the presence of a serotonergic agent:<br />1. IF (spontaneous clonus 1⁄4 yes) THEN serotonin toxicity 1⁄4 YES<br />2. ELSE IF (inducible clonus 1⁄4 yes) AND [(agitation 1⁄4 yes) OR (diaphoresis 1⁄4 yes)]<br />THEN serotonin toxicity 1⁄4 YES<br />3. ELSE IF (ocular clonus 1⁄4 yes) AND [(agitation 1⁄4 yes) OR (diaphoresis 1⁄4 yes)] THEN<br />serotonin toxicity 1⁄4 YES<br />4. ELSE IF (tremor 1⁄4 yes) AND (hyperreflexia 1⁄4 yes) THEN serotonin toxicity 1⁄4 YES<br />5. ELSE IF (hypertonic 1⁄4 yes) AND (temperature &gt; 38

Front 22

serotonin syndrome and neuroleptic malignant syndrome -- Compare and contrast

Back 22

• shared clinical features: o hyperthermia<br />o sweating<br />o tremor<br />• NMS is seen in patients on antipsychotic medications<br />• NMS is more common in young males, while serotonin syndrome is more common in the<br />elderly<br />• specific pharmacotherapy is available for NMS<br />o rigidity<br />o confusion o coma<br /><br><br>Features that are present in NMS and not serotonin syndrome are:[10]<br>Bradykinesia<br>Muscle rigidity<br>Laboratory values (WBC &amp; CPK)

Front 23

management of SSRI induced sexual dysfunction.

Back 23

• stimulation of 5-HT2a receptors in the spinal cord may inhibit spinal reflexes for orgasm and ejaculation, causing sexual dysfunction<br />• 50 to 80% of patients taking SSRI’s experience some sexual dysfunction, although few complain of it<br />• management: add medication or switch to a different antidepressant<br />o adding medications<br /> Bupropion<br /> sildenafil (Viagra): take one hour before intercourse<br /> Yohimbine: alpha-2 antagonist<br /> Cyproheptadine: antihistamine that is also antiserotonergic<br />o switching to medications with low rate of side-effects<br /> Bupropion<br /> Mirtazapine<br /><br />bupropion<br />yohimbine<br />moclobemide (correct answer; there is no evidence that it is helpful, and it leads to a risk of serotonin syndrome)<br />cyproheptadine (an antihistamine that has anti-serotonergic properties; reduces sexual side-effects by blocking 5-HT2a; brand name is Periactin; not to be confused with cyproterone)<br />sildenafil (Viagra)

Front 24

Neurolopetics -- five systems other than the CNS affected by conventional neuroleptics, and two side-<br />effects related to each of these symptoms.

Back 24

• gastrointestinal: increased appetite, weight gain, dyspepsia, nausea<br />• cardiovascular: postural hypotension, tachycardia, EKG changes<br />• sexual side effects: decreased libido, erectile dysfunction<br />• endocrine: elevated prolactin, SIADH<br />• ocular: retinitis pigmentosa, cataracts, lenticular pigmentation<br />• hematology: thrombocytopenia, Agranulocytosis

Front 25

A young woman with bipolar disorder is stable on valproic acid 750mg bid. She wishes to become pregnant, and wants to stay on her medication to avoid relapse. List four birth defects that are caused by valproic acid. What medication would you add to her treatment to reduce the risk of birth defects? [2000]

Back 25

• birth defects caused by Valproate:<br>• neural tube defects<br>• cleft lip / palate<br>• craniofacial abnormalities<br>• digital malformation<br>• cardiac abnormalities<br>• folic acid 1 to 4mg daily

Front 26

MOA -- sertraline, bupropion, nefazadone, venlafaxine, mirtazipine

Back 26

sert -- SSRI<br>bupr -- dopamine uptake block &amp; NE<br>nefaz<br>venlaf -- snri<br>mirtaz

Front 27

ten potential adverse effects caused by blockade of muscarinic acetylcholine receptors.

Back 27

CNS delirium, memory, impaired vision, dizzy/LH<br>RESP decr secretions (asthma exac)<br>CV bradycard<br>GI decr saliv, constip<br>autonom decr sweating (incr temp)<br>GU urinary retn, retro ejac

Front 28

Management of anticholinergic toxicity:

Back 28

• stop all anticholinergic medications<br />• expect improvement in 24 to 48 hours<br />• do not use Physostigmine unless cardiac monitoring and life support is available<br />• use benzodiazepines for management of agitation

Front 29

Neuroleptics = 5 systems other than the CNS affected by conventional neuroleptics, and two side-effects related to each of these symptoms. [COMBO-M]<br />

Back 29

gastrointestinal: increased appetite, weight gain, dyspepsia, nausea<br />cardiovascular: postural hypotension, tachycardia, EKG changes<br />sexual side effects: decreased libido, erectile dysfunction<br />endocrine: elevated prolactin, SIADH<br />ocular: retinitis pigmentosa, cataracts, lenticular pigmentation<br />hematologic: thrombocytopenia, agranulocytosis

Front 30

Drug Metabolism CYP

Back 30

there are five enzymes of significance: (two “A”s, two “C”s, and one “D”, listed in alpha-numeric order and numbered from 1 to 5) (no. 1) 1A2, (no. 2) 3A3/4,(no. 3) 2C9, (no. 4) 2C19, and (no. 5) 2D6; fluvoxamine inhibits three enzymes, fluoxetine two, and paroxetine and nefazadone one each<br>fluvoxamine: 1A2, 3A3/4, 2C19 (no. 1,2,4)<br>fluoxetine: 3A3/4, 2D6 (no. 2,5)<br>paroxetine: 2D6 (no. 5)<br>nefazadone: 3A3/4 (no. 2)<br><br>tertiary amines (eg. amitriptyline, clomipramine, imipramine) are metabolized by all P450 except 2D6, and secondary amines (eg. desipramine and nortriptyline) are metabolized by 2D6 (#5, which is inhibited by fluoxetine and paroxetine)<br>CYP2D6 and 2C19 have genetic polymorphisms; “poor metabolizers” can have TCA levels up to 30 times higher at the same dose as “extensive metabolizers”<br>CYP3A3/4 is the most abundant in humans, and is not subject to genetic polymorphism; this is inhibited by erythromycin, grapefruit juice<br>lamotrigine levels are decreased by all anti-epileptic drugs except for valproate, which increases them<br>

Front 31

Inducer of CYP

Back 31

warfarin (correct answer; warfarin is metabolized by 2C9 and others; I guess it also induces something)<br><br>1A2: cigarette smoking<br>3A4: carbamazepine, rifampin<br>

Front 32

Theophylline metabolism

Back 32

theophylline is metabolized by 3A4; its levels will be increased by fluvoxamine, as well as by erythromycin, grapefruit juice)<br>

Front 33

Fluoxetine metabolism

Back 33

fluoxetine increases the levels of clozapine (clozapine is metabolized by 1A2, 3A3/4, and 2D6; it’s levels are increased by fluvoxamine and other SSRIs, caffeine, erythromycin, cimetidine, and decreased by carbamazepine and nicotine)<br>nefazadone increases the levels of alprazolam (true; it blocks 3A3/4, which is involved in the metabolism of tertiary amines)<br>fluoxetine increases tricyclic antidepressant levels (true; it blocks both 3A3/4 and 2D6 – 2D6 metabolizes secondary amines and 3A3/4 is involved in the metabolism of tertiary amines)

Front 34

Fluvox metab cyp

Back 34

fluvoxamine is a potent inhibitor of CYP1A2, resulting in inhibition of clozapine metabolism (correct answer)<br><br>fluvoxamine decreases the levels of theophylline (correct answer; false; theophylline is metabolized by 3A4; its levels will be increased by fluvoxamine, as well as by erythromycin, grapefruit juice)<br><br>fluvoxamine increases the levels of haloperidol (true; haloperidol is metabolized by 1A2 and 2D6, and so its levels will be increased by fluvoxamine, fluoxetine, and paroxetine) <br>fluoxetine and norfluoxetine do not inhibit P450 2D6 (also a correct answer<br>

Front 35

most potent inhibitor of cytochrome P450 3A4

Back 35

nefazadone

Front 36

least histaminergic and alpha-adrenergic blockade

Back 36

desipramine (correct answer)

Front 37

bromocriptine indication / moa

Back 37

hyperprolactinemia (true; bromocriptine is a potent dopamine agonist; it is also used in Parkinson’s disease and acromegaliy)

Front 38

3a4 == ssri inhibitors

Back 38

fluvoxamine, fluoxetine, and nefazadone<br /><br />http://www.psychresidentonline.com/CYP450%20drug%20interactions.htm<br /><br />http://harvardpartnersinternational.staywellsolutionsonline.com/HealthNewsLetters/MensHealthWatch.pg

Front 39

maoi metabolizes what?<br>nsMOAI<br>MOAI-A<br>MOAI-B

Back 39

mono-amine oxidase A preferentially deaminates norepinephrine and serotonin<br>mono-amine oxidase B preferentially deaminates dopamine<br>non-selective MAOIs: phenelzine, tranylcypromine, isocarboxazid<br>MAO-A inhibitors: moclobemide, clorgyline<br>MAO-B inhibitors: selegiline, pargyline<br>

Front 40

non-revers MAOI side effects

Back 40

HTN <br>hepatotoxicity (can rarely occur with (Nardil) phenelzine; not seen with tranylcypromine)<br>cholestatic jaundice (mild jaundice has been reported)<br>ankle edema<br>worsening of hemolytic anemia (hemolytic anemia is a possible side-effect of (Parnate) tranylcypromine)

Front 41

Psychostimulant indications ?

Back 41

depression in the elderly (correct answer)<br>

Front 42

bzd moa

Back 42

potentiating the effects of GABA; they also inhibit the firing of the raphe-nucleus (decrease 5-HT)<br>their main sites of action are the brain stem reticular formation, the cortex, and the limbic system<br>

Front 43

BZD -- longest t1/2

Back 43

flurazepam

Front 44

bupropion MOA

Back 44

blocking the reuptake of norepinephrine and, to a lesser extent, dopamine<br>

Front 45

akathisia treatment

Back 45

lipophilic beta (prop)<br>???? bzd<br>clonidine / amant

Front 46

Li interactions

Back 46

thiazide diuretics (true; most diuretics, including thiazide, loop, and K sparing increase lithium levels)<br />ibuprofen (NSAIDs increase lithium levels)<br />renal failure (true; renal failure lower lithium clearance, increasing its levels)<br />caffeine (correct answer – caffeine lowers lithium levels, as do osmotic diuretics and carbonic anhydrase inhibitors)<br />low sodium diet (true; the body conserves sodium, and in the process will conserve lithium too, increasing its level)<br /><br />increase lithium levels: NSAIDs, thiazide diuretics, dehydration<br />increase toxicity: calcium channel blockers<br />the only things that decrease lithium levels are: osmotic diuretics, carbonic anyhydrase inhibitors, and xanthines (like caffeine)<br />

Front 47

VPA side effects

Back 47

hepatic toxicity<br />pancreatitis<br />coagulation disorders<br />agranulocytosis<br />gastrointestinal side effects<br />sedation<br /><br />common side-effects of valproate include: gastrointestinal side-effects, sedation, tremor, ataxia, dysarthria, weight gain, elevated liver tests (in up to 40%), and hair loss (in up to 10%)<br />the hair loss is temporary and can be treated with zinc and selenium

Front 48

AIMS test procedure

Back 48

observe the person in a relaxed, resting state<br>have the person remove everything from their mouth<br>have the person tap one palm, then the other (not part of AIMS)<br>observe the person sitting with their arms at their sides<br>FINGER TO NOSE TEST (NOT PART OF AIMS)<br>test their tone<br>have the person hold their hands out straight<br>flex the person’s arms<br>have the person tap the palms of their hands against each other (not a part of AIMS)<br>instructions for the AIMS<br>observe the patient unobtrusively at rest<br>ask patient to remove shoes/socks, anything in mouth<br>ask about current condition of teeth or if they wear dentures<br>ask if they notice any movements in mouth<br>observe entire body for movements while patient sits in chair with hands on knees, legs slightly apart<br>ask patient to sit with hands hanging between legs; observe<br>ask to open mouth; observe tongue at rest (do this twice)<br>ask to protrude tongue (do this twice)<br>ask patient to tap thumb with each finger for 10 seconds, each hand separately; observe for facial/leg movements<br>flex/extend arms, observing for rigidity<br>ask patient to stand up<br>ask patient to extend arms with palms down (observe trunk, legs, mouth)<br>have patient walk a few paces and return (do this twice, observing hands and gait)

Front 49

clozapine toxicity

Back 49

tachycardia, hypotension, lethargy/drowsiness, constipation, vomiting, seizures, agitation, delirium, mydriasis, diplopia, hyperreflexia

Front 50

clozapine agranulocyotosis incidence

Back 50

the rate of agranulocytosis is 1%<br>agranulocytosis is not dose dependent<br>duration of treatment is not a reliable predictor; most cases (75%) develop within the first six months, but some can develop years after starting treatment<br>

Front 51

phenothiazine s/e

Back 51

tachycardia<br>pigmented retinopathy<br>decreased seizure threshold<br>Parkinsonism<br>premature ejaculation<br>sedation<br>galactorrhea<br>photosensitivity<br>

Front 52

TD -- possible treatments???

Back 52

Decrease or d/c drug<br><br>The dopamine-depleting drug tetrabenazine has been used to treat tardive dyskinesia[8][9] and other movement disorders.<br>Zofran has shown some benefit in experimental studies on tardive dyskinesia and a variety of anti-Parkinsonian medications are used such as Aricept, Baclofen, Requip and Mirapex. Clonidine is used for dystonic spasms and can be of help. Botox injections are used for minor focal dystonia, but not in more advanced tardive dyskinesia.[10] A review paper found Benzodiazepines[N 3] to be effective in alleviating the symptoms of tardive dyskinesia.[11] However, like most anticonvulsants, benzodiazepines may cause tremors as well as benzodiazepine withdrawal syndrome upon rapid discontinuation.

Front 53

CBZ -- s/e

Back 53

side effects of carbamazepine include a rash, hyponatremia, hematopoietic alterations, peripheral neuropathy, and liver toxicity; benign transient neutropenia occurs in 20% of patients; agranulocytosis is rare; 3% of patients taking carbamazepine develop a hypersensitivity reaction consisting of a rash (erythema multiforme) and a fever – carbamazepine should be discontinued in such instances<br>side effects of valproate include alopecia, weight gain, nausea, vomiting, and at high doses thrombocytopenia (and possibly abnormal coagulation parameters); rarer side effects include hepatotoxicity, pancreatitis, and blood dyscrasias;

Front 54

Depot APs

Back 54

flupenthixol decanoate (Fluanxol)<br />fluphenazine enanthate (Moditen)<br />fluphenazine decanoate (Modecate)<br />fluspirilene (IMAP)<br />pipotiazine palmitate (Piportil LA)<br />haloperidol decanoate (Haldol LA)

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TCA toxicity

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main signs of TCA toxicity are anticholinergic signs, cardiac signs, and neurological signs<br>anticholinergic signs: blurred vision (mydriasis or pupillary dilation), fever, dry mouth, tachycardia, urinary retention, ileus, delirium (think: blind as a bat, dry as a bone, hot as Hades, mad as a hatter)<br>cardiac toxicity: tachycardia, hypotension, ECG changes, arrhythmias<br>neurological signs: confusion, myoclonus, seizures, coma<br>

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remeron MOA

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mirtazapine is an antagonist at alpha-2 receptors pre-synaptically on noradrenergic and serotonergic neurons, causing an increase in the release of both neurotransmitters; post-synaptically it inhibits 5HT-2 and 5HT-3, minimizing the sexual side effects and agitation that are seen with serotonergic stimulation<br>while it is anxiolytic, mirtazapine does not inhibit norepinephrine<br>

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features of neuroleptic induced acute dystonia

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dysphagia<br>retrocollis<br>torticollis<br>trismus<br>fasciculations (false; correct answer)

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clonidine s/e

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weight gain (probably the correct answer)<br>dry mouth<br>sedation<br>weakness<br>hypotension<br>clonidine is an alpha-2 agonist; works by reducing adrenergic tone; it may cause dry mouth, sedation, weakness, hypotension, irritability, impotence; weight gain can happen but is less common<br>

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Li intoxication

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diarrhea<br />ataxia<br />slurred speech<br />tremor<br />mydriasis (correct answer; I’m not sure what the pupils do in lithium toxicity; you can get blurred vision, however)<br />

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lithium side effects:<br>

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neurological: tremor (65%, coarse tremor may indicate toxicity), fatigue / weakness (33%), mild cognitive impairment<br>GI: nausea and vomiting (50%), weight gain (30%), diarrhea (20%)<br>cardiovascular: benign T-wave changes on EKG (30%)<br>renal: polyuria or polydipsia (40%)<br>dermatological: rash, pruritis, acne, thinning of hair<br>other: hypothyroidism, hyperparathyroidism (with hypercalcemia, in up to 40%)

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Li side effects

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normal blood levels: polydipsia, polyuria, dry mouth, weight gain, fatigue<br />occasional side effects: metallic taste, nausea/diarrhea, fine tremor, edema<br />less occasional side effects: hypothyroidism, hypokalemia, EKG changes, mental slowness, worsening of psoriasis, kidney changes, raised levels of ADH, goiter<br />mild toxicity: blurred vision, weakness, worsening GI side effects, CNS disturbances (coarse tremor, ataxia, dysarthria, nystagmus)<br />severe toxicity: hyperreflexia, convulsions, psychosis, syncope, oliguria, circulatory failure, coma<br><br>side effects long term<br>renal dysfunction (controversial, probably true)<br>hypothyroidism (true; 50% on long term lithium get an abnormal TRH response, and 30% have elevated TSH)<br>myasthenia gravis like reaction (true; can cause muscle weakness and fatigue; this is generally transient and may coincide with peaks in serum levels)<br>osteoporosis (correct answer; false; long term use of anticonvulsants, such as valproate, can increase the risk of osteoporosis)<br>EKG changes (true; benign changes are common; can also get ventricular and nodal arrhythmias)<br><br />

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NMS features

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diaphoresis (false)<br>blood pressure variability<br>elevated temperature<br>extrapyramidal side-effects<br>rigidity<br>autonomic instability<br>myoglobinuria<br>decreased catecholamines in urine (false)<br>laboratory findings: leukocytosis, elevated CK, ALT, AST, LDH; high levels of myoglobin and protein in the urine<br>risk factors include: previous NMS, male gender, young age (20-40)<br>the mortality rate is 20 to 30%<br>treatment: immediately stop antipsychotics, hydrate, try minor tranquilizers (benzodiazepines), try dantrolene or bromocriptine<br>

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NMS early sx

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catatonia<br>hyperthermia<br>bradycardia (correct answer; they get tachycardia)<br>dysphagia<br>rigidity<br>diaphoresis<br>

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muscarinic inhibition s/e

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<br>tachycardia (correct answer)<br>sexual side effects (also correct)<br><br>muscarinic anticholinergic effects include: blurred vision (mydriasis or pupillary dilation), fever, dry mouth, tachycardia, urinary retention, ileus, delirium (think: blind as a bat, dry as a bone, hot as Hades, mad as a hatter); muscarinic receptors are also involved in the modulation of erection and ejaculation/orgasm<br>histaminic: sedation and weight gain<br>alpha-1 adrenergic: orthostatic hypotension, dizziness, drowsiness, priapism<br>beta-adrenergic: erectile dysfunction<br>5-HT-2: agitation, akathisia, anxiety, insomnia, sexual function (delayed ejaculation or orgasm)<br>5-HT-3: nausea, diarrhea, emesis, migraine pain<br>

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Insomnia, arousals, energy, lethargy -- DDx Med (5) and Psych (5)

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Sleep - RLS, OSA, Central SA<br>Pain<br>Endo<br>Med / subst induced<br><br>MDD<br>GAD<br>Adj<br>PTSD<br>Panic<br>Dysthym<br>Somatoform

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Narcolepsy Criteria

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a. excessive sleepiness characterized by recurrent attacks of refreshing sleep during the day, for more than three months<br>b. the presence of cataplexy and/or REM intrusions (hypnopompic or hypnagogic hallucinations, or sleep paralysis)

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Sleep -- changes in depression

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A- Subjective sleep disturbance<br>Insomnia (90%) Hypersomnia<br>Disturbing dreams<br>Decreased slow wave sleep, shift to latter part of night Fragmented sleep<br>C -phase advance<br>Early morning wakenings**<br>B- Objective sleep disturbance<br>Abbreviated onset to REM sleep** Increased REM sleep, REM density

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Parasomnia -- define and 7 eg

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Parasomnias are disorders characterized by abnormal behavioural or physiological events occurring in association with sleep, specific sleep stages or sleep wake transitions. Unlike dyssomnias, parasomnias do not involve abnormalities of the mechanisms generating sleep-wake states nor of the timing of sleep and wakefulness. Rather, they represent the activation of physiological systems at inappropriate times during the sleep wake cycle (eg. autonomic nervous system, motor system or cognitive processes.<br><br>• Nightmare disorder<br>o Repeated awakenings from the major sleep period or naps with detailed recall of extended or<br>frightening dreams, usually involving some threat<br>o On wakening, the person rapidly becomes oriented and alert (unlike terrors)<br>o The dream experience or sleep disturbance that results causes significant impairment....<br>o The nightmares do not occur exclusively during the course of another mental disorder or<br>secondary to a substance/GMC<br>• Sleep terror disorder<br>o Recurrent abrupt awakenings from sleep usually occurring during the 1st 1/3 of sleep<br>episodes, and beginning with a panicky scream<br>o Intense fear and signs of autonomic arousal such as tachycardia, rapid breathing and sweating o Relative unresponsiveness to comfort during the episode<br>o No detailed dream recall and amnesia for the episode<br>o Significant distress<br>o Not due to a substance or GMC<br>• Sleepwalking disorder<br>o Repeated rising from the bed and walking about, usually during the 1st 1/3 of sleep<br>o While sleepwalking, person has a blank and staring face and is relatively unresponsive<br>o On awakening, is amnestic for this behaviour<br>o Within several minutes after awakening from the sleepwalking, person is not impaired (i.e. is<br>oriented, not confused)<br>o Not due to a substance or GMC<br>• Parasomnia not otherwise specified o Confusional arousals<br>o Sleep starts<br>o Sleep talking<br>o Nocturnal leg cramps<br>o Sleep paralysis<br>o Impaired sleep related penile erections<br>o Sleep-related painful erections<br>o REM sleep related sinus arrest<br>o REM sleep behaviour disorder (the people who kill people when they are &quot;sleeping&quot;) o Sleep enuresis<br>o Nocturnal paroxysmal dystonia<br>o Primary snoring

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Insomnia -- define and 8 DDx

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• Dyssomnias are primary disorders of initiating or maintaining sleep or of excessive sleepiness, and are characterized by a disturbance in the amount, quality or timing of sleep.<br>• Types of dyssomnias include:<br>o Primary insomnia<br>o Primary hypersomnia<br>o Narcolepsy<br>o Breathing related sleep disorder o Circadian rhythm sleep disorder o Dyssomnia NOS<br>• Insomnia is:<br>o Difficulty initiating or maintaining sleep or of nonrestorative sleep<br>o Lasts for at least 1 month<br>o Causes significant distress or impairment in social, occupational or other important areas of<br>functioning<br>o Primary if: does not occur exclusively during the course of another sleep disorder (eg.<br>narcolepsy, breathing related sleep disorder, parasomnia) or mental disorder o Not due to the direct effects of a substance or GMC<br>• Polysomnography may demonstrate poor sleep continuity<br>o Eg. increased sleep latency, increased intermittent wakefulness and decreased sleep efficiency<br>• Often night to night variability<br>• Oftn have elevated scores on self-report psychological or personality inventories<br>• More prevalent among women and with increasing age<br>• 1-year prevalence is 30-45%<br>• Differential diagnosis<br>o Another mental disorder<br>− Major depressive episode/disorder<br>− GAD<br>− PTSD<br>− Adjustment disorder<br>o Substance use<br>− Prescribed medication (eg. with ephedrine)<br>− Substances of abuse (eg. alcohol, cocaine)<br>− Caffeine, cigarettes<br>o Another sleep disorder<br>− Narcolpesy<br>− Circadian rhythm sleep disorder<br>− Breathing-related sleep disorder<br>− Parasomnia<br>o General medical condition<br>− Pain<br>− Cardiac disease<br>− Respiratory disease<br>− Etc.

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Insomnia -- Mgt

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Management<br>Sleep hygiene<br>• Regular sleep-wake cycle<br>• Daily exercise<br>• Insulate bedroom against excessive noise, light, cold, heat<br>• Light snack before bed if hungry<br>• Time to relax before bed<br>• Avoid strenuous exercise before bed<br>• Abstain from alcohol, tobacco, caffeine in the evening<br>• NoTVinbed<br>• Avoid chronic sleeping medication use<br>Stimulus Control Therapy<br>• Attempts to undo conditioned stimuli that interfere with sleep, condition stimuli that promote sleep, associate bed with rapid sleep onset<br>o Go to bed only when sleepy<br>o Use the bed only for sleeping<br>o Do not lie in bed and become frustrated if unable to sleep – get up, go to another room, do<br>something<br>o non-arousing, return to bed when sleepy<br>o Awaken at same time each morning, regardless of bedtime, total sleep o Avoid napping<br>Sleep Restriction Therapy<br>Restrict time in bed to closely approximate amount of sleep, when sleep efficiency is 85%, gradually increase time in bed<br>Relaxation therapy and biofeedback<br>Self-hypnosis, progressive relaxation, deep breathing<br>Pharmacotherapy<br>Imovane, trazodone, short-term benzos

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Hypersomnia -- Define &amp; DDx (7)

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• Hypersomnia is excessive sleepiness<br>• Primary hypersomnia is:<br>o Excessive sleepiness for at least 1 month as evidenced by either prolonged sleep episodes or by daytime sleep episodes occurring almost daily<br>o Causing significant distress<br>o Not occurring exclusively within another sleep disorder<br>o Not related to another mental disorder<br>o Not due to the direct effects of a substance or GMC<br>o Specifier - recurrent (episodes lasting at least 3 days occur several times a year for at least 2<br>years) • Features<br>o The quality of the sleep is often normal o Often difficult to awake<br>o Daytime naps tend to be long<br>o Often unrefreshed by sleep<br>o Sleepiness evolves gradually rather than a sleep attack per se<br>o Unintentional sleep episodes occur in low stimulation or activity situations (eg. TV or driving)<br><br>• Differential diagnosis<br>o Primary sleep related:<br>− Normal long sleepers<br>− Primary insomnia<br>− Inadequate nocturnal sleep<br>− Breathing related sleep disorder<br>− Circadian rhythm sleep disorder<br>o Non-primary sleep related<br>− Major depressive episode with atypical features<br>− Depressed phase of bipolar disorder<br>− Sleep disorder due to GMC, hypersomnia type<br>− Substance-induced sleep disorder, hypersomnia type

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Narcolepsy -- 4 sx

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Narcolepsy Tetrad<br>• Sleep attacks<br>• Cataplexy<br>• Sleep paralysis<br>• Sleep hallucinations

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Narcolepsy Pathophys

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Pathophysiology<br>• Narcolepsy results in part from genetic predisposition<br>o Almost 90% have HLA DQB1 on chromosome 6<br>• But, antigen is neigher necessary nor sufficient for narcolepsy/cataplexy<br>o 25% of the population have the same antigen, but less than 1% have narcolepsy o Only 1% of narcolepsy patients have affected 1st degree relative<br>o Only 25% MZ twin concordance<br>• Unidentified factor most likely triggers illness in those who are susceptible because they carry antigen<br>• Some cases of narcolepsy without tetrad have followed head trauma, MS or diencephalon tumor

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Narcolepsy -- Tx

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Treatment:<br>• First goal is to maintain awake at critical times (eg. driving, school)<br>• Ritalin and amphetamines ehance dopamine and reduce naps but have little effect on cataplexy<br>• Cataplexy often responds to clomipramine, imipramine, protriptyline and maybe SSRIs by<br>inhibiting noradrenergic uptake (??? SNRI???)<br>• Benzodiazepines help assure nighttime sleep<br>• Sleep hygiene like short daytime naps, regular bedtime

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FAS -- clinical features (10)

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a. growth retardation<br />b. facial features<br /> 1. short palpebral fissures (measured from inner to outer canthus; reflect underlying brain growth)<br /> 2. thin upper lip<br /> 3. long and flat philtrum<br />c. intellectual impairment<br />d. short attention span<br />e. difficulty with reasoning<br />f. mood and anxiety disorders<br />g. legal problems and conduct disorder<br />h. social problems<br />i. victimization<br />j. memory problems

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MR -- vulnerability contributions to psych

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a. 41% of children with MR meet criteria for at least one psychiatric disorder<br>b. 2 to 3% have schizophrenia (2 to 3 times the normal rate)<br>Biological vulnerability<br>a. neuropathology involved in MR may contribute to diathesis for psychiatric illnesss<br>b. there is an increased incidence of physical and sensory disability<br>Psychological vulnerability<br>a. are often unable to communicate needs<br>b. socially isolated<br>c. vulnerable to abuse<br>d. have poor coping skills<br>e. frequent care giver changes<br>f. institutionalization<br>g. poor self-esteem, self-image

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“Non-shared sibling environment” refers to environmental factors that are different for siblings in the same family. Describe briefly what these “non-shared” factors may be, how they may operate, and their significant in psychological development.

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• non-shared factors: o birth order<br />o gender<br />o peer group<br />o goodness of fit<br />o developmental stages at which family stressors occur<br />o accidents, abuse, etc • shared factors<br />o marital conflict or harmony o loss of a parent<br />o socio-economic class<br><br>defn = environmental differences between children in the same family <br><br>The KEY POINT = this is the major source of environmental variance for personality, psychopathology, and cognitive abilities ... probably genetic disease (read SCZ) too. Note the study title (url infra), basically = twins are not the same on in these domains. <br><br>Nonshared environment<br><br>Category Eg. <br>    Nonsystematic Accidents, illnesses, trauma<br>    Systematic <br>        Family composition Birth-order; gender differences<br>        Sibling interaction Differential treatment<br>        Parental treatment Differential treatment<br> Extrafamilial networks Peer groups; teachers; television<br>       <br>re SCZ = most likely environmental contributor, stress, may come from many sources and, apparently, may come during any stage of development. Prenatal or birth complications, early deprivations, broken homes, censuring parents, the death of someone close, failures in school, poor work or social relationships, childbirth, a bad drug trip, as well as all kinds ofgood fortune may have effects on a predisposed individual that are obvious only in retrospect. In prospect, it will be impossible to prophesy the events themselves, let alone their effects25<br><br>****<br>Re personality =&gt; Upper middle-class brothers who attend the same school and whose parents take them to the same plays, sporting events, music lessons, and therapists, and use similar child rearing practices on them are little more similar in personality measures than they are to working class or farm boys, whose lives are totally different. Now, perhaps this is an exaggeration of the known facts, but not by much.<br><br>****<br>for personality, psychopathology, and cognition, behavioral-genetic research converges on the conclusion that most behavioral variability among individuals is environmental in origin. For example, for schizophrenia, the concordance for first-degree relatives, whose coefficient of genetic relationship is .50, is less than 10%. Identical twins are less than 50% concordant for schizophrenia. <br><br>* n.b. siblings subjective perceptions may vary<br>* n.b. family therapists on systems theory in which the child is viewed as part of an organized family system,<br><br>http://ije.oxfordjournals.org.login.ezproxy.library.ualberta.ca/content/40/3/563.long#aff-1<br><br>

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factitious disorder by proxy -- characteristics suspect

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• the affected person has the “sick” person under their care (usually a mother)<br>• no secondary gain<br>• false medical history<br>• contamination of lab samples<br>• alteration of medical records<br>• induction of injury or illness in the child or dependent<br>• no other medical or psychiatric diagnoses to account for behavior<br>• features of patients:<br> demanding, difficult<br> accuse doctors of incompetence, threaten litigation  abruptly sign out from hospital<br> pattern of multiple hospital visits<br> history of true physical disorder<br> grudge against the medical profession<br> employment as a medical paraprofessional<br> important relationship with a physician in the past

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Delayed Language -- DDx

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a. mental retardation<br>b. autism<br>c. hearing impairment<br>d. specific language impairment (such as expressive language disorder)<br>e. neurological injury<br>f. maltreatment

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Enuresis -- Etiology

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Etiology of enuresis<br>primary enuresis is due to developmental factors; 75% of patients have a first degree relative who had enuresis<br>organic causes need to be ruled out – genitourinary (structural problems), diabetes, somnambulism<br>if enuresis is secondary, think of psychological causes

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Enuresis -- Tx

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Treatment options behavioral therapy<br>1. bladder training (drink less fluid, pee before going to sleep)<br>2. may be useful for comorbid conditions<br>3. family therapy may be helpful (psychoeducation, or improving family stressors in the case of<br>secondary enuresis)<br>2. bell and pad<br>pharmacotherapy<br>1. often not warranted; may be used for situations like sleepovers<br>2. imipramine (narrow therapeutic window, risk of cardiotoxicity)<br>3. desmopressin (antidiuretic hormone, may cause hyponatremia)<br>psychotherapy<br>1. not helpful on its own

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Autism -- DDx

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General differential<br> other pervasive developmental disorders (see below) <br> Rett’s disorder<br> childhood disintegrative disorder<br> Asperger’s disorder<br> mental retardation <br> hearing difficulties <br> speech difficulties<br>Differentiate from other pervasive developmental disorders A. Rett’s disorder<br>1. diagnosed only in females (Autism is more common in males)<br>2. loss of previously acquired purposeful hand skills; poor coordination of gait, trunk movements<br>B. childhood disintegrative disorder<br>1. a developmental regression that follows at least two years of normal development (developmental abnormalities in Autism are usually noted in the first year)<br>C. Asperger’s disorder<br>1. language development may be normal

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Reactive d/o -- mgt

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A. The first consideration in treating reactive attachment disorder is a child's safety.<br>B. The decision is whether to hospitalize or to attempt treatment while the child remains in the home.<br>C. Usually, the severity of the child's physical and emotional state or the severity of the pathological<br>caregiving determines the strategy.<br>D. Assessment of the nutritional status of the child and whether there is ongoing physical abuse or threat,<br>for cases in which malnourishment has occurred, hospitalization is necessary.<br>E. Along with an assessment of the child's physical well-being, an evaluation of the emotional condition is<br>important. Immediate intervention must address the parents' awareness and capacity to participate in<br>altering the injurious patterns that have ensued.<br>F. The treatment team must begin to alter the unsatisfactory relationship between the caregiver and the<br>child.<br>G. Extensive and intensive intervention and education with the mother or with both parents when possible.<br>H. Possible interventions include, but are not limited to, the following: psychosocial support services,<br>including hiring a homemaker, improving the physical condition of the apartment or obtaining more adequate housing, improving the family's financial status, and decreasing the family's isolation; psychotherapeutic interventions, including individual psychotherapy, psychotropic medications, and family or marital therapy; educational counseling services, including mother–infant or mother–toddler groups, and counseling to increase awareness and understanding of the child's needs and to increase parenting skills; and provisions for close monitoring of the progression of the patient's emotional and physical well-being. Sometimes, separating a child from the stressful home environment for a temporary period, such as in a hospitalization, allows the child to break out of the accustomed pattern.<br>I. A neutral setting, such as the hospital, is the best place to start for families who are genuinely available emotionally and physically for intervention.<br>J. If those interventions are unfeasible or inadequate or if they fail, placement with relatives or in foster care, adoption, or a group home or residential treatment facility must be considered.

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reactive attachment disorder. Name the two categories of this disorder, and describe two symptoms from each category. List five antecedents of reactive attachment disorder.

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A. Inhibited type: the child fails to initiate and respond to social interactions in a<br>developmentally appropriate way; shows a pattern of excessively inhibited, hypervigilant, or highly ambivalent responses (frozen watchfulness, resistance to comfort, or approach / avoidance)<br>B. disinherited type: child exhibits indiscriminate sociability, or lack of selectivity in choice of attachment figures<br>The diagnosis of reactive attachment disorder also requires antecedent “pathogenic care”, which can include:<br>1. Persistent disregard of child’s basic emotional needs (comfort, stimulation, and affection)<br>2. Persistentdisregardofchild’sbasicphysicalneeds(nutrition)<br>3. Repeated changes of primary care giver, such as frequent changes in foster care (preventing<br>the formation of stable attachments)<br>Situations that can predispose to the development of such “pathogenic care” include:<br>1. Prolongedhospitalizationofthechild 2. Extreme poverty<br>3. Parental inexperience

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Learning disabilities psychological and family problems associated with

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1. behavioral difficulties<br>2. externalizing behaviors (ODD, conduct)<br>3. emotional disorders<br>4. depression<br>5. anxiety<br>6. somatic symptoms<br>7. social skills and social competence problems<br>8. poor self-esteem and self-image<br>9. family problems (parent-child conflict) center around<br>10. homework<br>11. academic achievement<br>12. motivation<br>13. peer interactions

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School refusal - defn and tx

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A. not a separate diagnosis<br>B. in younger patients, likely a fear of separation; in older patients, likely a fear of teachers or peers<br>C. usually meet criteria for social phobia, specific phobia, depression, or abuse<br><br>A. psychiatric assessment for anxiety, mood disorders, abuse<br>B. psychoeducation for parents<br>C. cognitive therapy<br>D. coping skills training<br>E. exposure therapy<br>F. behavioral management training for parents and teacher<br>G. pharmacotherapy<br>H. SSRIs<br>I. imipramine

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adolescence -- devt challenge

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A. physical changes 1. puberty<br>2. neurobiological changes<br>3. appetite and sleep changes<br>B. cognitive changes<br>C. increasing independence from parents<br>D. identity consolidation<br>E. increasing dependence on relationships outside of the family

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BAD -- features obscure Adol dx

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• Adolescents are more likely to present with: o Mixed episodes<br />o Longer duration of episodes<br />o Lower interepisodic recovery<br />• Rapid cycling more likely in adolescents<br />• Adolescent bipolar disorder often looks like ADHD<br />• Adolescent bipolar disorder more likely than adult to have psychotic symptoms<br />• Adolescents often have comorbidity (ADHD, CD, Substance abuse) which makes diagnosis more<br />difficult<br /><br />A. there is a low base rate of mania in childhood<br />B. symptoms of bipolar disorder overlap with other more prevalent childhood disorders<br />1. ADHD<br />2. conduct disorder<br />C. mixed features may complicate the clinical presentation of mania in adolescents<br />D. psychotic symptoms may complicate the clinical presentation of mania in adolescents<br />1. hallucinations<br />2. paranoid thoughts<br />3. thought disorder<br />E. the presentation in adolescents is highly variable

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BAD -- Ddx

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∙ Substance abuse<br>∙ ADHD<br>∙ Borderline personality<br>∙ Conduct disorder/oppositional defiant disorder<br>∙ Schizophrenia/schizoaffective<br>∙ Medical illness/medications (eg. prednisone)

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BAD -- RF after MDE

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1. Acute onset<br>2. Psychomotor retardation<br>3. Family history<br>4. psychotic feature<br>5. Vulnerability to developed bipolar antidepressant<br><br>1. Family history of bipolardisorder<br />2. Mania or hypomania developing after treatment with antidepressants<br />3. Psychotic features inthe depression<br />4. marked psychomotor retardation during the depression <br />5. Rapid onset ofthe depression

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ADHD comorbidities

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<br />a. 30-40% have Oppositional Defiant Disorder (K and S)<br />b. 30-50% have Conduct Disorder (K and S) (only 14% in MTA study) (multimodal tx study)<br />c. 9-38% have depression<br />d. 25% have anxiety disorders (would have been nice if the big K and S was more specific!)<br />e. Association with bipolar disorder or mania is controversial<br />f. 9-30% have learning disorders<br /><br />• most common co-morbidities are ODD or conduct disorder<br />• may also have higher prevalence of:<br />o mood disorders<br />o anxiety disorders<br />o learning disorders<br />o communication disorders<br />• may precede diagnosis of Tourette’s disorder

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Adult ADHD -- 5 SSx

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A. anywhere from 22 to 80% of children with ADHD have persistent symptoms into adulthood<br>(about 50% have persistent symptoms) – childhood prevalence of ADHD is about 4%, making<br>adult prevalence about 2%<br>B. symptoms of ADHD in adulthood are the same as in childhood, but the focus seems to be more in<br>inattentive symptoms, as the symptoms of hyperactivity tend to improve<br>C. diagnosis requires:<br>1. establish current symptoms<br>2. establish past symptoms of ADHD in childhood<br>3. establish psychiatric, developmental, and family histories<br>4. perform physical examination<br>D. common comorbidities include: substance abuse, criminal behavior; adults with ADHD also have higher levels of anxiety and depression than the general population

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Adult ADHD -- how related to childhood (list sx)

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A. inattention symptoms (need six of nine): SOLID VCCF<br>1. starts things, but doesn’t finish them<br>2. organization is problematic<br>3. loses things<br>4. inattentive (trouble paying attention)<br>5. distracted easily<br>6. verbal instructions are difficult to follow<br>7. careless mistakes<br>8. concentration is avoided<br>9. forgetful<br>B. hyperactivity-impulsivity symptoms (need six of nine): WORST FAIL<br>1. waiting for things is frustrating<br>2. “on the go”<br>3. restless and jittery<br>4. sitting still is problematic<br>5. talkative (talks too much)<br>6. fidgets<br>7. acts before thinking things through<br>8. interrupts other people’s conversations<br>9. loud (trouble doing things quietly)

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Adult ADHD -- Tx

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A. pharmacotherapy<br>1. stimulants (methylphenidate and dextroamphetamine)<br>2. atemoxetine (Strattera): first medication to receive FDA approval for adult ADHD<br>3. noradrenergic antidepressants (bupropion, desipramine, venlafaxine)<br>B. psychoeducation<br>1. education about the deficits helps develop compensatory strategies<br>C. skills training<br>1. teach planning and organization skills<br>2. reduce distractions<br>3. break down large tasks into components<br>D. psychotherapy<br>1. individual: to deal with self-esteem, problems caused by impulsivity<br>2. family: to deal with conflict, problem-solving, communication

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ADHD -- modes of tx

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Biological<br>∙ Stimulants are 1st line (Ritalin, Dexadrine)<br>∙ Some evidence for antidepressants such as Bupropion, but careful if seizure history Psychological<br>∙ Play therapy suitable for young children if able to do it - can work through issues of self-esteem, etc.<br>∙ Behavioural techniques often used (eg. star charts for non-disruptive behaviour, sitting still)<br>∙ Group therapy often appropriate to enhance social skills and self-esteem Social<br>∙ Involve in activities which can increase self-esteem<br>∙ Liaise with teacher - often require classroom support or special class<br>∙ Liaise with parent to implement management strategies<br>∙ Psychoeducation Other<br>• Treat comorbid conditions (eg. learning disability, anxiety)

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Tourettes -- Dx criteria

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A. multiple motor tics and at least one vocal tic (not necessarily concurrent)<br>B. occur many times a day nearly every day or intermittently for a year with no more than three<br>months tic free<br>C. onset is before the age of 18<br>D. the disorder causes significant distress or impairment in social, occupational, or academic<br>functioning<br>E. the disorder is not due to a substance or a general medical condition

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Tourettes -- DDx

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A. transient tic disorder: motor and/or vocal tics lasting at least four weeks but not 12 months<br>B. Tourette’s disorder: motor tics and at least one vocal tic for more than 12 months; no more than<br><br>C. chronic motor or vocal tic disorder: motor or vocal tics (not both) for more than 12 months; no more than 3 months tic-free

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Tourettes - 3 comorbid

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A. obsessive-compulsive disorder<br>B. attention-deficit hyperactivity disorder<br>C. learning disorder

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Tourettes -- etiology

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• Emerging data suggest that the tic disorders are genetic disorders involving abnormal dopaminergic- excitatory amino acid interactions in neural circuits bridging parts of frontal cortex, basal ganglia and the thalamus<br>• Genetics<br>o Twin and family studies demonstrate patterns of inheritance consistent with autosomal dominant<br>disorder with incomplete penetrance<br>o Also, there is a consistent relationship between Tourette's, other tic disorders and OCD<br>• Neurochemistry<br>o The tic-suppressing effects of dopamine antagonists suggest that there is abnormal dopamine<br>transmission in Tourette's, often suspected to involve a hypersensitivity of D2<br>o Also, post-mortem studies of Tourette's patients suggest that they have higher concentrations of<br>glutamate in globus pallidus and other striatal areas<br>• Neuroimaging<br>o Has shown structural differences in Tourette's patients, including consistent volume reductions in the<br>region of the basal ganglia as well as loss of normal asymmetries in these structures o There is also reduction in the corpus callosum<br>o Taken all together, this may suggest some subtle disturbances in brain lateralization o Functional imaging studies have been less conclusive but show abnormalities<br>• May also be some link to autoimmune disease as there have been studies which demonstrate high levels of a lymphocyte antigen

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Family Therapy -- 5 models and goals

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A. structural (Minuchin); goal is a balance between connectedness and differentiation; focus is<br>on boundaries, hierarchies, engagement-enmeshment<br>B. family systemic (Bowen); goal is detriangulation and increased differentiation; focus is on<br>triangulation, differentiation of self<br>C. strategic (Erickson, Haley); goal is resolving presenting problem; focus is on symptom<br>maintaining sequences – uses paradoxical injuctions<br>D. narrative; goal is resolving presenting problem; focus is on constructivism, creation of<br>stories<br>E. psychodynamic-psychoanalytic: goal is improved insight; focus is on object relations,<br>projective identification

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“media history”. Name 2 environmental factors increasing chance of violence from media. Name 2 proven results of heavy metal music. Name 4 changes resulting from watching violence on television.

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Television<br>Do you have household rules about watching television?<br>Does your child have a television in his or her room?<br>Music and Videos<br>Do you listen to your child’s music or watch the music videos your child is watching? Do you and your child discuss lyrics or images you find objectionable?<br>Video, Computer and Internet Games<br>How long does your child spend playing video games each day?<br>Does your child ever exhibit aggression or hyperactivity, or experience staring spells after playing video games? Movies and Videos<br>Does your child ever experience nightmares or have trouble sleeping after watching movies?<br>Internet, E-mail, Instant Messaging<br>How long does your child spend using the Internet each day?<br>Does your child have access to the Internet in his or her bedroom.

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Safety assessment features

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1. full psychiatric assessment including history of substance abuse<br>2. Previous suicidal assessment and homicidal<br>3. 3- Environmental hazards<br>4. Sexual abuse risk<br>5. If child may need contact CAS

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Phobic d/o -- predisposing

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A. traumatic events (such as being attacked by an animal or trapped in a closet)<br>B. unexpected panic attacks in a certain situation<br>C. observation of others undergoing trauma or demonstrating fear (such as seeing someone fall<br>from a height, or seeing someone afraid of animals)<br>D. informational transmission (such as repeated parental warnings about the dangers of certain<br>animals, or media coverage of plane crashes)<br>E. feared objects or situations tend to involve things that may actually represent a threat, or have represented a threat at some point in human evolution<br>F. phobias that result from traumatic events, or from spontaneous panic attacks, tend to be particularly acute in their development<br>G. phobias of a traumatic origin do not have a characteristic age of onset (e.g. a fear of choking can develop at any age)<br>H. phobias that persist in to adult remit only infrequently (20% of cases)<br>I. phobias illustrate the interaction between a genetic constitutional diathesis and environmental stressors; children are constitutionally predisposed by having a temperament characterized by behavioral inhibition to the unfamiliar; full brown phobia results from a chronic environmental stress being imposed on the temperamental predisposition<br>J.examples of environmental stressors:<br>1. death of a parent<br>2. separation from a parent<br>3. criticism or humiliation by an older sibling<br>4. household violence

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PTSD -- predisposing

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• Biological vulnerability<br>o Eg. enhanced baseline sympathetic tone • Family factors<br>o Parental psychopathology<br>o Poor attachment<br>o Low SES<br>o Poor processing and modulation of anxiety<br>• Type of trauma<br>o Severe, repeated<br>o Relationship with perpetrator • Poor processing of trauma<br>o Eg. child blamed for event, shame, guilt • Lack of psychological treatment

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Sexual abuse -- behavioral factors

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Behavioural symptoms of sexual abuse<br>o Variety of behavioural responses to stress, including:<br>o Sexual acting out<br>o Aggression<br>o Declining school performance<br>o Regression (eg. return to thumb sucking, security blanket, enuresis/encopresis) o Sleep disturbance<br>o Depression<br>o Eating disturbance<br>• Most specific indicator of possible sexual abuse is sexual acting out

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Erikson stages

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Oral sensory (birth to 1y)<br>A. basic trust vs. basic mistrust<br>B. facilitated by: consistency, sameness of experience<br>C. consequences of failure: inability to trust<br>Muscular anal (2 to 3y)<br>A. autonomy vs. shame and doubt<br>B. sets stage for “holding on and letting go”<br>C. consequences for failure: self doubt (if parents overly shame child)<br>Locomotor (3 to 5y)<br>A. initiative vs. guilt<br>B. desire to mimic adult world; sibling rivalry is frequent<br>Latency (6 to 11y)<br>A. industry vs. inferiority<br>B. socially decisive age; danger of sense of inadequacy if child despairs of own tools and skills, and<br>status among peers<br>Adolescence (12 to 18)<br>A. identity vs. role confusion: adolescents make an effort to answer the question “who am I?”;<br>regarded by Erikson as the single most significant conflict a person must face<br>B. facilitated by: peer relationships, independence from parents<br>C. consequences of failure: inability to make decisions about vocation, confusion about sexual<br>orientation / identity<br>Young adulthood (19 to 40y)<br>A. intimacy vs. isolation<br>B. love relationships important; must develop intimacy, or suffer feelings of isolation<br>Middle adulthood (40 to 65y)<br>A. generativity vs. stagnation<br>B. find a way to support the next generation<br>Maturity (over 65)<br>A. ego integrity vs. despair<br>B. reflection and acceptance of one’s life

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MR -- epidemiology &amp; pathophys

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A. Trisomy 21; the most common chromosomal disorder<br>B. seen in 1 in 800 live births<br>C. 95% of cases caused by chromosomal non-disjunction; 3 to 4% caused by translocation<br>D. the average life expectancy is 55

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MR - features

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A. low muscle tone as newborns<br>B. transverse palmar creases (simian crease)<br>C. facial features<br>D. flattened nasal bridge<br>E. upward slanting eyes<br>F. epicanthal folds<br>G. high risk for the development of Alzheimer’s dementia<br>H. 20-fold risk of leukemia<br>I. increased risk of atlanto-occipital instability

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Strange situation - sequence

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A. 1: parent and infant enter unfamiliar room<br>B. 2: third person (stranger) joins dyad<br>C. 3: parent leaves, leaving stranger and infant<br>D. 4: parent returns, stranger leaves<br>E. 5: parent leaves, leaving infant alone<br>F. 6: stranger returns, leaving infant with stranger<br>G. 7: parent returns, stranger leaves

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Attachment -- define and describe 4 categories

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Definition of attachment<br>A. Bowlby: the propensity of human beings to make strong affectional bonds to particular others<br>B. as a behavioral system, attachment motivates the infant to seek proximity to an external<br>attachment figure<br>Types of attachment<br><br>1. 2.<br>  <br>B.<br>1. 2.<br><br><br>C.<br>1. 2.<br><br><br>D.<br>1. 2. 3.<br><br>secure<br>infant anticipates that the caregiver will be available for comfort when needed<br>strange situation:<br>infant may or may not cry when caregiver leaves the infant is easily comforted on reunion<br>the infant approaches the caregiver on reunion<br>avoidant<br>infants have learned to not express their distress externally in order to not elicit further rejection (mother rejecting)<br>strange situation:<br>do not protest when caregiver leaves the room<br>ignore caregivers on return<br>resistant<br>infants have ambivalent feelings towards caregivers (mothers inconsistent)<br>strange situation:<br>cry vigorously on separation<br>resist comforting on return; take a long time to settle down<br>disorganized<br>infants find caregivers frightening or frightened<br>they can not find a solution to the paradox of fearing the attachment figure strange situation<br>tend to have interrupted, confused, incomplete strategies for obtaining comfort from the attachment figure

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Devt theories -- Piaget vs Erikson

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Similarities<br>A. both tried to describe the process of normal development<br>B. both postulate that development occurs in a series of stages, with each stage building upon<br>successful resolution of the previous stage<br>C. each stage is postulated to occur at a particular age<br>Piaget<br>A. proposed a cognitive model of development<br>B. studied acquisition, modification, and development of abstract ideas and abilities, on the basis<br>of biological substrates<br>C. Piaget’s stages<br>1. sensorimotor: accommodative stance<br>2. pre-operations: divergent stance<br>3. concrete operations: abstraction begins; relies on logic<br>4. formal operations: representational logic; hypothetical-deductive reasoning<br>Erikson<br>A. psychosocial model of development<br>B. describes crucial steps in people’s relationships with the social world, based on interplay<br>between biology and society<br>C. each stage has one or more crises, which must be mastered before moving on to the next stage<br>D. Erikson’s stages:<br>1. trust vs. mistrust<br>2. autonomy vs. shame and doubt<br>3. initiative vs. guilt<br>4. industry vs. inferiority<br>5. identify vs. role confusion<br>6. intimacy vs. isolation<br>7. generativity vs. stagnation<br>8. integrity vs. despair

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Margaret Mahler’s theory about the process of separation and individuation

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• autistic (0 to 2 months): focus is on survival, not relatedness<br>• symbiotic (2 to 6 months): the child is able to smile, and follow the mother<br>• separation-individuation (6 months to 5 years, four subphases)<br>o differentiation or “hatching” (6 to 10 months)<br> the child becomes aware of the mother as a separate person  increased alertness; “prototypical biphasic visual pattern”<br>o practicing (10 to 16 months)<br> the child develops locomotor skills and begins to explore his environment  sense of omnipotence; experiences self as physically at one with mother<br>o rapprochement (16 months to 2 years)<br> the child develops a sharper awareness of separateness, and has a heightened sense<br>of vulnerability when separated<br> the child returns to the mother for reassurance<br>o object constancy (2 to 5 years)<br> consolidation of the child’s individuality<br> the child integrates his split views of the mother  the child develops a soothing inner presence

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Autism, aggression in patients with -- differential diagnosis and the management of . What medications can be used to manage aggression?

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 Axis I disorders (depression, anxiety, psychosis),<br> Axis III disorders (hypothyroidism, pain, seizures, other medical conditions),  Axis IV difficulties (changes in caregivers, instability in environment)<br><br> the management of aggression depends on the underlying cause:<br>a. for anxiety disorders or depression, use SSRIs at a low dose<br>b. for environmental causes, stabilize the environment<br>c. for medical causes, treat the underlying medical condition (such as seizures, hypothyroidism,<br>pain)<br>d. for behavioral management, a low dose of neuroleptics may be used

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Family Environment diff

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Alfred Adler<br>• Role of birth order<br>o First-born – lost position of only child, tend not to share, become conservative o Second children – change and become social activists<br>o Youngest – feel secure because never displaced<br>Birth order effects<br>First born/only child may benefit from more focused parental attention in early years, but inexperienced parents may also be more anxious or have higher/unrealistic expectations of the child.<br>Subsequent children, more closely spaced children may have less focused parental attention due to competing demands of other children, also may have decrease instrumental family resources (increased financial demands of more children), but experienced parents may be less anxious, children may benefit from learning/modeling from older siblings, or may alternatively be at risk for bullying/rivalry from older siblings.<br>Gender effects<br>Gender roles and expectations of culture are transmitted to children first by family. From birth, parents are noted to interact differently and use different language with boys and girls. Parents may choose gender-stereotyped toys and activities for children, and may differentially reinforce gender-stereotyped behaviours.

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psychological or behavioural adverse consequences of divorce in prepubertal children.

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∙ Blaming self for divorce<br>∙ Acting out, physical aggression (mostly in boys)<br>∙ Anger towards one or both parents<br>∙ Decreased school performance<br>∙ Fantasies of reuniting parents

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ODD- behav program

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The clinician should consider parent intervention based on one of the empirically tested interventions [MS].<br>The parent management training (PMT) in the use of contingency management methods to help them better handle disruptive behavior is one of the most substantiated treatment approaches in child mental health. The principles of these approaches are can be summarized as follows:<br>1. Reduce positive reinforcement of disruptive behavior.<br>2. Increase reinforcement of prosocial and compliant behavior. Positive reinforcement varies widely, but parental attention is predominant. Punishment usually consists of a form of time out, loss of tokens, and/or loss of privileges.<br>3. Apply consequences and/or punishment for disruptive behavior.<br>4. Make parental response predictable, contingent, and immediate.<br>These interventions are effective in community and clinical samples.<br>These interventions target one of the most studied causal processes by which children become oppositional, i.e., their coercive response to parental demands, and ways in which parents unwittingly reinforce the child’s noncompliance. Almost all of the best known and evidenced based PMT programs are variations of Hanf’s (1969) two-stage behavioral treatment model and are listed in Table 2. Defined as model programs by SAMSHA, these programs are available for dissemination and offer technical assistance and training by their developers. The programs have multi-media formats on videotape or DVD and are manual based. Other family therapies include models designed for prevention or intervention with youth with CD and/or substance use disorders. These therapies include Functional Family Therapy and Multisystemic Therapy. Issues associated with family or parental approaches are as follows: the use of mild forms of spanking, the high treatment dropout rates with these families and their children (sometimes up to 50%), and the existence of parental psychopathology, which impedes participation and progress. Adverse side effects<br>may be the misuse of the techniques to control children, especially in abusive homes, and the possibility of these intervention techniques resulting in increased or more severe confrontations between child and marginally controlled parents.

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Autism -- etiology

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a. Psychodynamic and Family Factors.<br /> Kanner noted that few parents of autistic children were warmhearted and that, for the most part, parents and other family members were preoccupied with intellectual abstractions and tended to express little genuine interest in their children. This finding, however, has not been replicated over the past 50 years.<br /> Other theories, such as parental rage and rejection and parental reinforcement of autistic symptoms, have also not been substantiated.<br /> Recent studies comparing parents of autistic children with parents of normal children have not shown significant differences in child-rearing skills.<br /> No satisfactory evidence indicates that any particular deviant family functioning or psychodynamic constellation of factors leads to the development of autistic disorder. Children with autism, as with children with other disorders, can respond with an exacerbation of symptoms to psychosocial stressors including family discord, the birth of a new sibling, or a family move. In fact, children with autistic disorder may be excruciating sensitive to a host of changes in their families and environment.<br />b. Neurological and Biological Factors.<br /> Autistic disorder and autistic symptoms are associated with conditions with neurological lesions, notably congenital rubella, phenylketonuria (PKU), tuberous sclerosis, and Rett's disorder.<br /> Autistic children show more evidence of perinatal complications than do comparison groups of normal children and those with other disorders.<br /> The finding that autistic children have significantly more minor congenital physical anomalies than do their siblings and normal controls suggests that complications of pregnancy in the first trimester are significant.<br /> Four to 32 percent of people with autism have grand mal seizures at some time, and about 20 to 25 percent show ventricular enlargement on computed tomography (CT) scans.<br /> Various (EEG) abnormalities are found in 10 to 83 percent of autistic children, and, although no EEG finding is specific to autistic disorder, there is some indication of failed cerebral lateralization.<br /> Recently, one magnetic resonance imaging (MRI) study revealed hypoplasia of cerebellar vermal lobules VI and VII, and another MRI study revealed cortical abnormalities. Those abnormalities may reflect abnormal cell migrations in the first 6 months of gestation. An autopsy study revealed decreased Purkinje's cell counts, and another study found increased diffuse cortical metabolism during positron emission tomography (PET) scanning.<br />c. Genetic Factors.<br /> 2 and 4 percent of siblings of those with autism also had autistic disorder, a rate 50 times greater than in the general population.<br /> The concordance rate of autistic disorder in the two largest twin studies was 36 percent in monozygotic pairs versus 0 percent in dizygotic pairs in one study and about 96 percent in monozygotic pairs versus about 27 percent in Dizygotic pairs in the second study.<br /> Clinical reports and studies suggest that the nonautistic members of families with autistic members have various language or other cognitive problems but less severely than does the person with autism.<br /> Fragile X syndrome appears to be associated with autistic disorder, but the number of persons with both autistic disorder and fragile X syndrome is unclear.<br />d. Immunological Factors.<br /> Some evidence indicates that immunological incompatibility between the mother and the embryo or fetus may contribute to autistic disorder.<br />e. Perinatal Factors.<br /> A high incidence of various perinatal complications seems to occur in children with autistic disorder,<br />although no complication has been directly implicated as causative.<br /> In the neonatal period, autistic children have a high incidence of respiratory distress syndrome and<br />neonatal anemia.<br /> Some evidence indicates a high incidence of medication usage during pregnancy in the mothers of<br />autistic children.<br />f. Neuroanatomical Factors.<br /> Recent MRI studies comparing autistic subjects and normal controls found that the total brain volume was increased in those with autism.<br /> The greatest average percentage increase in size occurred in the occipital lobe, parietal lobe, and temporal lobe.<br /> Although the specific implications and etiology of this enlargement are unknown, the increased volume can arise from three different possible mechanisms: increased neurogenesis, decreased neuronal death, and increased production of non-neuronal brain tissue such as glial cells or blood vessels. Although these data do not specifically identify a neuroanatomical deficit in autism, they suggest that brain enlargement itself may be a biological marker in autistic disorder.<br /> The temporal lobe has been suggested to be a critical area of brain abnormality in autistic disorder. This suggestion is based on reports of autistic-like syndromes in some people with temporal lobe damage. When the temporal region of animals is damaged, expected social behavior is lost, and restlessness, repetitive motor behavior, and a limited behavioral repertoire are seen.<br /> Another finding in autistic disorder is a decrease in Purkinje's cells in the cerebellum, a decrease potentially resulting in abnormalities of attention, arousal, and sensory processes.<br />g. Biochemical Factors.<br /> At least one third of patients with autistic disorder have elevated plasma serotonin.<br /> This finding is not specific to autistic disorder: People with mental retardation without autistic disorder<br />also display this trait.<br /> Patients with autistic disorder without mental retardation have a high incidence of hyperserotonemia.<br /> In some autistic children, increased cerebrospinal fluid (CSF) homovanillic acid (the major dopamine<br />metabolite) is associated with increased withdrawal and stereotypies.<br /> Some evidence indicates that symptom severity decreases as the ratio of CSF 5-hydroxyindoleacetic acid (5-HIAA, metabolite of serotonin) to CSF homovanillic acid increases. CSF 5-HIAA may be inversely proportional to blood serotonin levels; these levels are increased in one third of autistic disorder patients, a nonspecific finding that also occurs in mentally retarded persons.

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Autism -- mgt

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a. The treatment plan should address:<br>• Establishing goals for educational intervention.<br>• Establishing target symptoms for intervention.<br>• Prioritizing target symptoms/co-morbid conditions.<br>• Monitoring multiple domains of functioning (including behavioral adjustment, adaptive skills,<br>academic skills, social-communicative skills, and social interaction with family members and peers).<br>• Monitoring medication for efficacy and side effects, as appropriate<br>b. PSYCHOSOCIAL TREATMENTS<br>• Educational services (including special education, some forms of behavior modification, and other services) are the central and integral aspect of the treatment of autism in children and adolescents. Ancillary services are often required, that include speech-language therapy, occupational therapy and physical therapy. Sustained and continuous programming is more effective than episodic programming.<br>• Psychosocial interventions include parent training (e.g., in behavior modification techniques) and referral to parent/sibling support groups. Parental counseling may be appropriate or, for the affected individual, social skills training and/or highly structured individual counseling or psychotherapy may be indicated particularly for older and higher functioning individuals.<br>c. PHARMACOLOGICAL AND RELATED INTERVENTIONS<br>• Medications may be useful for symptoms, which interfere with participation in educational interventions or are a source of impairment or distress to the individual.<br>• The medications are not specific to autism and do not treat core symptoms of the disorder and their potential side effects should be carefully considered.<br>• The neuroleptics, selective serotonin reuptake inhibitors, tricyclic antidepressants, lithium and mood stabilizers, and anxiolytics have been used in these patients with varying degrees of success.<br>d. FOLLOW-UP ASSESSMENTS AND ONGOING TREATMENT<br>• Usually services are needed at different points in the child's development for various lengths of time. Coordination of services and family support are important aspects of ongoing care.<br>• The nature and intensity of such contact depend on the clinical situation and needs of the individual.<br>• More frequent contact is needed for individuals who receive psychotropic medication or who exhibit<br>behaviors which pose a danger to the individual or others or which interfere with the provision of an appropriate educational intervention program.<br>e. DEVELOPMENTAL ISSUES IN ASSESSMENT AND TREATMENT<br>• While early intervention undoubtedly is very helpful, important questions remain to be addressed, e.g., what features of the treatment are most important and what characteristics of the child are associated with greatest improvement.<br>• If medications are used in this age group, considerable caution should be exercised and the child monitored very closely.<br>• For school-aged children the eligibility for supportive services such as respite care may be important.<br>• For adolescents with autism and related conditions, there should be more emphasis on vocational and<br>prevocational skills as well as on adaptive skills.<br>• The latter are prerequisites for independent and semi-independent living.<br>• The clinician should help to identify areas of strength for vocational planning.<br>• Co-morbid conditions, such as depression in individuals with Asperger's disorder, may first be seen in adolescence.<br>• Among adults with autism and related conditions, the identification of community resources and<br>support in planning for long-term care is critical.

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temperament -- thomas and chess features

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1. Easy temperament (40%): Biological regularity, approach tendencies to the new, quick adaptability to change, and a predominantly positive mood of mild or moderate intensity.<br>2. Difficult temperament (10%): Biological irregularity, withdrawal tendencies to the new, slow adaptability to change, and frequent negative emotional expressions of high intensity.<br>3. Slow-to-warm-up temperament, (15%): Withdrawal tendencies to the new, slow adaptability to change, frequent negative emotional reactions of low intensity. Often labeled shy.<br>4. Neither (35%)<br><br>Trait<br><br><br>Description<br><br>Activity level<br>% of time spent in activities<br><br>Distractibility<br><br>Degree to which stimuli are allowed to alter behavior<br><br>Adaptability<br><br>Ease moving into change<br><br>Attention span<br><br>Amount of time spent in activity<br><br>Intensity<br><br><br>Energy level<br>Threshold of responsiveness<br>Intensity required for response<br><br>Quality of mood<br><br><br>Positive compared to negative behavior<br>Rhythmicity<br>Regulation of functions<br><br><br>

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RF -- foster care

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A. in foster care – relationship with foster parents<br>B. any previous suicidal ideation or attempts<br>C. belief about lethality of acetaminophen overdose<br>D. current plans for further suicidality<br>E. circumstances around separation from boyfriend<br>F. presence or absence of intoxication at party<br>G. family history of psychiatric illness<br>H. current major depression or other psychiatric illness

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RF - suicide

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SADPERSONS:<br>A. sex (male)<br>B. age (women plateaus at midlife, men biphasic peak – adolescence and old age)<br>C. depression<br>D. previous attempts<br>E. ethanol<br>F. rational thinking (loss of)<br>G. social supports lacking<br>H. organized plan<br>I. no spouse<br>J. sickness<br>NOHOPE:<br>A. no framework for meaning<br>B. overt change in clinical condition<br>C. hostile interpersonal environment<br>D. out of hospital recently<br>E. predisposing personality factors<br>F. excuses for dying

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SCZ -- suicide RF

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• being young<br>• having a chronic illness with many exacerbations<br>• having good insight<br>• recently being discharged<br>• being early in the course of illness<br>• having a high IQ<br>• experiencing command hallucinations

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Delirium -- RF

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<br />1- Elderly<br />2- History of delirium in the past<br />3- Hip replacement surgery (5-45%)<br />4- Baseline dementia<br />5- Presence of existence of medical conditions<br />6- Polypharmacy<br />7- Anticholinergic medication<br />8- Anesthesia<br />9- Anoxia<br />10- Dehydration<br />11- Bleeding and shock<br /><br />a. Advanced age more than six years<br />b. Pre-existing brain damage /cognitive impairment, hypoxia<br />c. Past history of delirium<br />d. Alcohol dependence and substance withdrawal<br />e. DM<br />f. Cancer<br />g. Malnutrition<br />h. Sensory impairment [hearing /visual impairment]<br />i. Post-operative complications (infections, lytes imbalance and pain)<br />j. Immobility

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Bereavement -- stages / tasks

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Bowlby’s stages of bereavement<br>A. acute despair<br>1. numbness, protest<br>2. anger, distress<br>3. denial<br>B. intense yearning and searching for person who has died<br>1. restlessness, preoccupation with the dead person<br>C. disorganization and despair<br>1. withdrawal, apathy, listlessness<br>D. reorganization<br>1. acute pain diminishes<br>2. patient returns to life<br>3. deceased person is remembered with joy and sadness<br>Grief therapy<br>A. patient encouraged to talk about feelings of loss<br>B. encouraged to recognize and express anger, or ambivalent feelings<br>C. therapist must be prepared to handle intense emotions<br>D. therapist must be active, and participate in decision making

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ECT -- consent

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• autonomy: the patient has the right to make their own decisions; they are assumed to be competent until proven otherwise, and their decisions should be respected<br>• education: in order for consent to be valid, the physician must educate the patient about the risks and benefits of ECT, alternative treatments available, and the option of no treatment<br>• non-maleficence: prior to obtaining consent for ECT, the physician should do a full psychiatric evaluation to ensure that ECT is indeed indicated, and that the patient is competent to consent<br>• the physician must ensure that the patient understands the information that has been provided to them, and address any questions that the patient may have<br>• the physician should be prepared to offer the patient access to another opinion about treatment, should the patient request it

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Li considerations in elderly

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general<br>A. safe and effective for older people<br>B. complicated by presence of other medical illnesses, and sensitivity to side effects<br>C. in many cases, lower lithium levels are needed<br>D. start at low dosages, switch less frequently, and allow a longer time before assuming steady<br>state levels have been reached<br>Lithium in the elderly – medical consideration<br>A. ensure good kidney function – consider 24 hour urine creatinine if patient has diabetes or<br>other diseases that may affect kidney function<br>B. perform EKG with a rhythm strip to rule out sick sinus syndrome<br>C. monitor side effects<br>D. check thyroid and renal status twice in first six months, and then every six months to year<br>Lithium in the elderly – drug interactions<br>A. lithium levels decreased by:<br>1. osmotic diuretics<br>2. xanthenes derivates: caffeine, theophylline<br>B. lithium levels increased by:<br>1. Thiazides, potassium sparing, and loop diuretics<br>2. NSAIDs<br>3. antipsychotics<br>4. anticonvulsants

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BAD -- elder vs younger pt diff

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A. elderly patients have longer acute episodes<br>B. elderly patients have more frequent episodes<br>C. euphoric mania is less common, and mixed episodes more common<br>D. elderly patients may present with delirious mania (with symptoms of delirium)<br>E. late onset mania has a high prevalence of associated neurological disorders<br>F. elderly patients are more likely to have obsessive thought patterns

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Antipsychotics in elderly -- consider

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1) in general psychosis in the elderly responds to much lower doses than those needed for younger patients<br>2) the elderly are more susceptive to the side-effects of antipsychotics than are younger patients extra-pyramidal side effects: elderly more susceptible to dyskinesias, and dyskinesias can<br>have more serious consequences in the elderly (e.g. stop walking, or swallowing) tardive dyskinesia: risk of TD increases with age; for patients over 65, a third develop TD at<br>1 year, a half a 2 years, and two-thirds at 3 years<br>cholinergic effects: (blind, hot, mad, dry) central toxicity can occur in older patients with<br>peripheral effects manifesting; low potency neuroleptics such as clozapine are highly<br>anticholinergic<br>adrenergic effects: orthostatic hypotension can lead to falls and fractured hips;<br>antipsychotics are highly associated with hip fractures<br>3) the elderly may need a longer time at a given dose to demonstrate response, so in general the<br>maxim “start low, go slow” should be used

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Aging -- 10 changes, one per organ system

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A. sensory: decreased visual and auditory acuity<br>B. neurologic: decreased cholinergic receptor density and decreased choline acetyltransferase<br>activity<br>C. gastrointestinal: decreased hepatic blood flow and liver size<br>D. renal: decreased creatinine clearance<br>E. sexual: longer refractory period in men, decreased lubrication in women<br>F. skeletal: loss of bone density (especially in women after menopause)<br>G. joints: stiffer and less flexible<br>H. immune system: decrease in immune function<br>I. skin: decreased strength and elasticity, slowed wound healing<br>J. body composition: increased body fat<br>K. endocrine: increased insulin resistance

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Adverse drug reactions elderly -- categories/causes (4)

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G. joints: stiffer and less flexible<br>H. immune system: decrease in immune function<br>I. skin: decreased strength and elasticity, slowed wound healing<br>J. body composition: increased body fat<br>K. endocrine: increased insulin resistance

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Multi-infarct dementia (5 non-cognitive features)

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DSM-IV diagnosis of dementia:<br>A. all DSM-IV diagnoses of dementia require (1) memory impairment (learning or recall), and<br>(2) one or more of aphasia, apraxia, agnosia, disturbed executive functioning<br>B. the only differences in the criteria are that for Alzheimer’s the course is gradual onset and continuing decline, for vascular there is evidence of cerebrovascular disease (neurological<br>signs or laboratory evidence), and for the others there is evidence of the other disease (HIV, Parkinson’s, head trauma, Pick’s, Huntington’s, CJD)<br>Subtypes of vascular dementia:<br>A. vascular dementia is a clinical syndrome of acquired intellectual and functional impairment<br>resulting from the effects of cerebrovascular disease<br>B. vascular dementia can be caused by multiple infarctions, strategic single infarctions, hypo-<br>perfusion of watershed areas, or small vessel disease<br>Clinical features:<br>A. focal neurological signs or symptoms<br>1. extensor plantar response<br>2. pseudobulbar palsy<br>3. gait abnormalities<br>4. exaggeration of deep tendon reflexes<br>5. weakness of an extremity<br>B. prior history of vascular disease (CVA, hypertension, atherosclerosis)<br>C. abrupt onset with step-wise deterioration<br>D. relative preservation of personality<br>E. somatic complaints<br>F. depression or mood lability<br>G. fluctuating course

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Aging -- pharmacokinetic changes

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a. decreased hepatic oxidation<br>b. decreased liver blood flow<br>c. decreased renal clearing<br>d. increased lipid storage<br>e. decreased plasma albumin

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depression with somatic complaints from hypochondriasis?

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a. in hypochondriasis, suicidal ideation is rare<br>b. in depression, somatic symptoms are episodic, or onset in late life (in hypochondriasis,<br>onset of somatic symptoms is early)<br>c. in depression there is a marked loss of interest or pleasure<br>d. in depression anger is directed inwards; hypochondriacs direct anger outwards<br>Diagnostic criteria for hypochondriasis:<br>A. preoccupation with fears of having, or the idea one has, a serious disease – based on<br>misinterpretation of bodily symptoms<br>B. persists despite adequate medical reassurance<br>C. not delusional, not restricted to belief about appearance<br>D. duration at least six months<br>E. note: up to 80% of patients with hypochondriasis may have a co-existing depressive or<br>anxiety disorder

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Pseudodementia vs dementia

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Differentiation of pseudodementia and dementia:<br>Pseudodementia (dr. shes, i’m a dip) pervasive Dysphoria (d)<br>Rapid decline in function (r) Suicidality (s)<br>High level of distress (h)<br>Emphasize own cognitive difficulties (e) social skills lost (hygiene) (s)<br>“I don’t know” answers (i)<br>recent and remote Memory affected (m) Am worse (a)<br>duration short before help (d) inconsistent MSE finding (i)<br>Dementia<br>Try hard to answer, or invent responses<br>minimize or deny deficits<br>slow, gradual decline in function consistently poor attention &amp; concentration<br>labile or shallow affect<br>not typically suicidal<br>long duration of decline before seeking help<br>past psychiatric history rare<br>low level of distress<br>preserved social skills<br>worse at night time<br>recent memory more affected; remote okay<br>past psychiatric history common (p)<br>1

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LBD -- 5 clinical features

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A. dementia syndrome (memory impairment and two of aphasia, apraxia, agnosia, or<br>dysexecutive) with two of the following three:<br>1. fluctuating cognition<br>2. visual hallucinations<br>3. Parkinsonism<br>B. associated clinical features<br>1. delusions<br>2. auditory hallucinations<br>3. hypersensitivity to neuroleptics<br>4. falls or syncopal episodes<br>5. depression<br>6. death in six to eight years

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Dementia -- subcortical vs cortical

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A. cortical: Alzheimer’s<br>1. can’t do (or learn)<br>2. early memory problems; they wander and get lost<br>B. subcortical: Frontotemporal, Parkinson’s<br>1. don’t know (forget)<br>2. late memory loss; wander, but come back<br>cortical (seven ‘A’s + visuospatial) amnesia – A1 criteria for dementia agnosia – A2 criteria for dementia apraxia – A2 criteria for dementia aphasia – A2 criteria for dementia<br>anomia<br>acalculia<br>loss of abstract ability<br>also: decreased visuospatial processing<br>subcortical (five ‘D’s)<br>dysmnesia (forgetfulness)<br>delayed (psychomotor slowing) depleted (apathetic, amotivated) dysexecutive (impaired planning, sequencing)<br>disinhibited<br>(visual spatial relatively preserved)<br><br>

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Alzheimers -- tx approach

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1.Educational Interventions for Patients with Dementia and Caregivers<br>a) Short-term programs directed toward educating family caregivers about AD should be offered to improve caregiver satisfaction.<br>b) Intensive long-term education and support services (when available) should be offered to caregivers of patients with AD to delay nursing home placement<br>2.Interventions Other Than Education for Patients and Caregivers. a) Functional Performance<br>o Behavior modification, scheduled toileting, and prompted voiding should be used to reduce urinary incontinence<br>o Graded assistance, practice, and positive reinforcement should be used to increase functional independence<br>o Low lighting levels, music, and simulated nature sounds may improve eating behaviors for persons with dementia, and intensive multimodality group training may improve activities of daily living, but these approaches lack conclusive supporting evidence (<br>b)Problem Behaviors<br>o Persons with dementia may experience decreased problem behaviors with interventions such as music, particularly during meals and bathing (Guideline)<br>o Walking or other forms of light exercise (Guideline)<br>o Although evidence is suggestive only, some patients may benefit from the following<br>(Practice Options):<br>• Simulated presence therapy, such as the use of videotaped or audiotaped family members • Massage<br>• Comprehensive psychosocial care programs<br>• Pet therapy<br>• Commands issued at the patient’s comprehension level<br>• Bright light, white noise<br>• Cognitive remediation<br>c) Care Environment Alterations<br>Although definitive evidence is lacking, the following environments may be considered for patients with dementia (Practice Options):<br>• Special care units within long-term care facilities.<br>• Homelike physical setting with small groups of patients, as opposed to traditional nursing homes<br>• Short-term, planned hospitalization of 1 to 3 weeks with or without blended inpatient and outpatient care<br>• Provision of exterior space, remodeling corridors to simulate natural or home settings, and changes in the bathing environment<br>d) Interventions for Caregivers<br>The following interventions may benefit caregivers of persons with dementia and may delay long-term placement (Guideline)<br>• Comprehensive, psycho educational caregiver training<br>• Support groups<br>Additional patient and caregiver benefits may be obtained by use of computer networks to provide education and support to caregivers (Practice Option), telephone support programs (Practice Option), and adult day care for patients and other respite services (Practice Option)

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Dementia -- reversible causes

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reversible causes of dementia, including<br>i. infections (check CBC)<br>ii. metabolic abnormalities (TSH, glucose, electrolytes)<br>iii. nutritional abnormalities (B12)<br>iv. normal pressure hydrocephalus, tumors (CT scan)

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Dementia -- ddx (other d/o that cause)

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A. Alzheimer's disease<br>B. Vascular dementia<br>Varieties: Multiple infarcts (called multi-infarct dementia)<br>Lacunae, Binswanger's disease, cortical microinfarction<br>C. Drugs and toxins (including chronic alcoholic dementia)<br>D. Intracranial masses: tumors, Subdural masses, brain abscesses<br>E. Anoxia<br>F. Trauma (Head injury, Dementia pugilistica (punch-drunk syndrome)<br>G. Normal-pressure hydrocephalus<br>H. Neurodegenerative disorders (( Parkinson's diseased, Huntington's diseased, Progressive supranuclear palsy, Pick's diseased, Amyotrophic lateral sclerosis, Spinocerebellar degenerations, Olivopontocerebellar degeneration, Ophthalmoplegia plus, Metachromatic leukodystrophy (adult form), Hallervorden-Spatz disease, Wilson's disease))<br>I. Infections ((Creutzfeldt-Jakob disease, AIDS, Viral encephalitis, Progressive multifocal leukoencephalopathy, Behcet's Behçet's syndrome, Neurosyphilis, Chronic bacterial meningitis, Cryptococcal meningitis, Other fungal meningitides))<br>J. Nutritional disorders ((Wernicke-Korsakoff syndrome (thiamine deficiency), Vitamin B12 deficiency, Folate deficiency, Pellagra, Marchiafava-Bignami disease, ?Zinc deficiency))<br>K. Metabolic disorders ((Metachromatic leukodystrophy, Adrenal leukodystrophy, Dialysis dementia, Hypothyroidism and hyperthyroidism, Renal insufficiency, severe, Cushing's syndrome, Hepatic insufficiency, Parathyroid disease))<br>L. Chronic inflammatory disorders ((Lupus and other collagen-vascular disorders with intracerebral vasculitis, Multiple sclerosis, Whipple's disease))

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Dementia -- workup

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a. Physical examination including thorough neurological examination<br>b. Vital signs<br>c. Mental status examination<br>d. Mini-Mental State Examination (MMSE)<br>e. Review of medications and drug levels<br>f. Blood and urine screens for alcohol, drugs, and heavy metals<br>g. Physiological workup<br>Serum electrolytes/glucose/Ca2+, Mg2+ Liver, renal function tests<br>SMA-12 or equivalent serum chemistry profile Urinalysis<br>Complete blood cell count with differential cell type count Thyroid function tests (including TSH level)<br>RPR (serum screen)<br>FTA-ABS (if CNS disease is suspected)<br>Serum B12<br>Folate levels<br>Urine corticosteroids<br>Erythrocyte sedimentation rate (Westergren) Antinuclear antibody (ANA), C3C4, Anti-DS DNA Arterial blood gases<br>HIV screen<br>Urine porphobilinogens<br> Chest radiograph<br> Electrocardiogram<br> Neurological workup<br> CTorMRIscanofhead  SPECT<br> Lumbarpuncture<br> EEG<br> Neuropsychological testing

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IPT question - what are 3 characteristics of IPT, Name two theoretical models that IPT is based. What is role of meds in IPT? 4 problem areas.

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A. characteristics of IPT<br> Character Assignment of sick role <br> Very structured treatment<br> Very active treatment<br>B. Name two theoretical models that IPT is based Triad of theoretical underpinnings<br>1. attachment theory – forms basis for formulating pt’s relationship difficulties &amp; informs clinicians about modifications they may need to make in therapy<br>2. communication theory describes ways in which patient’s maladaptive communication patterns may lead to difficulty in the here-and-now relationships<br>3. social theory – basis for understanding interpersonal context in which people interact with others &amp; the effect their social networks have on their interpersonal functioning<br>C. What is role of meds in IPT?<br>1. In geriatric patients with recurrent major depression, maintenance treatment with nortriptyline or IPT<br>is superior to placebo in preventing or delaying recurrence.<br>2. Combined treatment using both appears to be the optimal clinical strategy in preserving recovery.<br>D. What are the four problem areas?<br> role dispute –<br>1. identify the dispute,<br>2. plan of action ,<br>3. modify expectation and<br>4. improve communication<br> role transition –<br>1. mourn loss of role,<br>2. accept loss of role,<br>3. build new role,<br>4. Build self-esteem.<br> Grief –<br>1. facilitate mourning and<br>2. finding new life<br> ITP deficits –<br>1. build relationships,<br>2. diminish social isolation

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IPT -- List five elements of the opening phase of therapy, three elements of the middle phase, and two elements of the termination phase.

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Opening phase of treatment<br>A. definition of depression and explanation of diagnosis<br>B. relating depression to interpersonal factors, such as interpersonal disputes with mother,<br>boss, and husband<br>C. identification of goals of therapy (e.g. addressing interpersonal disputes)<br>D. explanation of rationale of interpersonal therapy, logistics of treatment<br>E. assignment of “sick role”<br>Middle phase of treatment<br>A. intermediate sessions for grief<br>1. facilitate mourning process<br>2. re-establish interest and relationships to substitute for loss<br>3. explore associated feelings<br>B. intermediate sessions for interpersonal disputes<br><br>2. understand and modify non-reciprocal role expectations<br>3. examine parallels in other relationships, and unspoken assumptions behind patient’s<br>behavior<br>C. intermediate sessions for role transitions<br>1. mourning and acceptance of the loss of the old role<br>2. help patient regard new role as more positive<br>3. develop sense of mastery regarding new roles<br>D. intermediate sessions for role interpersonal deficits<br>1. reduce patient’s social isolation<br>2. encourage formation of new relationships<br>3. explore repetitive patters in relationships<br>Termination phase of treatment<br>A. explicit discussion of termination<br>B. acknowledgement that termination is a time of grieving<br>C. moving towards patient recognition of independent competence

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Behavioral therapy -- indications

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A. obsessive-compulsive disorder<br>B. panic disorder<br>C. specific phobias<br>D. oppositional-defiant disorder<br>E. post-traumatic stress disorder<br>F. schizophrenia (social skills training)

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Brief Dynamic -- 4 models and descr.

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a. Brief focal ((Tavistock-Malan)<br>A. set termination date at beginning<br>B. examine defense, anxiety, impulse; focus on current, past, and transference<br><br>Selection criteria<br>Duration Focus Termination<br>Clarify the nature of the defense, the anxiety, and the impulse Link the present, the past, and the transference<br>Patient able to think in feeling terms High motivation<br>Good response to trial interpretation Up to one year, Mean, 20 sessions<br>Internal conflict present since childhood Set definite date at beginning of treatment<br><br>1. Patient is unavailable to therapeutic contact.<br>2. Therapist anticipates that prolonged work will be needed to<br>• generate motivation<br>• penetrate rigid defenses<br>• Deal with complex or deep-seated issues<br>• resolve unfavorable, intense transference, dependent or other, that may develop<br>3. Depressive or psychotic disturbance may intensify<br>c. Time Limited (Boston University-Mann)<br> exactly 12 sessions; deal with termination right from the onset Mann: Time-Limited Psychotherapy<br>Goal<br>Selection criteria<br>Duration Focus<br>Termination<br>Resolution of the present and chronically endured pain and the patient's negative self-image<br>High ego strength<br>Able to engage and disengage<br>Therapist quickly able to identify a central issue<br>Excludes major depressive disorder, acute psychosis, and borderline personality disorder<br>12 treatment hours<br>Present and chronically endured pain Particular image of the self<br>Specific last session set at beginning of treatment<br>Termination a major focus of the therapy work<br>d. Short-Term Dynamic Psychotherapy (McGill University-Davanloo)<br>• Resolution of Oedipal conflict; need to have had at least one significant past relationships<br>• should be psychologically minded and not have primitive defenses<br>• can have multiple foci<br>Davanloo: Short-Term Dynamic Psychotherapy<br><br>Selection criteria<br>Duration Termination<br>Resolution of oedipal conflict, loss focus, or multiple foci<br>Psychological-mindedness<br>At least one past meaningful relationship<br>Able to tolerate affect<br>Good response to trial transference interpretation High motivation<br>Flexible defenses<br>Lack of projection, splitting, and denial<br>5–40 sessions, usually 5–25, Longer durations for seriously ill<br>No specific termination date<br>Patient is told that treatment will be short<br>e. Short-Term Anxiety-Provoking Psychotherapy (Harvard University-Sifneos)<br> Resolution of Oedipal conflict; need to have had at least one significant past relationship Short-Term Anxiety-Provoking Psychotherapy<br><br>Selection criteria<br>Resolution of oedipal conflict<br>Above-average intelligence<br>At least one past meaningful relationship High motivation<br>Specific chief complaint<br>Able to interact with evaluator<br>Able to express feelings<br>Flexible<br>A few months, Average 12–16 sessions Oedipal (triangular) conflict<br>No specific date given<br>Duration<br>Focus<br>Termination<br>5) List and describe five cognitive errors that a cognitive therapist would identify to a patient. [2000]<br>1) catastrophizing: exaggerating negative consequences<br>2) selective abstraction: focusing on negative comments, ignoring positive ones<br>3) probability over-estimation: over-estimating the likelihood of negative events<br>4) dichotomous thinking: believing something must be either all good or all bad<br>5) excessive responsibility: believing yourself to be responsible for things<br>6) overgeneralization:<br>IPT area of focus – role transition (to a role as a single person rather than wife or mother), as this appears to be the precipitating event; could also consider grief – may have complicated bereavement; may be predisposing to this MDD<br>The sick role – psychoeducation around the diagnosis within a medical model; despite medical model, link to life events, especially difficulties within the interpersonal sphere; stress she is not responsible for causing the depression; encourage her to make allowances for herself in the early days/weeks of treatment, as she is not functioning at full capacity; however, also stress she has responsibilities to herself to participate in treatment to the best of her ability to regain her health and functional status.

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OCD -- Ax scale and meds

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a) What assessment scale would be useful in further evaluating this patient?<br> YBOCS<br>b) List two medications that you would use to treat this patient.<br><br> 1st line; Fluvoxamine, Fluoxetine, Paroxetine, Sertraline<br> 2nd line; clomipramine, Venlafaxine XR, Citalopram, Mirtazapine, adjunctive<br>risperidone<br> 3rd line; IV Clomipramine, Escitalopram, Phenelzine, tranylcypromine, Adjunctive<br>(Mirtazapine, olanzapine, quetiapine, haloperidol, Gabapentin, topiramate)

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OCD -- psychotherapy

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 CBT<br /> Component of CBT for OCD<br /> Education<br /> Educate about OCD, including typical obsessions, compulsions, and coping strategies  Describe the negative impact of some of the coping strategies<br /> Explain the procedure your are using<br /> Recommend self-help reading materials or manuals<br /> Exposure<br /> Offers in vivo (real life) exposure to situations that provoke anxiety and compulsive<br />behaviour (e.g., touching contaminated objects, driving past a cemetery)<br /> Offers imaginal exposure to feared obsessive thoughts (e.g., concerning religious,<br />aggressive, or sexual content)<br /> Offers imaginal exposure to catastrophic consequences of feared thoughts and actions<br />(e.g., exposure to thoughts about becoming gravely ill after touching a garbage can)<br /> Teaches response prevention, which is used at the same time as exposure so that<br />exposure takes place without engaging in rituals or other safety behaviours<br /> Teaches that exposure involves learning to tolerate, rather than avoid anxiety<br />experiences<br /> Response prevention<br /> Gradually reduces and eliminates;<br />i. Compulsive behaviour (hand washing) including mental compulsions or rituals<br />ii. Reassurance seeking (e.g., asking a family members if a task has been<br />completed correctly)<br />iii. Excessive safety behaviour (e.g., wearing gloves or other protective clothing to<br />avoid coming in contact with contaminated objects)<br /> Cognitive intervention<br /> Reappraisal of beliefs concerning the danger involved in situations that provoke<br />obsessions or compulsions. This involves estimation of the negative outcome<br />occuring and evaluation of the harm caused by these events<br /> Reappraisal of beliefs concerning the danger associated with the obsessions<br />themselves<br /> Reducing inflated sense of responsibility about creating harm<br /> Addressing belief that the occurrence of a thought makes it more likely that the feared<br />outcome will happen<br /> Dealing with problems of intolerance of uncertainty and perfectionism<br /> Family involvement<br /> Informing the family members about the problem and enlisting their cooperation with<br />treatment<br /> Family members are taught to stop their involvement in providing reassurance, safety behaviour (e.g., excessive cleaning and checking), and assisting with compulsive behaviours<br /> Problem solving<br /> OCD may cause severe disability, when there is improvement, there is often a need to<br />rebuild work life, social interactions, and family relationships<br /> Relapse prevention<br /> Prepare for period of increased anxiety when exposed to threatening experiences that<br />relate to the theme of the OCD (e.g., exposure to a new illness or source of contamination)

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Obsession vs delusion

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Definition of obsession:<br>1) recurrent and persistent thoughts, impulses, or images that are experienced as intrusive and inappropriate<br>2) they cause anxiety and distress<br>3) they are not simple excessive worries about real-life problems<br>4) the person attempts to ignore or suppress the thoughts, impulses, or images, or to neutralize<br>them with some other thought or action<br>5) the person recognizes them as products of his/her own mind<br>Definition of delusion:<br>1) a false belief, based on an incorrect inference about external reality, which is not consistent with the person’s intelligence and cultural background<br>2) the belief cannot be corrected by reasoning<br>Differences between obsessions and delusions:<br>1) obsessions are ego-dystonic, delusions are not<br>2) obsessions involve intact reality testing, whereas in delusions reality testing is impaired<br>3) obsessions cause anxiety and distress, whereas delusions do not always do so<br>4) obsessions involve compensatory thoughts or actions to neutralize them, whereas delusions do not

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OCD -- psych defenses

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regression, excessive use of intellectualization, and rationalization.<br /><br />1) isolation of affect<br />2) undoing: compulsive act performed in an attempt to prevent or undo the consequences<br />that the patient irrationally anticipate from a frightening obsessional thought or<br />impulse<br />3) reaction formation: manifest patterns of behavior and consciously experienced<br />attitudes that are exactly the opposite of underlying impulses<br />4) controlling: attempting to manage or regulate events or objects in the environment to<br />minimize anxiety and resolve inner conflicts

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OCD - comorbidities

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1. major depressive disorder<br>2. other anxiety disorders<br>3. specific phobia<br>4. social phobia<br>5. panic disorder<br>6. eating disorders<br>7. obsessive compulsive personality disorder<br>8. substance abuse<br>9. avoidant and dependent personality disorder<br>10. Tourette’s disorder (seen in 5 to 7% of OCD patients) – OCD is seen in 30 to 50% of patients with Tourette’s disorder

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OCD -- prognostic (good vs bad)

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Poor prognosis for OCD: (boy, do Ph.D.)<br>1) bizarre compulsions<br>2) onset in childhood<br>3) yielding to (rather than resisting) compulsions<br>4) delusional beliefs<br>5) overvalued ideas (some acceptance of obsessions and compulsions)<br>6) personality disorder (especially schizotypal)<br>7) hospitalization required<br>8) depression<br>Good prognosis for OCD:<br>1) good social and occupational adjustment<br>2) presence of a precipitating event<br>3) episodic nature of symptoms<br>4) note: content of obsessions is not related to prognosis

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PTSD -- 6 dx criteria

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A. The person has been exposed to a traumatic event in which both of the following were present: 2<br> (7) sense of a foreshortened future (eg, does not expect to have a career, marriage,<br>children, or a normal life span)<br>D. Persistent symptoms of increased arousal (not present before the trauma), as indicated by two (or more) of the following: 2<br> (1) difficulty falling or staying asleep<br> (2) irritability or outbursts of anger<br> (3) difficulty concentrating<br> (4) hypervigilance<br> (5) exaggerated startle response<br>E. Duration of the disturbance (symptoms in criteria B, C, and D) is more than 1 month. F. the disturbance causes clinically significant distress or impairment in social, occupational, or other important areas of functioning.<br> Specify if:<br> Acute: if duration of symptoms is less than 3 months<br> Chronic: if duration of symptoms is 3 months or more<br> Specify if:<br> With delayed onset: onset of symptoms at least 6 months after the stressor<br> (1) the person experienced, witnessed, or was confronted with an event or events that involved actual or threatened death or serious injury, or a threat to the physical integrity of self or others<br> (2) The person's response involved intense fear, helplessness, or horror. Note: in children, this may be expressed instead by disorganized or agitated behavior<br>B. The traumatic event is persistently reexperienced in one (or more) of the following ways: 1<br> (1) Recurrent and intrusive distressing recollections of the event, including images, thoughts, or perceptions. Note: in young children, repetitive play may occur in which themes or aspects of the trauma are expressed<br> (2) Recurrent distressing dreams of the event. Note: in children, there may be frightening dreams without recognizable content<br> (3) Acting or feeling as if the traumatic event were recurring (includes a sense of reliving the experience, illusions, hallucinations, and dissociative flashback episodes, including those that occur upon awakening or when intoxicated) Note: in young children, trauma-specific reenactment may occur.<br> (4) Intense psychological distress at exposure to internal or external cues that symbolize or resemble an aspect of the traumatic event.<br> (5) physiologic reactivity on exposure to internal or external cues that symbolize or resemble an aspect of the traumatic event<br>C. Persistent avoidance of stimuli associated with the trauma and numbing of general responsiveness (not present before the trauma), as indicated by three (or more) of the following: 3<br> (1) efforts to avoid thoughts, feelings, or conversations associated with the trauma<br> (2) efforts to avoid activities, places, or people that arouse recollections of the trauma  (3) inability to recall an important aspect of the trauma<br> (4) markedly diminished interest or participation in significant activities  (5) feeling of detachment or estrangement from others<br> (6) restricted range of affect (eg, unable to have loving feelings)

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PTSD -- one type of CBT and 3 components

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Education; by providing information about PTSD and its treatment Exposure;<br>help patients with gradually confrontation of feared situations, memory, emotions, images associated with the trauma until there is significant reduction in distress<br> imaginal exposure offers repeated review of the trauma based on memories of the experience and its aftermath, including the emotions accompanying the experience [either in imagination or by writing the trauma narrative]<br> in vivo exposure provides confrontation with avoided situations related to the event<br> eliminates unrealistic safety behaviors Cognitive approaches;<br> identify dysfunctional thinking pattern associated with anxiety, Depression, anger and shame<br> teach patient to challenge irrational cognition and replace them with functional, realistic believes<br> reduce hypervigilance by refocusing attention Emotion-Regulation approach<br> provide management skills to help cope with and to reduce the distress<br> provide relaxation approach such as muscle, breathing or imagery relaxation<br> refocus attention<br> practice acceptance-based approaches to reduce avoidance of difficult situations<br>Problem-solving<br> practices overcoming any social withdrawal and negative impact on relationships  addresses any excessive use of substances or other unhealthy Coping approaches  engages in positive activities and goals<br>Relapse prevention<br> practices prevention for trauma related events that may occur in the future<br> practices prevention for periods of increased distress related to reminders of the<br>trauma

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PTSD -- defense mech (3)

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1) denial<br>2) minimization 3) splitting<br>4) projective disavowal<br>5) dissociation<br>6) guilt (as a defense against underlying helplessness)

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PTSD -- comorbid (anx and non-anx)

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Non-anxiety disorder comorbid with PTSD:<br>1) depression<br>2) somatization<br>3) substance-related disorders<br>Anxiety disorder comorbid with PTSD:<br>1) panic disorder<br>2) agoraphobia<br>3) obsessive compulsive disorder

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Social Phobia -- criteria

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linical features of social phobia:<br />1) excessive, unreasonable fear of embarrassment or humiliation, such that exposure to performance situations leads to anxiety, and such situations are avoided or endured with distress<br />2) in individuals under the age of 18, the duration has to be at least six months

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Social Phobia -- meds / classes

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 Antidepressants<br>• SSRIs<br> Escitalopram .........1<br> Fluvoxamine IR ......1<br> Fluvoxamine CR .......1<br> Paroxetine IR ...........1<br> Paroxetine CR .........2<br> Sertraline ..............1<br> Citalopram .............2<br> Fluoxetine ...........+1 to -1<br>• TCAs<br> Imipramine..............-2<br> Clomipramine............3<br>• MAOI and (or) RIMA<br> Phenelzine.........1<br> Moclobemide ..........+1 to -1<br>• Other antidepressants<br> Venlafaxine XR ........1  Bupropion .............3  Mirtazapine............3<br> Anxiolytic<br>• Benzodiazepines<br> Alprazolam............2<br> Bromazepam..........2<br> Clonazepam...........1<br> Adjunctive clonazepam.......-2<br> Azapirones<br> Buspirone.......... -1<br> Adjunctive buspirone............3  Anticonvulsants<br> Gabapentin..........2<br> Pregabalin.........2<br> Divalproex.........+3 to - 3<br> Topiramate...........3<br> Levetiracetam...... -2<br> Adjunctive tiagabine..........3<br><br> Antipsychotics<br> Olanzapine................2<br> Quetiapine................3<br> Adjunctive risperidone ................3<br> Adjunctive Aripiprzaole ................32<br> Other therapies<br> Selegiline<br> Atenolol<br> Propranolol<br> St John's wort<br> Pergolide<br> Adjunctive Pindolol

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Social Phobia -- common components CBT

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 Education<br> Educates about the disorder and its treatment<br> Recommends self-help materials Exposure<br> Offers imaginal exposure to situations that are difficult to practice regularly in real life<br> Offers in vivo (real life) exposure to situations that provoke social anxiety during treatment sessions and homework<br> Provides exposure role-play simulations (for example, simulated conversations or interviews)<br> Reduces safety behaviours in social situations Cognitive restructuring<br> Aims to reduce negative beliefs about self and others<br> Works to reduce the excessive self-focus that is characteristic of social anxiety dis  Examines and changes perfectionist attitudes<br>Social skills training<br> Deals with any areas of weak social skills, such as eye contact or conversation skills<br> Addresses any interpersonal problems, including lack of social contacts and<br>friendships, improving social life, assertiveness, managing conflict, and dealing<br>with romantic relationships or problematic relationships<br>Emotion-regulation approaches<br> Offer relaxation approaches, acceptance of symptoms and anxiety

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Social Phobia / Anxiety d/o -- comorbid (5 dx, 3 cats)

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1) anxiety disorders: panic disorder, specific phobia<br>2) mood disorders: major depressive disorder<br>3) substance use disorders: alcohol abuse<br>4) personality disorders: avoidant personality disorder

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Social Phobia -- tx approaches

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1. selective serotonin reuptake inhibitors: first line [Escitalopram, fluvoxamine IR, Paroxetine IR or CR, Sertraline, Venlafaxine XR<br>2. Second line (Clonazepam, Alprazolam, Bromazepam, Gabapentin, Pregabalin, Citalopram, Phenelzine)<br>3. Third line (Fluoxetine, Bupropion, Mirtazapine, Moclobemide, divalproex, topiramate, olanzapine, quetiapine, clomipramine<br>4. Not recommended Atenolol, propranolol, buspirone, imipramine, [adjunctive Pindolol]<br>B. psychotherapy<br>provide cognitive explanation for social phobia<br>elicit maladaptive thoughts<br>exposure to simulated situations<br>cognitive restructuring to teach control of maladaptive thoughts <br>exposure to real social situations

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Panic -- medical ddx

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A. neurological: Meniere’s disease, transient ischemic attacks, Wilson’s disease<br>B. pulmonary: asthma, hyperventilation, pulmonary embolism<br>C. cardiovascular: paroxysmal atrial tachycardia, myocardial infarction, congestive<br>heart failure<br>D. endocrine: hyperthyroidism, pheochromocytoma, hypoglycemia<br>E. substance: intoxication or withdrawal<br>F. other: anaphylaxis

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Panic w/ phobic avoid -- cbt techniques

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A. cognitive therapy: education about the cognitive model of panic; cognitive restructuring around misinterpretation of bodily sensations, focusing on catastrophizing and probability over-estimation<br>B. applied relaxation: teaching progressive muscle relaxation, diaphragmatic breathing<br>C. interoceptive exposure: exposure to unpleasant bodily sensations<br>D. in vivo exposure: exposure and desensitization to feared stimuli<br><br> Education<br> Explains the development of panic attacks<br> Informs about the panic cycle—typical bodily reactions, thoughts, and behaviours<br>during panic attacks and related anxiety experiences<br> Presents a cognitive-behavioural model for panic attacks and PD<br> Recommends relevant self-help reading materials<br> Cognitive approaches<br> Illustrate the catastrophic thinking and other cognitive errors that often accompany<br>panic attacks (for example, belief that rapid heart beat means an impending heart attack)<br> Demonstrates strategies for replacing anxious thoughts with alternative interpretations<br>and coping thoughts<br> Offers behavioural experiments designed to challenge unrealistic anxious thoughts<br> Interoceptive exposure<br> Exposure to feared bodily symptoms experienced during episodes of panic.<br> Teaches strategies to produce the symptoms so that exposure may be practiced<br>repeatedly (for example, hyperventilation triggers feelings of dizziness, breathlessness,<br>and racing heart)<br> Real-life exposure to avoided situations<br> Offers graded and repeated exposure to situations that are feared and may be avoided<br>because they have become associated with panic attacks<br> Typically, exposure occurs in the context of assignments between treatment sessions,<br>although therapist-assisted exposure is common as well.<br> Emotion-regulation approaches<br> Comprise various relaxation approaches<br> Teach paced breathing to reduce hyperventilation<br> Recently developed approaches focus on acceptance and mindfulness, developing<br>tolerance of periods of increased anxiety<br> Problem solving<br> Practice coping with problems that were possibly involved in the development or<br>maintenance of PD—conflict, loss, overwork, perfectionism<br> Relapse prevention<br> Preparation for periods of increased anxiety or panic in the future

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Panic -- gorman's neuroanatomical hypothesis

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A. panic disorder involves three factors: panic attacks, anticipatory anxiety, and phobic<br>avoidance<br>B. Gorman postulates that these arise from distinct neuroanatomical substrates, and can be<br>targeted in distinct ways:<br>1. panic attacks: arise from brain stem, targeted by SSRI medications<br>2. anticipatory anxiety: arises from limbic system, targeted by benzodiazepines<br>3. phobic avoidance: arise from higher cortical centers (pre-frontal cortex), targeted by<br>exposure therapy<br>The amygdala also has caudal projections to monoaminergic loci such as noradrenergic neurons of the locus ceruleus, dopaminergic neurons of the ventral tegmental area, and serotonergic neurons of the raphe nuclei. The amygdaloid nuclei appear to have the appropriate connections to orchestrate the simultaneous elaboration of individual anxiety disorder correlates such as cognitive misappraisal and fear (cortical areas), escape and freezing behavior (periaqueductal gray), hyperventilation (parabrachial nucleus), sympathetic activation (lateral hypothalamus), endocrine activation (paraventricular nucleus of the hypothalamus), gastrointestinal distress (dorsal motor nucleus of the vagus), increased startle (nucleus caudalis pontis), and motor activation (striatum).

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Panic - 5 substances that induce

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A. panicogens (panic inducing substances) induce panic attacks in patients with panic disorder,<br>and also in a small percentage of normal individuals without a history of panic disorder or<br>panic attacks<br>B. respiratory substances (cause a shift in the acid-base balance)<br>1. carbon dioxide<br>2. bicarbonate<br>3. lactate<br>C. neurochemical substances (act via specific neurotransmitter systems)<br>1. Yohimbine (an alpha-2 antagonist)<br>2. m-chlorophenylpiperazine (serotonergic agonist; metabolite of nefazadone)<br>3. fenfluramine (promotes serotonin release)<br>4. caffeine

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GAD -- 3 categories of meds

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A. SSRIs (Paroxetine, Escitalopram, Sertraline)<br>B. novel antidepressants (Venlafaxine, Mirtazapine)<br>C. benzodiazepines (rapid relief, but chronic use can lead to tolerance and dependence)<br>D. buspirone (5-HT1a (presynaptic and post-synaptic) partial agonist)<br>E. tricyclic antidepressants (Imipramine)<br>F. Anxiolytics<br> Benzodiazepines (Alprazolam, Bromazepam, Lorazepam, Diazepam<br> Azapirones (Buspirone)<br>• Anticonvulsants (Pregabalin)<br>• Atypical antipsychotics (Adjunctive olanzapine, Adjunctive risperidone)<br>• Other agents (Hydroxyzine, Trazodone, Propranolol)

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Panic -- advantages of bzd 5

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a. Rapid relief of symptoms;<br>b. gives pt control of symptoms {good for CBT strategy},<br>c. has good evidence of efficacy;<br>d. minimal side effects,<br>e. inexpensive;<br>f. early relief while waiting for antidepressant to kick in;<br>g. early anxiety SE of some antidepressants;<br>h. residual anxiety symptoms (augment)

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Anxiety -- 10 med disorders associated with

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A. endocrine<br>1. hyper- or hypothyroidism 2. diabetes (hypoglycemia) 3. pheochromocytoma<br>B. respiratory 1. asthma<br>2. pulmonary embolism<br>3. chronic-obstructive pulmonary disease (COPD)<br>C. neurological<br>1. Huntington’s disease<br>2. Wilson’s disease<br>3. systemic lupus erythematosis<br>4. CNS tumors<br>5. strokes or transient ischemic attacks 6. seizure disorders<br>D. cardiovascular 1. cardiac arrhythmias<br>E. substance<br>1. substance intoxication or withdrawal

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PTSD -- clinical features

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• Onset of psychiatric symptoms following exposure to traumatic event (either witnessing or experiencing threatened death or injury/threat to physical integrity, response involves intense fear or horror)<br>• Symptoms in 3 domains:<br>o Reexperiencing the trauma (1/5) – intrusive memories, flashbacks, dreams, physiologic/psychologic<br>distress in response to stimuli linked to the trauma<br>o Avoidance of stimuli linked to the trauma (3/7) – efforts to avoid thoughts/activities/reminders,<br>amnesia for part of trauma, anhedonia, blunted affect, feelings of detachment or derealization,<br>foreshortened sense of future<br>o Symptoms of autonomic arousal (2/5) – sleep disruption, irritability/anger, difficulty concentrating,<br>hypervigilance, exaggerated startle • Symptoms persist at least one month

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Panic -- Epidemiology

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Exposure to traumatic event – 60.7% of men, 51.2% of women Rate of PTSD – 8.1% of men, 20.4% of women<br>Nature of trauma – men more combat and disasters, women more rape Men who are raped have same rates of PTSD as women who are raped<br>

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Panic -- RF

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Severity of trauma, ongoing stress, lack of current social support Gender, history of child abuse, prior adversity also play a role

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Panic -- pathogenesis theories

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Risk and resilience model<br>Initial response to fear is biologically mediated Normal response to fear<br>Sympathetic activation – adrenaline release, ↑HR, BP, glucose HPA axis – release of CRF → ACTH → cortisol<br>Returns to normal within several hours<br>In PTSD<br>Underlying vulnerability (?previous sensitization) leads to failure of normal dissipation of<br>response, long-term effects Individuals with PTSD show:<br>Increased acoustic startle, failure to habituate<br>Elevated HR at the time of the event, persists up to 1 week Lower cortisol levels after traumatic event<br>Subjective interpretation of the event is an important element, may modulate biological response Strongly influenced by previous history of trauma<br>Neurobiological hypotheses<br>• Increased activation of amygdala – involved in intense emotional states such as fear<br>• Failure of modulatory action of medial prefrontal cortex (anterior cingulate region) – fear response is not<br>modulated/tempered/organized adequately<br>• Hippocampal abnormalities – some studies show ↓ hippocampal volume in PTSD, but prospective studies<br>have not supported this<br>• Decreased activation of Broca’s area may be involved – may explain problems with verbalization of issues<br>related to the event

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Panic -- ddx

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Other responses to trauma – depression (ddx/comorbidity)<br>Other anxiety disorders – panic, GAD<br>GMC – head trauma<br>Phenomenologically similar disorders – borderline PD, dissociative disorders, factitious disorders

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Panic -- course and mgt

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Course and prognosis<br>After a traumatic event, majority of those exposed may experience post-traumatic symptoms After 9-12 months, 15-25% continue to be disturbed by symptoms<br>Management<br>Pharmacological (ISTSS Guidelines)<br>• SSRIs – Fluoxetine (level A evidence), sertraline/Paroxetine, fluvoxamine (level B o First-line treatment<br>o Reduce PTSD symptoms (all 3 clusters), produce global improvement, effective against comorbid disorders<br>• MAOIs – Phenelzine (level A evidence), Moclobemide (level B evidence)<br>o Most effective for reexperiencing symptoms and global improvement, some efficacy for avoidance<br>cluster symptoms<br>o Also effective antidepressant, antipanic agents<br>o Dietary restrictions may limit use<br>o Contraindicated in patients with alcohol/drug use<br>o Watch out for drug interactions, CV and hepatotoxic side effects o Reversible (Moclobemide) is safer<br>• TCAs – Imipramine/amitriptyline (level A evidence), desipramine (level B )<br>o Similar spectrum to MAOIs (reexperiencing, avoidance) but less effective<br>• Antiadrenergic agents – Clonidine/guanfacine/propranolol (level C evidence)<br>o Appear to reduce hyperarousal, reexperiencing, possibly dissociative symptoms, but not adequately<br>tested in clinical trials o Monitor BP<br>• Anticonvulsants – Carbamazepine/Valproate (level B evidence) o Both effective for hyperarousal symptoms<br>o Carbamazepine effective for reexperiencing symptoms o Valproate effective for avoidance symptoms<br>• Benzodiazepines – Alprazolam (level B evidence), clonazepam (level C evidence)<br>o Effective for reducing hyperarousal, but not for reexperiencing, avoidance<br>o Not recommended as monotherapy<br>o May be beneficial as time-limited adjunctive treatment of disrupted sleep or for quick relief of global<br>anxiety<br>• Other serotonergic agents – Nefazadone (level B evidence), trazadone (level C evidence),<br>Cyproheptadine/buspirone (level F evidence)<br>o Nefazadone – may be particularly effective in improving sleep and reducing anger<br>o Trazodone – may be useful adjunct to SSRIs (reverses SSRI-induced insomnia)<br>o Cyproheptadine, buspirone – only anecdotal evidence, not recommended first line at this time<br>• Antipsychotics – thioridazine/clozapine/risperidone (level F evidence)<br>o Not recommended first line – only a few anecdotal reports of effectiveness<br>o May prove to have a unique role for patients who are refractory to 1st and 2nd line treatments,<br>especially with extreme hypervigilance, paranoid symptoms, agitation or psychosis<br>Summary<br>The best evidence supports the use of SSRIs as first line drugs for PTSD. There is also good evidence suggesting that MAOIs are moderately, and TCAs mildly effective agents, although both may produce adverse side effects. Evidence supporting the use of antiadrenergic and anticonvulsants is not strong, not because of negative findings, but because there have been no randomized trials with either class of drugs. There is evidence to suggest that benzodiazepines are not useful for treating PTSD B or C symptoms. Finally, antipsychotic agents cannot be recommended as first line monotherapy at this time because only a few case reports have appeared in the literature.

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PTSD -- psychotherapy

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Stage-oriented trauma treatment (Judith Herman, 1992) • Stage 1 – Safety<br>o Assess risk, need for secure setting (suicidality, self-harm)<br>o Establish therapeutic alliance – empathy, validation, containment, tolerance of affect<br>o Develop plan and skills for coping with distress, maintaining safety<br>o May involve addressing complicating factors such as depression, substance abuse, other<br>comorbidities<br>o Techniques may include individual and group therapy, both supportive-expressive and symptom-<br>focused/skill building (eg. CBT)<br>• Stage 2 – Remembrance and Mourning<br>o Telling the story of the trauma, expressing associated affect<br>o Processing the experience in a way that can be integrated into patient’s identity/self-image/life<br>narrative<br>o Specific techniques include CBT (prolonged exposure) and EMDR<br>• Stage 3 – Reconnection<br>o Reintegration of patient into social roles and responsibilities o Reestablishing sense of self, relationships

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Panic -- features, comorbidity, approach to dx

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Panic Disorder is:<br>Presence of recurrent, unexpected panic attacks Followed by at least 1 month of: Persistent concern about having another panic attack OR<br>Worry about the possible implications/ consequences of having a panic attack Significant behavioural change related to the attacks<br>Panic attacks are not due to substance/GMC/another mental disorder<br>Common Comorbidities (90% have at least 1 other psychiatric disorder):<br>• Other anxiety disorders - phobias, agoraphobia, GAD, OCD<br>• Major depressive disorder<br>• Substance abuse<br>• Personality disorder<br>Biopsychosocial Approach to Differential Diagnosis<br>• Rule out medical disorder<br>o Complete history and physical<br>o Labs - CBC, lytes, BUN, creatinine, thyroid function, glucose, Ca, LFTs, drug screen,<br>urinalysis, ECG (± neuroimaging)<br>o Pay special attention to atypical symptoms<br>− Vertigo, loss of bladder control, loss of consciousness<br>− Late age of onset (&gt;45 years)<br>− Cardiac risk factors - do Holter, chest Xray, enzymes, stress test<br>o If suspicious<br>− 24 hour urine (carcinoid)<br>− Catecholamines (pheochromocytoma)<br>• Psychosocial factors<br>o Is panic attack unexpected vs. situationally based?<br>o Stressors?

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Panic -- mgt

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• Pharmacological<br>o SSRIs are 1st line treatment (also venlafaxine)<br>o TCAs are 2nd line<br>o Can use benzodiazepines as adjunctive treatment<br>Caution re: dependence, abuse--nstruct re: driving, dangerous equipment<br>o Treat for 12-16 weeks (acute phase), then maintain on medication for at least 1 year, then may<br>discontinue gradually over 2-6 months<br>• Psychotherapeutic<br>o CBT is 1st line<br>o May include psychoeducation, self-help manuals, exposure, cognitive restructuring, breathing retraining<br>o Information re: lifestyle, diet (eg. caffeine), other substances (if reduce, may have panic in withdrawal phase)<br>o Include spouse/partner/family

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OCD -- etiology

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Unique among the anxiety disorders - appears to be dominated by cognitive and behavioural symptomatology with autonomic dysregulation playing little role<br>Anxiogenic agents (lactate, caffeine, yohimbine, etc.) doe not induce much anxiety or panic in patients with OCD<br>• Neurotransmitters<br>o Serotonergic abnormalities<br>− Responds to SSRIs, clomipramine<br>− Some studies show high pretreatment CSF 5HIAA, a serotonin metabolite, decreases<br>with clinical improvement<br>− Platelets of OCD patients sometimes found to have reduced imipramine binding sites,<br>indicating abnormality of serotonin transporter<br>• Brain imaging studies<br>o Functional imaging<br>− Increased activity (metabolism and blood flow) in frontal lobes, basal ganglia (esp.<br>caudate) and cingulum<br>− Reverses after successful treatment with medications or CBT<br>o Structural imaging<br>− Bilateral decreased size of caudates<br>− Abnormality in frontal lobe<br>o Both types of imaging show that neurological procedures involving cingulum are sometimes effective in treating the condition<br>• Genetics<br>o Higher concordance in monozygotic twins o 35% of 1st degree relatives also have OCD<br>• Other<br>o Some EEG and neuroendocrine abnormalities similar to depression<br>− Decreased REM latency, nonsuppression response to dexamethasone in 30% with OCD<br>− Decreased growth hormone secretion with clonidine

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MDD -- standardized scales (3) and how use

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Rating scales for depression<br>A. Hamilton Rating Scale for Depression (HAMD)<br>2. physician administered scaled; 21 questions<br>3. &gt; 26 severe depression; 18-25 moderate depression; 8 to 17: mild depression<br>B. Beck Depression Inventory (BDI)<br>4. self rating scale; 21 questions<br>5. 15 to 30: moderate depression, &gt; 30 severe depression<br>C. Zung Self-Rating Depression Scale 6. 20 items; normal is &lt; 34, depressed is &gt; 50<br>D. Montgomery-Asberg Depression Rating Scale (MADRS)<br>7. 10 item scale, physician administered<br>8. 7 to 19: mild depression; 20 to 34: moderate depression; 35 to 60 severe depression<br>B. Montgomery-Asberg Depression Rating Scale (MADRS)<br>Main indications: Designed to be used in patients with major depressive disorder, both to measure the degree of severity of symptoms, and particularly as a sensitive measure of change in symptom severity during the treatment of depression.<br>Rating performed by: Trained interviewer.<br>Time period covered by scale: Clinical condition at the time of the interview. Does not specify a time<br>frame during which the patient should be rated.Time required completing rating: Approx. 15 minutes.<br>Remarks: Is a 10-item checklist. Widely used in drug-treatment trials, mainly because of its particular sensitivity to treatment effects. Since there is a comparative lack of emphasis on somatic symptoms, the scale is useful for the assessment of depression in people with physical illness. The following mean scores correlated with global severity measures, according to a study: very severe, 44; severe, 31; moderate, 25; mild, 15; and recovered, 7. each symptom scored (0-2-4 or6).<br>Using rating scales for depression<br>E. scales can be used for screening, and for monitoring response to treatment<br>F. they allow for reliable future comparison and communication

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MDD -- tx resistant: define and comorbid (med and psych) that may contribute

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Defining treatment resistance<br>G. Patient shows only partial or no response to an optimized dose of an antidepressant<br>medication for a therapeutic duration.<br>H. should ensure treatment adherence before documenting treatment resistance<br><br>I. psychiatric comorbidity<br>9. substance abuse<br>10. personality disorders<br>11. bipolar depression<br>J. medical comorbidity<br>12. thyroid dysfunction<br>13. infections (pneumonia in the elderly, or mononucleosis in adolescents)<br>14. cerebrovascular disease<br>15. tumors of the CNS

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MDD -- sleep cycle changes

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Sleep architecture changes<br>K. increased sleep latency (Time from lights out to onset of sleep)<br>L. early morning awakening<br>M. decreased sleep continuity (increased wake after sleep onset) N. decreased slow-wave sleep(stage 3 &amp;4)<br>REM sleep changes<br>O. decreased REM latency<br>P. prolonged first REM period<br>Q. increased REM density<br>The sleep pattern of a person with major depressive episode shows<br> decreased stage 2<br> increased stage 4<br> Increased total sleep time???????????  decreased REM latency<br> REM rebound

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MDD -- reasons immed rx vs not

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Reasons for not immediately prescribing an antidepressant<br>R. inadequate follow-up to monitor side-effects or response<br>S. cross sectional evaluation limited; may need to further clarify diagnosis<br>T. treatment of choice or treatment preferred by patient may be psychotherapy<br>U. patient may be unable to make informed decision regarding pharmacotherapy after<br>initial assessment, and may wish to consider it further<br>Reasons for immediately prescribing an antidepressant<br>V. diagnosis is clear and antidepressant is clearly indicated<br>W. adequate social and family support to ensure compliance and follow-up<br>X. adequate follow-up in place<br>Y. patient preference

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MDD vs anxiety (6)

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A. anxiety: nervous and fearful on MSE; depression: sad, tearful, withdrawn on MSE<br>B. anxiety: more often associated with somatic symptoms (tremor, palpitations,<br>tachycardia, dizziness)<br>C. anxiety: more future-focused, described as worry or apprehension<br>D. anxiety: no diurnal variation, guilt; depression: diurnal variation, guilt<br>E. anxiety: more episodic; depression: sustained mood<br>F. anxiety: more cognitive vigilance, easily started

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MDD - prognostic factor (5 poor)

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A. anxiety disorder symptoms<br>B. more than one previous episode<br>C. poor inter-episode recovery<br>D. long duration of episodes<br>E. temporal association between the mood disorder and the psychotic symptoms<br>F. poor premorbid history of social adjustment<br>G. personality disorder<br>H. mood incongruent<br>I. substance abuse

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MDD - subtypes

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1. Major depressive disorder, single episode<br>2. MDD, recurrent<br>3. MDD<br>4. Dysthymia 5.MDD, NOS<br> Specifiers<br>Chronic<br>with psychotic features poor prognosis; worse if psychosis is mood incongruent<br>with catatonic features<br>Most commonly associated with bipolar disorder type I. diagnosed if you have two of (EVEN I):<br>excessive motor activity (purposeless)<br>peculiarities of voluntary movement (posturing) echolalia or echopraxia<br>extreme negativism (motiveless resistance) or mutism motoric immobility (catalepsy or stupor)<br>4. with melancholic features<br>less likely to have premorbid personality disorder less likely to respond to placebo<br>less likely to have clear precipitant<br>more likely to respond to antidepressant treatment more likely in older individuals<br>criteria are (MAD GRADS)<br>motor retardation or agitation is marked<br>appetite severely decreased (anorexia or weight loss) diurnal variation<br>guilt is excessive<br>reactivity of mood is absent (this or anhedonia required) anhedonia (this or lack of reactivity required)<br>distinct quality of mood<br>sleep is characterized by terminal insomnia<br>5. with atypical features<br>More common in younger individuals and in females<br>More likely to have more chronic course with worse inter-episode recovery Respond better to MAOIs than to TCAs<br>Criteria are RAILS<br> reactive mood<br> appetite increased<br> interpersonal rejection sensitivity  leaden paralysis<br> sleep increased<br>6with post-partum onset<br>.onset within four weeks of delivery<br>.with psychotic features, occur in 0.1 to 0.2%<br>7. with seasonal pattern<br>Regular pattern of onset at a certain time of year<br>Regular pattern of remission at a particular time of year<br>Two seasonal major depressive episodes in the past two years; no non-seasonal major depressive episodes in past two years<br>Over lifetime, seasonal episodes much more common than non-seasonal episodes

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MDD -- Neuro ddx

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Neurological diseases that can present with depressed mood<br>• Parkinson’s disease(50-75 % present with depression)<br>• Huntington’ s disease<br>• Alzheimer’s dementia<br>• cerebral neoplasms (especially left frontal)<br>• stroke (especially left frontal)particularly in the two years after the episode<br>• multiple sclerosis<br>• Frontal lobe dementia or syndrome<br>• Interictal episode can mimic depression, especially if the epileptic focus in on the right side)<br>Other diseases that can present with depressed mood<br>• Hypothyroidism sleep apnea Wilson’s disease

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MDD -- female w/ sz d/o and CBZ ... 3 causes, factors re Rx

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 Female gender<br /> GMC (epilepsy) 30 to 50 % of all people with epilepsy have psychiatric difficulties<br />sometime during the course of their illness. The most common behavioral symptom of epilepsy is a change in personality; psychosis, violence, and depression (20-60%) occur much less commonly in epileptic disorders.<br /> Seizure medication. Carbamazepine (3A3-4)<br />Mood disorder symptoms are seen less often in epilepsy than are schizophrenia-like symptoms. They do occur tend to be episodic and appear most often when the epileptic foci affect the temporal lobe of the nondominant cerebral hemisphere. The importance of mood disorder symptoms may increase incidence of attempted suicide in epilepsy.<br><br> Antidepressants drug interaction as Tegretol is enzyme inducer<br> Close monitoring of seizure as antidepressant may lower seizure threshold, Prozac, Zoloft, Luvox, they increase carbamazepine level.

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Seasonal Affective -- tx and psychotherapy modes

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Seasonal affective disorder is characterized by recurrent depressions that usually begin in November and end in March. Symptoms of winter depression commonly include lethargy, decreased activity, and social withdrawal, loss of interest in sex, oversleeping, overeating, carbohydrate cravings, and weight gain. Sometimes the picture changes to an opposite one in the spring, with increased energy, increased activity, social engagement, increased libido, decreased need for sleep, decreased appetite, and weight loss. The ubiquitous role of melatonin as a chemical mediator of seasonal change in animals and the similarities between patients' symptoms and behaviors that melatonin triggers in animals led clinical investigators to hypothesize that photoperiod-induced change in the duration of melatonin secretion are part of the mechanism that drives the seasonal cycles of this disorder.<br>The efficacy of Fluoxetine in winter seasonal affective disorder (mood disorder with seasonal pattern) was evaluated in 68 outpatients with DSM-III-R recurrent major depression, seasonal (winter) type. Participants were randomly assigned to Fluoxetine (20 mg a day) or placebo for 5 weeks. Both groups exhibited clinical improvement, though the Fluoxetine group had a higher rate of clinical response (defined as greater reduction in the 29-item HAM-D scale between initiation and termination), 59 percent compared with 34 percent for placebo. Those who did not demonstrate some improvement by weeks 2, 4, or 6 but did respond by week 8 were 36.4, 18.9, and 6.5 percent of the patient population, respectively; suggesting that similar to observations with major depression, additional Fluoxetine treatment after 8 weeks does not lead to subsequent recovery .<br>Phototherapy typically involves exposing the afflicted patient to bright light in the range of 1,500 to 10,000 lux or more, typically with a light box that sits on a table or desk. Patients sit in front of the box for approximately 1 to 2 hours before dawn each day, although some patients may also benefit from exposure after dusk.<br>Phototherapy tends to be well tolerated. Some patients have complained of irritability and headache. Some people may experience mild nausea, headaches, eyestrain, or feeling “edgy” when they first start using light therapy. These effects usually get better with time or reducing the light exposure.<br>Using the 10,000 lux light box for about 30 minutes a day is usually enough for a beneficial response Psychotherapy: CBT

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MDD - failed trials: hx points (2), what clarify (3), best validated augment, combo strategies

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A. Two points of the history to clarify?<br />2. previous psychiatric history, particularly of unipolar vs. bipolar, and treatment response;<br />3. Family psychiatric history, particularly of unipolar vs. bipolar, and treatment response.<br />B. What two things would you like to know about previous treatment?<br />1. dose and duration of the med trials;<br />2. compliance with med trials and adherence to previous treatment<br />3. was there any side effects experienced by the patients<br />C. What are the two best validated augmentation strategies? Give the doses and the duration of treatment for both.<br /> Two best validated augmentation strategies: lithium and T3 (liothyroxine)<br />6. Lithium augmentation – metaanalysis suggest response in 50-60% of patients.<br />7. Triiodothyronine augmentation – starts at 25mcg daily and increase to 50 mcg/day<br />after 1 week if no response. Continue trial for 2 weeks at 50mcg dose; if no response,<br />d/c.<br />8. Adding atypical antipsychotic (Olanzapine, Risperidone)-Level II<br />9. Adding stimulants (methylphenidate 5-10mg/day)<br />10. Adding Buspirone 5-10mg tid. Level II<br />1. Combination Strategies (combing two antidepressants; preferably ones affecting different<br />neurotransmitter<br />1.SSRIs + Desipramine<br />2.SSRIs+ Bupropion (NE+DA)  Switching strategies<br />1.from one SSRIs to another one<br />2.from one class of antidepressant to a different class (SSRIs to TCAs) 3.switch from any antidepressant to ECT

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IPT areas of focus

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role transition or grief (ip conflict, ip &gt;&gt;&gt;&gt;)

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IPT -- sick role components

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• Sick role shifts blame from patient to illness<br>• Defines the patient as in need of help<br>• Frees patient from ruminative self-criticism<br>• The sick person is considered exempt from certain normal social obligations<br>• Person is exempt from certain types of responsibility<br>• Sick role allows patient to receive in a compensatory way the care that has not<br>adequately been received from others

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MDD -- cognitive dysfunctions underlying and process of CBT addressing

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Cognitive triad of depression:<br>• negative self-perception<br>1. experience self as deprived and undesirable (worthless, defective, inadequate)<br>• negative view of circumstances<br>1. experience world as negative and demanding<br>• negative view of future<br>1. expect future of ongoing deprivation (hardship, suffering) and failure<br>Processes in cognitive therapy:<br>• Elicit automatic thoughts (cognitive distortions) .The cognitive therapist will try to elicit automatic thoughts, which are thoughts that come spontaneously, seem plausible to the patient, and are associated with negative affect. Typical automatic thoughts are &quot;I'll never be happy&quot; or &quot;I'll lose control&quot; or &quot;I'm a failure<br>• test automatic thoughts (test their validity, find alternate thoughts)<br>• identify maladaptive assumptions (examine the patterns of automatic thoughts)<br>• test the validity of maladaptive assumptions

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BAD 1 -- comorbid

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1. substance<br>2. anxiety disorders<br>3. panic disorder<br>4. obsessive compulsive disorder<br>5. social phobia<br>6. post-traumatic stress disorder<br>7. ADHD

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BAD - prognostic

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Good prognostic factors<br>Short duration of mania. Few suicidal thoughts, few co-existing medical or psychiatric problems<br><br>Poor prognostic factors<br>• substance abuse psychotic features<br>• Male gender. poor pre-morbid function

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Mania -- organic ddx

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• neurologic<br>1. cerebral neoplasms<br>2. temporal lobe epilepsy<br>3. strokes<br>4. multiple sclerosis<br>5. Frontal lobe dementia<br>• medication<br>1. corticosteroids<br>2. levodopa<br>• endocrine<br>1. hyperthyroidism<br>2. Cushing’s syndrome

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BAD -- nonadherance factors and strategies in tx

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A. Patient factors: Young, single, male, no education, and lack of psychosocial support, family<br>interference<br>B. Illness factors: Hypomanic, psychosis, comorbid personality, substance abuse, poor insight<br>C. Treatment factors:<br>Side effects, unfavorable personal attitude towards treatment, poor therapeutic alliance with prescriber<br>Factors that can help maximize compliance:<br>• patient psychoeducation<br>• self-monitoring<br>• recurrence prevention<br>• family involvement and education<br>• management of side-effects<br>• identifying and managing stressors<br>• addressing believe system and attitude towards illness<br>• development of therapeutic alliance<br>• adjunctive psychotherapy

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BAD and Li -- predictors of response

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Predictors of a good response to lithium<br>• Elated mania<br>• previous good response to lithium<br>• family history a bipolar disorder, and response to lithium<br>• euphoric mania(mania- depression-euthymia)<br>• no neurological impairment<br>• no psychotic sxs<br>• no substance<br>• few episodes of illness<br>Predictors of a poor response to lithium)<br>• rapid cycling<br>• mixed episode<br>• substance abuse<br>• psychotic symptoms<br>• depression followed by mania-euthymia<br>• presence of depressive sxs<br>• multiple episodes<br>• no family history<br>• personality disorder

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BAD -- 4 classes of med alternative Li (maintenance!)

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1. anti-epileptic drugs: Valproate(level I), carbamazepine(level I) (note that lamotrigene works for depression, but not mania)<br>2. neuroleptics: Olanzapine, quetiapine(level I)<br>3. benzodiazepines: clonazepam(level II)<br>4. others: calcium channel blockers have been considered in the past, but there is no<br>evidence for them, haloperidol Level I, chlorpromazine Level I)<br>5. note that lithium is the only medication that has proven efficacy against the relapse of<br>mania; the others may be used, but have less evidence

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BAD -- characteristics of depr

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• psychotic features<br>• rapid onset of depressive symptoms<br>• psychomotor retardation<br>• hypersomnia<br>• more likely to have an onset post-partum<br>• (note that the first three are also listed as risk factors for bipolarity in adolescent depression)<br>• other risk factors: family history of bipolar disorder, hypomania in response to antidepressant

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BAD -- mixed state comorbid

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Definition of mixed-state:<br>• criteria are met for both a manic episode and a depressive episode nearly every day for one week<br>• mixed-like episodes clearly caused by depression treatment should not count towards the diagnosis of bipolar<br>Features and co-morbidities of mixed states<br>• mixed episodes are more likely in adolescents, young adults, and the elderly than in middle aged adults<br>• mixed episodes are more likely in males (this is questionable)<br>• mixed episodes are associated with substance abuse (and possibly head injury)<br>• anxiety disorder, personality (borderline)

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BAD -- rapid cycling =&gt; etiology and mgt

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Definition of rapid-cycling:<br>• four episodes of mood disturbance in previous 12 months; either separated by a period of partial or full remission for two months, or by a switch to opposite polarity; can be applied to both bipolar I and bipolar II<br>• all the patients can have rapid cycling except 5 (MDD single, MDD recurrent, Dysthymia, cyclothymia, not in bipolar I single manic episode<br>Etiology of rapid-cycling:<br>• rapid-cycling may be a phase of regular bipolar disorder, or it may be a distinct disorder in its own right; the epidemiology of rapid cycling differs from non-rapid cycling (it is more common in females), but there is no familial pattern to rapid cycling<br>• hypothyroidism, drug or alcohol use, or any antidepressant may contribute to rapid cycling<br>• External factors (stress, pharmacotherapy, substance abuse) involved in the etiology of rapid<br>cycling.<br>Management of rapid-cycling:<br>• stabilize sleep<br>• reduce or stop caffeine, nicotine, alcohol, other substances<br>• consider discontinuing antidepressants (especially TCAs)<br>• keep a mood chart to monitor moods and medication response<br>• first line: lithium, lamotrigene has the best support, and then divalproex<br>• second line: lithium + divalproex, lithium+carbamazepine<br>• third line: divalproex or lithium +topiramate, atypicals,Clozapine,levothyroxine,<br>oxacarbamazepine<br>• psychosocial management strategies:<br>1. psychoeducation 2.interpersonal (especially “social rhythm therapy” 3. Family therapy 4. cognitive behavioral therapy

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mixed anxiety-depressive d/o, five of 10 B criteria

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• a DSM-IV research disorder<br>• A: persistent or recurrent dysphoric mood for at least one month<br>• B: dysphoric mood is accompanied by four or more of the following ten:<br>1. five symptoms from depressive disorders (note that Dysthymia has six of the SIGECAPS symptoms – it does not have interest or psychomotor changes, and instead of suicidality it is characterized by hopelessness – SiGECApS – mixed anxiety-depressive disorder has these six except for appetite change)<br> sleep disturbance<br> feelings of worthlessness  low energy, fatigue<br> difficulty concentrating  feelings of hopelessness<br>2. five other depressive-anxiety symptoms  being easily moved to tears<br> irritability<br> worry<br> hypervigilance<br> anticipating the worst<br>• E: never had depression, Dysthymia, panic, or GAD; do not currently have other mood or anxiety disorder

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MDD - catatonic features, Ax, Tx, RF

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Motor immobility, purposeless motor activity, extreme negativism or mutism, peculiarities<br>of voluntary movement (ex posturing, mannerism, etc), echolalia/echopraxia<br><br>b. Most common dx, MDD R/O BAD<br>Among 100 pts w/ 2+ catatonic features, 50% are BAD, 25% are unipolar, 15% have<br>neurologic/GMC causing catatonia &amp; 10% are schizophrenic<br><br>b. Most common dx, MDD R/O BAD<br>Among 100 pts w/ 2+ catatonic features, 50% are BAD, 25% are unipolar, 15% have<br>neurologic/GMC causing catatonia &amp; 10% are schizophrenic<br>c. In ER, name 2 non-pharmacologic strategies for assessment/management:<br>History &amp; physical to rule out GMC/stroke; Blood work, CT head<br>Best treatment - short term is Lorazepam; ECT is best for MDE w/ catatonia<br>d. Risk factors - stroke, basal ganglia disease, PCP use, psychiatric illnesses (like BAD, MDE,<br>schizophrenia, frontal lobe disease), neuroleptic use, dehydration/malnutrition, female<br>gender, children.

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MDE w/ psych, prior med-induced hypo, substances. MLDx, 1st line tx

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A. Most likely diagnosis, MDD, Recurrent Episode with atypical features<br />B. 4 aspects on Hx suggest Dx: female gender, previous episode, current MDE, presence of<br />psychotic features in her previous episode.<br />C. Differential Dx: Dysthymia, Bipolar II, GMC (hypothyroidism)<br />D. 1st-line medication are SSRIs (Fluoxetine, meclobemide, Sertraline), 2nd line is phenelzine.<br />E. If not working, 2 blood tests; TSH, Hg anemia ( secondary to hypothyroidism)<br />F. Three approaches: 1- optimize the dose to max as tolerated<br />2- Switch to antidepressant with a different neurochemical action<br />3-augment with lithium or Cytomel<br />4-switch to antidepressant with similar action<br />5- Augment with buspirone or atypical antipsychotic<br />6-combine with another antidepressant (level III) Not recommended augmentation with atenolo<br />If she is not responding to this, ECT is indicated

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MDD -- RF in woman, sz, cbz

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a. woman<br>b. epilepsy<br>c. Perimenopausal<br>d. CBZ (risk for depression)<br>e. ? family dynamics (?couple issues)<br>f. ? infertility (hormonal, psychological)

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Mania w/ psychosis -- ddx, violence RF, mgt

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a. Differential Dx:<br> Bipolar disorder I with psychotic features  SCZ<br> Schizoaffective D/O<br> Substance induced bipolar (manic episode)<br><br>b. Risk factor for violence<br> Young age, male, low socioeconomic  Previous Hx of violence<br> Hx of substance abuse<br> Personality psychopathology<br> Psychosis, paranoid SCZ<br> Lower IQ (the lower IQ the higher the violence)<br>c. Management of violence:<br>Several steps can be taken to minimize the agitation and potential risk. The interview should be conducted in a quiet, non-stimulating environment. There should be enough space for the comfort of both patient and psychiatrist, with no physical barrier to leaving the examination room for either of them. During the interview, the psychiatrist should avoid any behavior that could be misconstrued as menacing: standing over the patient, staring, or touching. The psychiatrist must ask the questions necessary to complete an adequate evaluation but must attempt not to be provocative. It is certainly appropriate to allow the patient to drink water, use a bathroom, and, for extended evaluations in an emergency room, eat food. However, these should never be offered as bargaining chips (&quot;I'll let you get a drink of water if you'll tell me what happened just before the police brought you here.&quot;) The examiner must also avoid promising outcome in exchange for cooperation (&quot;If you'll just talk with me for another half hour, I'll make sure you don't have to go into the hospital.&quot;). The psychiatrist should ask whether the patient is carrying weapons and may ask the patient to leave the weapon with a guard or in a holding area. The psychiatrist should not request that patient hand over any weapons. Dangerous mishaps can occur during the transfer; moreover, the sudden shift in power created by an armed psychiatrist may feel extremely threatening to paranoid patients. If the patient's agitation continues to increase, the psychiatrist may need to terminate the interview. Depending on the setting, assistance from security personnel, physical, or chemical restraints may be appropriate. The physician's own subjective sense of comfort or fear should be heeded. A frightened, intimidated examiner may be incapable of an accurate professional evaluation.<br>A. Acute management:<br>Verbal approach, behavioral response to violent patient, seclusion and physical restrain chemical<br>(benzo, antipsychotic,)<br>B. Chronic or long term:<br>Pharmacology (mood stabilizer, b-blockers, atypicals, antidepressants [SSRIs], Anxiolytics) Behavioural; and Psychotherapy; individual or group<br>Violent behavior commonly occurs in patients with antisocial and borderline personality disorders; in the latter the violence is often self-directed as well as other-directed. Violent behavior may occur in epilepsy—although rarely during true ictal periods; in frontal lobe syndromes as a release phenomenon; and in association with abused substances, particularly disinhibiting sedatives such as alcohol or stimulants such as amphetamines and cocaine, which increase irritability, aggressiveness, and paranoia

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BAD -- RF for noncompliance (li / olz)<br> Discuss the side effects of these medications.<br> How would you differentiate between EPS and a lithium tremor?<br> How should the family doctor deal with the fact that the patient likes being high?  How can you help the family, if they are burnt out?<br> What changes could be made to the medications to maximize compliance?

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A. Factors that may contribute to noncompliance are;<br>o non-response<br>o partial response<br>o side effects<br>o comorbid psychiatric disorders o drug interaction and poor insight<br>o multiple dose regimen o financial reasons<br>o educational reasons<br>B. Side effects:<br>Olanzapine; weight gain 25%, sedation 14%, metabolic syndrome, DM, TGs, EPS, Lithium;<br>CNS; fine tremor (65%), weakness, fatigue, dysphoria, blunting, slurred speech,<br>CVS; bradycardia, EKG changes (20-30%), St flattened,<br>GI; diarrhea 20%, N/V, Metallic taste, thirst, weight gain 60%,<br>Endocrine; Hypothyroidism 34%, Goiter, hyperparathyroidism 10-40%, prolonged menstrual cycle in 15%<br>Renal; Polyuria, polydypsia 60%, DI (reversible), decrease GFR, interstitial fibrosis 26%, nephrotic syndrome rare<br>Dermatology; exacerbation of psoriasis, skin rash, pruritis, folliculitis, nail pigmentation<br>Others; sexual 10%, decrease libido, erectile dysfunction, priapism, anemia, leukocytosis<br>C. Differentiation between EPS and Lithium tremor<br>EPS: It has a regular frequency (3–6 cps), is usually suppressed during volitional action of the<br>involved body part, is exacerbated by stress and anxiety, and classically involves alternating contractions of opposing muscular groups (e.g., pronators and supinators of the forearm), seborrhea, and altered righting reflexes also can be present.<br>Tremor is a steady, rhythmic oscillation, 3 to 6 cycles per second, more prominent in the resting position. Tremor may affect extremities (unilateral or bilateral), head, jaw, mouth, tongue, or lips (&quot;rabbit syndrome&quot;). Parkinsonian tremor (i.e., a coarse, rhythmic, resting tremor with a frequency between 3 and 6 cycles per<br>second, affecting the limbs, head, mouth, or tongue)<br> Classification of tremor<br>Tremor is an involuntary, regular oscillation of a body part around a fixed point. Table 2.1–9 presents a classification of tremors including rest tremors, postural tremors, and kinetic tremors.<br>1. Rest tremors include the typical large-amplitude, low-frequency (approximately 4–6 Hz) tremor of Parkinson's disease and other parkinsonian states. This tremor disappears with sleep and is better characterized as a tremor of alert repose, occurring when the patient is alert but inactive. Rest tremor is suppressed by volitional movement.<br>2. The principal postural tremors (lithium) include exaggerated physiological tremors and essential tremors. These are small-amplitude, high-frequency (10–2 Hz) tremors that are absent at rest and occur during postural maintenance activities (holding the arms outstretched in front of the body, writing and so on). Exaggerated physiological tremors occur with fatigue, excitement, hypoglycemia, and Thyrotoxicosis as well as in metabolic encephalopathies and drug-induced toxic states (caused by lithium, tricyclic agents, Sympathomimetics, and so on).<br>3. Essential tremors are usually inherited but may occur sporadically.<br>4. Kinetic tremors are those that worsen with movement. Cerebellar intention tremors are the classic example of<br>kinetic tremors and are observed frequently in patients with multiple sclerosis.<br>

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BAD -- risk factors ????

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Risk for bipolar:<br>Sudden onset Adolescent onset Melancholic features<br>f. Family history of bipolar<br>g. Antidepressant switch<br>h. Psychomotor retardation<br>Factors associated with a poor prognosis for patients with mood disorder<br>1. long duration of episodes<br>2. temporal association between the mood disorder and the psychotic symptoms<br>3. poor premorbid history of social adjustment<br>5 factors that would increase likelihood of diagnosis of bipolar:<br>a. Sudden onset<br>b. Adolescent onset<br>c. Female onset with depression (males, manic)<br>d. Sleep disturbance - hypersomnia<br>e. Psychotic features

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MDE vs atypical / melancholic

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Melancholic depression has a picture of severe anhedonia or a lack of mood reactivity (pervasive nature of depressed mood). The neurovegetative features differ. These include a distinct quality to the depressed mood, mood worse in the morning, early morning wakening, marked psychomotor changes (agitation or retardation), significant anorexia or weight loss and excessive guilt. Treatment with medication is required.<br>Atypical depression is essentially the converse. There is notable mood reactivity. In addition there can be significant weight gain or appetite increase, hypersomnia, leaden paralysis and a long-standing pattern of interpersonal rejection sensitivity. MAOIs show efficacy. Avoid TCAs.<br>CPA Guidelines: Atypical Features<br><br>Atypical<br>First Line Treatments<br><br>Fluoxetine, Moclobemide, sertraline (Level 2 evidence)<br>Second line treatments<br>Phenelzine (Nardil 15mg to a max of 90mg/d) (Level 2 evidence)<br><br><br><br>Melancholic<br>First Line Treatments<br><br>Paroxetine, Venlafaxine (SSRI start 50 and Increase by 50 Q 4-7days to a max of 300mg (level 1 evidence)<br>Second line treatments<br>TCAs, Moclobemide, (level 1 evidence)<br><br>

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MDE -- biolological changes

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Biological changes in Depression:<br>a. Early morning wakening<br>b. Hypersecretion of cortisol (plus non suppression with DST in 50% -non specific)<br>c. 1/3 have blunted release of TSH in response to TRH<br>d. Blunted ACTH response to IV CRF challenge<br>e. ⇓ SRIF in CSF<br>f. BluntedGHresponse<br>g. Some depression is phase advance (a biological rhythm that begins earlier than usual)<br>h. Phase delay: a biological rhythm that begins later than usual.<br>i. Now thought that the disrupted circadian rhythms are likely 2° to ⇑ nocturnal arousal.<br>Sleep Changes in Depression:<br>1) Initial and terminal insomnia<br>2) Hypersomnia<br>3) Multiple awakenings<br>• ⇓ REM latency ⇑ REM density<br>4) ⇑ Length of first REM period<br>5) Delta (deep, slow wave) abnormalities (decreased)<br>

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MDE -- secondary, 10 causes

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Neurological Drugs<br><br>Infectious<br><br>Endocrine<br><br>Inflammatory<br><br>Metabolic<br><br>EP d/o: -Parkinsons 50% -Huntington’s 40% -Progressive<br>supra nuclear palsy<br>3° Syphylis<br>Cushing’s Syn- drome 80%<br>(⇑ cortisol agitated depression<br>SLE<br>Renal disease and uremia<br><br>Alzheimer’s 11% other dementia<br><br>HIV<br><br>Adrenal Addisons<br><br>RA<br><br>Porphyria<br><br>CVA esp. ant. hemispheric lesions 27% in left hemi. lesions<br>Toxoplasmosis<br>Hyper- aldosterone<br>Temporal arteritis<br>Wilson’s 20%<br><br>Tumors<br><br>Pneumonia<br><br>Menses<br>Sjogren’s<br><br><br>Trauma<br><br>Viral hepatitis<br><br>Hyper Parathyroid<br><br><br>Hydrocephalus<br><br>Mononucleosis<br><br>Post-partum<br><br><br><br>Sleep apnea<br>Thyroid +/- Hypo: 40%<br><br>Migraine<br><br><br>Hypopituitary<br><br><br>MS<br><br><br>Diabetes<br><br><br><br>Epilepsy 20-60% esp. TLE<br><br><br><br><br>Other<br>Vitamin Def.: -Folate -Thiamin -B12<br>-C -Niacin<br>Cancer 25% Disseminated<br>carcinomatosis<br>Klinefelter’s<br>Cardiac dx.<br>Systemic infections<br>D/c steroids<br>Pain<br>Anemias<br>substances<br><br>Cerebrovascular accidents: Silent subcortical strokes frequently assoc with depression.<br>Dementia: Depression may in part be organically induced in that the location of neuronal cell loss is an important factor in the development of depression. Dementia comorbid with MDD results in more severe cognitive deficits than either alone<br>Depression and infections: Depression reduces immune functioning in turn will increase the potential for infections. Several infectious states – AIDS, neurosyphilis, fungal infections, TB can precipitate depression. Hypercholesterolemia: Higher rates of depression are found in males with serum cholesterol levels greater than 160 mg/dL and serum TG levels greater than 500mg/dL

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MDE -- relapses Tx?

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????<br>Assess for safety, severity of episode. Is hospitalization required?<br>Always reassess diagnostic issues (e.g. subtype, comorbidity (Axis I, II, and III), bipolarity, substance use) Ensure she had been compliant with medication.<br>Rule out possible medical causes e.g. thyroid function, anemia, other meds<br>Optimize dose<br>Trial of another medication of the same class or other class/mechanism of action (preferred option)<br>Trial of another class of medication<br>Consider addition of psychotherapy (likely CBT or IPT)<br>Augment with Li, or T3.<br>Consider ECT especially if high suicide risk, severe or chronic illness, psychotic features, physical deterioration.

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treatment resistant depression -&gt; defn. List the co morbid psychiatric and medical conditions, which may contribute to

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• Inconsistently defined in the literature<br />• Lack of adequate remission of depressive symptoms after two or more trials of antidepressants from different medication<br />Classes given at therapeutic dosages for an adequate period of time (6 to 12 weeks); some authorities feel that a designation of<br />Treatment-resistant depression should only be made after the patient has also unsuccessfully undergone a trial of ECT. • Co morbid psychiatric conditions: anxiety disorders, substance use disorders, personality disorders, others including OCD,<br />Eating disorder and body dysmorphic d/o.<br />• Co morbid medical: hypothyroidism, medications, diabetes, coronary artery dx, HIV, cancer, chronic pain, fibromyalgia,<br />Chronic fatigue syndrome, irritable bowel syndrome Suggested terminology for treatment resistance depressions<br />Treatment refractory depression (TRD). Treatment non-response (i.e., persistence of significant depressive symptoms) despite<br />At least two treatment trials with drugs from different pharmacological classes, each used in an adequate dose for an adequate<br />Time period. Adequate dose. An oral dose that is close to the manufacturer’s recommended maximal dose. Adequate Dose may be smaller for elderly patients.<br />Adequate length of treatment. At least 4 consecutive weeks of treatment, during which the patient has had<br />an adequate dose for at least 3 weeks<br />Medication intolerance. Inability to achieve or maintain an adequate therapeutic dose of an antidepressant drug due to idiosyncratic reactions or side effects.<br />Steps in management:<br />1. Proper assessment including history, PE, Investigations to ensure proper diagnosis was made<br />2. Rule out psychiatric and medical co morbidities<br />3. Ascertain treatments already tried including tolerance, effectiveness, adequate dose, and length of treatment (at least 4<br />weeks) with particular attention to compliance, ongoing substance use, at all points consider the patient’s preference<br />4. The preferred method is switching to a different monotherapy, particularly to a medication in another class (benefits of<br />monotherapy include reduced cost, reduced drug interactions, better adherence)<br />5. Consider augmentation with Li, T3, buspirone, atypical antipsychotic, a psychostimulants, or a combination strategy<br />with another antidepressant with a different mechanism of action<br />6. Consider that the impact of pharmacological interventions may have been adversely affected by a poor therapeutic<br />alliance, low social support, life stress, chronic adversity, and cognitive or personality factors, for which one must<br />consider the use of depression-focused psychotherapies such as IPT and CBT<br />7. Consider ECT

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OD -- suicide Risk

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Differentiate parasuicidal Behaviour from suicidal intent.<br>• Interpersonal stress. Suicide attempters report five particular events significantly more frequently than controls: serious arguments with the spouse, having a new person in the home, serious illness of a family member, serious personal physical illness, and having to appear as a defendant in court. When event categories are examined, suicide attempters have more undesirable exit-and-entrance events (e.g., birth, marriage) and interpersonal arguments than controls.<br>• Attempters are often immature, egocentric, anxious, dependent, hostile, impulsive, and have difficulties in relationships.<br>• There are seven main items that may be helpful in identifying the patient at risk of making another suicide attempt: problems with alcohol, antisocial personality disorder, impulsivity, previous inpatient psychiatric treatment, previous outpatient psychiatric treatment, previous attempt that led to admission, and living alone.<br>• Follow-up studies show that factors associated with subsequent suicide include male gender, older age in women, being unemployed or retired; being separated, divorced, or widowed; living alone; having poor physical health; having received medical treatment within the last 6 months; having a psychiatric disorder, including alcoholism; having made many previous attempts by violent methods; the presence of a suicide note; and a history of previous attempts. A subgroup of suicide attempters who have severe personality disorder and interpersonal conflicts, and who often had alcohol or other substance dependence, commit suicide while acutely depressed.<br>

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Suicide -- personal / social correlates

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The psychiatric and social risk factors for suicide include a<br>. The immediate post discharge period is a time of increased risk. However, these risk factors identify too many false-positive and<br>false-negative patients to be useful in the long-range prediction of suicide.

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Li -- 5 tests for female patient

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• Common lithium pretreatment tests include serum electrolytes, BUN serum creatinine, urinalysis, thyroid function tests (TFTs) (e.g., TSH, T4, T3RU), and an ECG. Glucose and calcium were not listed in K+S but might be helpful because lithium can increase glc levels and can sometimes cause hyperparathyroidism.<br>• In patients with a history suggestive of possible kidney problems, a 24-hour urine test for creatinine and protein clearance is recommended, although some clinicians routinely order this test in patients about to begin lithium therapy.<br>• Some have argued that antithyroid antibody testing is helpful in assessing the potential of lithium-induced hypothyroidism.<br>• Because of the potential cardiac teratogenicity of lithium, a pregnancy test in potentially childbearing women should be ordered.<br>• Common initial: gastrointestinal discomfort, nausea, vertigo, muscle weakness and dazed feeling<br>• Common and persistent: fine tremor of hands, fatigue, thirst, polyuria, weight gain and nephrogenic diabetes insipidus<br>• Less common: acne and alopecia, hypothyroidism, hyperthyroidism, hyperparathyroidism, renal toxicity, ventricular arrhythmias, seizures with toxic levels<br>• Prodromal toxic signs: fatigue, muscular weakness, in coordination, drowsiness, coarse tremors, diarrhea, and vomiting<br>• Alternatives: valproic acid, atypical antipsychotics, carbamazepine<br>• Drug interactions: they should tell their doctor that they are on lithium if a new medication is going to be started because Li interacts with many medications, they should avoid NSAIDs (or monitor Li levels closely) because these can increase Li levels, they should avoid drinking large amounts of caffeinated beverages because caffeine can decrease Li levels, excessive salt intake can decrease Li levels and too little salt in diet can lead to Li toxicity.

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Alexithymia. Defn and How does it relate to the chronic pain patient?

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Alexithymia: Inability or difficulty in describing or being aware of one's emotions or moods; or elaboration of fantasies associated with depression, substance abuse, and posttraumatic stress disorder. (K&amp;S def’n)<br>I) Difficulty identifying feelings and distinguishing between feelings and bodily sensations of emotional arousal.<br>II) Difficulty describing feelings to other people.<br>III) Constricted, imaginal processes as evidenced by a paucity of fantasies and<br>IV) Astimulusboundexternallyorientedcognitivestyle.<br>Alexithymia is difficulty identifying, describing, and differentiating between feelings or distinguishing between feelings and physical sensations. Alexithymic individuals often have constricted imaginations and fantasies, are preoccupied with objects and events in the outside world, and have a limited private, personal internal life. When distressed, these patients are simply aware of not feeling well and usually complain of somatic symptoms, leading to frustrating interactions with their physicians who are unable to find physical causes for the presenting physical complaints. Some view Alexithymia as a condition in which affect is communicated through somatic language.

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PMS -- 10 clinical,

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Physical: (progestin deficiency and estrogen excess)<br><br><br><br>3. Breast tenderness, 5. Abdominal bloating,<br>Psychological:<br>2.lower abdominal pain including cramps, 4.headache,<br>6.fatigue,<br><br>12. Libido change, 13.fatigue, 14.suicidal ideation, 15.tension<br>Booklet also includes:<br>16. Unreality 17.vertigo 18.syncope 19.parasthesia 20.nausea/vomiting 21. Enuresis, urinary retention 23.glaucoma, increased capillary fragility 24. Poor concentration

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aging -- define and 5 possible losses

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Ageing: to grow old, to gradually develop changes in structure that are not due to preventable disease or trauma and that are associated with decreased functional capacity and an increased probability of death.<br>• Alienation: a condition characterized by lack of meaningful relationships with others, sometimes resulting in depersonalization and estrangement from others. Also defined by Eriksson and others as the feeling that one’s life has no meaning, that the human and natural world around one is impersonal, mechanistic, and unsympathetic<br>Losses suffered in ageing (role transitions):<br>1. Loss of identity 2.loss of status 3.loss of work/loss of income 4.loss of spouse<br>5. Loss of health 6.loss of independence 7.loss of supports/social network<br>Predictors of poor adjustment:<br>1. involuntary or unexpected retirement<br>2. low SES<br>3. health problems<br>4. competitive and highly achievement oriented personality (A type behavior pattern)<br>5. inability to set future goals<br>6. general difficulty in adjusting to change<br>Recent studies controlling for health status at retirement have failed to reveal any association between retirement and mortality

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MDE and epilepsy

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a) Epidemiology<br>• &gt;75% have first seizure before age 18<br>• 12 to 20% have positive family history of epilepsy60 to 70% of adult have a temporal focus Specifically for depression:<br>• 25% of all those with epilepsy and 50% with complex partial seizures have depression, psychosis, personality, hyposexuality.<br>• These problems are equally divided between ictal/periictal and Interictal<br>• Prevalence of depression in patients with epilepsy is 7.5 to 34%.<br>• Those with complex partial and poor seizure control more likely to suffer from mood d/o.<br>• Greater incidence of ideational orientation, self-criticism, and depression among epilepsy patients with a Lt<br>temporal focus.<br>• Depression is 2X as common in epilepsy patients as in comparably disabled populations.<br>• Most have a chronic Interictal depression or Dysthymia, frequently have accompanying psychotic symptoms.<br>• Patients with alternating depression experience relief with a seizure or ECT<br>• Rare occurrence of ictal depression may not only outlast the actual ictus but may lead to suicide.<br>• Episodic mood disturbances often with agitation, suicidal behavior, and psychotic symptoms occur with increasing<br>seizure activity.<br>• Postictal depression is common and a prolonged depressive state occasionally follows complex partial seizures even<br>when ictal experiences do not include depression.<br>• Mood d/o due to epilepsy with manic features or with mixed features is much rarer than mood d/o due to epilepsy<br>with depressive features or with major depressive-like features.<br>• Although a Rt temporal focus was suggested as the source of mania in epilepsy, this laterality has not been<br>established.<br>Suicide:<br>• Risk of completed suicide in epilepsy patients is 4 to 5X greater than among the general nonepileptic population. Those with complex partial of temporal lob origin have particularly high risk of up to 25X greater<br>• This increased risk of suicide continues even long after temporal lobectomy and successful control of seizures<br>• Most suicidal behavior among epilepsy patients not directly caused by reactions to psychosocial stressors of having<br>a seizure d/o but because of psychosis.<br>• Contributors to successful suicide include paranoid hallucinations, agitated compunction to kill self, and occasional<br><br><br>Depression/depressive symptoms can occur at all stages:<br>• Ictal: ictal depression has extended days or longer after the seizure has passed<br>• Periictal: before (prodromal and after (postictal) seizures as well as during intermittent seizure activity<br>• Some experience prodromal symptoms of irritability, depression, headache, confusion that lasts 10 min to 3<br>days, are continuous.<br>• Postictal: depression is common<br>• Interictal: depression can occur

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Rapid cycling BAD -- Definition, comorbidity and management

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• At least 4 episodes of a mood disturbance in the previous 12 months that meet criteria for a major depressive, manic, mixed, or hypomanic episode<br>• Episodes are demarcated either by partial or full remission for at least 2 months or a switch to an episode of opposite polarity<br>• Exclude episodes directly caused by a substance or a GMC<br>• Assess and treat hypothyroidism, drug/alcohol abuse, medication induced rapid cycling (particularly antidepressant),<br>• consider borderline personality disorder<br>• Valproate is superior to Li or carbamazepine<br>• First line acute treatment of depressive episodes in rapid cycling: Li or Valproate or lamotrigine or a combination of<br>these; antidepressants may worsen cycling and not help depression

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BAD -- med nonadhere, strategies

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1. Denial and lack of insight into the illness<br>2. Adverse effects of medications<br>3. Dislike of having medication control their moods<br>4. Dislike of the idea of having a chronic illness<br>5. Aversion to feeling depressed – more ego-syntonic attachment to hypomania 6. Substance abuse<br>7. Co-morbid d/o including personality d/o<br>8. Multiple daily dosing/complicated dosing schedules<br>Strategies:<br>1. Psychoeducation regarding nature of illness<br>2 Psychoeducation regarding medications – how they work and their side effects/benefits<br>3. Minimize adverse effects by starting low and titrating slowly, close monitoring<br>4. Simple medication regimen<br>5. Individual psychotherapy to increase insight<br>6. Dealing with the feelings of shame, guilt, and loss associated with the behavior that took place during manic<br>episode<br>7. Reduce psychic discontinuity – (i.e.) manic self split off from Euthymic self – by using videotapes or audiotapes<br>of the patient during the manic episode to help them integrate that aspect of themselves into the illness and<br>overcome their denial<br>8. Enlist family<br>9. Collaborate with patient 10. ACT team

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ECT -- 5 circumstances consider in severe MDE

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• Acutely suicidal<br>• Not responsive to multiple trials of meds (i.e. refractory)<br>• Pregnancy<br>• Medically compromised patient<br>• Patient preference<br>• Psychotic depression<br>• Severe physical/mental deterioration<br>

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MDD -- Name 3 standardized scales for the evaluation of mood symptoms AND how use

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• HAM-D: to monitor severity of depression focuses on somatic Sx. Completed by examiner based on patient interview or observation. Good to excellent reliability and good validity; used experimentally to evaluate the change in response to Rx.<br>• BDI: To rate severity of depression; focuses on behavioural and cognitive Sx. Main use = outcome measure in clinical trials of interventions. Not suitable for diagnosis. Rated by patient.<br>• Zung Self-Rating Depression Scale: covers broad range of depressive Sx. Self rated; Gives measure of severity; Used to follow Rx response.<br>• Geriatric Depression Scale: For severity of depression. Does not emphasise the vegetative symptoms of depression.

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Steps after pt suicide

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• Pronounce patient dead<br>• Complete death certificate.<br>• Call the coroner’s office<br>• Contact patient’s family<br>• Obtain a statement from each member of staff. • Provide support for other patients and staff<br>• Inform hospital director/chief of staff<br>• Arrange Morbidity&amp; Mortality rounds<br>• Alter practice/policy if necessary

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CBT -- basic premise and technique in Tx MDE

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 Basic premise is that distorted beliefs re-self, the world and the future maintain the depressive affect.<br> The technique is that of changing the patient’s automatic and maladaptive ways of thinking. Patient first<br>becomes aware of his thinking style, and then learns to respond in a more adaptive ways.  Typical course is 12-16 sessions, divided into 3 phases:<br>1.Early (1-4): Establish therapeutic relationship with patient; educate re-cognitive model and the influences on emotion; setting goals; eliciting and evaluating automatic thoughts.<br>2.Middle (5-12): Identify dysfunctional beliefs and patient’s compensatory strategies; identify core beliefs; practice skills at responding to depressogenic views.<br>3.Late (13-15): Preparation for termination; predicting high risk situations relevant to relapse; consolidating learning through self-treatment tasks.<br> Behavioral techniques incorporated throughout the therapy e.g. monitoring activities and rating the degree of satisfaction; setting homework in the form of increasing pleasurable activities; problem solving; self control training. Many studies (unfortunately!!) show CBT to be as effective as pharmacotherapy on the treatment of MDD.<br>Outline the basic premise of CBT and its techniques in the treatment of MDD.<br>• Cognitive theory posits that the way individuals interpret experience determines how they feel and behave,<br>and that biased information processing causes distorted interpretations.<br>• Specific psychiatric disorders are associated with characteristic cognitive distortions biases that result from<br>and contribute to impaired corrective function of higher-level cognitive processes. For example, in depression, people see themselves, their experiences and their futures in negatively biased ways, which in turn sustains or magnifies depressive symptomatology<br>• Cognitive behavioural therapy employs a combination of verbal interventions and Behaviour modification techniques designed to help the patient identify their dysfunctional cognitions, test whether they are based on logic and reality, and correct the distorted conceptualizations and dysfunctional thinking<br>Principles of therapy<br>Therapeutic relationship: Therapist functions as guide, coach, catalyst to promote corrective experiences outside of therapy. Style is genuine warmth and non-judgmental acceptance. Therapist's verbal statements are in the form of questions, reflecting the basic empirical orientation and the immediate goal of converting the patient's closed belief system into an open system. Case conceptualization: Formulation to identify person's core dysfunctional beliefs<br>Structure of therapy program<br>Behavioural techniques: Obtaining a completed daily schedule of activities form to get info re: baseline activity.<br>This report forms the basis by which the therapist and patient design and schedule homework. Scheduling of activities that help to mobilize the patient and help to counteract the inertia often present in depressed patients. Graded task experiences. Testing dysfunctional beliefs.<br>Cognitive techniques. When the patient is already active, more purely cognitive procedures may be used. Patients track &quot;automatic thoughts&quot;, particularly those that precede or follow negative affects. Fill out thought records. Objectively evaluate evidence for certain thoughts - reality testing. Help patients to identify the impact of particular core beliefs on their automatic thoughts and feelings<br>Homework. The design of appropriate homework assignments to test specific dysfunctional notions The cognitive triad:<br>Depression entails the activation of 3 major cognitive patterns that lead to individual patients viewing Themselves, Their experiences, their future, in negative biased ways. Motivation and behavioural symptoms of depression are derived from, maintained or exacerbated by negative cognitive patterns

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MDE -- relation to epilepsy

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• Most patients with epilepsy have chronic Interictal depression or Dysthymia.<br>• The experience of psychic auras, esp. those with cognitive content, may predispose to Interictal depression.<br>• Seizure often brings temporary relief of depression.<br>• Depression may be caused by the epilepsy (? Due to altered receptor sensitivity; kindling; Interictal<br>hypometabolism; down-regulation of associated areas.<br>• Complex partial seizures, esp. those in temporal lobe and those with a left sided focus are most associated<br>with depression.<br>• Poorly controlled seizures -&gt; increased incidence of depression<br>• Epilepsy can -&gt; learned helplessness, low self-esteem, weak defense mechanisms.<br>• Reaction to the illness: grief at loss of function, increased dependence, altered status.

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MDE -- 4 ways may be linked to physical illness

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• Depression may be secondary to the illness itself (e.g. hypothyroidism,CNS tumors)<br>• May be precipitated by diagnosis e.g. HIV, Cancer<br>• May be a result of effects of illness on quality of life (loss of function; of one’s role; shortened life<br>expectancy)<br>• May be result of treatment (e.g. steroids; narcotics; chemotx agents)<br>• Depression impacts on patient’s self-care e.g. patient no longer care enough to accept treatment or lose<br>insight.<br>• Depression can make it more difficult to cope with physical illness<br>• Depression increases time to recovery and length of stay in hospital

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Deep Sleep Treatment or Modified Narcosis

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This involved knocking the individual unconscious for a period of days or weeks, using Massive doses of psychiatric drugs, usually sedatives and/or barbiturates. Sometimes, daily electroshock treatment accompanied it. In the 1920s, it had a 4.8% mortality rate. During WWII narcosis was employed on a large scale for acute battle neuroses.59 the treatment carries with it grave risks, including pneumonia, blood clotting, cardio-respiratory problems and brain damage. The American Handbook of Psychiatry states that the results of the therapy were unpredictable, at best empirical, and the procedure was not without risks.60In Australia, deep sleep treatment was banned in 1983 because of its high death rate; in one private psychiatric hospital, 48 patients were killed as a result of the procedure. Manslaughter charges were eventually laid against several of the psychiatrists who administered it.

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Psychosurgery -- indications / contra

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Major depressive disorder and obsessive-compulsive disorder. In evaluating candidates several factors are considered:<br>1. Primary diagnosis. The patient must meet clinical criteria for the diagnostic indication, and this disorder should be a primary Cause of the patient's illness.<br>2. Severity. The patient must have chronic, severe, and debilitating illness; duration of the primary illness must exceed 1 year and typically Exceeds 5 years. Severity is gauged on standardized instruments (e.g., patients with obsessive-compulsive disorder typically have Yale-Brown Obsessive-Compulsive Scale scores of 25 or above; patients with depression typically have Beck Depression Inventory scores of 30 or above), while debility should be indicated by a low level of functioning (e.g., a Global Assessment of Functioning score &lt; 50) and a poor quality of life.<br>3. Adequacy of previous treatment. Patients must have already undergone an exhaustive array of other available treatments.<br>(RESISTANT TO OTHER TREATMENTS)<br>4. Psychiatric comorbidity. Appropriate treatment must have been rendered for any comorbid psychiatric disorder; the presence of psychoactive substance use or personality disorders are considered strong relative contraindications.<br>5. Medical comorbidity and surgical fitness. Structural brain lesions or significant central nervous system injuries are strong contraindications. Medical conditions that increase neurosurgical risks (e.g., cardiopulmonary disease) and age above 65 years are relative contraindications. A history of Past seizures are a risk factor for perioperative seizures and must be weighed in the overall risk-benefit assessment.<br>6. Access to postoperative care. Patients must have access to adequate postoperative care, including a psychiatrist (typically the referring physician) who will accept responsibility for managing them after discharge. Arrangements for postoperative care (e.g., intensive behavior therapy) should be confirmed ahead of time. Informed consent. Under no circumstances should psychiatric neurosurgery be performed on patients against their will.

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MDE vs uncomplicated bereavement

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Bereaved individual typically regards depressed mood as “normal” Certain symptoms not characteristic of a normal grief reaction include:<br>• Guilt about things other than actions taken or not taken at time of the death<br>• Thoughts of death other than the survivor feeling that he or she would be better off dead or should have died<br>with deceased person<br>• Morbid preoccupation with worthlessness<br>• Marked psychomotor retardation<br>• Prolonged and marked functional impairment<br>• Hallucinatory experiences other than thinking that he or she hears the voice of, or transiently sees the image<br>of, the deceased person

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MDE -- RF post-retirement

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When pre-retirement mental and physical health controlled for, there is no clear association between<br>retirement and subsequent mental and physical problems. However, factors that predict poor adjustment to retirement include:<br>• Involuntary or unexpected retirement<br>• Low socioeconomic status<br>• Health problems<br>• High achievement oriented personality<br>• Inability to set future goals<br>• General difficulty adjusting to change

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Possible psychological sequelae induced abortion

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Most women who undergo termination (particularly before 12th week) do not suffer significant psychological sequelae.<br>Second trimester abortions more psychologically traumatic than first trimester abortions because child often wanted (i.e. Pregnancy is being Terminated because of chromosomal abnormality)<br>NB. There was an article in CMAJ this year purporting an association between abortion and subsequent psychiatric hospitalization but this Study was criticized for methodological flaws.<br>Short note on postpartum blues:<br>CANMAT guidelines: onset 2-7 days post-delivery, self-remitting (usually within 2 weeks), occurs in 25-85% of new mothers, symptoms include tearfulness, fatigue, anxiety, sadness, treated with support and reassurance FATS

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Pregnancy -- psych aspects

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All psychiatric disorders can occur during pregnancy, it does not have a protective effect. Women are as likely to have first onset of a mental illness, and to have a recurrence of depression, mania or psychosis if they discontinue meds and they are at risk of having a post-partum illness. Therefore, the issue of discontinuing meds during pregnancy needs to be balanced carefully against the risk of doing so. Conversely, continuing meds is associated with some (albeit small for most meds) risk and the Woman needs to be fully informed about such risks so she can make an informed decision. Reaction to pregnancy range from Joy to fear, anxiety, resentment re loss of former way of life, concerns re finances, already having too many children. Such issues may be accentuated when the pregnancy was not planned. Support from the partner very important. Women often report feeling more in need of emotional support and reassurance during pregnancy. Primiparous women are more Concerned about the pain of childbirth, their ability to cope and getting pregnant again. Multips are more concerned about the Ability to care for the family, having more children than desired and contraception. Needless to say psychiatric complaints are More common in younger (&lt;20), single women with unplanned/unwanted pregnancies. A correlation between depression during pregnancy and fetal development has been noted. Teenage mothers are at increased risk for suicide. Rates of depression appear to be similar for pregnant and for non-pregnant women. During pregnancy approx 20% of women have some depressive symptomatology; and 10% develop an MDE.<br />Assessment of major depression during preg can be complicated by a failure to diagnose medical complications such as anemia, gestational diabetes, or autoimmune thyroiditis. Women with a hx of prior sexual abuse have higher levels of depression during pregnancy compared to women with no such hx. Also important risk factors include prior hx of dep, younger age, and limited social support, living alone, greater no. of children, and ambivalence about preg, negative life events and low SES<br><br>Recommendations for tx of depression during pregnancy<br>• First line:fluoxetine<br>• Second line; Citalopram, fluvoxamine, Paroxetine or sertraline<br>• Third line; TCAs, ECT, IPT<br>Pica: repeated ingestion of nonnutritive substances such as dirt, clay, starch, sand, and feces; seen in pregnant females in some subcultures, most notably among African-Americans in rural south, where eating of clay or starch (for example Argo) is common.<br>False pregnancy “pseudocyesis” is a rare condition; signs and symptoms of pregnancy include abdominal distension, breast enlargement and pigmentation, cessation of menses, morning sickness; negative results often result in reduction of symptoms when communicated to patient; Treatment in concert with patient’s ob/gyn/primary care physician; reality-based supportive psychotherapy is the treatment of choice; some respond to antipsychotics if continue to believe one is pregnant<br>Lithium and anticonvulsants (fetal cranio facial and neural tube defects in &lt;10%) some of most teratogenic drugs. Antidep/antipsych/anxiolytics are less clearly associated with birth defects, but should avoid if possible. Administration of psychoactive drugs at or near delivery may cause baby to be overly sedated at delivery, to need a respirator, or be physically dependent on the drug and require detoxification and treatment of a withdrawal Syndrome. Virtually all psychotropic drugs secreted in breast milk

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Li -- 5 classes meds alternative

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Medications used for Anti-Manic Prophylaxis:<br>1. Li (best evidence)<br>2. Valproic acid (modest evidence)<br>3. Alternatives: lamotrigine or carbamazepine (see #7) or Oxcarbazepine<br>4. If treated with atypical antipsychotic during preceding acute episode, antipsychotic should be discontinued unless required for control of persistent psychosis or prophylaxis against recurrence.<br>5. Maintenance therapy with atypical antipsychotic may be considered, “there is definite evidence...comparable to Li or Valproate.” 2003 study: suggests olanzapine effective in preventing relapse of mania (not depression); evidence now for atypicals<br>6. Antipsychotics: atypicals: Olanzapine, risperidone Clozapine; typical: CPZ, haloperidol, Pimozide<br>7. Carbamazepine: Five small RCTs initially suggested equivalence to Li in prophylaxis but two large recent RCTs suggested Li better; now felt too many SE, not use unless tried everything else<br>8. Calcium-channel blockers: Verapamil (some studies indicate that it may be less effective than Li)<br>9. Benzos: clonazepam, Lorazepam (best evidence is as an adjunct to treat agitation)<br>Clonidine may be effective for acute treatment, not prophylaxis<br>Thyroid hormone – unclear evidence; may be useful in rapid cycling

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Preg -- 3 physiological change and how may affect meds????

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Three pharmacodynamic/kinetic changes in pregnancy?<br>a. increased volume of distribution (changes in fat distribution)<br>b. increased blood volume<br>c. increased GFR<br>d. change in hepatic metabolism

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MDE -- perimenopausal factors

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Four causes of Perimenopausal depression:<br>a. hormonal changes (decreased estrogen, increased progesterone)<br>b. cultural pressure favoring younger women<br>c. sudden recognition of aging<br>d. decreased sleep

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MDE -- postpartum psychotic, DDx, Ax and competence to care

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Diagnosis:<br>• The Specifier “with post-partum onset” is used if there is onset of a depressive, manic, or mixed episode within four weeks of delivery; the Specifier can also be used for brief psychotic disorder.<br>• post-partum mood episodes with psychotic features occur in 0.1% to 0.2% of deliveries<br>• risk factors include: primiparity, prior mood disorder (especially bipolar disorder I); once a<br>woman has had a post-partum depression with psychotic features, the risk of recurrence with<br>subsequent pregnancies is 50%<br>• symptoms usually manifest within two weeks of delivery; there is a second peak 1 to 3<br>months after delivery<br>• the peak age of onset is 25 to 35<br>Differential Diagnosis:<br>• psychotic disorder due to a general medical condition (such as hypothyroidism, Cushing’s syndrome)<br>• substance induced psychotic disorder (such as secondary to pain medications)<br>• mood disorders with post-partum onset (major depressive disorder, bipolar disorder I, bipolar<br>disorder II)<br>• brief psychotic disorder<br>• post-partum blues (occur in up to 38-80% of women following childbirth)<br>Management:<br>• this is a psychiatric emergency<br>• the treatment of choice is antidepressants and lithium, sometimes along with an antipsychotic<br>1. Post-partum psychosis usually merits hospitalization, because of the level of dysfunction and high risk of suicide (5%) and infanticide (4%)<br>2. ECT may be needed for medication refractory cases<br>• Suicidal patients without psychosis may also require admission.<br>• The mother is usually helped by contact with the infant, but this should be closely monitored,<br>especially if the mother is preoccupied with thoughts of harming the infant.<br>• psychoeducation for the family, and supportive outreach and education for the father are also<br>helpful<br>• after the acute episode, psychotherapy addressing failure and guilt is helpful; group therapy<br>may be particularly helpful<br>Competence to care for newborn:<br>• assessment of competence requires collateral information<br>• the interactions between the child and mother should be observed while closely supervised<br>• the content of the psychotic material is important:<br>1. infanticide is most often associated with command hallucinations to kill the infant, or with delusions that the infant is possessed<br>2. however, it can occur without such specific hallucinations or delusions<br>• suicidal ideation should also be considered in assessment of competence to care for the<br>newborn

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MDE -- preg counselling re risks

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) What are four risks to herself or to the fetus as a result of developing a depressive episode?<br>Four risks as a result of developing a depressive episode (assuming it means during the pregnancy):<br>Risks to mother – Inadequate prenatal care, poor nutrition, obstetrical complications, postpartum depression, and increased risk of alcohol and substance abuse. Must also consider risks of suicide, psychosis.<br>Risks to fetus – lower birth weight, neonatal distress, and prematurity, possible consequences of<br>substance abuse.<br>b) What are four reasons why she is at higher risk for developing post-partum depression?<br>Four reasons why this woman is at higher risk for PPD: previous episode of depression, family history<br>of mood disorder, mood symptoms during the pregnancy, chronic stressors (assuming this unplanned pregnancy is a stressor); other risk factors for PPD, include inadequate social support, low SES, depression and high EE in partner, and previous PPD

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MDE -- breastfeeding counselling

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If pt wishes to breastfeed: Before jumping to breastfeeding, I would discuss with her the above, her risk for PPD, and possible treatment options. I would suggest close follow up. During the pregnancy, Psychoeducation and enhanced social supports might be enough to stay off a depressive episode. If she becomes depressed during the pregnancy, I would review options e.g. Psychotherapy (IPT perhaps best, CBT may be effective) and antidepressants, and help her do risk/benefit analysis. If she remains well during the pregnancy, I would continue close follow-up given her risk for PPD. Some evidence shows that women at risk for PPD may benefit from counseling enhanced social support and education prior to delivery. There is also evidence of the prophylactic benefits of antidepressants in women with a prior PPD. If she becomes depressed, again review tx options, with some evidence for IPT and CBT in post-partum period. Full informed consent is imperative. As a general principle, I would encourage breastfeeding for its many benefits. If pt chooses treatment with an antidepressant and wishes to breastfeed, I would choose Sertraline or Paroxetine. Review with her the state of info – no RCTs, but follow up studies do not show any negative effects, and studies of mother-infant nursing pairs reveal very low to undetectable serum drug levels in the infants. Consider partial breast feeding, with restriction to times when the dose of drug in the breast milk is likely lowest, with pump-and-dump method (requires very motivated mother). Facilitate her connecting with Mother Risk by phone to hear info from them. Review in general pros and cons of breast vs. bottle feeding. NB in other remembered versions of this question, pt is already on Paxil when she comes to you for the consult, so also need to include risks of worsening/relapse with discontinuation.

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VPA -- birth defects

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Birth defects with VPA: (K and S)<br>From CPS:<br>Neural tube defects 1-4 %<br>Congenital heart malformations (doesn’t specify which)<br>Cleft lip and or palate<br>Craniofacial abnormalities<br>Skeletal malformations and growth retardation in monkeys with Epival<br>• birth defects caused by Valproate:<br>• spina bifida and neural tube defects.......11%<br>• cleft lip / palate<br>• cerebral hemorrhage<br>• IUGR<br>• Developmental delay<br>• digital malformation<br>• cardiac abnormalities<br>• highest risk is still within the 1st trimester<br>• folic acid 1 to 4mg daily<br><br>Folic acid to decrease risk of neural tube defects. Also some evidence it decreases risk of cardiac anomalies in some at-risk patients. If family hx of ntd’s 4-5 mg per day, also if pt on VPA. 0.4 mg/day found to be adequate for pts with no family hx or medication risks for ntd’s.

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MDE - postpartum w/ psych, counsel GP re Ax and Tx

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a. Post-partum psychosis nearly always warrants hospitalization, due to the risk of suicide (5%) and infanticide (4%)<br>b. assessment of competence to care for the newborn:<br>i. get collateral information<br>ii. observe interactions between the mother and the infant<br>iii. review content of psychotic material (especially for command hallucinations, or<br>delusions that the infant is possessed)<br>iv. review suicidal ideation

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MDE in preg -- What is the risk for post-partum psychosis? How is post-partum psychosis managed? Discuss breastfeeding and antidepressants.

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a. the risk of post-partum blues is 38-80%, post-p depression 10 to 20%, and post-p psychosis 1- 2 per 1000<br>i. post-partum blues: usually starts 3 to 10 days after delivery, and resolves by two weeks; risk factors include a history of PMDD, primiparity, or past depression or family history of depression<br>ii. post-partum psychosis usually presents within the first two weeks, but can also present 1 to 3 months after pregnancy; often heralded by worsening insomnia<br>1. risk increases to 20 to 25% who has had a past depression unrelated to pregnancy<br>2. risk of recurrence with future pregnancies is 30 to 50%<br>3. the risk of infanticide is 4%, and is correlated with the severity of psychotic<br>symptoms<br>iii. post-partum depression develops more insidiously, often three or more weeks after<br>delivery<br>1. risk increases up to 40% in women who had a past depression; risk of<br>recurrence is 50%<br>b. To minimize the risk: reduce environmental stress, mobilize additional resources, educate<br>about “normal” post-partum blues, and monitor closely.<br>c. management of post-partum syndromes<br>i. post-partum blues: mild and transitory; observe or use short-acting sedatives; take complaints seriously and offer support<br>ii. post-partum depression: serotonergic antidepressants<br>iii. post-partum psychosis: usually merits hospitalization; antipsychotics, lithium (with<br>antidepressant), or ECT are all helpful<br>d. remember to screen for thyroid abnormalities (post-partum, there is a dramatic reduction in<br>blood flow to the anterior pituitary; in rare cases, this can cause anterior pituitary necrosis, or<br>Sheehan’s syndrome)<br>e. psychotropic medications and breast-feeding<br>i. lithium: present in breast milk at 30 to 50%; breast feeding is contraindicated<br>ii. Carbamazepine and Valproate: considered compatible with breast-feeding; watch for<br>neonatal Hepatotoxicity with Valproate<br>iii. benzodiazepines: in general discouraged; however, there may be a role for<br>intermittent use of short acting agents with no active metabolites (such as Lorazepam)<br>iv. Fluoxetine and Sertraline: considered okay<br>v. Nortriptyline, desipramine (secondary amines) and imipramine (tertiary amine): generally okay; minimize exposure by taking antidepressant immediately after breast feeding prior to infants longest period of sleep<br>vi. antipsychotics: breast feeding should be avoided

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Postpartum psychosis -- mgt

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a. in nearly all cases, post-partum psychosis necessitates hospitalization, because of the high risk<br>of suicide 5% and infanticide 4%<br>b. post-partum psychosis most often has a significant mood component; treatment options<br>typically include lithium, low-dose antipsychotics, or ECT<br>c. note that lithium is expressed at fairly high levels in breast milk; this is less so for Olanzapine<br>(one study showed minimal olanzapine in breast milk of nursing mothers with post-partum<br>psychosis, and no noted adverse effects on the infant)

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BAD vs BPD

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COMPARISON OF BPD AND BIPOLAR II DISORDER<br><br>Trait<br><br>BPD<br><br><br>Bipolar II<br>Mood lability/impulsivity<br><br>Due to interpersonal sensitivity<br>Autonomous and persistent (person acts out)<br><br>Collections of all short assays 151<br><br><br><br><br><br>Affect<br>Deep, intense; evoke strong empathic response<br><br>Lack depth, pain; hard to empathize with<br><br>Protoypical behaviour<br>Care seeking; seeks exclusivity, is sensitive to rejection<br>Begins energetic self-initiated activities that are left incomplete; requiring others to clean up<br>Defense<br><br><br>Splitting; polarizes realities and, if challenged, becomes angry at challenger or changes to opposite view<br><br>Denial; ignores undesirable realities and, if confronted with a reality, denies its emotional significance

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BAD -- RF in depr adolescents

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∙ Family history of bipolar disorder<br>∙ Depression with psychotic symptoms<br>∙ Prior history of switch to mania with antidepressants<br>∙ Sudden onset of symptoms<br>∙ Psychomotor retardation<br>∙ Atypical depression

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Mania -- organic ddx 5

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• Neurological disorders<br>o Huntington's, postencephalitic Parkinson's, Wilson's<br>• CNS infections<br>o encephalitis<br>• Multiple CNS conditions<br>o Neoplasm, trauma, multiple sclerosis, stroke, temporal lobe epilepsy<br>• Systemic illnesses<br>o Uremia, dialysis dementia, hyperthyroidism, pellagra, carcinoid syndrome<br>• Drugs<br>o Amphetamines, cocaine, corticosteroids, cyclosporine, opioid, PCP, yohimbine...

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Suicide -- steps after

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∙ Go to the unit where the patient has died to gather information re: what happened, review chart<br>∙ Notify next of kin, explain what has happened, be available to speak to them in person<br>∘ Offer consolation, ask how can be helpful, be non-defensive<br>∙ Call the coroner (patient died in hospital)<br>∙ Speak with the staff on the unit - offer support, debriefing as needed<br>∙ Consider meeting to inform other patients on the unit of what has occurred, address feelings with patients individually or in a group as indicated

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MDE CBT -- premise and technique

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• Cognitive theory posits that the way individuals interpret experience determines how they feel and behave, and that biased information processing causes distorted interpretations<br>• Specific psychiatric disorders are associated with characteristic cognitive distortions biases that result from and contribute to impaired corrective function of higher level cognitive processes<br>o For example, in depression, people see themselves, their experiences and their futures in negatively biased ways, which in turn sustains or magnifies depressive symptomatology<br>• Cognitive behavioural therapy employs a combination of verbal interventions and behavioural modification techniques designed to help the patient identify their dysfunctional cognitions, test whether they are based on logic and reality, and correct the distorted conceptualizations and dysfunctional thinking<br>• Principles of therapy<br>o Therapeutic relationship<br>− Therapist functions as guide, coach, catalyst to promote corrective experiences outside of therapy<br>− Style is genuine warmth and non-judgmental acceptance<br>− Therapist's verbal statements are in the form of questions, reflecting the basic<br>empirical orientation and the immediate goal of converting the patient's closed belief<br>system into an open system<br>o Case conceptualization<br>− Formulation to identify person's core dysfunctional beliefs • Structure of therapy program<br>o Behavioural techniques<br>− Obtaining a completed daily schedule of activities form to get info re: baseline<br>activity<br>• This report forms the basis by which the therapist and patient design and<br>schedule homework<br>− Scheduling of activities that help to mobilize the patient and help to counteract the<br>inertia often present in depressed patients<br>− Graded task experiences<br>− Testing dysfunctional beliefs<br>o Cognitive techniques<br>− When the patient is already active, more purely cognitive procedures may be used<br>− Patients track &quot;automatic thoughts&quot;, particularly those that precede or follow negative<br>affects<br>• Fill out thought records<br>• Objectively evaluate evidence for certain thoughts - reality testing<br>• Help patients to identify the impact of particular core beliefs on their<br>automatic thoughts and feelings<br>o Homework<br>− The design of appropriate homework assignments to test specific dysfunctional<br>notions • The cognitive triad<br>o Depression entails the activitation of 3 major cognitive patterns that lead to individual patients viewing<br>− Themselves<br>− Their experiences<br>− Their future<br>in negative biased ways<br>o Motivation and behavioural symptoms of depression are derived from, maintained or<br>exacerbated by negative cognitive patterns

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MDE -- factors re choosing AD

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• Symptom profile (e.g. atypical, seasonal)<br>• Severity<br>• Side effect profile<br>• Previous response to a particular antidepressant<br>• Other medication<br>• Response of a first degree relative to a particular antidepressant<br>• Co morbid medical conditions

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MDE -- sleep changes

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Subjective sleep disturbance<br>Insomnia (90%) Hypersomnia<br>Disturbing dreams<br>Early morning wakenings**<br>Objective sleep disturbance<br>Abbreviated onset to REM sleep**<br>Increased REM sleep, REM density<br>Decreased slow wave sleep, shift to latter part of night Fragmented sleep<br>**phase advance

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MAOI -- Depr, irritable, social w/d -- DDx, mgt w/ MAOIs incl s/e, serotonin syndrome and hypertensive crisis

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a. differential: Axis I (mood, anxiety, psychosis), Axis II (avoidant, schizoid, schizotypal), Axis III (endocrine abnormalities), Axis IV (school or family stressors)<br />b. management depends on diagnosis; presuming that the diagnosis is depression, the treatment would be psychotherapy or antidepressant medications<br />c. dietary restriction on MAOIs<br />i. tyramine is an amino acid that is normally deactivated in the gut by monoamine<br />oxidase; when this does not happen, tyramine displaces norepinephrine and epinephrine from nerve terminals, and can cause tremendous sympathetic stimulation, resulting in a hypertensive crisis (severe headaches, nuchal rigidity, palpitations, mydriasis, diaphoresis)<br />ii. the reaction depends on the amount of tyramine ingested – 6 to 10mg will cause a mild reaction, while over 10mg will cause a severe reaction<br />iii. foods to avoid:<br />1. red wines (especially Chianti) and vermouth (white wines okay less than<br />120ml); beer should also be avoided (except possibly for some domestic)<br />2. cheese (cream cheese and cottage cheese are okay)<br />3. sausage, pepperoni, bologna, salami<br />4. smoked or preserved fish (fresh fish is okay)<br />5. miso soup, beans, bean curd<br />6. caffeine is okay in limited amounts<br />iv. with appropriate restrictions, risk of hypertensive crisis is down to about 4%; treatment involves phentolamine<br />d. in terms of drug interactions, should avoid: decongestants, Demerol, other antidepressants, stimulants<br />The following is true about MAOI’s:<br />a) dietary requirements are usually not necessary with moclobemide........T<br />[MAO-A activity returns to normal within 16-hrs of last dose of RIMA Moclobemide – tyramine-induced pressor response normalizes within 3-days of cessation of moclobemide; but are necessary if &gt;900 mg daily]<br /><br />e) f)<br />• •<br />•<br />•<br />tranylcypromine and phenelzine are non-hydrazine compounds.......False<br />[phenelzine aka. Nardil ® is derivative of hydrazine, i.e. –NHNH2<br />tranylcypromine aka. Parnate ® is non-hydrazine; structurally related to amphetamine]<br />clorgyline and selegilene do not interact with tyramine..........T<br />[clorgyline – specific inhibitor of MAO-A – therefore does not interact with tyramine Deprenyl® / Selegilene – specific inhibitor of MAO-B – therefore does interact with tyramine<br />moclobemide inhibits MAO-A and B.........F<br />[MAO-A metabolizes 5-HT, NE, DA  MAO-A inhibition believed to improve depression MAO-B metabolizes DA]<br />moclobemide is weakly protein-bound (i.e. &lt;30%) are non-sedating<br />Pargyline was the first selective MAOI to receive FDA approval. Although it proved selective for the B isoenzyme and did not require dietary restriction of tyramine intake (the gastrointestinal tract contains predominantly MAOA), it was not an effective antidepressant.<br />Selegiline is also a B inhibitor at low doses, but even at therapeutic doses in antidepressant trials, the selectivity is diminished. Despite their selectivity, both pargyline and selegiline represent examples of irreversible selective inhibitors, in contrast to moclobemide with both reversibility and selectivity.<br />Tyramine, a substrate of MAO present in significant concentrations in certain fermented foodstuffs, causes a vasopressor response, an effect dramatically accentuated in patients taking an MAOI. This response is partly due to the MAO-inhibited patient's inability to deaminate tyramine (which is normally broken down by MAOA in the gut), resulting in displacement of intracellular stores of norepinephrine. When dietary restrictions are followed, the risk of a serious hypertensive problem is curtailed.<br />At usual therapeutic doses, the cheese effect should not be a problem with the selective MAOB inhibitor selegiline, but at higher doses this drug exhibits some inhibition of MAO-A, and dietary restrictions should be followed.<br />MAOs degrade biogenic amine neurotransmitters (not GABA) Attached to outer mitochondrial membrane<br />Two types:<br />- MAO-A  metabolizes NE, 5-HT<br />- - -<br />- MAO-Bmetabolizes DA

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SSRI induced sexual dysfn -- mgt

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• stimulation of 5-HT2a receptors in the spinal cord may inhibit spinal reflexes for orgasm and ejaculation, causing sexual dysfunction<br>• 50 to 80% of patients taking SSRI’s experience some sexual dysfunction, although few complain of it<br>• management: add medication or switch to a different antidepressant<br>1. adding medications<br> bupropion<br> sildenafil (Viagra): take one hour before intercourse<br> yohimbine: alpha-2 antagonist<br> cyproheptadine: antihistamine that is also antiserotonergic<br>2. switching to medications with low rate of side-effects  bupropion<br> Mirtazepine

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MDE characteristics incr risk BAD

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a. Acute sever episode<br>b. Presence of psychotic features<br>c. Psychomotor retardation<br>d. Family history of bipolar<br>e. Antidepressant induced mania/hypomania

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Preg -- 3 physiological and effects on meds

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A. Three physiological changes (three pharmacodynamic/kinetic changes in pregnancy)?<br> change in hepatic metabolism<br>B. How they affect the use of these medications?<br> Increase in volume will lead to decrease blood levels of medication<br> Increase in GFR will increase medication clearance and in turn decrease blood level<br>concentration<br> Changes in hepatic metabolism will affect efficacy of such medications<br> increased volume of distribution (changes in fat distribution)  increased blood volume<br> increased GFR

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Peri-menopause, 3 factors contrib to depr mood

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e. hormonal changes (decreased estrogen, increased progesterone)<br>f. cultural pressure favoring younger women<br>g. sudden recognition of aging<br>h. decreased sleep

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PPD psychotic -- DDx, Ax

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Diagnosis:<br>J. the Specifier “with post-partum onset” is used if there is onset of a depressive,<br>manic, or mixed episode within four weeks of delivery; the Specifier can also be<br>used for brief psychotic disorder<br>K. post-partum mood episodes with psychotic features occur in 0.1% to 0.2% of<br>deliveries (1 in 500 to 1 in 1000)<br>L. risk factors include: primiparity, prior mood disorder (especially bipolar disorder<br>type I); once a woman has had a post-partum depression with psychotic features,<br>the risk of recurrence with subsequent pregnancies is 50%<br>M. symptoms usually manifest within two weeks of delivery; however there is a second<br>peak 1 to 3 months after delivery<br>N. the peak age of onset is 25 to 35<br>Differential Diagnosis:<br>O. psychotic disorder due to a general medical condition (such as hypothyroidism,<br>Cushing’s syndrome)<br>P. substance induced psychotic disorder (such as secondary to pain medications)<br>Q. mood disorders with post-partum onset (major depressive disorder, bipolar disorder<br>type I, bipolar disorder type II)<br>R. brief psychotic disorder<br>S. post-partum blues (occur in up to 80% of women following childbirth)<br>Management:<br>T. this is a psychiatric emergency<br>U. the treatment of choice is antidepressants and lithium, sometimes along with an antipsychotic<br>16. Post-partum psychosis usually merits hospitalization, because of the level of dysfunction and high risk of suicide (5%) and infanticide (4%)<br>17. ECT may be needed for medication refractory cases<br>V. suicidal patients without psychosis may also require admission<br>W. the mother is usually helped by contact with the infant, but this should be closely<br>monitored, especially if the mother is preoccupied with thoughts of harming the<br>infant<br>X. psychoeducation for the family, and supportive outreach and education for the<br>father are also helpful<br>Y. after the acute episode, psychotherapy addressing failure and guilt is helpful; group<br>therapy may be particularly helpful<br><br>Z. assessment of competence requires collateral information<br>AA. the interactions between the child and mother should be observed while closely<br>supervised<br>• the content of the psychotic material is important:<br>18. infanticide is most often associated with command hallucinations to kill the infant, or with<br>delusions that the infant is possessed<br>19. however, it can occur without such specific hallucinations or delusions<br>• suicidal ideation should also be considered in assessment of competence to care for the<br>newborn

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Preg and depr -- risks, PPD and breastfeed

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Four risks because of developing a depressive episode (assuming it means during the pregnancy):<br> Risks to mother<br> inadequate prenatal care,<br> poor nutrition,<br> obstetrical complications,<br> postpartum depression,<br> and increased risk of alcohol and substance abuse.<br> Risks to fetus<br> Lower birth weight,<br> neonatal distress,<br> and prematurity,<br> plus possible consequences of substance abuse.  Must also consider risks of suicide, psychosis.<br>b. What are four reasons why she is at higher risk for developing post-partum depression? Four reasons why this woman is at higher risk for PPD:<br> previousepisodeofdepression,<br> family history of mood disorder,<br> mood symptoms during the pregnancy,<br> chronic stressors (assuming this unplanned pregnancy is a stressor);<br> other risk factors for PPD, which may or may not apply in her case, include inadequate social<br>support, low SES, depression and high EE in partner, and previous PPD<br><br><br> <br><br>  <br>What do you tell her when she wants to breastfeed? If pt wishes to breastfeed:<br>Before jumping to breastfeeding, I would discuss with her the above, her risk for PPD, and possible treatment options.<br>I would suggest close follow up.<br>During the pregnancy, Psychoeducation and enhanced social supports might be enough to stay off a depressive episode.<br>If she becomes depressed during the pregnancy, I would review options eg. Psychotherapy (IPT perhaps best, CBT may be effective) and antidepressants, and help her do risk/benefit analysis.<br>If she remains well during the pregnancy, I would continue close follow-up given her risk for PPD.<br>Some evidence shows that women at risk for PPD may benefit from counseling enhanced social support and education prior to delivery.<br>There is also evidence of the prophylactic benefits of antidepressants in women with a prior PPD.<br> If she becomes depressed, again review tx options, with some evidence for IPT and CBT in post-partum period.<br> Full informed consent is imperative.<br> As a general principle, I would encourage breastfeeding for its many benefits.<br> If pt chooses treatment with an antidepressant and wishes to breastfeed, I would choose<br>Sertraline or Celexa. Review with her the state of info – no RCTs, but follow up studies do not show any negative effects, and studies of mother-infant nursing pairs reveal very low to undetectable serum drug levels in the infants.<br> Consider partial breast-feeding, with restriction to times when the dose of drug in the breast milk is likely lowest, with pump-and-dump method (requires very motivated mother).<br> Facilitate her connecting with Mother Risk by phone to hear info from them.<br> Review in general pros and cons of breast vs. bottle-feeding.<br> NB in other remembered versions of this question, pt is already on Paxil when she comes<br>to you for the consult, so also need to include risks of worsening/relapse with discontinuation.

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Preg and depr -- risk for ppd w/ psychosis, mgt, breastfeed and antidepr

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a. the risk of post-partum blues is 50%, post-partum depression 10 to 20%, and post-partum<br>psychosis 1 to 2 per 1000<br>i. post-partum blues: usually starts 3 to 10 days after delivery, and resolves by two weeks; risk<br>factors include a history of PMDD, primiparity, or past depression or family history of<br>depression<br>ii. post-partum psychosis usually presents within the first two weeks, but can also present 1 to<br>3 months after pregnancy; often heralded by worsening insomnia<br>1) risk increases to 20 to 25% in a woman who has had a past depression unrelated to pregnancy<br>2) risk of recurrence with future pregnancies is up to 70 %<br>3) the risk of infanticide is 4%, and is correlated with the severity of psychotic symptoms<br>iii. post-partum depression develops more insidiously, often three or more weeks after delivery 1) risk increases up to 40% in women who have had a past depression; risk of recurrence is 50%<br>b. to minimize the risk:<br> Reduce environmental stress,<br> mobilize additional resources<br> educate about “normal” post-partum blues, and monitor closely<br>c. management of post-partum syndromes<br>i. post-partum blues: mild and transitory; observe or use short-acting sedative; take<br>complaints seriously and offer support<br>ii. post-partum depression: serotonergic antidepressants<br>iii. post-partum psychosis: usually merits hospitalization; antipsychotics, lithium (with antidepressant), or ECT are all helpful<br>d. remember to screen for thyroid abnormalities (post-partum, there is a dramatic reduction in blood flow to the anterior pituitary; in rare cases, this can cause anterior pituitary necrosis, or Sheehan’s syndrome)<br>e. psychotropic medications and breast-feeding<br>i. lithium: present in breast milk at 30 to 50%; breast feeding is contraindicated<br>ii. Carbamazepine and Valproate: considered compatible with breast-feeding; watch for neonatal Hepatotoxicity with Valproate<br>iii. benzodiazepines: in general discouraged; however, there may be a role for intermittent use of short acting agents with no active metabolites (such as Lorazepam)<br>iv. fluoxetine and Sertraline: considered okay<br>v. Nortriptyline, desipramine (secondary amines) and imipramine (tertiary amine):<br>generally okay; minimize exposure by taking antidepressant immediately after breast<br>feeding prior to infants longest period of sleep<br>vi. antipsychotics: breast feeding should be avoided

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PPD w psychosis -- mgt

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e. in nearly all cases, post-partum psychosis necessitates hospitalization, because of<br>the high risk of suicide and infanticide<br>f. post-partum psychosis most often has a significant mood component; treatment<br>options typically include lithium, low-dose antipsychotics, or ECT<br>g. note that lithium is expressed at fairly high levels in breast milk; this is less so for olanzapine (one study showed minimal olanzapine in breast milk of nursing<br>mothers with post-partum psychosis, and no noted adverse effects on the infant)

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VPA -- birth defects and 4 alternative classes

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Birth defects with VPA: (K and S)<br>1a. spina bifida and neural tube defects 11%, (1-4 % risk of Spina bifida) (note to all that<br>ntd’s also encompass anencephaly (no brain formation, just brainstem), and<br>iniencephaly (neural tube open all the way down)<br>2a. cleft lip / palate<br>3a. cerebral hemorrhage<br>4a. IUGR<br>5a. Developmental delay<br>6a. digital malformation<br>7a. cardiac abnormalities<br>8a. highest risk is still within the 1st trimester<br>9a. Increased pulmonary adenomas and fibrosarcomas in rats – no evidence in humans<br>From CPS:<br>Neural tube defects<br>Congenital heart malformations (doesn’t specify which) Cleft lip and or palate<br>Craniofacial abnormalities<br>One report of an infant born with afibrinogenemia IUGR and death in mice given Epival<br>Skeletal malformations and growth retardation in monkeys with Epival<br> What medication would you add to her treatment to reduce the risk of birth defect (doesn’t specify dose)<br>1a. Folic acid to decrease risk of neural tube defects.<br>2a. In addition, there is some evidence that it decreases risk of cardiac anomalies in some<br>at-risk patients.<br>3a. If family hx of ntd’s 4-5 mg per day, also if pt on VPA.<br>4a. 0.4 mg/day found to be adequate for pts with no family hx or medication risks for<br>ntd’s.<br><br>Disorders<br>Postpartum Psychosis Postpartum Depression Bipolar I Disorder<br>Major Depressive disorder<br>Risk of Relapse at Future Pregnancy 70%<br>50%<br>20–50%<br>30%

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AP -- most likely wt gain, blood test, 5 do/counsel

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a. Which two novel antipsychotic medications are most likely to cause weight gain?<br> Two novel antipsychotic are Olanzapine and Clozapine<br>b. What three blood tests would you do in someone who has weight gain?<br> FBS<br> Lipid profile<br> TGs &amp; LFTs<br>c. List five things that you would either do or counsel the patient to do to help<br>with weight loss. [2002]<br> 5-steps approach to help with weight loss<br> (behavioural modification)Increase exercise and decreased caloric intake<br> Consider switching to a lower risk weight gain medication<br> Adding medication approved for weight loss (orlistat [Xenical] 120 mg tid,<br>or by adding medications that promote weight loss (H2-blockers – Nizatidine 150 mg bid, topiramate 25-100 mg bid, Modafinil 50-200 mg, Metformin (Glucophage) 500 mg bid, tid.<br> Psychoeducation about the risk of weight gain

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DDx -- delusional, withdrawn, decr comm<br>Most impt lab test, investigations

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a. List five diagnoses that you would include in the differential.<br> Brief Psychotic Disorder<br> Depression with psychotic features<br> Schizophrenia<br> Substance induced psychosis<br> Bipolar Disorder, Manic episode with psychotic features<br>b. What is the single most important laboratory test to perform?<br> Urine/drug tox screen<br>c. List what investigations you would do before beginning an atypical<br>antipsychotic.<br>Name four lab/physical exam parameters that would perform in order to monitor specific side effects of atypical antipsychotic:<br> Fasting glucose<br> Fasting lipids<br> Liver function tests<br> Weight and Waist measure<br> Pulse and blood pressure<br> ECG<br> AIMS

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SCZ -- cogn deficits (4) and implications

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Cognitive deficits seen in schizophrenia<br>A. attention: involuntarily drawn to irrelevant environmental elements (seen on stroop test)<br>B. abstraction: appreciation of nuances of meaning<br>C. executive function: impaired SOAP (Sequencing, Organization, Attention,<br>Planning)<br>D. memory: impaired working and short term spatial memory<br>Implications for treatment<br>A. cognitive enhancers may have a role in treatment<br>B. cognitive test scores are better outcome predictors for psychosocial interventions<br>than positive symptoms<br>C. because of impaired abstraction and executive function, specific social skills<br>training and vocational training may be required<br>D. deficits in attention suggest that psychoeducation done repetitively over a number<br>of sessions may be more helpful<br>Memory: The clinical assessment of memory should test three periods, which have distinct anatomical correlates<br>1. Immediate memory functions over a period of seconds; immediate memory is implicit in the concept of attention and the ability to follow a train of thought. This ability has been divided into phonological and visuospatial, and functional imaging has localized these components of immediate memory to the left and right hemispheres, respectively.<br>2. recent memory applies on the scale of minutes to days;<br>3. Remote memory encompasses months to years.<br>4. Working memory is incorporating immediate and recent memory, working memory is defined<br>as the ability to store information for several seconds, while other, related cognitive operations take place on this information. Recent studies have shown that single neurons in the dorsolateral prefrontal cortex not only record features necessary for working memory, but also record the certainty with which the information is known and the degree of expectation assigned to the permanence of a particular environmental feature. Some neurons fire rapidly for an item that is eagerly awaited, but may cease firing if hopes are dashed unexpectedly. The encoding of the emotional value of an item contained in the working memory may be of great usefulness in determining goal-directed behavior. Some researchers localize working memory predominantly to the left frontal cortex. Clinically, however, bilateral prefrontal cortex lesions are required for severe impairment of working memory.<br>5. Memory is divided into short term and long term; long-term memory is also known as recent memory, recent past memory, remote memory, and secondary memory. Short-term memory— also called immediate memory, working memory, primary memory, and buffer memory—is adversely affected by chronic emotional stress, psychological exhaustion, or too much input. Short-term and long-term memory differs in the amount of information that can be stored. The capacity of short-term memory is limited (five to nine bits of information).<br>

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SCZ -- tx resistant, Kane criteria (4 illness related features, 4 tx related)

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Illness related features of treatment resistance<br>A. no periods of good functioning in the past five years<br>B. a clinical global impression score (CGI) of at least 4 (moderately ill)<br>C. a BPRS score of at least 45<br>D. a score of at least four (moderately severe) on two of: conceptual disorganization,<br>unusual thought content, suspiciousness, hallucinatory behavior<br>Treatment related features of treatment resistance<br>A. during the past five years, the patient has been treated with doses of antipsychotics<br>equal to or greater than 1000mg of chlorpromazine daily<br>B. has tried at least two different classes of antipsychotics for at least six weeks each<br>without significant clinical relief<br>C. a six week prospective trial of haloperidol up to 60mg daily fails to decrease BPRS<br>by 20% (or to below 35), or to decrease CGI score to 3 (mildly ill)

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SCZ -- prognostic

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• poor prognosis: IF SPY SAP (3 RANNT)<br>Good prognosis<br>acute onset<br>family history of mood disorders married<br>precipitants are present<br>older age at onset<br>support systems are good<br>mood symptoms<br>premorbid functioning is good<br>Poor prognosis<br>insidious onset (I)<br>family history of schizophrenia (F) single, divorced, or widowed (S) precipitants are lacking (P)<br>young age at onset (Y)<br>support systems are poor (S) autistic or withdrawn behavior (A) premorbid functioning is poor (P)<br>3 years without remission (3) relapses frequent (R)<br>assaultiveness in history (A) negative symptoms (N)<br>neurological signs or symptoms (N) trauma at perinatal time (T)

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SCZ -- psychosocial interventions

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social skills training<br />social performance within the family and outside the family; teaching eye contact, reciprocity<br />cognitive therapy: correct cognitive distortions, errors in judgment, enhance coping strategies<br />family therapies: one of the most effective at preventing relapse; reduce expressed emotion<br />case management: coordinate multidisciplinary teams, with home visits, assisting community living, patient advocacy<br />group therapy: decreases social isolation, helps self-esteem<br />psychoeducation: teach about illness, risks of relapse, early identification of relapse supportive psychotherapy: support problem solving<br /><br />1) Medication Adherence and Psychoeducation<br /> Despite the effectiveness of psychopharmacological interventions in producing improved outcomes in schizophrenia,<br />Medication nonadherence occurs frequently (in up to 50% or more of cases) for various reasons.<br /> A recent comprehensive review identified that the lack of awareness of illness was a key factor in medication nonadherence.<br /> Such lack of insight has been hypothesized to be a cognitive impairment associated with schizophrenia itself<br /> Other issues contributing to nonadherence include concurrent alcohol or drug abuse, problems with the therapeutic alliance, medication side effects and complicated dosage schedules, problems with access to treatment, and financial obstacles to obtaining medication.<br /> The impact of nonadherence is costly, for the person and his or her family and more generally the health care system.<br /> Psychoeducational interventions that are aimed at increasing knowledge about the illness have shown some effectiveness in conveying facts, but have not been found to show increased adherence unless accompanied by motivational enhancement and the use of specific “behavioural tailoring” strategies such as reminders, prompting, and self-monitoring cues.<br /> The importance of introducing concrete coping aids and behavioural compensation methods, such as keeping medication regimens as simple as possible, “pillbox” dosette use, establishing a regular medication routine and monitoring it regularly, and including home visits as needed.<br /> Motivational strategies emphasize the links between adherence and benefits in the individual’s life circumstances as well as the heightened risk of relapse when medications not taken.<br />2) Vocational Interventions<br /> Employment rates among individuals with schizophrenia and related disorders are substantially lower than in the general population.<br /> Employment status appears likely to have substantial impact on the economic circumstances of many patients and influences many aspects of quality of life.<br /> In the past, there was considerable emphasis on providing extensive preparation for employment before an individual was placed in a job setting; more recently, the emphasis appears to placing individuals in competitive employment sooner and offering considerable after placement job-support services.<br /> The supported employment approach includes the following elements:  Developing job opportunities appropriate for the individual,<br /> Rapid placement that emphasizes competitive employment,<br /> Providing ongoing support after job placement, and<br /> Integrating vocational and mental health services.<br /> Recent metaanalysis findings concluded that the supported employment approach leads to better<br />employment rates, although long-term job retention rates may be less positive.<br /> There is no evidence that employment obtained with these methods leads to increased stress or<br />exacerbation of symptoms; there is some, but not entirely consistent, evidence that such beneficial effects on employment status may have positive impacts on self-esteem, on aspects of psychiatric symptoms, and on the likelihood of relapse.<br />3) Skills Training<br /> Schizophrenic Individuals frequently have difficulties related to social interaction and coping with aspects of independent living.<br /> Such difficulties may result from several factors, including early onset, which interferes with development of social and living skills; the impact of some aspects of impaired cognitive functioning; and the impact of the illness and its associated stigma.<br /> Interventions used to address these issues include social skills and life skills training.<br /> Social skills training uses methods based on learning theory and attempts to improve<br />interpersonal skills related to conversational skills, making friends, and social interaction.<br /> Methods include instruction about the significance of various verbal and nonverbal aspects<br />of social behaviour, modeling, role-playing, behavioural rehearsal, corrective but supportive feedback, and behavioural homework and practice to increase generalization to the individual’s daily environment.<br /> Life skills training focuses on skills related to practical aspects of living, such as managing money and domestic skills, and personal self-care, such as grooming and hygiene.<br />° The results of recent metaanalysis of true RCTs have indicated caution regarding their impact. Pilling and others examined the outcomes of 9 RCTs and concluded that there was no clear evidence that patients who received social skills training had better outcomes, compared with other active treatment conditions, on any of various measures, including relapse rates, global adjustment, social functioning, or quality of life.<br />° When Robertson and others examined the literature on life skills training, they found only two studies that met criteria for an unbiased RCT, and the results of the metaanalysis (based on only 38 patients) did not demonstrate clear effects.<br />° Individual reports suggest the potential of these interventions (particularly social skills training) to improve outcomes and it would be contentious (controversial, debatable) to suggest that results of metaanalysis of rigorously (thoroughly, strictly, carefully) selected RCTs should be the only evidence examined with reference to their effectiveness.<br />4) Cognitive-Behavioural Interventions:<br /> Cognitive behavioural techniques are effective in the treatment of several forms of Psychopathology, including anxiety and affective disorders.<br /> When applied to schizophrenia and related disorders, the most frequently used cognitive- behavioural interventions include:<br /> development of a collaborative understanding of the nature of the illness, which encourages<br />the patient’s active involvement in treatment<br /> identification of factors exacerbating symptoms<br /> learning and strengthening skills for coping with and reducing symptoms and stress<br /> reducing physiological arousal<br /> testing of key beliefs that may be supporting delusional thinking<br /> development of problem-solving strategies to reduce relapse<br /> Both individual and group formats have been used, although most research on impact has<br />involved evaluation of individualized treatment approaches.<br /> There has been variation in the frequency and duration of treatment (varying between 6 and 50<br />sessions). It appears that weekly or biweekly sessions over a period of 4 to 9 months are typical<br />of the trials.<br /> There have been several reviews of the evidence concerning the effectiveness of such<br />interventions, the most recent being a Cochrane Review metaanalysis.<br /> The evidence available at this point suggests that, as well as reducing psychiatric symptoms,<br />adding cognitive-behavioural interventions to standard care (including medication) can have an impact on time to discharge from hospital and on general psychological functioning.; one recent trial using cognitive behavioural interventions focused on dealing with early signs of relapse has reported promising results in this respect.<br /> Studies in this field have focused on demonstrating symptom reduction in patients who are otherwise considered treatment-resistant.<br /> The extent to which cognitive-behavioural interventions lead to better outcomes regarding symptoms and mental state, compared with less specific supportive psychotherapy, is unclear. Many reviewers have reached different conclusions.<br /> Bechdolf and others reported a CT comparing group-administered CBT with a simpler psychoeducation intervention. They found that, while the CBT condition had fewer post- intervention hospitalizations, the two groups did not differ significantly on indices of clinical relapse, symptoms, or adherence to medication.<br /> The opinion of authoritative commentators suggests that cognitive-behavioural treatment of schizophrenia and related disorders requires substantial training and experience and has to occur within the context of a good therapeutic relationship characterized by trust.<br /> One controlled trial suggests that community psychiatric nurses who received 10 days’ training in CBT were able to provide interventions that reduced overall symptoms (as assessed by the Comprehensive Psychopathology Rating Scale), reduced depression, and improved insight but did not have an impact on symptoms specific to schizophrenia.<br /> Only the change in insight was sufficient to be considered clinically significant by the authors.<br />5) Family Interventions<br /> Families are often the primary caregivers and that they can consequently experience a burden from those demands.<br /> Regardless of whether the patient with schizophrenia is actually living with his or her family in the community, most families provide support and assistance to their ill relative.<br /> Families are often left in the position of assuming the role of caregiver, for which they are neither trained nor psychologically prepared. As well, professionals do not always accurately understand what factors caregivers find burdensome (onerous, troublesome, heavy) when coping with an ill relative.<br /> The degree and nature of burden has been found to vary with the phases of the disorder.<br /> In the early phase, families are faced with feelings of uncertainty and emotional shock. In later<br />phases, families face dealing with the everyday impact of negative symptoms, such as lack of<br />interests and loss of initiative.<br /> Treatment efficacy can be enhanced and relapses can be prevented when family members<br />participate in a structured program of family psychoeducation, which has been shown to relieve<br />caregiver distress.<br /> There are core curriculum components to Psychoeducational family treatment, an approach that<br />offers empathy, knowledge sharing, and problem-solving skills training. Home visits are a part<br />of some programs.<br /> Family Psychoeducational interventions should be introduced during the early phases of<br />treatment when a patient is experiencing a first episode. There is some evidence that multiple-family groups may have more enduring benefit than individual approaches during the first<br />episode.<br /> However, many families will not attend groups and need individualized treatment and outreach.<br />Educational interventions may need to be supplemented, depending on individual circumstances<br />such as the needs of siblings and needs related to the illness phase.<br /> In working with family members, sensitivity to confidentiality issues is required, including the<br />use of appropriate information-release forms, to maintain a trusting relationship with the patient.<br /> However, family members should not be underused: they provide a valuable consultation<br />resource for mental health professionals, and they are allies in patient recovery efforts.<br /> Working with families should include listening to family members’ concerns, exploring family<br />expectations about treatment and their understanding of the patients’ illness, making adjustments that acknowledge and respect family culture and values, assessing family members’ capacity to cope with and support their ill relative, and developing a crisis plan.<br /> Mental health practitioners can also assist in linking family members to other ongoing supports as needed, including family organizations such as the Schizophrenia Society of Canada (www.schizophrenia.ca) or the Canadian Mental Health Association (CMHA, www.cmha.ca).<br />6) Cognitive Remediation<br /> Individuals with schizophrenia and related disorders not only have disturbing and pathological thought content related to delusions and hallucinations, they can also have anomalies in thought form or information processing, such as difficulties with attention, learning, memory, executive functioning, and planning.<br /> When they occur, such cognitive deficits are often related to negative symptoms, appear to have substantial implications for an individual’s daily functioning, and may compromise the individual’s ability to benefit from psychosocial interventions.<br /> Recently, there has been increased interest in the possibility of developing interventions to help patients reduce such cognitive difficulties and (or) their impact, and these efforts are referred to by varying terms, the most common of which are cognitive remediation, cognitive training, and cognitive rehabilitation.<br /> Such efforts usually involve one or more of 3 strategies:<br /> restorative approaches, in which efforts are made to reduce the underlying cognitive<br />deficits;<br /> compensatory strategies, which aim to help patients work around or compensate for<br />cognitive deficits;<br /> Environmental approaches, which try to provide situational supports, such as external<br />reminders, to decrease the impact of cognitive deficits.<br /> Several studies have examined the impact of cognitive remediation training strategies on<br />standardized neuropsychological tests, but of greater clinical significance would be studies<br />assessing the impact of such Strategies on daily functioning.<br /> There is currently no clear and consistent evidence that such interventions have a significant<br />effect in such domains.<br />7) Peer Support, Self-Help, and Recovery<br /> The “recovery vision” focuses on “consumer” involvement (empowerment) in setting rehabilitation goals leading to improved community functioning (not just stability of symptoms) and on the development of a “recovery-oriented system” that advocates for supports beyond standard health care.<br /> Key components of system-level change have been the introduction of self-help programs, including peer-run services, the use of peer-support workers or peer providers as staff members of multidisciplinary teams.<br /> Critical ingredients of peer-provider services hold promise for benefits beyond typical practices.<br /> These include their use of experiential knowledge (“street smarts”) to enhance pragmatic<br />support efforts and the positive impact of social role modeling.<br /> Peer-assistant workers, including graduates of previous training groups, have been incorporated into skills training groups to deliver some of the training, such as social skills role-play instruction or training as worker-assistants in collective kitchens.<br /> There are modest findings of some benefits, including improvements in self-esteem and increased social networks.<br /> Peer services and, more generally, recovery oriented practitioner perspectives work toward maintaining and inspiring a sense of hope, levels of which have been consistently found to be unrelated to the actual severity of the psychotic symptoms.<br /> There have been some suggestions from a CMHA survey (195) that peer supports provide patients with increased satisfaction regarding their community adjustment and with increased feelings of self-worth.

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SCZ -- SSx in adolescent (prodrome)

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• functional deterioration, deteriorating academic performance<br>• social withdrawal<br>• decreased hygiene and self-care<br>• dysphoria, and non-specific anxiety or depressive sxs.<br>• bizarre behaviors, odd beliefs<br>• substance abuse<br>• aggression or other conduct problems

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SCZ -- structural / neurophysiological abn

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• neuropathology<br>o limbic system changes<br> decreased amygdala size<br> decreased hippocampus size<br> decreased parahippocampal gyri<br>o basal ganglia changes<br> increased D2 receptor sites in the caudate, putamen<br> increased D2 receptor sites in the nucleus accumbens<br>• brain imaging<br>o ventricular enlargement<br>o decreased cortical volume<br>o abnormal symmetry<br>o impaired activation of DLPFC with Wisconsin card sorting test<br>Wisconsin Card Sorting Test, an abstract problem-solving test requiring attention and working memory (The Wisconsin Card Sorting Test is a problem-solving task that is known to be sensitive to focal lesions of the frontal lobes and to diffuse cerebral injury). Where the patient sorts cards according to a series of criteria designated by the examiner such as color, shape, or number. The patient must discover and apply the sorting criteria through trial-and- error observations. Critical brain regions are the prefrontal cortex and anterior cingulate.<br>• neurophysiological<br>o decreased alpha-waves<br>o increased slow waves<br>o impaired smooth pursuit (saccadic intrusions) o small and late evoked potentials

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SCZ -- 5 neuro findings

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• while there are no pathognomic findings, increased localizing and non-localizing neurological signs have been reported in patients with schizophrenia when compared to patients with other psychiatric diagnoses; these are associated with a poor prognosis and a<br>more severe illness<br>• signs:<br>o dysdiadochokinesia<br>o astereognosis<br>o tics and stereotypies<br>o abnormal motor tone and poor fine motor skills o disorder of smooth ocular pursuit<br>o increased blink rate

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SCZ -- RF noncompliance

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• lack of insight has been hypothesized to be a cognitive impairment associated with schizophrenia itself<br>• Medication side effects<br>• concurrent alcohol or drug abuse<br>• Lack of adequate follow up and problems with the Therapeutic alliance<br>• medication side effects and complicated dosage schedules<br>• Problems with access to treatment, and financial obstacles to obtaining medication.<br>• comorbid depression or anxiety

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Delusional d/o -- RF (3) and (favorable) prognostic (2)

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Risk factors for delusional disorder<br>A. advanced age<br>B. sensory impairment<br>C. social isolation<br>D. recent immigration<br>E. personality features<br>Favorable prognostic factors<br>F. acute onset<br>G. clear precipitants<br>H. female<br>I. being married<br>General notes<br>J. Delusional disorder is rare (prevalence 0.025 to 0.03%)<br>K. the average age of onset is 40<br>L. the prevalence is slightly higher in females<br>M. It is not associated with increased rates of mood disorders or schizophrenia in the<br>family; the diagnosis remains stable over time.<br>N. the most common type is persecutory

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SCZ -- historical

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1. Eugen Bleuler is the first who called it schizophrenia<br>2. Manfred Bleuler (Eugen’s son, conducted follow-up studies)<br>3. Emil Kraeplin coined the term ‘dementia praecox’<br>4. Adolph Meyer, proposed DSM-I, developed “psychobiology” theory<br>5. Kurt Schneider, proposed “first rank” symptoms<br>6. Pierre Janet, described body dysmorphic disorder

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SCZ -- double bind theory

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The “double-bind” theory was proposed by Bateson, Jackson, Haley, and Weakland in the mid 1950’s; it proposes that schizophrenia results from a child being exposed to conflicting injunctions (orders, command) without the opportunity to either respond to them or to escape; for example, a mother who tells a child she loves him while turning her head away with an expression of disgust

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SCZ - oneroid state

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patients feel and behave as though they were in a dream. (Oneiros is the Greek word for dream). Patients may be deeply perplexed (Puzzled, confused) and not fully oriented in time and place. During the state of clouded consciousness, they may experience feelings of ecstasy and rapidly shifting hallucinated scenes. Illusionary distortions of their perceptional processes (including time perception) and the symptomatic picture may resemble those of a hysterical twilight state. During oneiroid reactions, the observer can most clearly detect the patient's peculiar &quot;double bookkeeping&quot;—patients may be convinced that they are traveling through space on a satellite and at the same time conscientiously follow the regular hospital routine. The patient with oneiroid schizophrenia acknowledges everyday realities but gives priority to contingencies of reality. Oneiroid states are usually limited in duration and occur most frequently in acute schizophrenic episodes.

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SCZ - Late onset

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Late-onset schizophrenia is usually defined as an illness that is clinically indistinguishable from schizophrenia but has an onset after age 45. Since DSM-IV no longer uses an age cutoff, this distinction may no longer be relevant. This condition tends to appear more frequently in women and tends to be characterized by a predominance of paranoid symptoms. The prognosis is favorable, and these patients usually do well on antipsychotic medication. This term refers to cases of late-onset paranoid symptomatology not characterized by the presence of dementia, confusion, or mood disorder<br>The classic “late-onset” schizophrenia is characterized by<br>1. insidious onset<br>2. women over the age of 60, never married<br>3. more likely to have been married and have had a job than other schizophrenics, but they tend to<br>have<br>4. pre-morbid paranoid or schizoid personalities<br>5. absence of dementia<br>6. no clear stronger association with family history<br>7. partition(dividing wall) delusion which is electricity is going through the wall is common

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SCZ -- first rank (3 from ABCD)

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a. initially there were described eight first rank symptoms (as suggested by the mnemonic above) – the “control” symptoms, however, have been further sub-classified by some, as noted below<br>b. “second-rank” symptoms are all other forms of hallucinations<br>c. auditory –audible thoughts, voices arguing, voices commenting:<br>1. audible thoughts are defined as: the patient’s own thoughts are experienced as an audible (hallucinated) voice (the voice is typically not your own)<br>2. arguing: two voices arguing about the patient in the third person<br>3. commenting: commenting on patient’s actions as they occur<br>d. broadcasting – broadcasting, withdrawal, insertion<br>1. broadcasting: inner thoughts are no longer private; have escaped and are known to everyone (also known as “thought diffusion”)<br>2. insertion: alien thoughts have been placed in one’s mind<br>3. withdrawal: own thoughts have been stolen from mind<br>e. control – in general, feelings of external influences playing on the body; have been further<br>sub-categorized by some into three areas: “made acts”, “made feelings”, somatic hallucinations<br>1. made acts: delusions of actions being under the control of external forces<br>2. made feelings: delusions of feelings being under the control of external forces<br>3. somatic passivity: unwanted bodily sensations (somatic hallucinations) attributed to<br>an external agent<br>f. delusional perception – a non-hallucinated sensory perception whose meaning is significant in a delusional thought or system<br>1. a delusional perception is a real perception followed by an unrelated delusional idea, often having a theme of self-reference; this is a two-stage process<br>2. primary delusions appear suddenly, and with full conviction; a delusional perception is an example of a primary delusion<br>3. “secondary delusions” are derived from abnormal mental phenomenon – for example, believing that you are Jesus because a hallucinatory voice of God tells you so<br>4. According to a different definition, a primary delusion refers to and is synonymous with an autochthonous delusion, one that takes form in an instant, without identifiable preceding events, as if full awareness suddenly burst forth in an unexpected flash of insight, like a bolt from the blue. These delusions may be quite elaborate.<br>5. Delusional percept refers to the experience of interpreting a normal perception with a delusional meaning, one that has enormous personal significance to the patient. Delusional atmosphere or delusional mood is a state of perplexity, a sense that something uncanny (eerie, strange, weird) or odd is going on that involves the patient, but in unspecified ways. Ordinary events may take on heightened (sharp, keen) significance but the delusional interpretations are fleeting (brief, transitory, short- lived) whereas the uncanny feeling lingers (remain, stay behind, hold on). Typically, after a period of time full-blown delusions develop, replacing the delusional mood. Delusional memory is the memory of an event that is clearly delusional. As an example, a patient &quot;remembered&quot; his fourth-grade teacher slipping lysergic acid diethylamide (LSD) into his apple juice; this memory served to explain his psychotic disorder. The elaboration of false memories and their subsequent fixed beliefs may assume delusional proportions.

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SCZ - course

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 Recovery rates 10-60%<br> Likely 20-30% has somewhat normal lives<br> About 20-30% has moderate symptoms<br> But 40-60% remains significantly impaired for life (as opposed to 20-25% of mood disorder<br>patients who are significantly impaired)

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SCZ -- type I vs II

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Dividing schizophrenia into positive or negative symptoms<br> Type I – mostly positive, normal brain structures on CT, mostly better response to Tx<br> Type II – mostly negative, brain abnormalities, mostly worse response Additional category<br> Disorganized – disorganized speech, behavior, cognitive defects, attention deficits

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SCZ -- 5 non-demographic RF suicide

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10 to 15 percent of schizophrenic patients die by suicide during a 20-year follow-up period. I. The non-demographic risk factors include:<br>The major risk factors for suicide among people with schizophrenia include the following:<br>1. Presence of depressive symptoms, high levels of premorbid functioning (especially a<br>college education, overly high ambitions).<br>2. People in this risk group may realize the devastating significance of their illness more<br>than do other groups of schizophrenic patients and may see suicide as a reasonable<br>alternative.<br>3. Other precipitants of suicide include feelings of absolute emptiness, a need to escape from<br>mental torture, or auditory hallucinations that command patients to kill themselves.<br>4. Also other risk factors for suicide considered are the patient's awareness of the illness, a change in the course of the disease, an improvement after a relapse, dependence on the hospital (Up to 50 percent of suicides among patients with schizophrenia occur during the first few weeks and months after discharge from a hospital; only a minority commit suicide while inpatients).<br>5. Previous suicide attempts early in the course of the illness (50 percent have made a previous suicide attempt), and living alone.<br>II. The demographic risk factors include: Young age, and male sex, college education.<br>1.<br>2.<br>3.<br>4. 5.<br>The onset of schizophrenia is typically in adolescence or early adulthood, and most of these patients commit suicide during the first few years of their illness; therefore, schizophrenic patients who commit suicide are young.<br>Thus, the risk factors for suicide among patients with schizophrenia are young age, male gender, single marital status, a previous suicide attempt, a vulnerability to depressive symptoms, and a recent discharge from a hospital.<br>Having three or four hospitalizations during their 20s probably undermines (weaken, challenge, destabilize) the social, occupational, and sexual adjustment of possibly suicidal schizophrenic patients.<br>Consequently, potential suicide victims are likely to be male, unmarried, unemployed, socially isolated, and living alone—perhaps in a single room.<br>After discharge from their last hospitalization, they may experience a new adversity or return to ongoing difficulties. As a result, they become dejected, experience feelings of helplessness and hopelessness, reach a depressed state, and eventually act on, suicidal ideas.

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SCZ -- differential mannerisms/beliefsm, how approach consistently refused tx

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1. Schizophrenia<br>2. SCHIZOTYPAL PERSONALITY DISORDER<br> People with schizotypal personality disorder are strikingly odd or strange, even to laypersons.<br> Magical thinking, peculiar notions, ideas of reference, illusions, and derealization are part of a schizotypal person's everyday world.<br> Is diagnosed based on the patients' peculiarities of thinking, behavior, and appearance.<br> Thinking and communicating are disturbed. Although frank thought disorder is absent, their speech may be distinctive or peculiar, may have meaning only to them, and may often need interpretation.<br> They are superstitious or claim powers of clairvoyance and may believe that they have other special powers of thought and insight.<br> Their inner world may be filled with vivid imaginary relationships and childlike fears and fantasies.<br> They may admit to perceptual illusions or macropsia and confess that other people seem to them to be wooden and all the same.<br> Because people with schizotypal personality disorder have poor interpersonal relationships and may act inappropriately, they are isolated and have few, if any, friends.<br> Patients may show features or borderline personality disorder, and indeed, both diagnoses can be made.<br> Under stress, patients with schizotypal personality disorder may decompensate and may develop psychotic symptoms, but these are usually of brief duration. In patients severely affected by the disorder, anhedonia and severe depression may be<br>present.<br>3. Borderline personality disorder<br>4. Autistic disorder<br>5. OCD<br><br><br>HOW WOULD YOU APPROACH????

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psychotic sx -- differential

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1. Axis I: psychotic disorders (brief psychotic disorder, Schizophreniform disorder, schizophrenia, schizoaffective disorder, delusional disorder)<br>2. Axis I: mood disorder (major depressive disorder or bipolar disorder with psychotic features)<br>3. Axis I: substance use disorder (intoxication)<br>4. Axis I: delirium (dementia unlikely in young woman)<br>5. Axis II: Schizotypal personality disorder<br>6. Axis III: medical causes (metabolic like; diabetes; thyroid problems; Porphyria; neurologic;<br>like Huntington’s, Parkinson’s Wilson’s, stroke, connective tissue; like lupus, infectious; like meningitis, UTI, pneumonia)

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Meds -- 5 years psychosis free wants d/c

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o Discuss risks of relapse following discontinuation, and if patient wishes to proceed with stopping Meds<br>o Suggest involving family/caregivers<br>o Continue close follow-up, and discuss early warning signs of relapse o Recommend no drug/alcohol use/abuse<br>o Taper gradually the meds over a period of 1-2 months<br>o Restart Meds if there is worsening.

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TD -- sx, RF, Tx

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A. Symptoms of tardive dyskinesia<br>v. Primarily characterized by involuntary movements of the tongue, lips, or jaw; the movements disappear during sleep<br>vi. Assessment of tardive dyskinesia can be done through the AIMS test<br>1. Remove things from mouth<br>2. Ask about teeth or dentures<br>3. Ask about patient noticing movements in face, mouth, hands, feet<br>4. Observe patient seated, feet flat, knees apart, hands on knees<br>5. Observe patient seated with hands hanging freely<br>6. Ask patient to open mouth, look at tongue (twice)<br>7. Ask patient to stick out tongue (twice)<br>8. Ask patient to tap fingers with right hand then left, as fast as possible<br>9. Flex and extend patients arms<br>10. Ask patient to stand<br>11. Ask patient to extend arms, palms down (observe trunk, legs, mouth)<br>12. Have patient walk, turn, walk back to chair (twice)<br>B. Risk factors for tardive dyskinesia<br> The main risk factors are advanced age, female gender, and mood disorder<br> Duration of exposure to antipsychotics is also a risk factor<br>C. Management of tardive dyskinesia:<br>1) Assess severity with AIMS scale <br>1. If mild (AIMS score of 2 or less)<br>a. Observe with serial assessments if no distress<br>b. If upsetting, switch to atypical antipsychotic, or if already on atypical, switch<br>to Clozapine<br>2. if severe<br>a. Try Clozapine; if improves, maintain on Clozapine (Clozapine has been shown to reverse persistent tardive dyskinesia after six to 12 months)<br>b. Consider referral to movement disorders clinic

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Cloz -- use, s/e, monitor

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A.<br>The use of Clozapine:<br>o The most effective antipsychotic drug for partial or non-respondent treatment-resistant schizophrenia<br>o Significant improvements in both positive and negative psychotic symptoms<br>o Its beneficial use in several disorders including psychosis secondary to dopaminergic<br>therapy or coexisting psychiatric disorders in Parkinson's disease, other psychotic disorders, affective disorders, dyskinesias and related disorders, dementia, mental retardation, and polydipsia/ hyponatremia.<br>o There are reports, showing its dramatically beneficial effect in the patients with severe personality disorder.<br>o There are case reports and small studies show marked reduction in self harming behaviour, aggression and intensive affective response.<br>o The duration of an adequate trial with Clozapine is considered to be 4 to 6 months<br>o Clozapine may improve social functioning, occupational functioning and quality of life,<br>and that it may also reduce affective symptoms, hospitalization, secondary negative<br>symptoms and tardive dyskinesia.<br>o Clozapine is introduced at a dose 12.5 to 25.0 mg, Incremental dosage range, mg ↑ 12.5<br>to 25.0 mg on the second day, ↑ up to 25.0 to 50.0 daily with Usual target dosage (300 to<br>600), up to a maximum dose of 900 mg.<br>Its side effects:<br>1. The most serious adverse effect of Clozapine is Agranulocytosis (0.5-2%)<br>2. Other important side effects include postural hypotension and tachycardia, sedation,<br>seizures,<br>3. weight gain and abdominal obesity<br>4. Impairment in Glucose Regulation and Diabetes<br> insulin resistance, hyperglycemia, exacerbation of type 1 diabetes, new onset of type 2 diabetes mellitus, and diabetic Ketoacidosis.<br> In Canada, all SGAs carry a warning for potential glucose abnormalities.<br>5. Rebound psychosis.<br>6. Clozapine can also cause:<br>o Nausea, vomiting and constipation.<br>o Elevation of liver enzymes (frequency up to 10%)<br>o Hypersalivation (frequency 12-40%)<br>o Confusion or delirium<br>o Incontinence frequency/urgency, hesitancy, urinary retention, or impotence (6%) o Benign hyperthermia (5-15%)<br>o Development or exacerbation of OCD symptoms (Baker et al, 1992; Patil,<br>1992; Meltzer, 1993)<br><br>Clozapine Side Effect Profile<br> Clozapine is associated with several serious and potentially fatal side effects, including Agranulocytosis (0.5% to 2.0%), seizures (2% to 3%), and rare occurrences of myocarditis and cardiomyopathy.<br> It is also associated with significant weight gain and glucose and lipid disturbances.<br>Among other side effects, Clozapine may also induce Sialorrhea, significant sedation, hypotension, tachycardia, and significant anticholinergic side effects such as constipation, dry mouth, blurred vision, gastroparesis, and enuresis.<br>It does not elevate prolactin levels or induce EPSEs.<br>Risk of Agranulocytosis is higher in the first 6 months of treatment, requiring a weekly assessment to ensure that white blood count (WBC) and absolute neutrophils counts remain over 3000/mm3 and 1500/mm3, respectively. Thereafter, blood monitoring of complete blood count (CBC) and differential is reduced to every 2 weeks.<br>A monitoring program has been shown to reduce Agranulocytosis risk to less than 0.5%. Certain medications such as carbamazepine may increase the risk of Clozapine-induced Agranulocytosis and should be avoided.<br>Clozapine may induce seizures at a higher dosage (≥500 mg). Lower dosages and slower titration may reduce risk of seizure.<br>Adjunctive anticonvulsants can be considered to manage seizures. Smoking cessation has been associated with seizures, since it may significantly reduce metabolism (via CYP1A2) and increase Clozapine levels. Preventive dosage reduction (up to 50%) in case of smoking cessation would be judicious (sensible).<br>Patients taking Clozapine should be advised to contact their physician if signs of infections occur (that is, fever, chills, and sore throat).<br>Signs of myocarditis (such as fever, chest pain, peripheral edema, tachycardia, and respiratory distress) should also be known by patients and their family.<br><br>Its monitoring:<br>Pretreatment Assessment. Once a physician has determined that a trial of Clozapine is warranted for a particular patient, the risks and benefits of Clozapine treatment must be explained to the patient and the family.<br>The informed consent procedure should be documented in the patient's chart.<br>The patient's history should include information about blood disorders, epilepsy, cardiovascular disease, and hepatic and renal diseases.<br>Baseline body weight (BMI, WAIST measure)<br>FBS and Fasting lipid profile, Baseline ECG and pulse and BP then as indicated. EEG<br>The presence of a hepatic or renal disease necessitates the use of low starting dosages of the drug.<br>The laboratory examination should include an ECG, several complete blood counts (CBCs) with WBCs, which can then be averaged, and liver and renal function tests.<br>Start low and go slow principle with every week blood monitoring for the first 6-months, then switch to every two weeks thereafter<br><br>Guidelines for the Management of Patients on Clozapine<br>1.Patients should have a thorough medical history and physical examination prior to initiation of<br>treatment.<br>2.Testing for tuberculosis should be performed and testing for HIV offered to any patient with risks<br>for either disease. (Risk factors include prolonged residence in an institutional facility, group home, shelter, etc). Treatment with Clozapine may begin before test results are available if the patient lacks physical signs or symptoms of illness. If either condition is diagnosed, appropriate consultation should be obtained regarding the risks and benefits of continuing Clozapine.<br>3.It is advisable to begin Clozapine therapy with a small dose (eg, 12.5-25 mg) and build up gradually, over a 30-day period, to a therapeutic level of 500 mg or more per day.<br>4.The physician must complete a three-part National Registry WBC Reporting Form (provided by Sandoz).<br>5.The physician keeps one copy and forwards the remaining two copies to the patient's pharmacist. 6.The pharmacist may dispense a maximum of 7 days ‘supply of medication, provided three criteria<br>are met:<br>a. The patient's current WBC is recorded.<br>b. The initial WBC is at least 3,500 per mm3.<br>c. Subsequent WBCs, obtained weekly, are at least 3,000 per mm3.<br>7.Benign Neutropenia is not typical with Clozapine. The following thresholds must be observed in<br>monitoring WBC levels:<br>a. Treatment should not be initiated if the WBC is less than 3,500 per mm3.<br>b. If subsequent WBCs are between 3,000 and 3,500 per mm3, twice-weekly WBCs with<br>differentials should be obtained.<br>c. If the total WBC falls below 3,000 per mm3, therapy should be interrupted and the patient<br>closely monitored.<br>d. If the total WBC falls below 2,000 per mm3, therapy should be discontinued, and the patient<br>should never be rechallenged with Clozapine.<br>e. If a weekly WBC falls 30% from the previous level, the WBC should be repeated. If the<br>repeat level shows the WBC continuing to fall significantly, appropriate consultation from Sandoz and/or another expert (i.e., psychiatrist, hematologist, or infectious disease specialist) should be obtained.<br>f. A gradual progressive decrease in the WBC from the time of initiation of therapy with Clozapine should be monitored closely and consideration should be given to obtaining consultation as above.<br>

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EPS -- total body tremor ddx

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a. What are the Different types of movement disorders are acutely that may be contributing to this<br>i. The acute movement disorders that occur as manifestations of effects of neuroleptics and other dopamine antagonists include akathisia, acute dystonia, and other hyperkinetic dyskinesias.<br>ii. Acute effects of dopamine antagonists also include Parkinsonian syndromes that are manifested by (bradykinesia, rigidity, and pill rolling tremor).<br>iii. The acute movement disorders resulting from exposure to dopamine antagonists are commonly termed extrapyramidal syndromes (EPS).<br>b. Some movements decrease and others get worse indicate that<br>The occurrence of acute movement disorders upon exposure to dopamine antagonists is increased in female patients and older patients. Use of potent dopamine antagonists, prolonged exposure to dopamine antagonists, and prior occurrence of acute movement disorders on exposure to dopamine antagonists are also associated with an increased risk for the occurrence of acute movement adverse effects. Withdrawal dyskinesias may also occur as when treatment with dopamine antagonists is decreased or withdrawn. They are often refractory to all therapeutic modalities.

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TD -- define, 3 factors, 5 differential dx

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a. Definition of tardive dyskinesia:<br>A. Abnormal, involuntary, irregular choreoathetoid movements of the head, limbs, and<br>trunk<br>B. A delayed effect (after six months) of antipsychotic treatment<br>C. Peri-oral movements most common<br>1. Darting, twisting, protruding movements of the tongue<br>2. Chewing and lateral jaw movements<br>3. Lip puckering<br>4. Facial grimacing<br>D. Exacerbated by stress, and disappears during sleep<br>E. Not provoked by urges to move<br>b. Epidemiology<br>A. Occurs in about 10 to 20% of patients who are treated for more than one year with<br>typical antipsychotics<br>B. More common in women, mood disorders, brain damage, and children<br>C. Assessed with the AIMS<br>c. Differential diagnosis<br>A. Mannerisms and stereotypies<br>B. Meige’s syndrome and other senile dyskinesias<br>C. Dental problems (ill fitting dentures)<br>D. Sydenham’s chorea<br>E. Drug toxicity (e.g. Levodopa)<br>

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FGA -- MOA on positive, da pathways

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a. Antipsychotic medications reduce the positive symptoms of schizophrenia through the blockade of D2- dopamine receptors in the mesolimbic pathway<br>b. Mesolimbic pathway: reward pathway (from ventral tegmental area to nucleus accumbens)<br>c. Mesocortical pathway: learning and memory, negative symptoms (from substantia nigra and ventral tegmental area to amygdala, septal nuclei, anterior cortex, olfactory tubercle); there is a high density of 5-HT2a receptors in this pathway; the blockade of 5- HT2a by atypical antipsychotics reverses some of the effect of dopamine blockade in this pathway, which may be why the atypicals are somewhat effective in negative symptoms (normally, serotonin inhibits dopamine release; blockage of 5-HT2a therefore increases dopamine release)<br>d. Nigrostriatal pathway: movement (from substantia nigra to caudate and putamen); again, the blockade of 5-HT2a in this pathway counteracts the D2 blockade, leading to less EPS and tardive dyskinesia<br>e. Tuberoinfundibular pathway: prolactin elevation; normally dopamine inhibits prolactin increase – blockade of dopamine causes prolactin elevation; the reverse is true for serotonin

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FGA -- AEs 5 systems other than CNS

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• Gastrointestinal: increased appetite, weight gain, dyspepsia, nausea<br>• Cardiovascular: postural hypotension, tachycardia, EKG changes<br>• Sexual side effects: decreased libido, erectile dysfunction, retrograde ejaculation<br>• Endocrine: elevated prolactin, SIADH<br>• Ocular: retinitis pigmentosa, cataracts, lenticular pigmentation<br>• Hematological: thrombocytopenia, Agranulocytosis

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NMS -- 3 dx criteria, 2 assoc features, 3 interventions

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A. Diagnostic criteria for NMS<br> Muscular rigidity and elevated temperature in response to Neuroleptic treatment; usually occurs within four weeks of starting or increasing dose<br> Diagnosis requires rigidity, fever, and two of: MIDWEST CDC 1. Mutism<br><br>3. Diaphoresis<br>4. White count (leukocytosis)<br>5. Elevated or labile blood pressure<br>6. Shaking (tremor)<br>7. Tachycardia<br>8. Changes in level of consciousness<br>9. Dysphagia<br>10. CPK elevated<br>B. Differential Diagnosis:<br> Anticholinergics induced hyperthermia (dilated pupil, dry skin, but not the rigidity seen in NMS<br> Heat stroke<br> Septic shock<br> Thyrotoxicosis<br> Serotonin syndrome (triad of altered mental status, autonomic dysfunction, and<br>neuromuscular abnormalities) - it requires exposure to serotonin agonist.<br> Malignant hyperthermia<br> Neurological disorders with associated fever (e.g., brain abscess, encephalitis,<br>meningitis)<br>C. Investigations: white count, CPK, renal and liver function, electrolytes (can get<br>dehydration, acidosis)<br>D. Treatment:<br>1. Discontinue Neuroleptic (antipsychotic and anticholinergics)<br>2. Supportive therapy-hospitalization on a medical intensive care unit and provision of<br>hydration and fever-reduction measures (antipyretic, cooling blanket) i.e. (IV fluids,<br>cooling, monitoring)<br>3. Trials of DA agonist (e.g., dopamine agonist bromocriptine or amantadine), muscle<br>relaxants (e.g., Dantrolene, Baclofen, benzodiazepines)<br> Note that NMS is less likely with low potency, anticholinergic antipsychotics  Usually develops within four weeks of starting an antipsychotic<br> Other laboratory abnormalities<br>1. 2. 3. 4. 5. 6.<br>Note: leukocytosis and elevated CPK are the only ones that are part of the criteria Renal failure: myoglobinuria and proteinuria, elevated BUN and Creatinine<br>Liver failure: elevated transaminases<br>Electrolyte changes: low calcium, magnesium, phosphate<br>Acidosis Dehydration

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ddx -- 20yo F psychosis, inv menstrual irreg?

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A. Differential Diagnosis<br>1. consider puerperal psychotic illnesses in women (postpartum psychosis)<br>2. Brief reactive psychosis<br>3. Bipolar disorder, manic episode with psychotic feature<br>4. Substance induced psychosis<br>5. Psychosis secondary to GMC<br>6. Schizoaffective disorder<br>7. Schizophrenia<br>B. Investigation or approach of Menstrual irregularities  Long (missed) cycles (anovulation)<br>1. Stress<br>2. Low body fat<br>3. Hormonal imbalance<br>a. hyperprolactinemia<br>° irregular menstruation, galactorrhea, loss of libido<br>° note prolactinomas can cause eye problems or headaches (these<br>symptoms are more common in men because the clear-cut menstruation<br>symptoms are not seen)<br>° treatment is usually with bromocriptine<br>b. abnormal levels of LH, FSH c. hyperthyroidism<br>d. Cushing’s syndrome<br>4. polycystic ovary syndrome<br>5. menopause<br> Short cycles or heavy bleeding (menorrhagia)<br>1. pregnancy<br>2. hypothyroidism 3. clotting disorders<br>h. To manage medication induced hyperprolactinemia,<br>o Lower the dose of medication, switch medication, or add a dopamine agonist (like bromocriptine)<br>E. Weight gain on neuroleptic medications can best be managed through psychoeducation and lifestyle changes; issues to consider include general health (mental health, physical health), nutrition (healthy diet, nutritionist consult), group support (weight reduction, education)

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Risp -- risk of DM

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a. Patients with schizophrenia have two-fold higher baseline risk for type 2 diabetes; this risk is amplified with atypical antipsychotics<br>b. The increased risk may be due to in large part to weight gain, but there is insulin resistance independent of weight gain (dysregulation may be due to hypothalamic effects)<br>c. All of the atypicals have a higher risk of diabetes, but Risperidone is probably the least risky of them; one study found the risk to be 40% higher with Olanzapine than with no medication; the risks with quetiapine and Risperidone were no different than no medication

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SGA -- adv (3) vs. disadv

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A. Three advantages of atypical<br> Lower rates of extrapyramidal side effects<br> More helpful in treating the negative symptoms of SCZ<br> They are beneficial in the treatment of the anhedonia, flat affect, and avolitional state<br> Have benefits in treating the cognitive disturbance and executive dysfunction that can be disabling in SCZ<br> They have more mood stabilizing properties<br>B. Listthedisadvantagesofatypicals<br> The cost as they are expensive meds<br> Their metabolic side effects (enhanced risk of hyperglycemia and DM, enhanced risk of<br>weight gain, enhanced the risk of CVA), increased in cholesterol profile (HDL, LDL, TGs)

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APs -- What adverse side effect requires weekly blood monitoring? What is the incidence of this side effect? List three other adverse side effects. If the patient starts the medication, then stops smoking, then develops sexual side effects, describe why sexual side effects might be emerging now? What would be your first step in addressing this issue?

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a. Agranulocytosis and its incidence =0.38% with Clozapine and 0.05% with other atypicals<br>b. The other three side effects: are Seizure, constipation, drooling, hypotension, sedation and weight gain, and DM/ hyperlipidemia<br>c. After stopping smoking when started on medication and developed sexual side effects; Nicotine is an enzyme inducer of CYP 1A2/3A4 and Clozapine is a substrate for this enzyme and its level will be decreased, however when stop smoking the Clozapine levels rises up<br>d. 1st step to take is further hx, PE, to R/O out other possible causes, then decrease Clozapine gradually

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Cloz -- 2 most serious AE, and guidelines

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a. The two most serious side effects are<br>i. Agranulocytosis<br> Rate of 0.5 to 2%<br> Most common in the first six months, but can occur at any time  Risk factors: increasing age, female gender<br> Dose-independent<br>ii. Seizures<br> Dose dependent<br> Rates: 5% if &gt; 600mg, 3-4% if 300 to 600mg, 1-2% if &lt; 300mg<br> Myoclonus can be a precursor to seizures<br> Management: temporary stop, and then restart at 50% dose, gradually<br>increasing the dose; add anticonvulsant (not Carbamazepine, due to combined Agranulocytosis risk)<br>b. Baseline measures and monitoring<br>i. Baseline: CBC, renal function, ECG, liver function, CT-head, abdominal X-ray<br><br>ii. Monitoring: weekly WBC and differential for six months, then biweekly<br>iii. React to either WBC or ANC – yellow if ANC 1.5 to 2 or WBC 2 to 3.5 (red if lower, green if higher)<br>iv. For yellow: twice-weekly CBC until return to green<br>v. For red: stop Clozapine, monitor blood work and clinical signs for four weeks

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Cloz -- AE, interactions

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° Do not combine with other drugs that may cause Agranulocytosis (e.g. Carbamazepine,<br>propylthiouracil, sulfonamides, Captopril)<br>° Caution in combination with other drugs that may cause seizures<br>• Clozapine is metabolized by many isoenzymes; o 1A2, the primary one<br>o3A4<br>o2D6<br>o 2C9<br>o 2C19<br>• Cytochrome P450 (CYP) isoenzyme 1A2 (CYP 1A2) activity accounts for 70 % of the<br>variance in Clozapine clearance. This suggests that fluvoxamine (Luvox), a potent inhibitor of CYP 1A2, will elevate Clozapine concentrations, while Fluoxetine (Prozac) may only lead to changes in higher dosage ranges.<br>• Clozapine is metabolized by many pathways including 1A2, 3A4<br>• While phenytoin (Dilantin) and Carbamazepine induce CYP 2C9??? and 3A4 hepatic<br>isoenzymes and may decrease concentrations of Clozapine (≤50 percent).<br>Clozapine rule:<br> If red flag<br>a) WBC&lt;2.0*109<br>b)<br>ANC &lt;1.5<br> Stop Clozaril therapy immediately<br> Monitor CBC and Diff. q daily until WBC comes back to 3.0 and then twice a week until<br>WBC comes back to 3.5<br> Notify Clozaril registry of patients<br> Don’t challenge<br> If Yellow (which)<br>A. 2.0x10/L≤ WBC≤3.5X10/L<br>B. 1.5X10≤ANC≤2.0X10/L<br>C. Flu-like complaints<br>D. Fever<br>E. Single fall or sum of falls in WBC count ≥3.0X10/L is measured in the last 4-weeks, reaching a<br>value &lt;4.0X10/L<br>F. Single fall or sum of falls in ANC count ≥1.5X10/L is measured in the last 4-weeks, reaching a<br>value &lt;2.5X10/L<br> Monitor twice a week until WBC resume to normal and meanwhile continue Clozaril<br> Cholinergic rebound leading to nausea, vomiting, and diarrhea<br> Dopaminergic rebound leading to withdrawal dyskinesia<br> Clozapine substrate is 1A2 which also substrate for Caffeine and 1A2 main inhibitor is Luvox,<br> So it will be lowered by cigarette smoking, phenytoin, and Phenobarbital via (1A2 and 3A4<br>isoenzyme induction)<br> C/I in patients with Hx of Agranulocytosis, or myeloproliferative disorders especially if patient is<br>immunocompromised secondary to HIV infection or TB<br> It should not be used with Carbamazepine (Agranulocytosis) or benzos (increased potential for<br>cardiac or pulmonary arrest)

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Mvt d/o

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a) Ballistic movements<br>a. Ballismus usually occurs as hemiballismus following infarction of the subthalamic nucleus. Hemiballismus is a dramatic disorder in which the patient manifests large- amplitude flinging movements of the arm and leg contralateral to a lesion of the subthalamic nucleus; with time, the movement may evolve into hemi chorea.<br>b. Ballismus is a high-amplitude, violent shooting of the limb from the shoulder or pelvis. It is an extreme version of chorea and is seen in Sydenham's chorea and lupus erythematosus.<br>b) Choreoathetosis<br>a. Dyskinetic movements observed in tardive dyskinesia are a special instance of chorea.<br>c) periodic tachypnea<br>a. Is the less common but more severe Truncal dyskinesia, the torso moves in thrusting motions, and respiratory dyskinesia is characterized by grunting and irregular breathing patterns.<br>b. These include<br>1. Facial grimacing;<br>2. Blinking of the eyes,<br>3. Movement of the eyelids;<br>4. Choreoathetoid movements of the fingers, wrists, ankles and toes;<br>5. Axial hyperkinesia, rocking or torsion movement of neck and trunk or both;<br>6. Diaphragmatic involvement resulting in grunting (glottal dyskinesia) and difficulty<br>breathing.<br>d) Tremor<br>a. Rabbit Syndrome is uncommon medication-induced extrapyramidal syndrome is often misdiagnosed as tardive dyskinesia. It most closely resembles a limited expression of a Parkinsonian tremor. Patients make rapid chewing movements similar to those made by rabbits, ordinarily faster and more regular than the orofacial tics of tardive dyskinesia. The tongue is spared.<br>e) Retrocollis<br>37.<br>•<br>•<br>•<br>Presentation<br>•<br>The diagnosis of primary Erotomanic delusions requires at least one month's duration of the delusion, otherwise generally normal appearance and behaviour and the exclusion of schizophrenia, mood disorder,<br>a. Common types of dystonia include opisthotonos, a rigid contraction of the back muscles with arching; retrocollis and torticollis of the neck; oculogyric crisis, a spasm in which an eye or both eyes are turned upward; macroglossia and tongue protrusion, which can lead to choking; and laryngeal dystonias. Rarely, dystonias of laryngeal or pharyngeal muscles can lead to sudden death.

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ADH / antivasopressin ????

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 AVP or (antidiuretic hormone [ADH]) is a posterior pituitary hormone that maintains plasma osmolarity through regulation of renal water excretion. AVP release is triggered by pain, emotional stress, dehydration, increased plasma osmolarity, or decreases in blood volume.<br> Profound alterations in fluid ingestion and excretion have been observed in psychiatric patients throughout most of the twentieth century. Polydipsia occurs in 10 to 15 percent of hospitalized psychiatric patients and is unrelated to diagnosis.<br> In many cases, the syndrome is secondary to inappropriate secretion of AVP, which occurs as a feature of the altered behavioral state itself and resolves with treatment or, conversely, is precipitated by a variety of antidepressant or antipsychotic agents.

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Erotomania formulation

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De Clerambault's syndrome 1927 Gaetan Gatian de Clerambault<br />Synonyms: erotomania (a delusion of passion), erotomanic delusion, paranoia erotica, psychose passionelle.<br />A form of paranoid delusion with an amorous quality.<br />Age at onset is usually middle or late adulthood, and the course is v<br />Social:<br />- The patient, often a single woman, believes that an exalted person is in love with her. - often isolated, unemployed, and with few social contacts<br />- Functional deterioration<br /> Biological:<br />- Familial transmission is suspected,<br />Epilepsy and a left frontal lobe lesion. Psychological:<br />- Co-morbidity (frequently mood disorders) may exist mood disorder, substance-induced toxicity, and medical disease, schizo-affective disorder, major depression, bipolar disorder or Alzheimer's disease<br />- Patients are unaware of the psychiatric nature of the condition.<br />may develop delusions of persecution<br />Violent against those they believe stand in the way of their delusional love.<br /><br />Presentation<br />The diagnosis of primary Erotomanic delusions requires at least one month's duration of the delusion, otherwise generally normal appearance and behaviour and the exclusion of schizophrenia, mood disorder, substance-induced toxicity, and medical disease. Typically, patients are unaware of the psychiatric nature of the condition.<br />Usually the supposed lover is inaccessible, e.g. a famous television performer who she only sees whilst watching the television.<br />The patient often believes that it is the subject of her delusion that is more in love with her than she with him is, and takes great pride in this. She may feel that the subject cannot live happily without her.<br />The patient may believe that the subject of her delusion cannot make his feelings known because of various reasons, for example difficulties in approaching her.<br />This type of delusional disorder may lead to stalking or other potentially threatening and dangerous behaviour. The police may get involved in trying to keep her from pestering the subject, but this may be perceived as a paradoxical sign of affection.<br />The patient may continue to pester the subject and may develop delusions of persecution following the delusions of passion.<br />They may also be violent against those they believe stand in the way of their delusional love.<br />A thorough psychiatric evaluation is essential in diagnosis and assessment of possible co-morbity. <br /><br />A perpetrator of child sexual abuse is, despite all medical definitions, commonly assumed to be a<br />pedophile, and referred to as such; however, there may be other motivations for the crime (such as stress, marital problems, or the unavailability of an adult partner), much as adult rape can have non- sexual reasons. Thus, child sexual abuse alone may or may not be an indicator that its perpetrator is a pedophile; most perpetrators of it are in fact not primarily interested in children.<br />Those who have committed sexual crimes against children, but do not meet the normal diagnosis criteria for pedophilia, are referred to as situational, opportunistic, or regressed offenders, whereas offenders primarily attracted toward children are called structured, preferential, or fixated pedophiles, as their orientation is fixed by the structure of their personality. It is estimated that only 2 to 10 percent of child sexual abuse perpetrators meet the regular criteria for pedophilia. There are generally large distinctions between the two types of offenders' characteristics. Situational offenders tend to offend at times of stress; have a later onset of offending; have fewer, often familial victims; and have a general preference for adult partners. Pedophilic offenders, however, often start offending at an early age; often have a large number of victims who are frequently extrafamilial; are more inwardly driven to offend; and have values or beliefs that strongly support an offense lifestyle.<br />Most cases of father-daughter incest are believed to involve fathers who are situational offenders, rather than pedophiles. Attempts have been made to use &quot;profiling&quot; to identify pedophiles; however, these methods have come under sharp criticism for making claims that are far in excess of what the evidence supports.<br /><br />&quot;Diagnostic criteria for Pedophilia&quot;:<br />• Over a period of at least 6 months, recurrent, intense sexually arousing fantasies, sexual urges, or behaviors involving sexual activity with a prepubescent child or children (generally age 13 years or younger).<br />• The person has acted on these urges, or the sexual urges or fantasies cause marked distress or interpersonal difficulty.<br />• The person is at least age 16 years and at least 5 years older than the child or children in Criterion A.<br />Three other specifications figure in this classification system: (1) whether the client is sexually attracted to males, females, or both; (2) whether the offenses are limited to incest; and (3) whether the client is an “exclusive” (attracted only to children) or “nonexclusive” type<br />Schneiderian first rank symptoms and include delusions of being controlled by an external force, the belief that thoughts are being inserted into or withdrawn from one's conscious mind, the belief that one's thoughts are being broadcast to other people and hearing hallucinated voices which comment on one's thoughts or actions, or may have a conversation with other hallucinated voices.

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DDx -- obs thoughts / comp rituals bizarre; +/- del of reference. Psychosis tx vs ocd. Risk of atypical. How obs / del distinguished? how neg sx and dept disting? how manage if want to d/c meds?

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a. The differential diagnosis of obsessive-compulsive disorder includes: 1. Depressive disorders,<br>For example, the ruminative thoughts of depressed patients may be differentiated from obsessive preoccupations in that depressed patients usually do not consider their thoughts absurd or alien and not attempt to block or avoid them. The patient with depression who is preoccupied with the thought &quot;I am worthless&quot; experiences this thought as reasonable and accepts it as part of himself or herself. On the other hand, the patient with obsessive-compulsive disorder who is preoccupied with the thought &quot;If I touch a public telephone I will become contaminated and infect my children&quot; will often consider this thought absurd and foreign.<br>2. Generalized anxiety disorder and<br>Patients with generalized anxiety disorder may present with excessive worries that resemble obsessive thinking; however, they usually consider these worries to be realistic and appropriate rather than absurd. Sometimes the patient with obsessive-compulsive disorder has obsessional concerns that become so intense and irrational that the patient may appear to be psychotic. However, true obsessions are usually accompanied by some form of compulsive ritual, whereas this is not usually the case in patients with delusional thinking.9<br>3. Hypochondriasis.<br>Of particular importance in the family practice setting is the ability to differentiate between obsessive- compulsive disorder and hypochondriasis. Patients with hypochondriasis may present with unrealistic preoccupations with physical disease that closely resemble obsessive ruminations. In addition, somatic checking rituals and frequent visits to the physician's office for reassurance may play an anxiety-reducing role similar to that of compulsive rituals. Typically, however, the patient with hypochondriasis will not present with apparent compulsive rituals. In those cases where the patient does present with ritual behavior designed to decrease the anxiety associated with the somatic ruminations, a diagnosis of obsessive-compulsive disorder may be appropriate.<br>4. Other psychiatric disorders A. Anorexia nervosa<br>B. Body dysmorphic disorder<br>May have obsessive preoccupations with physical appearance, but these are not considered manifestations of obsessive-compulsive disorder because they occur in the context of another psychiatric disorder. The &quot;compulsive&quot; behavior of pathologic gamblers or substance abusers differs from true compulsions in that the patient typically finds them pleasurable, at least initially. The diagnosis of obsessive-compulsive personality disorder, with its preoccupation with orderliness and perfectionism, is often confused with obsessive- compulsive disorder but may be distinguished from it by its lack of obsessions or compulsions and by its unresponsiveness to psychotropic medications<br>b. What if the person also endorses delusions of reference?<br>1. OCD and psychosis may coexist by chance and may be unrelated.<br>2. An obsession may become a delusion or vice versa.<br>3. A reactive delusion of guilt or persecution may develop.<br>4. An obsession may trigger a psychotic episode or vice versa.<br>5. Obsessions may be misdiagnosed as delusions or hallucinations.<br>6. Recognition and treatment of OCD may improve the outcome of psychosis<br>c. What are the treatments for OCD and for psychosis (guidelines)<br>d. Risk of starting an atypical antipsychotic<br>1.CNS antagonist H1, Ach, α1..........Headache 10-15% Outpatient 19%<br>A. cognitive: sedation first 2 weeks<br>Sedation<br>Insomnia, nightmares<br>Confusion, disorientation, toxic delirium, concentration Dysphoria<br>Improve cognition: 5HT1a, attention, information processing<br>Exacerbate OCD<br>Anxiety agitation, hypomania, mania, panic, aggression (OLNZ) Sleep walking, sleep eating disorder<br>B. Neurological D2 antagonist EPS binding &gt;80%<br>1. Seizures: SIADH, ↓ threshold: CLOZ 1%-300, 2.7%-600, 4.4%&gt;600 60%EEG, 0.8% QTB, 0.3% RESP<br>2. Motor ticks, myoclonus jerks, cataplexy<br>3. EPS: OLNZ 38%, 28% RES, 13% QTP lowest CLOZ, QTP<br>4. Akathesia 38%<br>5. Pisa syndrome (dementia), Rabbit syndrome (CLOZ), loss gage reflex, Dysphagia, Sialorrhea<br>(CLOZ)<br>6. Urinary incontinence, enuresis (42% CLOZ) , pain (8% CLOZ), paresthesias<br>7. TD (dementia RESP 2.6%)<br>8. CVA, TIA death (RES, OLNZ dementia).<br>2.Anticholinergic antagonism : muscarinic Ach<br>1. dry mouth , blurred vision, constipation, urine retention,<br>2. disorientation, confusion, memory, fever<br>3.CVS block α1 and muscarinic<br>1. hypotension<br>2. bradycardia (i.m OLNZ)<br>3. ECG: T, QT (female age lytes CAD), ST, MI (OLNZ), Death (arrhythmia Torsades de<br>pointes)<br>4. cardiomyopathy, myocarditis, pericarditis, CHF, mitral valve NOT USE with severe<br>heart disease<br>4.GI : 5HT 1b,2c, α1, H1<br>1. weight gain: due to: prolactenemia, gonadal, adrenal steroid imbalance, high leptin, insulin resistance, carbohydrate craving (thirst): 50% gain 20% of there (low BMI, first 6 wk except CLOZ, females, mental R, dose related, polycystic ovaries, plateau RESP QTP), lead to CAD , hyperglycemia, sleep apnea<br>2. anorexia, nausea, diarrhea, dyspepsia, Dysphagia, vomiting, constipation, esophagitis (11% CLOZ), Sialorrhea M4 muscarinic, α2 (80%CLOZ)<br>5.Sexual: D2, Ach, α1, H1 5HT2<br>1. libido, impotence, ejaculation, erectile, Priapism<br>2. Rx: neostigmine, Cyproheptadine,<br>6.Endocrine<br>1. prolactin: if 50-75% D2 occupancy normalize 12-24h except RISP (8-15%), related to dose of OLNZ&gt;20mg, Rx : carbergoline<br>2. breast enlargement, gynecomastia<br>3. Hyperinsulinemia, metabolic syndrome: obesity, hyperlipidemia: Cholesterol (CLOZ 48%, OLNZ,<br>QTP 25%, And RIS 21%) Triglyceride ( CLOZ 48% M 35% F, OLNZ 38%, QTP 40%, REP 31%)<br>highest with CLOZ, OLAZ lowest Ziprasidone, hypertension, disturbed glucose and insulin<br>4. PIP: polydipsia, hyponatremia, psychosis 6-20% (elderly, smokers, alcoholics)<br>5. tT4, fT4 increase (QTP)<br>7.ocular lens changes estropia (strabismus) 8.Hypersensitivity<br>1. cholestatic jaundice 0.1% reversible<br>2. high liver enzymes OLNZ 6%, CLZP 37%, QTP 9%<br>3. Agranulocytosis 1-2% COLZ CYP3A4<br>4. eosinophilic transient 5.7%<br>5. leukocytosis 41% with COLZ<br>6. NMS : any time any dose ( Polypharmacy, organic brain, mood, dehydration, low Na , exhaustion,<br>Agitation) 0.2% CLOZ mortality 4% Rx ECT Dantrolene amantadine bromocriptine<br>9.Temperature transient increase 55% with CLOZ 10. Epistaxis Rhinitis<br><br>OCD<br><br>Delusions<br><br>ego-dystonic&quot;<br><br><br>Ego syntonic<br><br>thoughts resistance<br>Defend the thoughts<br><br>intrusive<br><br><br>inserting<br>hear the thoughts inside their head<br>outside<br><br>Absurdity, senselessness<br><br><br>Insight<br><br><br><br><br>e. How are negative symptoms and depression distinguished?<br>The negative symptoms of schizophrenia include symptoms such as deficiencies in emotional responsiveness, spontaneous speech and volition. Around a half to three-quarters of people with chronic schizophrenia, exhibit some features of negative symptoms of schizophrenia.<br>Primary negative symptoms; are shown in flattening of affect, poverty of speech, lack of volition and drive, loss of feeling, social withdrawal and decreased spontaneous movement.<br>Negative syndrome in schizophrenia is a distinct dimension of psychopathology. The core negative symptoms such as flattened affect and poverty of speech may be particularly stable over time and less responsive to treatment. Negative symptoms occur in those with bipolar disorder and major depression as well as those with schizophrenia.<br>Primary and secondary negative symptoms<br>There is an overlap between negative symptoms, depressive features and neuroleptic side-effects, particularly somnolence and bradykinesia due to drug-induced parkinsonism. It may be very difficult to distinguish between persistent, primary negative symptoms that are component of the illness, and negative symptoms secondary to depressive features, drug side-effects or positive symptoms.<br>Withdrawal, Loss of Motivation and Ambivalence (Avolition)<br>This may involve lack of energy, apathy or seeming absence of interest in what were usually routine activities. People experiencing Avolition may be inattentive to grooming, personal hygiene, have difficulty making decisions and have difficulty persisting at work, school or household chores.<br>Loss of Feeling or an Inability to Experience Pleasure (Anhedonia)<br>This may manifest itself through having a lack of interest in social or recreational activities or through failure to develop close relationships. It may mean that the simple pleasures of life, like appreciating a beautiful sunset, being no longer enjoyed.<br>Poverty of Speech (Alogia)<br>The person's amount of speech is greatly reduced and tends to be vague or repetitious. People showing signs of alogia may be slow in responding to questions or not respond at all.<br>Flat Presentation (Affective Flattening)<br>Unchanging facial expressions, poor or no eye contact, reduced body language and decreased spontaneous movements. A person experiencing affective flattening may stare vacantly into space and speak in a flat, toneless voice. Flat affect refers to the outward expression of emotion and not the inner experience.<br>Some people with schizophrenia experience negative symptoms prior to and after an acute episode of the illness. However, the negative symptoms are difficult to assess because they may be caused by a variety of other factors such as medication side effects, mood disorders or the demoralization often felt as a consequence of a mental illness.

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scz and cannabis

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Marijuana is the most commonly abused illicit drug in the United States. A dry, shredded green/brown mix of flowers, stems, seeds, and leaves of the hemp plant Cannabis sativa, it usually is smoked as a cigarette (joint, nail), or in a pipe (bong). It also is smoked in blunts, which are cigars that have been emptied of tobacco and refilled with marijuana, often in combination with another drug. It might also be mixed in food or brewed as a tea. As a more concentrated, resinous form, called hashish and, as a sticky black liquid, hashes oil. Marijuana smoke has a pungent and distinctive, usually sweet-and-sour odor. There are countless street terms for marijuana including pot, herb, weed, grass, widow, ganja, and hash, as well as terms derived from trademarked varieties of cannabis, such as Bubble Gum, Northern Lights, Fruity Juice, Afghani #1, and a number of Skunk varieties.<br>The main active chemical in marijuana is THC (delta-9-tetrahydrocannabinol). The membranes of certain nerve cells in the brain contain protein receptors that bind to THC. Once securely in place, THC kicks off a series of cellular reactions that ultimately lead to the high that users experience when they smoke marijuana.<br>Effects on the Brain<br>Scientists have learned a great deal, about how THC acts in the brain to produce its many effects. When someone smokes marijuana, THC rapidly passes from the lungs into the bloodstream, which carries the chemical to organs throughout the body, including the brain. In the brain, THC connects to specific sites called cannabinoid receptors on nerve cells and influences the activity of those cells. Some brain areas have many cannabinoid receptors; others have few or none. Many cannabinoid receptors are found in the parts of the brain that influence pleasure, memory, thought, concentration, sensory and time perception, and coordinated movement.<br>The short-term effects include problems with memory and learning; distorted perception; difficulty in thinking and problem solving; loss of coordination; and increased heart rate. Long-term marijuana abuse can cause changes in the brain as those seen in other major drugs. For example, cannabinoid (THC or synthetic forms of THC) withdrawal in chronically exposed animals leads to an increase in the activation of the stress-response system and changes in the activity of nerve cells containing dopamine. Dopamine neurons are involved in the regulation of motivation and reward, and are directly or indirectly affected by all drugs of abuse.<br>Effects on the Heart<br>One study has indicated that an abuser's risk of heart attack more than quadruples in the first hour after smoking marijuana. This suggest that such an effect might occur from marijuana's effects on blood pressure and heart rate and reduced oxygen-carrying capacity of blood.<br>Effects on the Lungs<br>People who smoke marijuana frequently but do not smoke tobacco have more health problems and miss more days of work than nonsmokers. Many of the extra sick days among the marijuana smokers in the study were for respiratory illnesses. Smoking marijuana possibly increases the likelihood of developing cancer of the head or neck. A study comparing 173 cancer patients and 176 healthy individuals produced evidence that marijuana smoking doubled or tripled the risk of these cancers. Marijuana abuse also has the potential to promote cancer of the lungs and other parts of the respiratory tract because it contains irritants and carcinogens. In fact, marijuana smoke contains 50 to 70 percent more carcinogenic hydrocarbons than tobacco smoke. It also induces high levels of an enzyme that converts certain hydrocarbons into their carcinogenic form—levels that may accelerate the changes that ultimately produce malignant cells. Marijuana users usually inhale more deeply and hold their breath longer than tobacco smokers do, which increases the lungs' exposure to carcinogenic smoke. These facts suggest that, puff for puff, smoking marijuana may be more harmful to the lungs than smoking tobacco.<br>Effects of Heavy Marijuana Use on Learning and Social Behavior<br>Research clearly demonstrates that marijuana has the potential to cause problems in daily life or make a person's existing problems worse. Depression, anxiety, and personality disturbances have been associated with chronic marijuana use. Because marijuana compromises the ability to learn and remember information, the more a person uses marijuana the more he or she is likely to fall behind in accumulating intellectual, job, or social skills. Moreover, research has shown that marijuana’s adverse impact on memory and learning can last for days or weeks after the acute effects of the drug wear off. The ability of long-term heavy marijuana abusers to recall words from a list remained impaired for a week after quitting, but returned to normal within 4 weeks. Thus, some cognitive abilities may be restored in individuals who quit smoking marijuana, even after long-term heavy use. Workers who smoke marijuana are more likely than their coworkers to have problems on the job are.<br><br>Several studies associate workers' marijuana smoking with increased absences, tardiness, accidents, workers' compensation claims, and job turnover. A study among postal workers found that employees who tested positive for marijuana on a pre-employment urine drug test had 55 percent more industrial accidents, 85 percent more injuries, and a 75-percent increase in absenteeism compared with those who tested negative for marijuana use. In another study, heavy marijuana abusers reported that the drug impaired several important measures of life achievement including cognitive abilities, career status, social life, and physical and mental health.<br>Effects of Exposure during Pregnancy<br>Research has shown that some babies born to women who abused marijuana during their pregnancies display altered responses to visual stimuli, increased tremulousness, and a high-pitched cry, which may indicate neurological problems in development. During the preschool years, marijuana-exposed children have been observed to perform tasks involving sustained attention and memory more poorly than nonexposed children do. In the school years, these children are more likely to exhibit deficits in problem-solving skills, memory, and the ability to remain attentive.<br>Addictive Potential<br>Long-term marijuana abuse can lead to addiction for some people; that is, they abuse the drug compulsively even though it interferes with family, school, work, and recreational activities. Drug craving and withdrawal symptoms can make it hard for long-term marijuana smokers to stop abusing the drug. People trying to quit report irritability, sleeplessness, and anxiety. They also display increased aggression on psychological tests, peaking approximately one week after the last use of the drug.<br>Genetic Vulnerability<br>Scientists have found that whether an individual has positive or negative sensations after smoking marijuana can be influenced by heredity. A 1997 study demonstrated that identical male twins were more likely than nonidentical male twins to report similar responses to marijuana abuse, indicating a genetic basis for their response to the drug. (Identical twins share all of their genes.)<br>It also was discovered that the twins' shared or family environment before age 18 had no detectable influence on their response to marijuana. Certain environmental factors, however, such as the availability of marijuana, expectations about how the drug would affect them, the influence of friends and social contacts, and other factors that differentiate experiences of identical twins were found to have an important effect.<br>Treating Marijuana Problems<br>Marijuana was the primary drug of abuse in about 15 percent of all admissions to treatment facilities in the United States. Marijuana admissions were primarily male (75 %), White (55 %), and young (40 % were in the 15-–19 age range). Those in treatment for primary marijuana abuse had begun use at an early age; 56 percent had abused it by age 14 and 92 percent had abused it by 18.<br>One study of adult marijuana abusers found comparable benefits from a 14-session cognitive-behavioral group treatment and a 2-session individual treatment that included motivational interviewing and advice on ways to reduce marijuana use. Participants were mostly men in their early thirties who had smoked marijuana daily for more than 10 years. By increasing patients' awareness of what triggers their marijuana abuse, both treatments sought to help patients devise avoidance strategies. Abuse, dependence symptoms, and psychosocial problems decreased for at least 1 year following both treatments; about 30 percent of the patients were abstinent during the last 3-month follow-up period. Another study suggests that giving patients vouchers that they can redeem for goods—such as movie passes, sporting equipment, or vocational training—may further improve outcomes.<br>What if he finds the antipsychotic too sedating?<br>Management of Side Effects Canadian guidelines 2005<br>1. Weight Gain and Abdominal Obesity<br>All antipsychotics may increase body weight, but a differential liability is well known among agents. Clozapine and olanzapine have been associated with significant weight gain; risperidone and quetiapine have been associated with moderate weight gain. Detailed mechanisms underlying body fat, particularly visceral fat, and<br><br>accumulation are unknown. Lean persons as well as young patients seem to be particularly vulnerable to<br>dramatic weight gain, but no clinical tool is yet available to predict such an effect. Combinations with some psychotropic drugs such as lithium, Valproate, and some antidepressants may significantly worsen the weight- gain profile. Preventive lifestyle strategies should be encouraged, even if it is well known that, such strategies<br>are difficult to implement, not only in patients with schizophrenia but also in the general population. Benefits of physical activities and good nutrition habits should be emphasized both to the patient and to his or her family. If prevention is insufficient to limit weight gain, a change to an antipsychotic with a lower weight-gain liability could be considered. In such cases, modification of lifestyle habits should still be a goal. (The Canadian<br>Task Force on Preventive Health Care recommendations on the detection, prevention, and treatment of obesity are available on-line at www.ctfphc.org/Tables/Obesity_tab.htm.)<br>Impairment in Glucose Regulation and Diabetes<br>Many glucose abnormalities have been reported with atypical antipsychotic treatment: insulin resistance, hyperglycemia, exacerbation of type-I diabetes, new onset of type-II diabetes mellitus, and diabetic Ketoacidosis. Additional studies are required to determine the differential liability of glucose impairment among agents and the differences in liability possibly owing to genetic factors. It is possible that there are differential responses between atypical agents; however, this is a subject of active debate. In Canada, all SGAs carry a warning for potential glucose abnormalities. If diabetes is diagnosed, the Canadian Diabetes Association Guidelines should be followed. A switch of antipsychotic could be considered in some cases, although few studies have directly assessed the impact of a switch on metabolic parameters.<br>Dyslipidaemia<br>Second-generation antipsychotics may elevate lipids. Clinical experience and published reports indicate that Clozapine and olanzapine can be associated with hyperlipidemia. A few cases have also been reported with<br>the use of quetiapine, while risperidone appears to be more neutral.<br>The 2003 update of Canadian recommendations for the management of Dyslipidaemia should be followed when lipids abnormalities are detected. A switch of antipsychotic could be considered in some cases, but advantages still need to be confirmed. (Clinical guidelines on dyslipidemia are available on-line. Psychiatrists should participate in the implementation and follow-up of both nonpharmacologic and pharmacologic treatment in such cases.<br>QT Prolongation<br>Prolongation of the QT interval is an ECG abnormality that can lead to torsades de pointes, arrhythmia, syncope, ventricular fibrillation, and sudden death. Risk seems to be greater with QTc values over 500 ms. Thioridazine<br>has for some time not been permitted as a first-line antipsychotic, owing to concerns about QT prolongation, and<br>is now off the market. FGAs such as mesoridazine and Pimozide should be avoided in patients with heart disease, familial history of death at an early age (aged 40 years and under), and congenital long QT syndrome.<br>Endocrine and Sexual Side Effects<br>In women, changes in libido, delayed or absent orgasm, menstrual changes, or galactorrhea and, in men, changes<br>in libido, erectile or ejaculatory troubles, or galactorrhea are among frequently experienced side effects, especially with FGAs.<br>III. Pharmacotherapy<br>Hyperprolactinemia may lead to decreased production of gonadal hormones in both men and women and may in part explain sexual side effects, along with modulation of neurotransmitters. Prolonged hyperprolactinemia and decreased hormonal levels may increase risk of osteopenia, osteoporosis, and impaired reproductive function in women. SGAs show a lesser degree of elevation of prolactin levels, with the exception of risperidone, which is frequently associated with marked and sustained hyperprolactinemia, particularly if higher dosages are used. Transient prolactin elevation is possible with olanzapine. Quetiapine and Clozapine are considered prolactin-sparing agents. Still, sexual dysfunctions may be seen with all available antipsychotics, regardless of their propensity to induce prolactin elevation. In the presence of signs and symptoms of endocrine disturbance or impaired sexual functioning, a dosage reduction of the antipsychotic may be attempted. If unsuccessful, a switch to a prolactin- sparing agent should be tried. If adjunctive medication, particularly a selective serotonin reuptake inhibitor, is also being prescribed, the need for these medications should be reassessed. Careful attention should be paid to issues of birth control for women changing from an FGA or risperidone to a prolactin-sparing agent, since fertility level may be unexpectedly restored.<br><br>Cognitive Side Effects and Sedation<br>FGAs induce sedation, and many patients complain of a subjective dulling effect. Cognitive testing has shown no benefit in cognitive functioning with FGAs. SGAs appear to show statistically significant improvements in cognitive performance. Significant sedation may still occur, at least transiently, mainly with Clozapine but also to a lesser extent with olanzapine and quetiapine. It is worse during the titration phase and may remit over time, but in some patients, increased sleep time and excessive diurnal sedation persist. Risperidone may be associated with both mild sedation and insomnia in some cases. High risperidone dosages (and to a lesser extent, high olanzapine dosages) increase EPSs, which in turn may impair cognitive performance. Concomitant agents such as anticholinergics or anticonvulsants may increase cognitive problems. The therapeutic goal should be to at least prevent any cognitive harm and, ideally, to promote cognitive performance. In case of persistent cognitive dulling or sedation, dosage reduction should be tried. If insufficient, a switch to another agent should be considered.<br>Extrapyramidal Side Effects<br>EPS are particularly associated with FGA medications. Acute reactions occurring in the first days or weeks of treatment include dystonia, Parkinsonism (akinesia or bradykinesia, tremor, and rigidity), and akathisia. Chronic side effects, some irreversible and appearing months or years after treatment, include TD and tardive dystonia. Neurologic side effects are the major burden of FGAs and a limitation to their use. When used in the recommended dosage range, risks of neurologic side effects from SGAs are minimal, but subtle signs of tremor, rigidity, and akathisia still can be detected and could be easily mistaken for anxiety, agitation, or negative symptoms. Higher dosages of Risperidone (and to a lesser extent olanzapine) are associated with a higher risk of EPSEs. If neurologic symptoms are detected, a dosage reduction of the antipsychotic should be tried, or switch to another SGA. A Benzodiazepine or beta-blocker can be prescribed for akathesia if a dosage reduction is insufficient. Anticholinergic medication is usually not recommended with the use of SGAs. The annual risk of TD with FGAs is about 4% to 5%, with a cumulative risk of up to 50%, even when low dosages are used. SGAs are possibly associated with a reduced risk, where Clozapine exhibits the lowest risk and may improve existing TD. Symptoms are not alleviated by antiparkinsonian medication and may worsen. A switch to an SGA is recommended, and a Clozapine trial should be considered in the presence of persistent symptoms of TD. There is no evidence-based treatment formally indicated for TD, so prevention is the preferred strategy.<br>Neuroleptic Dysphoria<br>Neuroleptic dysphoria includes various subtle, unpleasant, subjective changes in arousal, mood, thinking, and motivation. It is associated with noncompliance, substance abuse, poor clinical outcome, increased suicidality, and compromised quality of life. SGAs are less likely to induce such dysphoric responses.<br>Neuroleptic Malignant Syndrome<br>Neuroleptic malignant syndrome (NMS) is a rare and severe condition with symptoms of rigidity, tachycardia, and hyperthermia, elevated levels of serum creatine kinase, autonomic dysfunctions, and altered consciousness. It can occur with any antipsychotic agent, at any dosage, and any time. NMS constitutes a medical emergency with a high mortality rate. Risk factors include young age, male sex, neurologic disabilities, dehydration, exhaustion, agitation, and rapid or parenteral administration of antipsychotic. This side effect is potentially fatal if not managed promptly. Antipsychotic medication should be stopped and supportive therapy instituted. Agonists such as dantrolene, bromocriptine, or amantadine may improve symptoms.<br>His family doctor has told him that mixing marijuana and the antipsychotic would kill him–how do you respond to that<br>Cannabis use has been associated with a doubled the risk of psychosis onset, according to a comprehensive review. For the long-term stable phase of the illness, specialized interview methods should be considered to identify concurrent substance abuse. In terms of psychosocial treatments, difficulties in even engaging the patient in therapy pose the first and seemingly biggest obstacle to recovery. Mental health workers familiar with the stages of change model recognize that many individuals who abuse substances are not even considering making a change in their substance use lifestyle, a phase termed Precontemplation. Motivational interviewing is a technique that has been shown to be effective in moving patients toward considering making changes (contemplation phase) and eventually taking action such as entering treatment. The most effective outpatient treatment for substance abuse disorders involves a comprehensive, integrated approach. The historical dual-treatment team approach not only lacks cohesiveness but also has in the past provided discrepant messages on issues such as the role of medications in recovery and the failure to accommodate the addiction therapy to the cognitive learning deficits associated with schizophrenia. Integrated residential treatment, especially over a period of up to 1 year, has also proven to be successful, especially for those who do not respond to outpatient intervention. The prevalence of “legal” drug use, including nicotine, caffeine, and alcohol, has been found to be higher among individuals with schizophrenia. Significant associated health hazards exist, including complications with psychopharmacologic intervention. Specialized behaviour based interventions for smoking cessation has been tailored successfully for schizophrenia patients. There are suggestions that patients treated with Clozapine, and possibly other atypical antipsychotics, may smoke less after being switched from a first-generation treatment.<br>While the typical antipsychotics are of limited value in controlling substance use in schizophrenic patients, previous studies suggest that the novel antipsychotic Clozapine (CLOZ) may decrease their substance use. We describe a retrospective study of the effects of the novel antipsychotics risperidone (RISP) and Clozapine on alcohol and cannabis use in patients with schizophrenia or schizoaffective disorder and comorbid alcohol and/or cannabis use disorder. While the limitations of this retrospective study must be recognized, the data suggest that comorbid patients treated with Clozapine are more likely to abstain from alcohol and cannabis use than are those treated with risperidone. Further prospective studies will be required to confirm these intriguing results.<br>Patients were evaluated with multiple efficacy and safety measures at baseline and then monthly thereafter. Statistically significant improvement was noted in psychopathology, levels of hope, and safety measures. Seventy percent (n = 21) of the patients achieved early full substance abuse remission at the end of the study period, while 30% (n = 9) achieved early partial substance abuse remission. Our results indicate that olanzapine treatment improved psychopathology, increased hopefulness, and reduced antipsychotic-associated side effects. The benefits observed with olanzapine treatment may contribute to the patients’ substance abuse remission<br>Research on the optimal pharmacotherapy for people with schizophrenia and co-occurring substance use disorders remains in its infancy. This report reviews existing data and provides an update on recent research. The confluence of findings is consistent with a model of a reward dysfunction inherent in the neuropathology of schizophrenia, leading to a heightened vulnerability of people with schizophrenia to substance use disorders. Studies indicate that patients with dual disorders have difficulty tolerating conventional antipsychotics, have higher rates of medication nonadherence, and have greater impulsivity and sensation seeking. Limited evidence suggests that Clozapine treatment may be associated with reduced substance abuse, with weaker evidence suggesting that other novel antipsychotics may have similar, but potentially less potent, effects. Controlled trials to test the effects of these medications are underway. A number of recent studies indicate that Bupropion can facilitate reduced tobacco smoking among patients with schizophrenia. The preferential use of novel antipsychotics, a lower threshold for prescription of Clozapine, the use of Bupropion for smoking cessation, careful monitoring of compliance and possible use of other medications for substance use disorders when indicated are recommended in pharmacologic management for people with co-occurring substance use disorders and schizophrenia.

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SCZ -- catatonic define, ddx

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2 of:<br />a. motoric immobility evid by catalepsy (incl. waxy flexibility) or stupor<br />b. excessive motor activity (purposeless / not influenced by external stim)<br />c. extreme negativism (motiveless resist to all instructions or maint. rigid posture vs attempts) or mutism<br />d. peculiarities of voluntary mvt evid by posturing, stereotyped mvt, prominent mannerisms, or prominent grimacing<br />e. echolalia or echopraxia<br /><br />Differential Diagnosis;<br />1. Elective mutism; is usually associated with preexisting personality disorder, identifiable stressors, and no other catatonic features. Lorazepam (or amobarbital) challenge, to which 50%–70% of patients with catatonia respond, may not resolve elective mutism<br />2. metabolic-induced stupor<br />3. Parkinson’s disease; also resembles catatonia. Patients with akinetic Parkinsonism may be mute and immobile and<br />may posture. This condition usually occurs after years of illness with Parkinsonian symptoms and dementia.<br />Benzodiazepines do not relieve akinetic Parkinsonism, but anticholinergic drugs may provide some benefit.<br />4. Malignant hyperthermia; looks like malignant catatonia and has been associated with neuroleptic malignant<br />syndrome. Malignant hyperthermia is an autosomal dominant transmitted muscle sensitivity to inhalation anesthetics<br />and depolarizing muscle relaxants that is confirmed by muscle biopsy.<br />5. Locked-in syndrome; the mutism of the locked-in syndrome is associated with total immobility except for vertical<br />eye movements and blinking. These patients typically try to communicate by these movements, whereas patients with catatonia make little or no effort to communicate. Unlike the primary akinetic mutism of catatonia, the mutism of locked-in syndrome is accompanied by no other catatonic features, does not respond to Lorazepam challenge, and is usually associated with lesions in the ventral pons and both cerebellar peduncles.<br />6. Stiff-person syndrome is similar to but distinguishable from catatonia; is associated with painful spasms that are precipitated by touch, noise, or emotional stimuli. Baclofen, which can relieve stiff-person syndrome, may induce catatonia<br />Distinguishing catatonic excitement from manic excitement is problematic. Both states seem purposeless, are sudden in onset, and are of short duration. Both are associated with psychosis. That so many patients with catatonia meet the criteria for manic- depressive illness further blurs distinctions. Kahlbaum characterized catatonic excitement by &quot;hystrionic exaltation, expansive mood permeating all speech [with] constant declamations and recitations accomplished by lively gesticulations [and] sudden short-lived joy&quot;. Bleuler described catatonic excitement as a &quot;hyperkinetic [state] with flight of ideas [during which the patient will] cry, sing, verbigerate, laugh, curse, scream, and spit. They grimace, showing sadness, happiness or horror.&quot; Other than, by the presence of catatonia, the mania associated with catatonia cannot be distinguished from mania without catatonia. A parsimonious conclusion is that the validity of catatonic excitement is unproven, and the presence of excitement during a catatonic episode indicates an underlying manic-depressive illness.<br />Cause of Catatonia a. Mood Disorder<br />despite the historic linkage of catatonia with schizophrenia, catatonic episodes are most commonly associated with mood disorder, particularly mania. The more severe the mania, the more likely that catatonic features will also be present. Most catatonic episodes were preceded by episodes of depression and mania. Bleuler commented that &quot;as a rule catatonic symptoms mix with the manic and the melancholic conditions&quot; (emphasis ours). Kraepelin reported that nearly 50% of catatonic attacks begin with a depressive episode that catatonia is often associated with mania, and that dementia praecox patients with catatonia were likely to recover. Many authors link catatonia to manic-depressive illness. Their findings suggest that 25% or more of manic patients have enough catatonic features to meet the DSM criteria and that more than half of catatonic patients have manic-depressive illness.<br />b. General Medical and Neurologic Conditions<br />Catatonia is a feature of many general medical conditions. Metabolic disturbances, Endocrinopathies, viral infections (including HIV), typhoid fever, heat stroke, and autoimmune disease, all of which are commonly associated with delirium, are also associated with catatonia. Drug intoxications and withdrawals may induce catatonia. These drug-related conditions include exposure to antipsychotic drugs and illicit recreational drugs, withdrawal from benzodiazepines and dopaminergic drugs and opiate intoxication. Neurologic conditions associated with catatonia include postencephalitic states, parkinsonism, bilateral globus pallidus disease, thalamic and parietal lobe lesions, frontal lobe disease, and general paresis. In children, catatonia may be caused by a developmental or seizure disorder.<br />c. Nonaffective Psychoses<br />about 10%–15% of patients with catatonia meet the criteria for schizophrenia when the diagnosis requires no past or present episodes of mood disorder. Catalepsy, mannerisms, posturing, and mutism are the features traditionally associated with catatonic schizophrenia.<br />d. Genetic Form of Catatonia<br />German psychopathologists, beginning with Wernicke, Kleist, and Leonhard, and more recently students at the University of Würzburg, defined putative subsyndromes of catatonia that are not delineated in the DSM or ICD. One form of catatonia has been described as familial and as having a suspected major gene effect. A follow-up study of these patients found their prognosis to be poor, and benzodiazepines and ECT were deemed unhelpful. The fact that so many catatonic patients have manic-depressive illness, which is itself highly heritable, makes interpretation of the Würzburg findings difficult, and it is unclear how best to integrate their subdivision of catatonia into general classification systems.<br />Treatment<br />No study of treatment efficacy for catatonia has fully met current standards for evaluating therapies. The systematic trials with meaningful sample sizes are either naturalistic or refer to the more malignant forms of catatonia. A meta-analysis or other statistical analysis for pooling multiple-source databases has also not been done. Despite these shortcomings, the literature is remarkably consistent—from the first reported patient treated with amobarbital in 1930 to the first dementia praecox patient (with catatonia) treated with convulsive therapy in 1934 to the many positive reports in the past decade. It has compelling face validity. Modern investigators of catatonia conclude that drugs with anticonvulsant properties, particularly benzodiazepines and barbiturates, and ECT effectively relieve or resolve catatonic episodes regardless of their severity or etiology. The number or pattern of catatonic features does not affect outcome, and the syndrome has an excellent acute treatment prognosis. The patient’s long-term prognosis depends on the underlying condition that elicited catatonia. Exposure to either typical or atypical antipsychotic drugs, however, usually worsens catatonia or induces the malignant form.

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Competency -- to refuse treatmsent

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Competency to consent<br><br>is the patient currently psychotic, and in need of psychiatric intervention does the patient understand the medical condition<br>does the patient understand the risks and benefits of treatment<br>does the patient understand the risks of refusing treatment<br>does the patient have a rationale for refusing treatment (is the rationale influenced by psychosis)

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Delirium post-op, slow recovery, irritable, agitated, morphine -&gt; refusal of treatment. Most important issue re timing Ax, most important ruleout, 4 factors in competency ax

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A. What is the most important issue about the timing of this evaluation?<br> Would want to see later in the day to see possible sundowning.<br> Also better to see at different times of day since can fluctuate.<br>B. What is the most important thing to rule out?<br> Diagnosis of Delirium<br>C. Give four factors involved in competency assessment in this male if PEG feeding<br>percutaneous endoscopic gastrostomy (PEG) feeding is to be considered?<br>1. The patient’s understanding of the overall problem.( Understanding the condition that the<br>patient has)<br>2. The patient’s understanding of the nature of the proposed procedure. (Understands reason<br>for treatment)<br>3. The patient's understanding of the purpose of the procedure. (Why do you think that you<br>need an operation, why do the surgeons think that you need an operation?)<br>4. The patient's understanding of the risks of the procedure. (Appreciate cons of taking<br>treatment)<br>5. The patient's understanding of the risks of not having the procedure. (Appreciate cons of not<br>taking treatment)

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Chronic Pain d/o -- 5 criteria dx, 5 tx

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Diagnosis of chronic pain disorder:<br>A. pain in one or more sites that is the focus of clinical presentation<br>I. pain disorder on Axis I (with psychological factors, or both psychological factors and a general medical condition) can be acute (less than six months) or chronic (longer than six months)<br>J. pain disorder symptoms can be a part of conversion or somatization, but these diagnoses take precedence, and pain disorder is not diagnosed if they are present<br>Treatment modalities for pain disorder:<br>A. pharmacotherapy: SSRIs, TCAs<br>B. behavioral therapy: biofeedback, hypnosis, transcutaneous nerve stimulation<br>C. psychotherapy: psychodynamic, cognitive<br>D. pain control programs: group therapies, physiotherapy, exercise<br>E. limit investigations, be supportive<br>B. psychological features are judged to have an important role in the onset, severity, or<br>exacerbation or maintenance of pain<br>C. the symptom or deficit is not intentionally produced<br>D. remember: pain disorder = unintentional, psychological pain<br>E. pain causes significant distress or impairment is social, occupational, or other areas<br>of functioning<br>F. not better explained by another mood, anxiety, or psychotic disorder, and does not<br>meet criteria for dyspareunia<br>G. note: pain disorder is one of six somatoform disorders (somatization,<br>undifferentiated somatoform, conversion, pain, hypochondriasis, body dysmorphic<br>disorder), and of course somatoform disorder NOS<br>H. pain disorder can be:<br>1. associated with psychological factors<br>2. associated with both psychological factors and a general medical condition<br>3. associated with a general medical condition (coded on Axis III, not Axis I)

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AIDS -- 6 psych comorbidities

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A. adjustment difficulties at diagnosis<br>B. anxiety symptoms<br>C. depression<br>D. cognitive deficits (dementia)<br>E. psychosis<br>F. personality change<br>G. substance abuse<br>H. delirium<br>I. suicidality<br>J. (note: just about anything, except mania)

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Thyroid dz -- psych manifestations

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4. depression<br>5. mania<br>6. anxiety<br>7. psychosis<br>8. delirium<br>9. personality change<br>Hyperthyroidism<br>A. agitated depression<br>B. pressured speech, manic excitement<br>C. nervousness, irritability, excitability<br>D. delusions and hallucinations<br>E. confusion, impaired memory<br>F. personality change<br>G. insomnia<br>Hypothyroidism<br>A. depression or depressed affect<br>B. hypomania or manic-like psychosis<br>C. irritability<br>D. delusions, hallucinations, paranoia<br>E. cognitive impairment, delirium<br>F. personality change<br>G. lethargy

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Neoplastic dz -- possible etiologic factors depression

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Epidemiology<br>A. the rate of depression in patients with cancer is almost uniformly higher than that in the general population<br>B. pancreatic, oropharyngeal, and breast cancer are the most highly associated with depression<br>Etiology<br>A. psychosocial stressors related to the illness<br>1. loss of autonomy<br>2. threatened loss of life<br>B. biological factors<br>3. chronic pain<br>4. paraneoplastic syndromes<br>1) for example, tumor proteins in pancreatic cancer appear to elicit alterations in serotonergic<br>neurotransmission and the activity of the hypothalamic-pituitary axis

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5 most likely reasons consult hemodyalisis unit

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• depression<br> suicidal ideation is common in this population<br> somatic and vegetative symptoms of depression may overlap with uremia and therefore<br>psychological symptoms should be carefully examined<br>• sexual difficulties<br>• dementia<br>• delirium<br>• psychological difficulties<br>• problems with adaptation to chronic illness<br>• assessment of competency<br>• note that dialysis is schedule three times a week and takes four to six hours, leading to a<br>significant disruption of living routines, and possibly struggles with independence and dependence

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Neoplasm refused tx -- discuss mgt

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 Assess capacity to consent to treatment<br>• Assist treating team in assessing any psychiatric factors that may attribute to her refusal of treatment (e.g. delirium, cognitive impairment, psychosis) that may impair her capacity to understand and appreciate the nature and prognosis of her illness,<br>• Assess her capacity in understanding the risks and benefits of the treatment recommended as well as alternative treatments<br> Assess psychiatric contribution to decision to refuse treatment<br>• E.g. depression, anxiety may not alter cognitive understanding and appreciation, but may<br>affect hopefulness about treatment or fear/reluctance to endure potentially noxious<br>treatment.<br>• Offer treatment for any psychiatric comorbidity.<br>If capable patients continue to decline treatment, remain empathic and respectful of their autonomy. Provide opportunity for psychotherapeutic intervention re: coping with chronic illness, end of life issues where appropriate

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AIDS -- clinical presentation / tx of organic mental d/o assoc. with

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• Delirium<br>o Most common acute mental disorder, reportedly noted in 20-57% of hospitalized AIDS<br>patients seen in consultation<br>o Treatment of delirium is always primarily the treatment of the underlying medical cause o Antipsychotic treatment may be useful for symptomatic relief<br>o Important HIV-specific causes of delirium include:<br>− Cryptococcal meningitis<br>− Herpes encephalitis<br>− Toxoplasmosis<br>− Lymphoma<br>− Medications including analgesics, retrovirals, antibiotics<br>• Cognitive disorders<br>o HIV-AIDS dementia complex<br>− Progressive subcortical dementia (in later stages cortical involvement)<br>− Has cognitive, behavioural and affective symptoms, therefore can mimic any<br>psychiatric disorder<br>− Diagnosis requires that symptoms significantly interfere with activities - i.e. clinical<br>diagnosis (not neurological/imaging/neuropsychiatric)<br>− Incidence in the late 1980's ranged from 20-60%<br>− Likely secondary to both immunosuppression and CNS HIV infection<br>• Signs and symptoms<br>• Decreased memory and concentration<br>• Apathy, anergia, Abulia (abnormal lack of ability to act or to make decisions)<br>• Social withdrawal<br>• Psychomotor retardation<br>• Headache<br>• Gait, balance disturbance<br>• Pyramidal tract signs<br>• Seizures<br>• Incontinence<br>• Paraparesis<br>• Dysphasia, dyspraxia<br>− AZT may reverse the course of ADC with improved cognitive functioning,<br>decreased lability<br>− Neurological diagnostic criteria include impairment of at least 2 areas of cognition,<br>impairment<br>In work or ADLs, no clouding of consciousness and exclusion of delirium.<br>o HIV-AIDS associated minor cognitive motor disorder<br>− This term seems to be less used than the above one<br>− The main idea is that it is a milder, less impairing form of cognitive impairment where<br>there is Some combination of gait, balance, personality and/or cognitive change causing mild as Opposed to major impairment with no evidence of CNS opportunistic infection, malignancy and not attributable to another psychiatric disorder<br>• Approach - General principles<br>o All new onset neuropsychiatric symptoms to be considered organic until proven otherwise o Organic mental disorder can be present even if work-up is negative, which is true for ADC o Organic mental disorder signs and symptoms can precede evidence of primary CNS disease o Careful history and detailed mental status examination essential<br>o Early neurology or medical referral should be the standard of practice<br>o Assessment should involve<br>− Ruling out other CNS disease<br>− Immunological status testing<br>− History of pattern of deficits<br>− Neurological and mental status examination<br>− Head CT/MRI - frequently normal or only cortical atrophy ± enlarged ventricles or<br>white matter abnormalities.<br>− CSF studies<br>− Neuropsychiatric testing

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Neoplasia -- possible etiologic factors contributing to depr

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Biological<br>o Drugs<br>− Chemotherapeutic (prednisone, vincristine, interferon......) − Narcotics<br>− Benzodiazepines<br>o Tumor effects<br>− Hormone secreting tumors (paraneoplastic syndromes)<br>− CNS tumors/mets<br>o Associated medical conditions − Uremia<br>− Viral encephalitis<br>− Electrolyte imbalance<br>• Psychological<br>o Fear of death<br>o Fear of disfigurement<br>o Fear of abandonment<br>o Loss of independence<br>o Fear of disrupted relationships, role functioning, financial standing o Denial, anxiety, anger, guilt<br>• Social<br>o Loss of income<br>o Withdrawal of social circle/family - especially if culturally stigmatized<br>o Functional decline, unable to engage in work, ADLs, enjoyable activities

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HIV -- ER agitated and confused, most impt considerations re DDx and Tx

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• Differential diagnosis<br>o HIV/AIDS related<br>− HIV associated dementia<br>− Neuropsychological testing - AIDS dementia rating scale, finger tapping test, trails A&amp;B<br>• Treatment<br>o Containment and safety<br>− Verbal reassurance, physical/chemical restraints as needed o Low dose atypical neuroleptics<br>− Used in advanced HIV for symptom control<br>− High risk for EPS with high potency typicals<br>− Increased risk of cognitive side effects with low potency typicals<br>o Treat reversible causes of confusion<br>o Address risk of transmission of HIV to others, especially if IV drug use<br>o Consider ability to comply with antiretroviral regimen given confusion and high risk<br>of furthering drug resistancealization of Neuropsychiatric Syndromes<br><br>Aphasia finger agnosia,<br>without alexia)<br>Ideomotor apraxia<br>Depression (LR)<br>or to make decisions)<br>altered sexual hypermetamorphosis,<br>Right Hemisphere<br>Delusions with Schneiderian First-rank Symptoms<br>Primary progressive aphasia Alexithymia, Aprosodia<br>Capgras syndrome, Mania Nonverbal amnesia, Social<br>Impropriety, Visuospatial Abnormalities (RL)<br>Bilateral<br>Gerstmann's syndrome (acalculia, right/left disorientation, agraphia<br>Verbal amnesia<br>Abulia (abnormal lack of ability to act<br>Klüver-Bucy syndrome (placidity, behavior, visual agnosia,<br>Hyperorality) Severe amnesia<br>• Usually CD4 &lt; 50<br>• CD normal count (750±250), when the total count &lt;200 μl indicates underlying opportunistic infection<br>• Subcortical dementia - apathy, inertia, irritability, emotional lability, impaired judgment, socially inappropriate Behaviour, disinhibition<br>− Delirium<br>• CNS infections (usually CD4 &lt; 100) - toxoplasmosis, Cryptococcus, progressive<br>multifocal leukoencephalopathy, mycobacterium tuberculosis encephalitis, herpes<br>simplex encephalitis, neurosyphilis<br>• CNS neoplasm - lymphoma, Kaposi's sarcoma<br>• Medical complications - pneumonia, renal failure, metabolic abnormalities<br>• Medications - zidovudine, efavirenz at high doses, narcotics<br>− Mania, psychosis - if without personal/family history, may present at later stages of HIV, usually in association with cognitive-motor impairment<br>o Non HIV/AIDS related<br>− Drugs - intoxication or withdrawal<br>− Psychiatric illness<br>− Delirium<br>• Investigations<br>o Physical/neurological examination<br>− Focal deficits may indicate space-occupying lesion (e.g. CNS lymphoma, toxoplasmosis, progressive multifocal leukoencephalopathy)<br>o Labs<br>− CBC + diff, electrolytes, VDRL, B12, folate<br>− CT<br>− Lumbar puncture

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Ganser's Syndrome

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is a syndrome of approximate answers that may be a manifestation of malingering, confusional state, or disinhibition syndromes. Patients with Ganser's syndrome will respond to items on mental status examinations in such an approximately correct fashion as to raise suspicion of duplicity (deceit, deception, betrayal) (e.g., &quot;five quarters in a dollar, 13 months in one year.&quot;)

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BPD -- disruptive inpatient, how deal w/ reactions? Outline plan for staff?

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a) How would you deal with these reactions?<br> Other components of effective therapy for patients with borderline personality disorder include managing feelings (in both patient and therapist)<br> Promoting reflection rather than impulsive action<br> Diminishing the patient’s tendency to engage in splitting<br> In addition, setting limits on any self-destructive behaviors.<br>b) How to handle patient who uses splitting on the inpatient ward?<br> As previously noted, splitting is a major defense mechanism of patients with borderline personality disorder.<br> Management of patient’s own transference reaction and further education to the staff of how to use them as away of understanding the patient.<br> Frequent staff meeting and help the patient to perceive what is going on<br> Staff meeting with patient based on 5-10 minutes for further discussion and understanding<br>the patient<br> More Psychoeducation to staff that patient’s reactions of transference has no personal means.<br> The self and others are often regarded as “all good” or “all bad.” This phenomenon is closely related to what Beck and Freeman call “dichotomous thinking” and what Linehan refers to as “all or none thinking.”<br> Psychotherapy must be geared to helping the patient begin to experience the shades of gray between the extremes and integrate the positive and negative aspects of the self and others.<br> A major thrust of psychotherapy is to help patients recognize that their perception of others, including the therapist, is a representation rather than how they really are.<br>Nevertheless, specific transference-countertransference enactments are at high risk for occurring with patients with borderline personality disorder. If a patient has experienced neglect and abuse in childhood, he or she may wish for the therapist to provide the love that the patient missed from parents. Therapists may have rescue fantasies that lead them to collude with the patient’s wish for the therapist to offer that love. This collusion in some cases leads to physical contact and even inappropriate physical contact between therapist and patient. Clinicians should be alert to these dynamics and seek consultation or personal psychotherapy or both whenever there is a risk of a boundary violation. Sexual interactions between a therapist and a patient are always unethical.<br>

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Somatization d/o -- postulated etiology, mgt plan

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Etiology<br>Psychosocial Factors.<br>The cause of somatization disorder is unknown. Psychosocial formulations of the cause involve interpretations of the symptoms as social communication, the result of which is to avoid obligations (for example, going to a job a person does not like), to express emotions (for example, anger at a spouse), or to symbolize a feeling or a belief (for example, a pain in the guts).<br>Strict Psychoanalytic interpretations of symptoms rest on the hypothesis that the symptoms substitute for repressed instinctual impulses.<br>A behavioral perspective on somatization disorder emphasizes that parental teaching, parental example, and ethnic mores may teach some children to somatize more than do others.<br>In addition, some patients with somatization disorder come from unstable homes and have been physically abused.<br>Social, cultural, and ethnic factors may also be involved in the development of symptoms.<br><br>Biological Factors.<br>Some studies point to a neuropsychological basis for somatization disorder. These studies propose that the patients have characteristic attention and cognitive impairments that result in the faulty perception and assessment of somatosensory inputs.<br>The reported impairments include excessive distractibility, inability to habituate to repetitive stimuli, the grouping of cognitive constructs on an impressionistic basis, partial and circumstantial associations, and lack of selectivity, as indicated in some studies of evoked potentials.<br>A limited number of brain-imaging studies have reported decreased metabolism in the frontal lobes and in the nondominant hemisphere.<br>Genetic data indicate that in at least some families the transmission of somatization disorder has genetic components.<br>The data indicate that somatization disorder tends to run in families and occurs in 10 to 20 percent of the first-degree female relatives of patients with somatization disorder.<br>Within these families, first-degree male relatives are prone to substance abuse and antisocial personality disorder.<br>One study also reported a concordance rate of 29 percent in monozygotic twins and 10 percent in Dizygotic twins, an indication of a genetic effect.<br><br> Research into cytokines, a new area of basic neuroscience study, may be relevant to somatization disorder and other Somatoform disorders.<br> Cytokines are messenger molecules that the immune system uses to communicate within itself and with the Nervous system, including the brain. Examples of cytokines are interleukins, tumor necrosis factor, and interferons.<br> Some preliminary experiments indicate that cytokines may help cause some of the nonspecific symptoms of disease, especially of infections, such as hypersomnia, anorexia, fatigue, and depression.<br> Although no data yet support the hypothesis, abnormal regulation of the cytokine system may result in some of the symptoms seen in somatoform disorders.<br>B. management plan<br>o Is best treated when the patient has a single identified physician as primary caretaker.<br>o Primary physicians should see patients during regularly scheduled visits, usually at monthly<br>intervals. The visits should be relatively brief, although a partial physical examination should be<br>conducted to respond to each new somatic complaint.<br>o Additional laboratory and diagnostic procedures should generally be avoided.<br>o Once somatization disorder has been diagnosed, the treating physician should listen to the somatic<br>complaints as emotional expressions rather than as medical complaints.<br>o Physicians must always use their judgment about what symptoms to work up and to what extent.<br>o A reasonable long-range strategy for a primary care physician is to increase the patient's awareness<br>of the possibility that psychological factors are involved in the symptoms until the patient is willing<br>to see a mental health clinician, probably a psychiatrist, on a regular basis.<br>o Psychotherapy, both individual and group, decreases these patients' personal health care<br>expenditures by 50 percent, largely by decreasing their rates of hospitalization.<br>o In psychotherapy settings, patients are helped to cope with their symptoms, to express underlying<br>emotions, and to develop alternative strategies for expressing their feelings.<br>o Giving psychotropic medications whenever somatization disorder coexists with a mood or anxiety<br>disorder is always a risk, but psychopharmacological treatment, as well as psychotherapeutic<br>treatment, of the coexisting disorder is indicated.<br>o Medication must be monitored, because patients with somatization disorder tend to use drugs<br>erratically (intermittently, irregularly) and unreliably.<br>

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Hypochondriasis -- etiology, mgt plan

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a) Definition; is defined as a person's preoccupation with the fear of contracting, or the belief of<br>having, a serious disease and this fear or belief arises when a person misinterprets bodily symptoms or functions.<br>b) Etiology<br>A first theory; A reasonable body of data indicates that people with hypochondriasis augment and<br>amplify their somatic sensations; they have lower than usual thresholds and a lower tolerance of physical discomfort. For example, what people normally perceive as abdominal pressure, people with hypochondriasis experience them as abdominal pain; they may focus on bodily sensations, misinterpret them, and become alarmed by them because of a faulty cognitive scheme.<br>A second theory is that hypochondriasis is understandable in terms of a social learning model. The symptoms of hypochondriasis are viewed as a request for admission to the sick role made by a person facing seemingly insurmountable (impossible, overwhelming) and insolvable problems. The sick role offers an escape that allows a patient to avoid noxious obligations, to postpone unwelcome challenges, and to be excused from usual duties and obligations.<br>A third theory about hypochondriasis is that it is a variant of other mental disorders, among which depressive disorders and anxiety disorders are most frequently included. An estimated 80 percent of patients with hypochondriasis may have coexisting depressive or anxiety disorders. Patients who meet the diagnostic criteria for hypochondriasis may be somatizing subtypes of these other disorders.<br>The psychodynamic school of thought has produced a fourth theory of hypochondriasis.<br><br>According to this theory, aggressive and hostile wishes toward others are transferred (through repression and displacement) into physical complaints. The anger of patients with hypochondriasis originates in past disappointments, rejections, and losses, but the patients express their anger in the present by soliciting the help and concern of other people and then rejecting them as ineffective. Hypochondriasis is also viewed as a defense against guilt, a sense of innate badness, an expression of low self-esteem, and a sign of excessive self-concern. Pain and somatic suffering thus become means of atonement and expiation (undoing) and can be experienced as deserved punishment for past wrongdoing (either real or imaginary) and for a person's sense of wickedness and sinfulness.<br><br>management plan;<br>Patients are usually resistant to psychiatric treatment although some accept this treatment if it takes place in a medical setting and focuses on stress reduction and education in coping with chronic illness.<br>Among such, group psychotherapy is the modality of choice, in part because it provides the social support and social interaction that seem to reduce their anxiety.<br>Individual insight-oriented psychotherapy may be useful, but is generally unsuccessful. Frequent, regularly scheduled physical examinations are useful to reassure patients that their physicians are not abandoning them and that their complaints are being taken seriously. Invasive diagnostic and therapeutic procedures should only be undertaken, however, when objective evidence calls for them.<br>When possible, the clinician should refrain from treating equivocal or incidental physical examination findings.<br>Pharmacotherapy alleviates hypochondriacal symptoms only when a patient has an underlying drug-responsive condition, such as an anxiety disorder or major depressive disorder.<br>When hypochondriasis is secondary to another primary mental disorder, that disorder must be treated in its own right.<br>When hypochondriasis is a transient situational reaction, clinicians must help patients cope with the stress without reinforcing their illness behavior and their use of the sick role as a solution to their problems.

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Delirium -- mgt plan

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A. Non-Pharmacological Management<br>1. Treatment of all correctable contributing causes of the delirium should be done in a timely, effective manner.<br>2. Establish and maintain cardiovascular stability, a normal temperature, adequate oxygenation, normal fluid and electrolyte balance, normal glucose levels, and an adequate intake of nutrients. Biochemical abnormalities should be promptly corrected.<br>3. A daily multivitamin should be considered in older persons with delirium who are at risk for micronutrient deficiencies (e.g., thiamine).<br>4. Aim for regular voiding during the day and a bowel movement at least every two days.<br>5. Urinary retention and fecal impaction should be actively looked for and dealt with if discovered.<br>6. Continuous catheterization should be avoided whenever possible. Intermittent catheterization is preferable.<br> Mobility and function n s: Non-Pharmacological Management – Mobility and Function (p. 36)<br>1. Maintain and improve the older person’s self-care abilities, mobility and activity pattern. Allow free movement (provided the older person is safe) and encourage self-care and other personal activities to reinforce competence and to enhance self-esteem.<br>2. The implementation of intensive rehabilitation that requires sustained attention or learning from the delirious older person is not likely to be beneficial and may increase agitation. It should be delayed until the older person is able to benefit from the intervention.<br><br> Safety<br>1. Take appropriate measures to prevent older persons from harming themselves or others. The least restrictive measures that are effective should be employed.<br>2. Attempt to create safe environment that is as hazard free as possible.<br>3. Although it is often necessary to increase supervision during delirium, it would be preferable if security personnel did not provide this unless it is necessary for safety reasons. Given the older delirious person’s difficulties in reasoning and their tendency to see even innocuous behaviours as aggressive, the presence of security personnel may entrench delusional thinking and agitation. If family cannot stay with the older person and staff cannot provide the required degree of surveillance, consider the use of a private-duty nurse (also known as a nurse sitter, personal care attendant or patient companion).<br> Communication<br>1. Given difficulties in sustaining attention, when communicating with a delirious older person ensure that instructions and explanations are clear, slow-paced, short, simple, and repeated. The older person should be addressed face-to-face.<br>2. Avoid abstract language/ideas and do not insist that the older person appreciate the information that is being given. Do not engage in discussions that the older person cannot appreciate.<br>3. Discuss topics that are familiar and/or of interest, such as hobbies and occupation, with the older person.<br>4. Routinely provide orienting information in the context of care. For example, frequently use the older person’s name and convey identifying information (e.g., “I’m your nurse”).<br>5. When providing care, routinely explain what you are about to do. This is to reduce the likelihood of isinterpretation. 6. Keep your hands in sight whenever possible and avoid gestures or rapid movements that might be misinterpreted as aggressive. Try to avoid touching the older person in an attempt to redirect him/her.<br>7. Evaluate the need for language interpreters and ensure their availability if required.<br>8. Reminding older persons of their behaviour during episodes of delirium is not generally recommended. Many older persons with delirium retain memories of the fear they experienced during a time of delirium. Others become embarrassed of their behaviour during delirium.<br> Non-Pharmacological Management – Behavioural Management<br>Those caring for a delirious older person should convey an attitude of warmth, calmness and kind firmness. They should acknowledge the older person’s emotions and encourage verbal expression. Strategies for managing the behaviour of a delirious patient should be derived from an understanding of the neurocognitive/ neurobehavioural features of delirium and behavioural management principles.<br>Given difficulties in sustaining attention with delirium, present one stimulus or task at a time to the older person.<br>If agitation occurs, use behavioural management strategies to identify triggers for agitation. This information should be used to modify the older person’s environment and/or delivery of care in order to reduce the incidence of agitation. Any interventions implemented will require evaluation to confirm their effectiveness.<br>Do not directly contradict delusional beliefs, as this will only increase agitation and not likely orient the person. If there is a question of safety, attempt to use distraction as a way of altering behaviour.<br>Avoid confrontations with the older person even when they say inaccurate/inappropriate things. Disagreements with the older person can lead to increased agitation and is not likely to be effective in altering perceptions or behaviour. If the older person is becoming agitated, try distracting him/her. If it is important to correct the older person, wait and try offering the required information at another time in a calm, matter-of-fact tone of voice. Ignore the content of their statements when it is not necessary to correct them.<br>In complex cases, referral to geriatric psychiatry, neuropsychology, psychology and/or psychiatry for behavioural management strategies is recommended.<br> Recommendations: Non-Pharmacological Management – Care Providers/Caregivers<br>Effective care of the delirious older person requires interdisciplinary collaboration.<br>Request family members, if available, to stay with the older person. They can help re-orientate, calm, assist, protect, and support the older person. As well, they can help facilitate effective communication and advocate for the older person. To fulfill their role in an effective manner, family members do require introductory education about delirium and its management.<br>If family cannot stay with the older person and staff cannot provide the required degree of surveillance, consider the use of a private-duty nurse (also known as a nurse sitter, personal care attendant or patient companion). Please note<br><br>that their use does not obviate the need to ensure adequate staffing in health care facilities. Any person engaged in this activity requires appropriate training on the assessment and management of delirium.<br> Recommendations: Non-Pharmacological Management - Environment<br>1. Avoid both sensory deprivation (e.g., windowless room) and sensory overload (e.g., too much noise and<br>activity).<br>2. The older person’s room should be quiet with adequate lighting. Over-stimulation is a common antecedent of<br>agitation.<br>3. Implement unit-wide noise-reduction strategies at night (e.g., silent pill crushers, vibrating beepers, quiet<br>hallways) in an effort to enhance sleep.<br>4. Check if the older person wants a radio or television for familiar background stimulation and arrange for it, if<br>requested and possible. Allow delirious older persons to listen to music of their choice. If it is felt that these devices are distracting, disorientating and/or disturbing to the older person when used, they should be removed from the room.<br>5. Ensure that the older person’s room has a clock, calendar and/or chart of the day’s schedule. Give the older person frequent verbal reminders of the time, day and place.<br>6. Attempt to keep the older person in the same surroundings. Avoid unnecessary room changes.<br>7. Obtain familiar possessions from home, particularly family pictures, sleepwear and objects from the bedside, to<br>help orient and calm the older person.<br>8. It is generally not recommended to put older persons with delirium (especially if hyperactive-hyperalert) in the<br>same room. Agitation tends to be reinforced by the presence of agitation in other individuals. The exception to<br>this would be if delirious persons are being congregated in order to provide enhanced care.<br>Recommendations: Management -<br>B. Infections, Pain Management, and Sensory Deficits<br>• If there is a high likelihood of an infection, antibiotics should be started after appropriate cultures have been taken.<br>• The antibiotic or antibiotics initially selected should be ones that are likely to be effective against the established or presumed infective organism.<br>C. Recommendations: Management - Pain Management<br>• Adequately manage the older person’s pain. This can be complicated by the observation that some of the medications used to treat pain can also cause delirium. The treatment goal is to control the older person’s pain with the safest available intervention(s).<br>• Non-pharmacological approaches for pain management should be implemented where appropriate.<br>• Local or regional drug therapies (e.g., local blocks, epidural catheters) for pain that have minimal systemic<br>effects should be considered.<br>• For persistent severe pain, analgesics should be given on a scheduled basis rather than administered as-needed.<br>• Non-narcotic analgesics should be used first for pain of mild severity and should usually be given as adjunctive<br>therapy to those receiving opioids in an effort to minimize the total dose of opioid analgesia required.<br>• If opioids are used, the minimum effective dose should be used and for the shortest appropriate time. Opioid<br>rotation (or switch) and/or a change in the opioid administration route may also be helpful.<br>• The opioid Meperidine should be avoided, as it is associated with an increased risk of delirium.<br>• The practitioner should be always alert to the possibility of narcotic induced confusion.<br>D. Recommendations: Management - Sensory Deficits<br>• Sensory deprivation is a frequent contributor to a delirium, especially in an acute care setting. If present, take steps to eliminate or, if not possible, minimize its impact.<br>• Glasses and hearing aids used by the older person should be available and worn by them. For deaf patients consider the use of a pocket amplifier to facilitate communication.<br>E. Recommendations: Management – Medications: Precipitating or Aggravating a Delirium<br>• Withdraw all drugs that might be contributing to the delirium whenever possible.<br>• Psychoactive medications, those with anticholinergic effects, and/or drugs recently initiated or with a dosage<br>change are particularly suspect as inciting causes.<br><br>• If suspect drugs cannot be withdrawn, the lowest possible dose of the suspected medication(s) should be used or substitution with a similar but lower risk medication should be considered.<br>• Monitor for potential adverse drug-disease interactions and drug-drug interactions.<br>• Regularly review the medication regimen in an attempt to simplify it by eliminating those not needed. Avoid<br>adding unnecessary medications.<br>• Avoid the routine use of sedatives for sleep problems. Try to manage insomnia by taking a Nonpharmacologic<br>approach with the patient and modifying the environment so as to promote sleep.<br>• Ensure that medication schedules do not interrupt sleep.<br>• Diphenhydramine should be used with caution in older hospitalized persons and its routine use as a sleep aid<br>should be avoided.<br>• Use of anticholinergic medications should be kept to a minimum.<br>• Restarting a formally consumed sedative, hypnotic or anxiolytic should be considered for a delirium that<br>developed during, or shortly after, a withdrawal syndrome.<br>F. Recommendations: Pharmacological Management - General Principles<br>• Psychotropic medications should be reserved for older persons with delirium that are in distress due to agitation or psychotic symptoms, in order to carry out essential investigations or treatment, and to prevent older delirious persons from endangering themselves or others.<br>• In the absence of psychotic symptoms causing distress to the patient, treatment of hypoactive delirium with psychotropic medications is not recommended at this time.<br>• The use of psychotropic medications for the specific purpose of controlling wandering in delirium is not recommended.<br>• When using psychotropic medications, aim for monotherapy, the lowest effective dose, and tapering as soon as possible.<br>• The titration, dosage, and tapering of the medication should be guided by close monitoring of the older person for evidence of efficacy of treatment and the development of adverse effects.<br>1. Recommendations: Antipsychotics<br>• Antipsychotics are the treatment of choice to manage the symptoms of delirium (with the exception of alcohol<br>or benzodiazepine withdrawal delirium)<br>• High potency antipsychotic medications are preferred over low potency antipsychotics.<br>• Haloperidol is suggested as the antipsychotic of choice based on the best available evidence to date.<br>• Baseline electrocardiogram is recommended prior to initiation of haloperidol.<br>• For prolongation of QTc intervals to greater than 450 msec or greater than 25% over baseline electrocardiogram<br>(ECG), consider cardiology consultation and antipsychotic medication discontinuation.<br>• Initial dosages of haloperidol are in the range of 0.25mg to 0.5 mg od-bid. The dose can be titrated as needed,<br>and severely agitated persons may require higher dosage.<br>• Benztropine should not be used prophylactically with haloperidol in the treatment of delirium.<br>• Atypical antipsychotics may be considered as alternative agents as they have lower rates of extra-pyramidal<br>signs.<br>• In older person’s with delirium who also have Parkinson’s Disease or Lewy Body Dementia, atypical<br>antipsychotics are preferred over typical antipsychotics.<br>• Droperidol is not recommended in the elderly.<br>2. Recommendations: Benzodiazepines<br>Benzodiazepines as monotherapy are reserved for older persons with delirium caused by withdrawal from alcohol/sedative-hypnotics. As benzodiazepines can exacerbate delirium, their use in other forms of delirium should be avoided.<br>3. Recommendations: Management of Alcohol Withdrawal Delirium<br>• Sedative-hypnotic agents are recommended as the primary agents for managing alcohol withdrawal delirium.<br>• Shorter acting benzodiazepines such as Lorazepam are the agents of choice in the elderly.<br>• Antipsychotics may be added to benzodiazepines if agitation, perceptual disturbances, or disturbed thinking<br>cannot be adequately controlled with benzodiazepines alone.<br>• Antipsychotics may be considered when other medical causes of delirium complicate AWD.<br>• The dosage of medication should be individualized with light somnolence as the usual therapeutic end point.<br><br>• Older persons should be frequently re-evaluated for the control of symptoms and the development of excessive sedation.<br>• Benzodiazepines should be tapered following AWD rather than abruptly discontinued.<br>• Parenteral administration of thiamine is recommended to prevent or treat Wernicke encephalopathy or<br>Wernicke-Korsakoff syndrome.<br>• Older persons with alcohol withdrawal are best treated in closely supervised settings.<br>Recommendations: Capacity<br> Delirium can impair capacity; older persons with delirium who are being asked to provide consent for treatment require a review to ensure they have the capacity to provide informed consent.<br> Clinicians should be familiar with relevant provincial legislation regarding capacity (including capacity to consent to treatment) and the identification of a substitute decision-maker if the older person is deemed to lack capacity.<br> Capacity assessments must elicit sufficient information to allow for the determination of the older person’s capacity as defined by the appropriate provincial legislation.<br> Measures of neurocognitive functions known to underlie capacity (i.e., attention, language, verbal learning/memory and higher order cognitive functions) should be included as part of an in-depth assessment.<br>It is recommended that brief measures of neurocognitive functions (e.g., Mini Mental Status Examination) be supplemented by other cognitive measures that also assess judgment and reasoning.<br> The clinician should strive to make the assessment as brief as possible while still obtaining the required<br>information.<br> In view of the fluctuating nature of delirium, serial evaluations may be necessary as treatment decisions arise.<br> Screening for psychotic features relevant to decision-making capacity is recommended.<br> The use of a structured interview with known reliability and validity is recommended for the assessment of<br>capacity when there is uncertainty.<br> The use of The MacArthur Competency Assessment Tool – Treatment is recommended for the assessment of<br>capacity to consent to treatment in cases where there is uncertainty.<br> The use of The MacArthur Competency Assessment Tool – Clinical Research is recommended for the<br>assessment of capacity to participate in research in cases where there is uncertainty.<br> If uncertainty regarding capacity persists after the clinician in charge has assessed the older person,<br>neuropsychological consultation is recommended.<br>Recommendations: Physical Restraints<br>Avoidance of physical restraints is an important component of interdisciplinary interventions to prevent the development of delirium in an older person.<br>Physical restraints for older persons suffering from delirium should be applied only in exceptional circumstances. Specifically this is when:<br>a) There is a serious risk for bodily harm to self or others; OR<br>b) Other means for controlling behaviours leading to harm have been explored first, including pharmacologic treatments, but were ineffective; AND<br>c) The potential benefits outweigh the potential risks of restraints.<br>The use of physical restraints to control wandering behaviour or to prevent falls is not justified.<br>The least restrictive physical restraint that is appropriate for the situation should be attempted first.<br>Frequent monitoring, re-evaluation, and documentation are necessary to justify the continued use of physical restraints. Restraints should be applied for the least amount of time possible. Restraints should be discontinued when the harmful behaviour(s) is controlled, when there is a less restrictive alternative which becomes viable (e.g., a sitter for constant supervision), or when there are physical complications arising from the continued use of restraints.<br><br>

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Delirium -- lab workup

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A. Standard studies<br>1. Blood chemistries (including electrolytes, renal and hepatic indexes, and glucose)<br>2. Complete blood count with white cell differential<br>3. Thyroid function tests<br>4. Serologic tests for syphilis<br>5. Human immunodeficiency virus (HIV) antibody test<br>6. Urinalysis<br>7. Electrocardiogram<br>8. Electroencephalogram<br>9. Chest radiograph<br>10. Blood and urine drug screens<br>B. Additional tests when indicated<br>1. Blood, urine, and cerebrospinal fluid (CSF) cultures<br>2. B12, folic acid concentrations<br>3. Computed tomography or magnetic resonance imaging brain scan<br>4. Lumbar puncture and CSF examination

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CAD -- risk of depression

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The interactions of personality traits, psychiatric symptoms and syndromes, and environmental stressors with the cardiovascular system have long intrigued investigators interested in the factors that contribute to the development and progression of atherosclerotic heart disease. Increasing evidence is accumulating suggesting that major depression a mood disorder, is associated with drastically elevated morbidity and mortality after an index (MI) and also acts as an independent risk factor in the development of atherosclerotic heart disease.<br>Depressive syndromes and major depression are exceedingly common.<br>The most recent comprehensive study done in the United States, the National Comorbidity Study, reported life-time prevalence rates of major depression and Dysthymia of 13 percent and 5 percent, respectively.<br>In patients with CAD, depression predicts future cardiac events and hastens mortality. Since the 1960s, multiple cross-sectional and longitudinal studies have scrutinized the association of cardiovascular disease (CVD), especially CAD and congestive heart failure (CHF), with depressive symptoms is well as major depression.<br>Early studies reported the prevalence of depression to be 18 to 60 % in patients with CAD. Later studies reported relatively consistent prevalence rates of depression in patients with CVD (patients with CAD) ranging from 16 to 23 percent (mean, 19 percent; median,18 percent)<br>PATHOPHYSIOLOGY<br>Hypothalamic-Pituitary-Adrenocortical and SympathomeduLLary Hyperactivity<br>Diminished Heart Rate Variability<br>Alterations in Platelet Receptors and/or Reactivity<br><br><br>Depression in patients with coronary artery disease (CAD) can be reduced with a combination of clinical management and the selective serotonin reuptake inhibitor (SSRI) Citalopram, but not through psychotherapy, study findings show.<br>&quot;Since the early 1990s, studies have reported prevalences of major depression between 17% and 27% in hospitalized patients with CAD,”.<br>To evaluate the efficacy of treatments for this group of patients, the researchers carried out the Canadian Cardiac Randomized Evaluation of Antidepressant and Psychotherapy Efficacy (CREATE) trial. This involved 284 patients with both CAD and major depression, all of whom had a Hamilton Depression Rating Scale score of 20 or above.<br>The participants underwent two separate randomizations, with four separate treatment groups: interpersonal psychotherapy plus clinical management and Citalopram; interpersonal psychotherapy plus clinical management and placebo; clinical management and Citalopram; and clinical management and placebo.<br>Clinical management involved weekly sessions with information about depression and medication use provided, along with reassurance and encouragement to adhere to medication. Interpersonal psychotherapy sessions dealt with problems common in patients with CAD, such as interpersonal conflicts, life transitions, grief, and loss.<br>Over the 12 weeks of treatment, Citalopram proved superior to placebo, with an average 3.3-point greater reduction in HAM-D scores.<br>The response rate, defined as a 50% or greater reduction in HAM-D scores, was higher among patients receiving Citalopram, at 35.9% compared with 22.5% for those given placebo. Similarly, the respective rates of remission, defined as a HAM-D score of 8 or below, were 52.8% versus 40.1%.<br>The benefits of Citalopram also extended to perceived social support and daily function, the team notes.<br>In contrast, Lespérance et al failed to find a beneficial effect of interpersonal psychotherapy over that of clinical management alone. The average reduction in HAM-D scores favored clinical management, at an average difference of 2.26 points.<br>&quot;Citalopram... should be considered for the initial acute-phase treatment for major depression in patients with CAD,&quot;

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frontal lobe dementia - list the characteristics you would see of the syndrome using modern investigation techniques.

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A. Computed tomography (CT) or magnetic resonance imaging (MRI) may be initially normal.<br>Cortical atrophy and ventricular enlargement may be symmetrical or asymmetrical; severity<br>increases over time [Foster et al 1997, van Swieten et al 1999].<br>B. Single photon emission computed tomography (SPECT) shows decreased cerebral perfusion<br>anteriorly that is present early in the disease, preceding CT or MRI findings.<br>C. In Frontotemporal dementia, both hypoperfusion and hypometabolism have been shown in frontal lobes and in the anterior part of temporal lobes. However, this pattern is not specific because similar pictures can be observed in other pathological entities, such as severe<br>depression, schizophrenia, and progressive supranuclear palsy.<br>D. As the name suggests, patients with FTD have dysfunction of the brain’s prefrontal regions,<br>temporal lobes, or both. In many cases, there may be significant atrophy easily visible with MRI specific to the affected regions; in other instances, the abnormalities may be functional rather than structural. Mild ischemic white matter changes consistent with normal aging may be present as well. Although some patients have Pick bodies, most do not. It is controversial whether those with semantic deficits have atrophy of the anterior hippocampus to the degree seen in Alzheimer’s disease.<br>E. Neuroimaging studies including computerized tomography (CT or CAT scans) and magnetic resonance imaging studies (MRIs) of the brain can support the diagnosis of Pick's disease. Atrophy (shrinkage) of the frontal and temporal regions (front half of the brain) is seen.<br>F. PET or SPECT studies, which measure brain metabolism and blood flow, may also support the diagnosis of Pick's disease.

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Dementia -- dx workup

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Comprehensive Workup of Dementia<br>1. Physical examination including thorough neurological examination<br> RPR (serum screen)<br> FTA-ABS (if CNS disease is suspected)<br> Serum B12<br> Folate levels<br> Urine corticosteroids<br> Erythrocyte sedimentation rate (Westergren)<br> Antinuclear antibody (ANA), C3C4, Anti-DS DNA  Arterial blood gases<br> HIV screen<br> Urine porphobilinogens<br>8. Chest radiograph<br>9. Electrocardiogram 10. Neurological workup<br> CT or MRI scan of head  SPECT<br> Lumbar puncture<br> EEG<br>11. Neuropsychological testing<br>2. Vital signs<br>3. Mental status examination<br>4. Mini-Mental State Examination (MMSE)<br>5. Review of medications and drug levels<br>6. Blood and urine screens for alcohol, drugs, and heavy metals<br>7. Physiological workup<br> Serum electrolytes/glucose/Ca2+, Mg2+<br> Liver, renal function tests<br> SMA-12 or equivalent serum chemistry profile<br> Urinalysis<br> Complete blood cell count with differential cell type count  Thyroid function tests (including TSH level)

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Dementia -- Compare and contrast: different major dementing disorders (Alzheimer’s, Picks, vascular,<br />Lewy body, frontal)

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Causes Signs Symptoms Treatments Vascular Dementia<br>Vascular dementia is the term given to dementia that occurs when the blood supply carrying oxygen and nutrients to the brain is interrupted, blocked or diseased. Damage to the vascular system, the network of blood vessels, results in brain damage when the brain cells die. The death of the brain cells causes various symptoms of dementia depending on the location of the damage.<br>Vascular Dementia Facts<br>

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cortical Vs subcortical dementia

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Distinguishing Features of Subcortical and Cortical Dementias<br>Characteristic Language<br>Naming test vocabulary test<br>Memory<br>memory scale; Symbol Learning<br>Subcortical Dementia<br>No aphasia (anomia if severe)<br>Cortical Dementia<br>Aphasia early<br>Recommended Tests<br>FAS test, Boston WAIS-R<br>Attention and immediate<br>digit span<br>impaired<br>Impaired<br>involved early<br>Digit, Paired Associate<br>(Brandt)<br>WAIS-R<br>Picture<br>And Block design;<br>Mini-Mental State<br>Recall<br>Visuospatial skills Impaired<br>arrangement, object assembly<br>WAIS subtests<br>Calculation Preserved until late<br>Impaired recall (Retrieval) &gt; Recognition<br>(Encoding)<br>Recall and recognition Wechsler<br>Frontal systems abilities disproportionately affected Degree of impairment Wisconsin Card Sorting Test; Odd<br>Collections of all short assays<br>219<br>(Executive function)<br>Picture Absurdities<br>Speed of cognitive<br>Paced Auditory<br>Processing<br>(PASAT)<br>Personality<br>MMPI<br>Mood<br>consistent with other<br>Man out test:<br>Hamilton depression scales<br>Unconcerned Euthymic<br>Articulate until late<br>upright Normal until late<br>Normal<br>Slowed early<br>Apathetic, inert Depressed<br>Involvement Normal until late in disease<br>Trail making A and B: Serial Addition Test<br>Beck and Verbal fluency<br>Speech Dysarthric (Rosen, 1980)<br>Posture Bowed or extended Coordination Impaired<br>Motor speed and control<br>Finger-tap; grooved pegboard<br>Adventitious movements Abstraction<br>Category test (Halstead Battery)<br>Slowed<br>Chorea, tremor tics, dystonia Absent (Alzheimer's dementia— Some myoclonus)<br>2

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frontal lobe syndromes 3

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1. Orbitofrontal syndrome - DISINHIBITION<br>• Flamboyant (showy , colorful)<br>• Disinhibited<br>• Tactless (thoughtless, insensitive, inconsiderate)<br>• Impulsive<br>• Irritable mood<br>• Labile<br>• Fatuous (idiotic, stupid, silly) euphoria<br>• Inappropriate jocularity<br>• Insensitive humor<br>• Lack of social restraint<br>• Overfamiliarity with strangers<br>• Often no or few other neuropsychiatric deficits<br>• Can occur with post-traumatic encephalopathy, frontal tumors, anterior cerebral artery<br>stroke/aneurysm rupture, Multiple sclerosis, neurodegenerative diseases (Pick's)<br>• Often associated with olfactory deficits because of proximity to those nerves<br>• Phineas Gage<br>2. Medial frontal syndrome - APATHETIC-AKINETIC<br>• Severity extends from akinetic mutism to a mild amotivation<br>• Occurs with bilateral medial frontal lesions<br>• May improve with dopamine agonist, suggesting some involvement of dopaminergic fibers<br>3. Frontal convexity syndrome - NEUROPSYCHOLOGICAL DEFICIT AND MOTOR<br>PROGRAMMING<br>• Produce abnormalities of sequential Behaviour including perseveration, deficits in shifting sets, poor judgment, concrete thinking/Behaviour<br>• Tumors, stroke, trauma, frontal degeneration

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dementia and pseudodementia.

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<br><br>Pseudodementia<br><br>Dementia<br><br>History and Clinical Course<br><br>Family often unaware of dysfunction and severity-- Onset can be dated back--Short duration before medical help sought<br>Rapid progression, Usually past depressions<br>Family very aware--Onset slow and vague--Long duration before medical help sought, Slow progression<br>Usually no past depressions<br><br>Complaints and Clinical Behaviour<br>Patient complains of cognitive loss--Patient emphasizes disability and highlights failures-- Behaviour and loss of social skills incongruent with degree of cognitive dysfunction-Little effort to perform even simple tasks<br>Patient complains little-- Complaints vague and patient conceals disability--Struggle to perform tasks and delights in accomplishments--Affect often shallow--Social skills retained. Relies on notes, calendars, etc.<br><br><br>Cognitive Dysfunction<br>Attention and concentration usually well preserved--&quot;don't know&quot; answers Memory loss severe for recent and remote events--Memory gaps for specific events Marked variability on tasks of similar difficulty<br>

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Gaucher's disease:

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1. Inherited storage disease, Autosomal Recessive sphingolipidosis, Mutations in glucocerebrosidase<br>gene on 1q21 (also known as acid beta glucosidase).<br>2. Lipids accumulate in such body tissues as the liver, the spleen, the bone marrow, and the nervous<br>system.<br>3. Often progressive damage to the nervous system causes profound developmental disability and<br>death within a few years.<br>4. Gaucher's disease are uncommon, and types II and III are quite rare.<br>5. Type I is highly concentrated in Ashkenazi Jews. ( as often as 1 in 1,000 births)<br>6. Some may be asymptomatic<br>7. Anemia, easy bruising, the joints may ache, and the bones may break easily.<br>8. The level of the normal enzyme can be measured from parental blood cells or from fetal cells<br>collected by amniocentesis. A very low level indicates an affected individual, one who produces little or no normal enzyme. An intermediate level indicates a carrier, a person who has one normal and one abnormal gene and produces about half the usual enzyme.<br>9. The missing enzyme can be replaced via injections.

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Gerstmann's Syndrome;

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1. Neurological disorder characterized by four primary symptoms:<br>a. a writing disability (agraphia or dysgraphia),<br>b. lack of understanding of the rules for arithmetic (acalculia or dyscalculia),<br>c. inability to distinguish right from left<br>d. Inability to identify fingers (finger agnosia).<br>2. In adults, the syndrome may occur after a stroke or in association with damage to the parietal lobe. In addition to exhibiting the above symptoms, many adults also experience aphasia, (difficulty in expressing oneself when speaking, in understanding speech, or in reading and writing).<br>3. A few reports of the syndrome, sometimes called developmental Gerstmann's syndrome, in children. The cause is not known. Most cases are identified when children reach school age, a time when they are challenged with writing and math exercises. Generally, children with the disorder exhibit poor handwriting and spelling skills, and difficulty with math functions, including adding, subtracting, multiplying, and dividing. An inability to differentiate right from left and to discriminate among individual fingers may also be apparent. Many children also suffer from constructional apraxia, an inability to copy simple drawings. Frequently, there is also impairment in reading. Children with a high level of intellectual functioning as well as those with brain damage may be affected with the disorder.<br>4. In adults, many of the symptoms diminish over time. Although it has been suggested that in children symptoms may diminish over time, it appears likely that most children probably do not overcome their deficits, but learn to adjust to them.

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left and to discriminate among individual fingers may also be apparent. Many children also suffer from constructional apraxia, an inability to copy simple drawings. Frequently, there is also impairment in reading. Children with a high level of intellectual functioning as well as those with brain damage may be affected with the disorder.<br>4. In adults, many of the symptoms diminish over time. Although it has been suggested that in children symptoms may diminish over time, it appears likely that most children probably do not overcome their deficits, but learn to adjust to them.

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6) Absence of voluntary motor movement or speech in a patient who is apparently alert (as evidenced by eye movements).<br>7) Akinetic mutism is a state of silent, alert-appearing immobility. The patient's eyes are open and may follow environmental events; there are regular sleep-wake cycles. The patient may be completely inert or may have occasional brief movements to adjust posture spontaneously or in response to vigorous stimulation<br>8) characterized by mutism and very limited spontaneous movement. The patients, however, appear alert, have their eyes open, exhibit ocular following movements of environmental events, will eat when fed, and may move with persistent stimulation<br>9) Seen in psychotic depression, catatonic states<br>10) Lesion location:large frontal lobe injuries, bilateral cingulate gyrus damage, and midbrain<br>pathology; bilateral medial frontal lesions<br>11) bilateral anterior cerebral artery occlusions, trauma, hydrocephalus, bilateral thalamic infarction<br>12) midline tumors of the thalamus, third ventricle, hypothalamus, and pituitary.

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Postcardiotomy Delirium

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The incidence of postcardiotomy delirium has remained fixed at approximately 30 % for the past 30 years and shows only a slight correlation with age. Several consistent features of postcardiotomy delirium emerge from meta-analysis of the reported literature. Illness variables associated with delirium reveal a higher prevalence of delirium in patients with non-congenital heart disease. Patients with congenital heart disease spend less time on bypass, which may be a factor. Patients with calcified mitral or aortic valves are reported to have more neuropsychiatric abnormalities, which are attributed to increased embolic events, although these patients are typically older and have longer times on bypass. Preoperative variables associated with delirium include the severity of illness assessed by New York Heart Association Functional Class or the preoperative presence of brain damage, organicity, or the presence of preoperative neurologic signs. Interestingly, the meta- analysis reported that preoperative psychiatric intervention was the single most predictive variable (negative correlation) and was associated with a low prevalence of postoperative delirium, which suggests opportunity and implications for prevention. Intraoperative time on bypass was found to have an inconsistent relationship with the development of delirium. A recent study of delirium in patients who have undergone coronary artery bypass revealed an incidence of 32% and identified a history of stroke, longer duration of bypass, and a postoperative low cardiac output as risk factors. Thus, postcardiotomy delirium remains a common problem without consistently defined risk factors and should be anticipated in one third of cases.

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Somatization -- define and list six disorders where somatization is likely a prominent feature of the clinical presentation.

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Definition of somatization<br />C. a defensive conversion of psychic derivatives to bodily symptoms; a tendency to react<br />with somatic rather than psychic manifestations<br />Disorders where somatization is prominent D. somatoform disorders<br /><br />6. hypochondriasis<br />7. pain disorder<br />8. conversion disorder<br />9. body dysmorphic disorder<br />10. undifferentiated somatoform disorder<br />11. somatoform disorder NOS<br />E. major depressive disorders<br />F. panic disorder<br />G. borderline personality disorder<br /><br />GUIDING FACTS/PRINCIPLES ON SOMATIZATION DISORDER:<br />o Clinical presentation is polysymptomatic, recurrent and chronic, with a “sickly” past; patients characteristically evidence a profusely positive review of symptoms, have multiple clinical contacts, and have had many surgeries<br />o Onset is at a young age, with female predominance 5-20:1, and a 5-10% incidence in primary care populations; prevalence is estimated at 0.2-2% of women and 0.2% of men; it is more common among individuals with lower education and lower income<br />o Management strategy focuses on building therapeutic alliance and organizing regular appointments (i.e. not driven by spontaneous symptom-emergence); management also involves crisis intervention<br />o Personality disorders are commonly comorbid (1/2 to 2/3 patients with avoidant, paranoid, self- defeating or obsessive-compulsive features); mixed views regarding likelihood of comorbid substance abuse (i.e. K&amp;S Syn p.644 vs p.645)<br />o Prognosis is poor to fair<br />o Suicide threats are common; actual suicide is rare<br />o Primary differential for any future illness presentation includes both physical disease and MDE o Psychological processes contributing to the patient’s symptoms are unconscious, cultural and<br />developmental; the motivation for symptom production is unconscious 31. QUESTIONS FROM THE GROUP:<br />1. NURSE: It’s absurd that she’s getting me to help her with bedpans and the like. I want to know, if she’s not actually physically disabled, should I just leave her there and tell her she should be doing it for herself? Maybe she’d snap out of it.<br />2. SURGEON:<br />a. I’m tempted to refuse to see her again. No one is going to want to see her twice. b. Can I be sued for having operated on her?<br />3. INTERNIST: Shouldn’t she be fined or something? Think of all the money that has gone into her.<br />4. GP:<br />a. How am I supposed to manage her in the community?<br />b. This seems like a very unusual condition. Shouldn’t her care be based out of a psychiatrist’s<br />office, involving me only peripherally?<br />5. ANYONE: Are you going to recommend medications for her? Would an antipsychotic work?<br />Sample “answers” [focus is really whether the candidate conceptualizes the patient’s condition as a disorder requiring ongoing concern and attention, provides some clinical information about the condition, and helps to refocus caregivers on the process of providing due care and diligence]:<br />Collections of all short assays 223<br />1. NURSE: It’s absurd that she’s getting me to help her with bedpans and the like. I want to know, if she’s not actually physically disabled, should I just leave her there and tell her she should be doing it for herself? Maybe she’d snap out of it.<br />It is important to realize that the patient is at least as confused as her caregivers. Her symptoms are not consciously produced. It is very important to distinguish somatization disorder from malingering, where the patient would be doing this for a specific, conscious reason, like getting out of police prosecution, or getting drugs to sell on the street. Likewise, her life is suffering the greatest consequences of her actions. I wonder if, as a nurse, you could gently encourage whatever gradual, stepwise, functional improvements you see day to day, encouraging the patient to work with you. Other teammembers will need to help, and it will be important to involve OT and PT in helping her to set and achieve functional goals and recovery.<br />2. SURGEON:<br />a. I’m tempted to refuse to see her again. No one is going to want to see her twice.<br />A patient with this disorder will receive the best care from a consistent team of caregivers. I don’t<br />know if you feel able to take on this challenge, that is something you’ll need to sort out. One of the hardest things about this disorder is recognizing that it is happening. Once you have established that, it helps to support your clinical decision-making, when the symptoms and results of investigations simply don’t add up.<br />b. Can I be sued for having operated on her?<br />This is a very difficult diagnosis to make, and those past surgeries, with benign results, are part of what helps us to recognize the disorder. In the past, you assessed her clinical presentation as any surgeon would, and treated her with due diligence and care. In the future, she will need to be treated with the same diligence. She may present in future with a true surgical condition, and it will be important that she get that surgery. What this diagnosis really tells us, is that, when clinical assessment and investigations don’t match up with symptomatic report, we can feel more justified in proceeding with “conservative management” until the situation declares itself. Anyone can sue anyone, but given that this situation is about somatization disorder, not malingering, it would be unusual for the case to go in that direction.<br />3. INTERNIST: Shouldn’t she be fined or something? Think of all the money that has gone into her.<br />I can appreciate your frustration; it is somewhat similar to the frustration many people feel facing the costs associated with the medical complications of smoking, or type II diabetes. As essence, this patient actually suffers from a very serious condition, and will herself suffer more than anyone else unless she can somehow find her way through this to other ways of coping. It would be hard to justify suing her, given that she does not actually consciously control what is happening, and that she is suffering from a disorder herself.<br />Collections of all short assays 224<br />4. GP:<br />a. How am I supposed to manage her in the community?<br />The key to management is building therapeutic alliance and maintaining regular appointments, including during times that the patient does not have any acute or changing symptoms. I would recommend that you consider scheduling regular appointments every 1-2 weeks. It can help to assure her that you will investigate symptoms as clinically appropriate, and to keep in mind that true medical conditions are likely to emerge over time. You can also identify that the regular appointments are being made because her overall diagnosis, somatization disorder, means that she is likely to experience symptoms and impairments that are not due to physical changes in her body, and that experience shows us that regular contact will help to keep her functioning as well as possible in her life. Encourage her to set functional goals for herself, and to see physical symptoms as possible clues that the goals she is setting may need to be re-evaluated (e.g. intense migraines whenever getting together with an old boyfriend).<br />b. This seems like a very unusual condition. Shouldn’t her care be based out of a psychiatrist’s office, involving me only peripherally?<br />This condition is both common, and uncommon. 5-10% of patients in primary care settings actually meet criteria for the disorder, with an estimated prevalence of 0.2-2%, with higher rates of picking up on the diagnosis in women. Certainly, if the patient is able to engage in this, we can look at psychiatric interventions to improve her coping skills and self-awareness, such as individual therapy, CBT, IPT, and day hospital. A common comorbidity for somatization disorder is clinical depression, and it will be important to treat that if she develops a clinical depression. The cornerstone of treating a patient like this, however, is at the primary care level, where her symptoms can be appropriately assessed and worked up as appropriate.<br />5. ANYONE: Are you going to recommend medications for her? Would an antipsychotic work?<br />There is no evidence that an antipsychotic would be helpful over the long-term, as this is not a psychotic illness. It would place her at risk for serious side-effects such as tardive dyskinesia, similar to the risk of dependence which she suffered when she was put on opioids for her pain complaints. In general it is important to be conservative in managing patients with somatization disorder, and to seriously weigh the potential harms of proposed treatments against the often- minimal benefits. The most likely medication to benefit, with the least risk of harm, would be an antidepressant, such as an SSRI. I will look into this, although we should realize that there is no magic pill for this condition. The main thing we can do for her is providing a stable, therapeutic environment, and attempt to contain her, minimizing the cost of this disorder to the patient, as well as the system. Caregivers will need to be aware that she has this condition, but also work up her symptoms as appropriate when they emerge. Communication, and continuity of care, are key.

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cocaine -- clinical presentation and mgt of abuse

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Diagnosis of cocaine intoxication:<br>A. recent use of cocaine, followed by behavioral changes and physical changes<br>B. behavioral changes can include euphoria or affective blunting, change in sociability, anxiety, impaired judgment<br>C. physical changes include two of: (3 ‘p’, 2 heart, 2 stomach, 2 muscular)<br>1. pupillary dilation (mydriasis)<br>2. perspiration or chills<br>3. psychomotor agitation or retardation<br>4. bradycardia or tachycardia<br>5. elevated or lowered blood pressure<br>6. nausea or vomiting<br>7. evidence of weight loss<br>8. muscular weakness, respiratory depression, chest pain, cardiac arrhythmias<br>9. seizures, dystonia, dyskinesia, confusion or coma<br><br>Management of cocaine abuse:<br>A. attain abstinence<br> complete or partial hospitalization with frequent, unscheduled urine drug screens<br>B. psychological interventions<br> focus on dynamics leading to use; meet at least twice a week<br>C. medications<br> dopaminergic medications: amantadine (causes dopamine release), bromocriptine (dopamine agonist)<br> tricyclic antidepressants: desipramine<br> other: Bupropion, carbamazepine, methylphenidate – help manage withdrawal<br>D. behavioral contract with positive reinforcement for negative urine drug screens<br>2) List five symptoms of cocaine withdrawal. [2003][1996] Diagnosis:<br>A. cessation of or reduction in cocaine use that has been heavy and prolonged, leading to dysphoric mood and two or more of THeSPiaN (tired, hungry, sleep disturbance, psychomotor disturbance, nightmares) – mnemonic: dysphoric THeSPiaN<br>B. withdrawal symptoms end within 18 hours if use was mild to moderate; can last up to a week if use was heavy; withdrawal is characterized by intense and powerful cravings<br>C. the criteria described are generally the “intermediate phase” of withdrawal<br><br><br> <br>immediate (crash): intense craving, acute dysphoria, irritability, restlessness intermediate: as above<br>late: intense cravings, conditioned triggers for cravings, depression<br> ON THE OTHER HAND, you do it this way<br>Immediate (the “crash” period): lasts from 9 hours to 4 days. It initially produces agitation, depression, anorexia and high cocaine craving, and later it is associated with fatigue, depression, insomnia, no craving, and finally exhaustion. →intense craving, acute dysphoria, irritability and restlessness<br>Themiddleorintermediatephase,“withdrawal,”lastsfromoneto10weeksand swings from initial low anxiety and craving; to high anxiety and cravings in the latter stages.<br>Thethirdandfinalphase,“extinction,”isanindefiniteperiodandfeaturesa normal mood but episodic craving, which can be triggered by conditioned cues learned during past cocaine use. → intense cravings, conditioned triggers for cravings, depression<br><br>

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Etoh abuse - factors raising suspicion, 70M alone

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A. criteria for substance dependence: WASTED 1. withdrawal<br>2. amounts (large, long periods)<br>3. social activities replaced by time spent acquiring substance<br>4. tolerance<br>5. efforts to cut down unsuccessful<br>6. despite adverse consequences, keeps using<br>B. features in history:<br>1. seizures, blackouts<br>2. esophagitis, gastritis<br>3. family history of alcoholism<br>4. history of legal charges<br>5. collateral from friends or family<br>C. physical findings<br>1. gynecomastia<br>2. spider angiomata<br>3. ascites<br>4. abnormal gait<br>D. laboratory tests<br>1. elevated GGT<br>2. increased MCV<br>3. ALT over AST ratio of greater than two<br>4. carbohydrate-deficient transferrin test

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hallucinogen of the ergot type. ER -- Describe the two most likely behavioral / psychological changes that would support your diagnosis, and three clinical signs you would expect to find

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Criteria for hallucinogen intoxication<br>A. psychological changes (anxiety, depression, ideas of reference, paranoia)<br>B. perceptual changes (e.g. hyperesthesia, Synesthesia, illusions, depersonalization)<br>C. clinical signs (ECSTASY):<br>1. eyes wide open (pupillary dilation)<br>2. cardiac – palpitations<br>3. sweating<br>4. tachycardia<br>5. ataxia (incoordination)<br>6. shaking (tremors)<br>7. blurry vision<br>Synesthesia: Condition in which the stimulation of one sensory modality is perceived as sensation in a different modality, as when a sound produces a sensation of color. Hyperesthesia: Increased sensitivity to tactile stimulation.

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alcohol withdrawal delirium in a 50-year-old man, and briefly describe the treatment of the disorder

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Features<br>A. within hours to days of stopping alcohol use, development of (ALC’HOLIC):<br>1. anxiety<br>2. listlessness (psychomotor agitation)<br>3. “c” – seizures<br>4. hand tremor increased<br>5. autonomic instability (tachycardia or diaphoresis)<br>6. loss of reality (hallucinations or illusions)<br>7. insomnia<br>8. c-sickness (nausea, vomiting)<br><br><br>safety: do a full history and physical to rule out other disorders<br>B. disposition (inpatient vs. outpatient) – outpatient only if patient reliable, has supports, and<br>no medical complications<br>C. monitoring – use clinical institute for withdrawal assessment (CIWA) scale, or check<br>autonomic signs<br>D. medications<br>1) 2)<br>3) 4) 5) 6)<br>6) What are<br>outpatient: fixed dosing schedule of Lorazepam or diazepam<br>inpatient: front load dosing of long acting benzodiazepine, or symptom triggered dosing (such as hourly benzodiazepine until sedated but rousable)<br>thiamine 100mg IV or IM then orally for one week<br>multivitamins<br>folic acid<br>magnesium if low<br>

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Substance abuse RF (made up question???)

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a.<br>  <br> <br>b.<br>    <br>c.<br>  <br>d.<br>  <br>e.<br> <br>f.<br>  <br>genetic influences on drug dependence;<br>Most genetic work has been done with twin and adoption studies.<br>Higher rates of susceptibility to Etoh use is found in children with alcoholic parents.<br>Genetic susceptibility is a risk factor for future abuse, but it must be combined with environmental factors to be expressed<br>↑ Risk of dependence is found with: a phenotype where Etoh has a decrease physical impact on the user and increased +ve effect from use. (e.g., increase endorphin release)<br>↓ risk of dependence is found with: a phenotype which causes ill effects from Etoh consumption<br>family issues: found in families characterized by acceptance of drug and Etoh within the family conflict between family members<br>lack of supervision or parental rejection<br>sexual or physical abuse poor communication<br>school factors<br>unfair rules<br>norms conducive (contributing to, encouraging, favorable) to drug use lack of school “bonding”<br>peer group factors<br>bonding to an antisocial peer group delinquent behaviour<br>social marginalization<br>community factors<br>poverty unemployment<br>societal factors<br>Degree of social acceptance.<br>Social upheaval.<br>The price of a drug is inversely proportional to its prevalence of use

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Substance abuse -- psych comorbidities (self made???)

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i. comorbidity of psychiatric illness and substance abuse:<br>1. antisocial personality disorder: 60 to 80%<br>2. bipolar disorder 30-50%<br>3. schizophrenia 47%<br>4. post-traumatic stress disorder: 30 to 50%<br>5. panic disorder: 36%<br>6. any anxiety disorder: 36% 7. ADHD: 23%<br>8. depression: 17%<br><br>ii. patients with schizophrenia have a 4x risk for alcohol, 5x for marijuana, 6x for opiates, and 13x for cocaine

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Ego defenses -- 5 statements drunken etohic admit for GIB

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“I don’t have a problem; they’re just out to get me”<br>“I’m not an alcoholic, I hate drunks”<br>“Think of war, famine &amp; the world - what does my drinking matter in comparison” “Drinking helps me by....”

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Etoh Depend -- Name four medications evidence to help w/ abstinence &amp; prevent relapse. Name 4 factors associated with late onset alcohol dependence. Name four psychosocial therapies that a psychiatrist can do (evidenced based to decrease drinking &amp; prevent relapse).

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A. Name four medications evidence to help w/ abstinence &amp; prevent relapse. 1. Naltrexone<br> An opiate receptor antagonist act by preventing the opiate receptor mediated euphoric and rewarding effects of alcohol, diminishing the rewarding aspects of alcohol-induced dopamine release, and blunting the subsequent craving for alcohol.<br> Metaanalysis have found it to be more effective than placebo in promoting abstinence, reducing heavy drinking days, and decreasing rates of relapse.<br> Several studies have indicated that naltrexone works best when combined with a relapse prevention approach, such as coping skills or CBT<br>2. Disulfiram<br> Aimed at motivating abstinent alcoholic individuals to resist alcohol consumption, 250 mg/day, range 125-500 mg/day.<br> When aldehyde dehydrogenase is inhibited by disulfiram, alcohol consumption causes toxic levels of acetaldehyde to accumulate, which in turn is associated with a host of unpleasant and potentially dangerous signs and symptoms, including a sensation of heat in the face and neck, headache, flushing, nausea, vomiting, hypotension, and anxiety.<br> Chest pain, seizures, liver dysfunction, respiratory depression, cardiac arrhythmias, myocardial infarction, and death have also been reported.<br> a meta-analysis showed only some diminution in drinking with disulfiram<br> Patients who are intelligent, motivated, and not impulsive and whose drinking is often<br>triggered by unanticipated internal or external cues that increase alcohol craving are the<br>best candidates for disulfiram treatment.<br> Disulfiram should never be used without the patient's knowledge and consent Patients<br>taking disulfiram must be advised to avoid all forms of ethanol (including, for example,<br>that found in some cough syrups).<br> Disulfiram requires hepatic metabolism to convert it into an active medication. A<br>metabolite of disulfiram is an inhibitor of CYP 450 3A4 and can interfere with the metabolism of a variety of psychotropic and other medications that are substrates for CYP 450 3A4.<br> It should be used cautiously in patients with moderate to severe hepatic dysfunction, peripheral neuropathies, renal failure, and cardiac disease.<br> Disulfiram is eliminated from the body slowly. Ingesting alcohol even 1-2 weeks after the last dose of disulfiram could cause an alcohol-disulfiram reaction<br>3. Acamprosate<br> It is an amino acid derivative of taurine that is thought to work at brain glutamate receptor sites and stabilize glutamatergic function.<br> As such, it has been hypothesized that it might normalize an aberrant glutamate system present during early abstinence that may be the basis of protracted withdrawal and early abstinence craving<br> Those who relapsed had more abstinent time before their first drinking day and also more overall abstinent days during a year or more of treatment.<br> acamprosate was more effective than placebo in increasing the number of abstinent days<br> It would appear that, although not specifically studied, a number of days (perhaps 7 or<br>more) of abstinence prior to starting acamprosate might be needed for acamprosate to be<br>most effective.<br> There is also some evidence that acamprosate and naltrexone can be given together<br> At a dosage of two 333-mg pills t.i.d. (total dose of 1,998 mg),<br> acamprosate is well tolerated, with generally self-limited and symptomatically treated<br>diarrhea being the main adverse effect<br> acamprosate is excreted by the kidneys and not metabolized by the liver, caution must be<br>taken with patients who have renal impairment. Acamprosate has minimal if any negative<br>interaction with alcohol<br>4. Medications acting on the serotonin system<br> SSRIs also may reduce psychiatric symptoms or syndromes (e.g., anxiety, depression) that might influence drinking behavior<br> several randomized, double-blind, placebo-controlled human studies with nondepressed heavy drinkers found that SSRIs reduce short-term alcohol consumption by 15%-20%<br>5. Lithium is not recommended as a primary treatment in patients who do not have co-occurring bipolar disorder.<br>B. Name 4 factors associated with late onset alcohol dependence.<br>1.<br>2.<br>Late onset: type A,<br>° Few childhood risk factors<br>° mild dependence<br>° few alcohol related problems<br>° little or less psychopathology-anxiety comorbidity,<br>° good prognosis Early onset: Type B,<br>o many childhood risk factors<br>o severe dependence<br>o early onset of Etoh-related problems<br>o much psychopathology<br>o a strong family history of Etoh abuse<br>o frequent polysubstance abuse<br>o a long history of alcohol treatment and high number of severe life stresses and poor<br>prognosis<br>C. Name four psychosocial therapies that a psychiatrist can do (evidenced based to decrease drinking &amp; prevent relapse).<br>1. Cognitive-behavioral therapies<br> CBT and relapse prevention therapies aimed at improving self-control and social skills have been consistently found to reduce drinking; such cognitive-behavioral therapies, as well as MET and TSF, are therefore recommended for use in individuals with an alcohol use disorder.<br> Cognitive therapy interventions that are focused on identifying and modifying maladaptive thoughts but that do not include a behavioral component are not as effective.<br> CBT: focuses on appropriate ways to cope with life experiences without drinking.<br> In-group settings, CBT approaches are similarly effective, although treatment benefits<br>may vary with patient characteristics.<br> Finally, most studies show efficacy for social skills training, which focuses on learning<br>skills for forming and maintaining interpersonal relationships, being assertive, and<br>refusing alcohol<br> MET and motivational interviewing are typically brief therapies that last one to four<br>sessions and are aimed at maximizing the patient's intrinsic desire to change or<br>enhancing a patient's adherence to more intensive or extended treatment.<br>2. Behavioral therapies<br> Individual behavioral therapy, particularly involving positive reinforcements for targeted behaviors, has been found to be effective for patients with an alcohol use disorder and is a recommended treatment approach.<br> Also effective are behavioral contracting and the community reinforcement approach, which uses behavioral principles and usually includes conjoint therapy, training in job finding, counseling focused on alcohol-free social and recreational activities, monitoring of disulfiram use, and an alcohol-free social club.<br> When compared with usual outpatient treatment or disulfiram plus a behavioral adherence program, community reinforcement led to significantly better patient outcomes<br>3. brief therapies<br> Brief therapies have been shown to be effective in reducing alcohol use and improving general health and social functioning<br>4. Self-help groups and T2-step-oriented treatments<br> large number of studies have documented that greater AA participation is associated with greater rates of abstinence from alcohol as well as with better drinking outcomes<br> The only requirement for membership is a desire to stop drinking<br>5. Marital and family therapies<br>6. Self-guided therapies<br> Strong evidence is available to support the efficacy of self-monitoring of drinking patterns<br>7. psychotherapy (individual, marital, and group)...focuses on reasoning for drinking and dealing with stressors<br>8. Aftercare<br> A patient's involvement in aftercare after completing inpatient treatment for an alcohol use disorder is an important predictor of outcome.<br> The lowest rates of relapse have been noted in those completing an aftercare program, with some evidence that completion rates vary with therapists' efforts to maintain patients in the aftercare program<br><br>10) Discuss the reporting of patients who are drinking and driving. Discuss treatment for the withdrawal of alcohol. What are the roles of naloxone and naltrexone?<br> reporting issues:<br>a. transportation issues:<br>1. aeronautics act: mandatory reporting<br>2. motor vehicle act: voluntary reporting (physician protected if they<br>report)<br>b. protective services<br>1. adult protection act: mandatory reporting of elderly abuse<br>2. children and family services act: mandatory reporting of child abuse or<br>neglect<br> naltrexone is an opioid antagonist; was approved by the FDA for the treatment of alcoholism<br>in 1994 (the first medication to receive approval for this since disulfiram in 1948) – <br><br><img src=pasteVgipYz.png /><br>

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recent immigrants or refugees and their families -- psych probs may suffer

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E. adjustment disorder (with depressed mood, anxiety, or both)<br>F. post-traumatic stress disorder<br>G. major depressive disorder<br>H. anxiety disorders<br>I. acculturation problems (v-code)<br>J. culture-bound syndromes

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ED -- treatment: 4 reason inpatient, outpatient, 2 reasons involuntary hosp,

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1. Weight loss greater than 20% of normal weight for age, height and bone structure.<br>2. History of repeated hospitalizations for anorexia nervosa or underweight greater than 6 months<br>3. Psychotic depression or serious suicide attempt<br>4. Incapacitating obsessions and compulsions related and/or not related to eating disorder<br>5. Serious co-morbid medial conditions such as edema, hypoproteinemia, severe anemia<br>b) Give four reasons for the inpatient treatment of a person with bulimia nervosa.<br>1. All of the above plus<br>2. Binging that requires all meals to be supervised<br>3. Severe disabling symptoms that don’t respond to outpatient TX<br>4. Severe concurrent alcohol/drug abuse<br>c) Give two reasons for the involuntary treatment of an eating disorder. Indications for forced hospitalization<br>1. Life threatening medical condition (Imminent risk of death due to medical complications)<br>2. Acutely suicidal (Imminent risk of suicide)<br>3. Judged incapable of consenting to treatment due to cognitive impairment, and at imminent<br>risk?

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AN -- 5 complications, one per body system

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Complications of anorexia nervosa<br>A. endocrine: amenorrhea (low LH, FSH), decreased growth hormone, low T3,<br>hypercholesterolemia<br>B. hematological: leukopenia<br>C. skeletal: osteoporosis<br>D. dermatologic: lanugo hair<br>E. neuropsychiatric: depression<br>F. cardiac: arrhythmias<br>G. gastrointestinal: constipation<br>Complications of binge eating or purging (bulimia)<br>A. metabolic: electrolyte abnormalities (low potassium)<br>B. gastrointestinal: pancreatic inflammation, esophagitis, elevated amylase<br>C. dental: eroded dental enamel, tooth decay<br>D. neurological: seizures, weakness<br>E. psychiatric: suicide (higher rate of impulsivity in bulimics than in anorexics)<br>Laboratory abnormalities<br>A. CBC: decreased white count (leukopenia)<br>B. electrolytes: low magnesium<br>C. glucose low<br>D. renal function impaired (elevated BUN)<br>E. elevated amylase<br>F. low thyroid function<br>G. EKG abnormalities<br>H. elevated cholesterol<br>I. non-suppression on dexamethasone suppression test

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BN -- ax and manage as outpatient

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Diagnosis and Epidemiology:<br>A. being overly concerned with body shape and weight, leading to recurrent episodes of binge<br>eating (eating more than normal in a discrete period of time, and experiencing a loss of control during this) and compensatory behavior at least twice a week for three consecutive months<br>B. can be purging type (vomiting or laxatives, enemas, diuretics) or non-purging type (exercise, fasting)<br>C. prevalence of 1 to 3% in adolescent females; ten times less common in men<br>D. usual onset in late teens<br>E. weight usually normal<br>F. unlike anorexia, commonly have suicide attempts and substance abuse<br>G. course is chronic, with multiple relapses<br><br>Physical findings:<br>A. dizziness, postural hypotension<br>B. parotidomegaly<br>C. dental problems<br>D. abrasions of knuckles (Russell’s sign) caused by repeated contact of hands with incisors<br>during self-induced vomiting<br>Laboratory tests:<br>A. with chronic vomiting, amylase may be elevated and potassium decreased<br>B. may show dexamethasone non-suppression (it is a stressed state)<br>C. should also check CBC, lytes, liver function, fasting blood sugars, and TSH<br>Management:<br>A. pharmacotherapy<br>1) A number of antidepressants have been shown to be superior to placebo, including: Fluoxetine, desipramine, imipramine, phenelzine and have been conducted in normal-weight outpatients with bulimia nervosa.<br>2) The dosage used was similar to that used for the treatment of depression.<br>3) In all trials, the drugs were significantly more effective than placebo in reducing binge eating.<br>4) In addition, the medication improved mood and reduced eating disorder symptoms such as<br>preoccupation with shape and weight.<br>5) The majority of patients were still symptomatic at the end of treatment and in long-term<br>studies over 80 % of patients relapse.<br>6) The medications used for the treatment should be continued for 6 months to prevent relapse.<br>7) One large multicenter collaborative study showed Fluoxetine in doses of 60 mg a day to be<br>effective in reducing episodes of binge eating and purging.<br>8) Cognitive-behavioral therapy plus medication was superior to cognitive-behavioral therapy<br>alone.<br>9) abstinence is not usually the outcome<br>B. psychotherapy<br><br>cognitive behavioral therapy<br>Cognitive-behavioral therapy should be considered the benchmark, first-line treatment for bulimia nervosa.<br>Found to be the most effective treatment in over 35 controlled psychosocial studies.<br>About 40 to 50 % of patients are abstinent from both binges eating and purging at the end of treatment (16 to 20 weeks).<br>Improvement by a reduction in binge eating and purging occurred in a range from 70 to 95 % of patients.<br>Another 30 percent of those who did not show improvement immediately post-treatment showed improvement to full recovery 1 year after treatment.<br>Cognitive-behavioral therapy implements a number of cognitive and behavioral procedures to interrupt this self-maintaining behavioral cycle of bingeing and dieting<br>interpersonal therapy – findings suggest that interpersonal therapy has a delayed but powerful<br>psychodynamic psychotherapy<br>family therapy; Not widely used because most patients with bulimia nervosa are in their 20s and live away from their family of origin<br>nutritional counseling

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ED and families, 5 psych dx more common

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• family members have increased rates of mood disorders and eating disorders<br>Anorexia:<br>A. Depression (65%)<br>B. Social phobia (34%)<br>C. Obsessive-compulsive disorder (26%)<br>Bulimia<br>A. Depression (50%)<br>B. substance abuse (especially cocaine and amphetamines)<br>C. suicide attempts<br>D. personality disorders<br>5) What is the prognosis of ED’s ?<br>° Earlier age of onset (under age 18)<br>° No previous hospitalization for the illness ° No binging or purging behaviors.<br>° No co-morbid BN,OCD,Mood disorder ° Good pre-morbid adjustment<br>° No severe somatic complaints<br>° Lack of general medical complications<br>° Good social supports

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30 yo chronic schizophrenia has a long history of sexually inappropriate behavior that has been unrelenting. After a violent sexual assault of a 10-year-old boy, he was sentenced to one<br><br>Collections of all short assays 236<br>year in jail. After he has completed 10 months of this sentence, you have been asked to see him to give an opinion on the risk of him re-offending if he should be released from jail.

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A. Five factors to consider in risk for future violence: (MacArthur study)<br> Substance use<br> Mental disorder with substance abuse<br> Antisocial personality disorder<br> Male more than female<br> Prior history of violence<br> Father who was substance abuser or criminal  Physically abused as child<br> Violent thoughts<br>B. Five treatment approaches in preventing future sexual assaults:<br> CBT (relapse prevention based) treatment program  Teaching coping skills<br> Booster sessions<br> SSRI can decrease libido<br> Anti-androgens<br> Hypothalamic leutinizing- releasing hormone

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DDx rambling speech &amp; delusional/grandiose. 3 criteria re fitness stand trial

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Most likely disorders:<br>• Bipolar disorder type I in manic episode with psychotic features<br>• substance induced psychotic disorder<br>• schizophrenia<br>Criteria for fitness:<br>A. understand the nature of the proceedings<br>1) understand the charges against him<br>2) understanding what a judge, lawyer, prosecutor, jury all do<br>3) understand what it means to take an oath<br>4) understand the consequences of lying in court<br>B. understand the possible consequences of the proceedings<br>1) who makes the final decision<br>2) what can you plea<br>3) what are the possible outcomes of the trial<br>C. to be able to instruct counsel

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DDx -- 22M tall obese sparse facial hair a poor educational vocational record sexual assault<br>A. What are the three most Likely diagnoses<br>B. Recidivism risk factors

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What are the three most Likely diagnoses  Pedophilia<br>diagnosis:<br>1. over six months of recurrent, intense, sexually arousing fantasies, urges, or behaviors<br>involving sexual activity with a prepubescent child or children (usually under age 13)<br>2. the person is at least 16 years old, and at least five years older than the child<br>3. specify if attraction is to boys, girls, or both<br>4. specify if limited to incest<br>5. specify if exclusive (attracted only to children) or non-exclusive<br> Mental retardation<br>1) impaired judgment and understanding<br>2) inability to delay gratification<br><br>Impulse control disorder not otherwise specified<br><br><br>A. What are the risk factors for recidivism you would consider in this patient?<br>A. offense variables<br>1) use of force vs. coercion in the act<br>2) range of paraphilias<br>B. offender variables<br>1) developmental delay<br>2) substance abuse<br>3) prior sexual offender<br>4) deviant arousal<br>5) failed response to prior treatment<br>6) psychosis<br>7) denial of responsibility

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assisted suicide is controversial. Present four arguments for and four arguments against the involvement of physicians in assisted suicide.

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Arguments for assisted suicide<br>A. physicians are obligated to relieve pain and suffering<br>B. physicians are obligated to promote dignity and autonomy of dying patients<br>C. to provide effective palliative care, physicians may be required to provide treatments that<br>hasten death<br>D. physicians can respect a patients decision to withhold life-sustaining treatment (such as<br>mechanical ventilation)<br>E. physicians are best trained to assist painless suicide<br>Arguments against assisted suicide<br><br>C.<br>D. E.<br>nearly every code of professional ethics opposes physician assisted suicide<br>suicidal ideation is nearly always associated with a mental illness and/or intolerable pain, both of which require treatment<br>suicidal ideation may represent a patient’s wish to not be a burden, in which case family therapy may be indicated<br>patients may be coerced by their families to end their lives<br>physician assisted suicide is a crime

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doctor-patient confidentiality -- 3 circumstances necessitate breaching

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A. child abuse<br>B. risk to patient (suicidality)<br>C. risk to society (Smith vs. Jones; clarity, severity, and imminence of risk)<br>D. operating a motor vehicle

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NCR criteria

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A. unable to appreciate, by reason of mental disorder, the nature and consequences of the act, or omission of the act<br>B. unable to know, by reason of a mental disorder, that the act is wrong (legally or morally)<br>Assessment process<br>A. presence of mental disorder<br>B. did the mental disorder cause either:<br>1) failure to appreciate nature and consequences of act or<br>2) failure to know act was wrong (legally or morally)

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MR -- 3 criminal offenses commonly associated with

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A. physical assault<br><br>C. pyromania (arson)

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Competence -- financial, criteria

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 appreciates the importance of being financially competent and understands purpose of examination<br> has some realistic appreciation of own strengths and weaknesses in area of financial competence<br> understands nature of own assets and liabilities<br> has demonstrated sound judgment in the past and can be expected to do so in the foreseeable<br>future<br> has used available resources appropriately in the past, and indicates willingness to do so in the<br>future

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Testamentary Capacity

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The testator must know<br>1) the nature and extent of their property<br>2) the nature of the act they are about to perform<br>3) the name and identity of any person who is to be the object of their bounty<br>4) their relations to the person<br>5) must have sufficient mind and memory to understand all of these acts<br>6) must be able to relate these facts to one another<br>7) must recall the decision he/she has made

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noncustodial parent for a 14 yr old with ADHD -- make decisions with? Can we share info with noncustodial parent without involving other parent?

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 You would need to assess capacity if there is a doubt.<br> Due to the age you probably have reason.<br> If capable you don't need to the custodial or noncustodial parent.<br> I would have to look up the revised statues to answer the custodial parent question.  As you can imagine it is not something I have to address often.

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incompetent for TX decisions on an admission, and then goes home, how long does the incompetence last? What about for $? I know a lot of this is provincial, but it does seem to come up a lot on past exams

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 If someone is found to be incompetent to consent to treatment, HCCA, they remain incapable until<br>this condition is reversed.<br> This applies to the treatment at the facility where the chart is opened.<br> There is no stop date to incapacity.<br> A person may contest their finding of incapacity and if they lose can recontest every six months.<br> If someone is found to be incompetent to consent to management of property or finances and a<br>continuance (continuation, prolongation, persistence) is issued, a letter is sent to the PGT office.<br> If a valid POA for Finance exist, the PGT office advises the POA to act and no further action is<br>taken (i.e. no letters are sent to financial institutions or lawyers etc).<br> If no POA exists for finances then the PGT freezes the assets, takes a percentage and manages<br>things.

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SDM -- 12 yo anorexia, refusing admit, when is parent automatically SDM

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 If the person is 15 and is refusing admission, your two options are to admit the person as an informal patient (person is incapable and an SDM agrees) or certify the patient.<br> Technically you should certify the patient because the involuntary status of the informal patient poses some difficulty.<br> Only with regards to the MHA is a person who is younger than 16 considered incapable.<br> This has nothing to do with treatment but only admission.<br>

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OCPD - clinical characteristics, Give 2 psychodynamic/unconscious conflicts at play, list 4 defense mechanisms at play

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1- Externalization,<br>2- Isolation of affect,<br>3- Rationalization,<br>4- Displacement and<br>5- Reaction formation<br>6- Undoing<br>OCPD defenses are intellectualization, isolation of affect, undoing, reaction formation, displacement, and regression<br>Psychodynamic theories are:<br> There is a conflict between the superego and the Id<br> obsessional behavior is described as a fixation at the anal stage of psychosexual development;<br>as a result, these client's are characterized as being anal-retentive  Parents are harsh and controlling<br>Discuss 3 psychodynamic issues that may arise in therapy<br>6. Regression to an anal fixation in response to castration anxiety encountered in the<br>oedipal phase.<br>7. As psychoanalytic theory has focused less on anal character traits and more on<br>difficulties in self-esteem, management of dependency and anger, cognitive style, and problems with intimacy. Psychoanalytic treatment reveals the entrenched conviction that they were not loved or valued by their parents.<br>8. Intense anger directed at the parents and dependent longings are frequently defended against through reaction formation and isolation of affect.<br>9. They often feel that, if they could just do enough, they will finally win the parental approval that they missed in childhood.<br>10. Most patients with obsessive-compulsive personality disorder prefer work to the unpredictable intimacy of personal relationships.

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BPD -- want admission to hospital. If their request is denied, they may become very demanding. Rate suicide, 3 reasons admit, not admit, alternatives (3)

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a) What is the rate of completed suicide associated with this diagnosis? 10 % peak in middle thirties due to lack of medical support<br>b) Give three reasons why you would admit such a person to hospital.<br>a. Dangerous impulsive behavior not managed as outpatient<br>b. Non-adherence to outpatient treatment &amp; deteriorating clinical picture c. Complex co-morbidity that requires intensive clinical assessment<br>d. imminent danger to others<br>e. Loss of control, serious suicide attempt<br>f. Transient psychotic episode with loss of impulse control<br>c) Give three reasons why you would not admit such a person to hospital. A. Tendency towards regression in hospital<br>B. Can worsen suicidal behavior in some patients<br>C. Minor attempt<br>D failure previous treatment<br>d) Give three alternatives to hospital admission.<br>1. Day hospital program 2. Outpatient program 3. Residential treatment<br>4. Psychotherapy

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5 inclusion criteria PD generally

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DSM-IV General Diagnostic Criteria for a Personality Disorder<br>A. An enduring pattern of inner experience and behavior that deviates markedly from the expectations of the individual's culture. This pattern is manifested in two (or more) of the following areas:<br>(1) Cognition (i.e., ways of perceiving and interpreting self, other people, and events)<br>(2) Affectivity (i.e., the range, intensity, lability, and appropriateness of emotional response)<br>(3) Interpersonal functioning (relationship)<br>(4) Impulse control<br>B. The enduring pattern is inflexible and pervasive across a broad range of personal and social situations. C. The enduring pattern leads to clinically significant distress or impairment in social, occupational, or other important areas of functioning.<br>D. The pattern is stable and of long duration and its onset can be traced back at least to adolescence or early adulthood.<br>E. The enduring pattern is not better accounted for as a manifestation or consequence of another mental disorder.<br>F. The enduring pattern is not due to the direct physiological effects of a substance (e.g., a drug of abuse, a medication) or a general medical condition (e.g., head trauma).

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splitting. What disorder does this frequently? Describe 2 other defences used by that disorder. Name 4 management strategies on inpatient unit to deal with splitting.

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a- What disorder does this frequently<br>Borderline personality disorder.<br>b- Describe 2 other defences used by that disorder.<br>1- splitting,<br>2- acting out ,<br>3- identification,<br>4- dissociation<br>5- Distortion<br>C -Name 4 management strategies on inpatient unit to deal with splitting<br>1- Management patient’s own transference reaction and further education of how to use them<br>as away of understanding the patient.<br>2- Frequent staff meeting and help the patient to perceive what is going on<br>3- Staff meeting with patient based on 5-10 minutes for further discussion and understanding<br>the patient<br>4- More Psycho-education to staff that patient’s reactions of transference has no personal<br>means.<br>5- The self and others are often regarded as “all good” or “all bad.” This phenomenon is<br>closely related to what Beck and Freeman (19) call “dichotomous thinking” and what<br>Linehan (17) refers to as “all or none thinking.”<br>6- Psychotherapy must be geared to helping the patient begin to experience the shades of gray<br>between the extremes and integrate the positive and negative aspects of the self and others. A major thrust of psychotherapy is to help patients recognize that their perception of others, including the therapist, is a representation rather than how they really are.

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DBT differs from psychodynamic therapy (3 ways)

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1- Therapist is active &amp; non-neutral;<br>2-no free association/dynamic interpretations;<br>3-no resolution of unconscious conflict or interpretation of transference; 4-DBT says behaviors, thoughts &amp; feeling are learned<br>Four issues &amp; behaviors addressed in Stages 1 &amp; 2<br>Stage 1 target is Stability &amp; control - suicidal behaviors, therapy interfering behaviors, quality of life-<br>interfering behaviors, behavior skills (mindfulness, interpersonal effectiveness, emotion<br>regulation, distress tolerance, and self-management)<br>Stage 2 target is Emotional processing of the past -

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DBT differs from psychodynamic psychotherapy (3 ways) Describe 4 issues/behaviors addressed in DBT stages 1 and 2.

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Three areas of transference to medication<br>Idealization &amp; devaluation of med, splitting therapist against medication, noncompliance as a displacement against the therapist, furtherance of resistance to insight believing that illness is only biologic needing meds;<br>2 possible countertransference therapists has while prescribing meds<br>Rescue fantasies from medication; anger at devaluation/failure of therapy; feelings of inadequacy that therapy isn’t working; Paternalism/authoritarian omnipotence at “prescribing” what pt should do<br>Three ways to approach using meds in BPD pt<br>Use non lethal meds in non-lethal doses; be aware &amp; educate pt about limits of medication effectiveness; set target symptoms [ex SSRI to decrease impulsivity]; avoid polypharmacy

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BPD, identify: 3 areas of transference to medication, 2 possible countertransference reactions which the therapist might have when prescribing medication, 3 ways to approach using medications in a patient with BPD.

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a) 3 areas of transference to medication<br>1. Idealization &amp; devaluation of med,<br>2. Splitting therapist against medication,<br>3. Noncompliance as a displacement against the therapist,<br>4. Furtherance of resistance to insight believing that illness is only biologic needing meds;<br>b) 2 possible countertransference therapist has while prescribing meds<br>1. Rescue fantasies from medication;<br>2. Anger at devaluation/failure of therapy;<br>3. Feelings of inadequacy that therapy isn’t working;<br>4. Paternalism/authoritarian omnipotence at “prescribing” what pt should do<br>c) 3 ways to approach using meds in BPD pt<br>1. Use non lethal meds in non-lethal doses;<br>2. Be aware &amp; educate pt about limits of medication effectiveness; 3. Set target symptoms [ex SSRI to decrease impulsivity];<br>4. Avoid Polypharmacy

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BPD vs BAD II

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COMPARISON OF BPD AND BIPOLAR II DISORDER<br><br>Trait<br><br>BPD<br><br><br>Bipolar II<br>Mood lability/impulsivity<br>Due to interpersonal sensitivity<br>Autonomous and persistent (person acts out)<br>Affect<br><br>Deep, intense; evoke strong empathic response<br><br>Lack depth, pain; hard to empathize with<br>Protoypical behaviour<br>Care seeking; seeks exclusivity, is sensitive to rejection<br>Begins energetic self-initiated activities that are left incomplete; requiring others to clean up<br><br><br>

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BPD -- How to undertake a therapeutic contract

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• Agreement to treatment framework that promotes therapeutic alliance<br>• Goals of treatment and roles of each participant in working towards goals<br>o Eg. symptom reduction, improvement in functioning<br>o Roles of both participants – take responsibility for own behaviour, behave in a way that is<br>respectful of other person, non-aggressive and non-violent<br>o Patient’s role – share experience as honestly as possible<br>o Therapist’s role – offer understanding, undistracted attention, compassion, feedback that can<br>help patient to attain their goals<br>• Therapy sessions – when, where, frequency of sessions – procedure for cancelling sessions,<br>consequences of missed sessions (fee if appropriate)<br>• Therapist availability outside sessions<br>• Plans for crisis management<br>o Monitoring risk (suicidality/self-injury)<br>o Measures to manage risk – strategies and resources, hospitalization when necessary

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NPD -- Compare and contrast Kohut and Kernberg

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• Background<br>o For the past 2 decades, principal controversy surrounding the theoretical understanding of<br>narcissistic personality disorder has revolved around the models of Kohut and Kernberg o Kohut<br>− Believed that narcissistically disturbed individuals are developmentally arrested at a stage where they require specific responses from persons in their environment to maintain a cohesive sense of self, without which fragmentation of the self occurs<br>− Kohut understood this as the result of the parents' empathic failures<br>− These failures manifest themselves in the patient's tendency to form a mirror,<br>twinship or idealizing transference<br>o Kernberg<br>− Saw borderline as similar to narcissism while Kohut saw them as very different<br>− Viewed the narcissist as different only by his grandiosity, but that otherwise, they used the same primitive defenses as the borderline (splitting, devaluation,<br>idealization)<br>− Suggested that whereas borderline patients tend to have alternating self-<br>representations that make them look very different form day to day, narcissistic patients have a smoother, more consistent level of functioning based on an integrated pathological self<br><br>Feature<br><br><br>Kohut<br><br>Kernberg<br>Patient population<br>Based on relatively well functioning people whose self-esteem is vulnerable<br>All outpatient<br>Based on mixture of inpatients and outpatients<br>Most primitive, aggressive, grandiose<br><br>Comparison to borderline PD<br><br><br>Differentiates sharply between NPD and BPD<br>Defines NPD as similar to BPD but with slightly better ego functioning<br>Discussion of inner functions<br><br>Does not define inner world as emphasis on deficits<br>Delineates primitive defenses and object relations akin to BPD<br>Self-definition<br>Self defined as developmentally arrested<br>Self defined as highly pathological structure composed of fusion of ideal self, ideal object and real self<br><br>Defenses<br>Views self as non-defensive<br>Views grandiose self as being defensive against investment or dependency on others<br><br>Aggression<br><br>Views aggression as secondary to narcissistic injury, not primary<br>Emphasizes envy and aggression<br>Idealization<br><br>Accepts idealization at face value as normal developmental phase making up for missing psychic structure<br>Views idealization as defensive against rage, envy, contempt

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normal pressure hydrocephalus. Define and List its clinical features.

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Definition<br>• cerebral ventricular dilation with normal lumbar CSF pressure<br>• often no clear etiology<br><br>• dementia<br>• apraxia of gait<br>• urinary incontinence

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ER violence RF -- ten non-demographic, patient-related features that suggest there is an increased risk

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Patient-related features (non-demographic) suggestive of risk of violence in ER<br>• previous history of violence<br>• substance intoxication or withdrawal (drunk)<br>• delirium<br>• mental retardation<br>• paranoia<br>• command hallucinations to harm<br>• neurological disorder (head trauma)<br>• poor impulse control<br>• dementia<br>• history of childhood abuse<br>Demographic factors suggestive of risk of violence in ER<br>• young age<br>• male gender<br>Situational factors suggestive of risk of violence in ER<br>• needs not met in emergency room<br>• not being allowed to smoke

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MSE -- 10 obs mental status of a mute 35 year old man. The patient has been brought to the emergency room by his spouse, who tells you he has been mute for the past three days.

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Mental status (aseppttic jims)<br>• appearance<br>3) hygiene, grooming<br>4) facial asymmetry<br>5) pupillary abnormalities<br>6) eye contact<br>• speech<br>7) Do they nod, or respond in non-verbal ways?<br>• emotions (affect and mood)<br>8) affect – sad, anxious, flat<br>• perceptions<br>9) do they appear to be reacting to internal cues (possibly hallucinating) • psychomotor features<br>10) agitated vs. immobile<br>11) any abnormal motor activity<br>12) echopraxia<br>• thought form (none)<br>• thought content (none)<br>• insight (none)<br>• cognition (none)<br>• judgment (none)<br>• intellect (none)<br>• memory (none)<br>• suicidality (none)<br><br>• catatonia<br>13) bipolar disorder<br>14) schizophrenia<br>15) depression<br>• voluntary mutism (fear of spouse)<br>• neurological disorders<br>• substance abuse

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Somatization -- List six disorders where somatization is likely a prominent feature of the clinical presentation

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Definition of somatization<br>• a defensive conversion of psychic derivatives to bodily symptoms; a tendency to react with somatic rather than psychic manifestations<br>Disorders where somatization is prominent<br>• somatoform disorders<br>16) somatization disorder<br>17) hypochondriasis<br>18) pain disorder<br>19) conversion disorder<br>20) body dysmorphic disorder<br>21) undifferentiated somatoform disorder<br>22) somatoform disorder NOS<br>• major depressive disorders<br>• panic disorder<br>• borderline personality disorder

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criteria you would regard as important in evaluating the quality of a psychiatry review article.

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• Who are the authors, are they respected?<br>• What is the impact rating of the journal?<br>• How recent is the publication?<br>• What methods were used in the review?<br>• Were the articles in the review assessed on the basis of level of evidence?<br>• do the conclusions follow rationally from the results<br>• What level of industry sponsorship is present?<br>• Do the authors take into account the clinical populations that were studied, and whether<br>these apply to real-life clinical situations in every day practice?

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DDx -- 29M violent impulses/compulsions

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• obsessive compulsive disorder<br />• panic disorder with agoraphobia<br />• post-traumatic stress disorder<br />• bipolar disorder, manic state (irritability)<br />• Schizophrenia (is he paranoid?)<br />• general medical conditions<br>23) migraine aura<br>24) partial complex seizures<br>25) brain injury leading to personality change

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catatonia -- DDx

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Psychiatric differential<br>• bipolar disorder is the most common<br>26) catatonic excitement in mania<br>27) retarded catatonia in depression<br>• depression<br>• schizophrenia<br>• dissociative disorder<br>• obsessive compulsive disorder<br>• malingering<br>Medical differential<br>• infectious (encephalitis)<br>• neoplastic<br>• seizure (status epilepticus)<br>• neuroleptic malignant syndrome<br>• serotonin syndrome

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Tx plan -- 22m, family brought, organic syndrome associated with a brain injury at the age of 15?

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• safety<br>o safety of family from patient<br>o safety of patient from family<br>o consider appropriate setting for management of patient (home vs. facility)<br>• treatment of co-existing psychiatric difficulties (depression, anxiety)<br>• treatment of co-existing medical illnesses (headaches, pain)<br>• pharmacotherapy of behavior<br>o gabapentin o quetiapine o lithium<br>• psychotherapy for behavior

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Aggr behavior -- 5 meds for long term mgt, one clinical eg each

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neuroleptics (risperidone): schizophrenia, mania<br>anticonvulsants (divalproex): epilepsy, mental retardation lithium: mania<br>benzodiazepines (clonazepam): mania, ADHD, mental retardation antidepressants (fluoxetine): depression<br>antiandrogens (lupron): sexual aggression<br>stimulants (methylphenidate): aggression in children, ADHD

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Cholinesterase inhibitors such as Donepezil (Aricept) are used in the treatment of Alzheimer’s disease. [2002]<br>a) List five common side effects (from at least three different systems) of these medications.<br>b) Name two relative contraindications.<br>c) Name three areas that you would assess for improvement to see if treatment was<br>effective.

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Common side effects<br>1. Gastrointestinal: nausea, vomiting, diarrhea<br>2. Neuropsychiatric: insomnia, fatigue, headaches<br>3. Cardiovascular: hypertension, syncope<br>Relative contraindications<br>1. Sick sinus syndrome<br>2. gastro-intestinal bleeding<br>Three areas to be assessed for improvement:<br>1. Cognitive (memory, calculation)<br>2. Behavioral (agitation, aggressiveness)<br>3. Functional (ADL’s and IADL’s).

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Aricept -- Describe three systems affected and five adverse side effects, 3 contraindications and 3 domains to follow the response to treatment.

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Donepezil (Aricept) - cholinesterase inhibitor – reduces cleavage and inactivation of acetylcholine in the synapse, thus potentiate cholinergic transmission.<br>- tabs of 5 and 10 mg<br>- may have less GI effects that Rivastigmine and Galantamine Others: Rivastigmine – Exelon<br>Galantamine – Reminyl<br>Tacrine – Cognex * liver toxicity<br>- mild sides effects are dose related and time dependent (usually resolve in 3 wks)<br>- Numerous well-controlled studies show efficacy in long term in slowing progression of<br>memory loss, diminishing apathy, depression, hallucinations, anxiety, euphoria and<br>purposeless motor behaviors.<br>- LESS effective in: preserving ‘functional autonomy (ADL and IADL’s) = but we<br>generally assume that use of them may ‘delay or reduce need for Nursing home placement.<br>‘Most common side-effects’: &gt; 5 % of cases (often 10-15%) and &gt; double placebo rate. Most common side effects are due to cholinomimietic activity:<br> N/V/D<br> Muscle cramps  Fatigue<br> Anorexia<br>Contraindications: sensitivity to piperidine Caution with:<br> known seizures (lowers seizure threshold)<br> Ulcers (increases GI secretion in theory)<br> Cardiac disease (vagotonia induces bradycardia)<br> ? sick sinus syndrome, LBBB, RBBB, CHF, CAD, syncope (no studies)<br>Three systems affected:<br>1. cognitive – enhances memory and goal directed thought<br>2. GI – can get nausea, vomiting, anorexia<br>3. cardiac – bradyarrhythmias, syncope<br>Five adverse side effects:<br>1. GI – nausea, vomiting, diarrhea, anorexia<br>2. CNS – insomnia, fatigue, headache, dreams, agitation, TIA, seizures<br>3. CV – dizziness, syncope, AFib, arrhythmias, 1st degree AV block, DVT<br>4. Resp – nasal congestion, dyspnea<br>5. Vision – blurred<br>6. Dermatological – flushing, pruritis<br>7. MSK – muscle cramps, pain<br>Three contraindications:<br>1. anesthesia – exaggeration of muscle relaxation<br>2. Epilepsy – reduction of seizure threshold<br>3. Parkinson’s or severe Alzheimer’s<br><br>Three domains to follow response to treatment<br>1. Cognitive<br>2. Behavioral<br>3. Functional (IADL’s, ADL’s)<br>4. Physical (for side effects)

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You are about to start a patient on an antidepressant. List five factors to consider in choosing an antidepressant.

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• previous trials of antidepressants<br>• drug interactions<br>• symptom profile<br>• patient preference<br>• cost<br>• side effects profile

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Nort &amp; Bupr -- Tx resistant depression. Eventually put on nortriptyline, which controls depression. Smoking, so Dr starts Bupropion. Presents w/ tachycardia, high anxiety, and confusion &amp; QTc prolongation. Describe the metabolism of both drugs &amp; explain how interact (6pts). Why is his cardiac probs happening? Explain why he is now complaining of worsening psychiatric symptoms.

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A. How are these two drugs metabolized?<br> Nortriptyline is metabolized by 2D6, Wellbutrin is metabolized by 2B6.<br>B. List how they can interact with each other<br> Wellbutrin is enzyme inhibitor of 2D6, so thereafter Nortriptyline will not be metabolized and its level will be increased and becomes toxic as it has narrow therapeutic window.<br>C. What could be causing his medical symptoms?<br> Medical symptoms are mainly through the increased level of Nortriptyline (anticholinergic effects) and additive effects of Wellbutrin on the heart.<br> It is also of significance that Wellbutrin is seizure inducer and Nortriptyline decrease seizure threshold, so patient will be at higher risk of developing seizure<br>D. What could be causing his depression?<br> Curvilinear Nortriptyline dose-response curve

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mechanism of action of the following drugs:<br>SSRI – selective serotonin reuptake inhibitor<br>SNRI – serotonin and norepinephrine reuptake inhibitor SARI – serotonin 2 antagonist reupt inhibitor<br>NDRI – norepi dop reup inhib<br>NaSSA- nonadrenergic specific serotonergic antidepressant RIMA – reversible inhibitor monoamines<br>venlafaxine nefazadone<br>Bupropion Mirtazapine<br>Moclobemide

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SSRIs:<br>1) Unlike TCA have non-linear dose response curve ---<br>2) 90% of clinical response at starting dose, increase dose and just increase side effects.<br>3) No Norepinephrine/dopamine reuptake inhibition, no antihistamine, no alpha-adrenergic<br>4) Paxil &gt;30 mg/d  anticholinergic effects.<br>5) SSRI blocks reuptake of serotonin on the presynaptic nerve terminals- and the<br>6) MAO cannot degrade the 5HT which is outside the nerve terminal (and MAO is inside!)<br>1. Sertraline – SSRI<br>a. Specific activity in the inhibition of serotonin reuptake without effects on NE or DOP reuptake. Clinical efficacy is associated with 70-80% of the occupancy of serotonin transporters. Inhibition of reuptake raises synaptic concentrations of serotonin, which bind to and activate receptors.<br>b. SSRI’s are essentially devoid of agonist and antagonist activity on any Neurotransmitter receptors.<br>2. Venlafaxine SNRI<br>a. Potent inhibitor of serotonin and NE reuptake and a weak inhibitor of DOP reuptake.<br>b. It does not have activity at muscarinic, nicotinic, histaminergic, opioid, or adrenergic<br>receptors.<br>3. Bupropion NDRI<br>a. Mechanism or action poorly understood. Was initially thought to act through blockade of dopamine reuptake; however, CNS concentrations are probably not sufficient to result in significant dopamine reuptake inhibition. Some data indicate it increases the functional efficiency of the noradrenergic systems.<br>b. For smoking cessation, it is a noncompetitive inhibitor of nicotinic acetylcholine receptors and may interfere with the addictive actions of nicotine.<br>4. Mirtazapine NaSSA<br>a. Acts as an antagonist of central presynaptic alpha–2-adrenergic receptors with the CNS, where it has a net effect of increasing synaptic levels of NA and 5HT.<br>b. A potent antagonist of 5HT2 and 5HT3 receptors<br>c. A potent antagonist of H1 receptors<br>d. Moderately potent antagonist of alpha –1-adrenergic and muscarinic receptors.<br>5. Nefazodone SARI<br>a. inhibitor of serotonin uptake and , less so, of norepinephrine uptake b. antagonist at 5HT2a receptors<br>c. may selectively activate 5HT1a

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DDx mood swings in a bipolar patient on divalproex and venlafaxine? What are the risks and benefits of mood stabilizer use during pregnancy? What are the risks and benefits during breast-feeding? What are the rates of switching from depression to mania with antidepressants? Discuss the use of folic acid during pregnancy.

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1. Differential diagnosis:<br>A. Rapid cycling bipolar disorder<br>B. Bipolar Disorder (Mixed Episode)<br>C. personality disorder<br>D. medical illness (Hypothyroid)<br>E. psychological or social stressors<br>2. Risk and Benefits during pregnancy<br> Risk of relapse after discontinuing medication in pregnancy is three-fold higher than<br>for non-pregnant women;<br> there is a particularly high risk of symptom exacerbation in the immediate post-partum<br>period;<br> the risks of mood stabilizer use include fetal risks (teratogenesis, fetal growth effects,<br>neonatal toxicity, and neurobehavioral toxicity) and maternal risks (fluctuations in<br>plasma levels)<br>3. Risk and Benefits during breast feeding<br> Breast-feeding is contraindicated with lithium, as relatively high levels of this are<br>expressed in breast milk;<br> breast-feeding is generally okay with Valproate and carbamazepine<br>4. switching with antidepressant use:<br> Paroxetine, Bupropion: similar to placebo if taken with mood stabilizer (about 6%); risk for SSRIs is higher if taken without mood stabilizer (about 25%)<br> imipramine: significantly higher (11% to 25% with mood stabilizer, 50% if taken without mood stabilizer)<br>5. folic acid is protective against neural tube defects; doses taken during pregnancy can be up to 5mg daily (significantly higher than usual dose of 1mg daily)

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Lithium

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 lithium has no clinically important protein-binding properties and no metabolites<br> Lithium is over 95% eliminated unchanged by the kidney.<br> A substantial amount of filtered lithium is reabsorbed (primarily in the proximal tubules), although<br>it is considerably longer in the elderly because of the age-related decrease in Glomerular filtration rate (GFR). Consequently, elderly patients tend to need lower than usual doses to reach a given serum concentration and require longer than usual to reach steady state.<br> It is reabsorbed in the proximal tubules and to a lesser extent in the loop of Henle.<br> Li level is increased by : via decreasing its clearance<br>o Thiazides diuretics<br>o ACE inhibitors; Captopril, Enalapril, Lisinopril o NSAIDs (except ASA and Sulindac)<br>o Metronidazole<br>o Spectinomycin<br>o Tetracycline<br> Li level is decreased by: via increasing its clearance o Aminophylline<br>o Theophylline<br>o Urinary alkalization (acetazolamide, sodium bicarbonate) o Sodium chloride<br>o Osmotic diuretics (Mannitol, urea)

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1. cbz AEs?<br><br>2. Elderly woman, previous MDE treated w/ ECT now presents not caring for self, not eating. In the ER, she is immobile &amp; staring, unresponsive.<br />A. List 5 Catatonic features

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Carbamazepine Dosage-Related Adverse Effects Double or blurred vision<br />Vertigo<br />Gastrointestinal disturbances<br />Task performance impairment Hematological effects-- mild leukopenia in 1-2%<br />Bipolar SAQ<br />Idiosyncratic Adverse Effects<br />Agranulocytosis – 1 in 250,000 via inhibiting CSF (colony stimulating factor) Stevens-Johnson syndrome<br />Aplastic anemia<br />Hepatic failure<br />Rash – in 12-16%, usually macular popular rash within initial 3-weeks of therapy Pancreatitis<br /><br><br><br /> Motor immobility<br /> purposeless motor activity<br /> extreme negativism or mutism<br /> peculiarities of voluntary movement (e.g., posturing, mannerism, etc)<br /> echolalia/echopraxia<br />B. Most common dx?...................... BAD<br />Among 100 pts w/ 2+ catatonic features, 50% are BAD, 25% are unipolar, 15% have<br />neurologic/GMC causing catatonia &amp; 10% are schizophrenic<br />C. In ER, name 2 non-pharmacologic strategies for assessment/management:<br /> History &amp; physical to rule out GMC/stroke;<br /> Blood work, CT head<br />D. Best treatment - short term is Lorazepam; ECT is best for MDE w/ catatonia<br />E. Risk factors - stroke, basal ganglia disease, PCP use, psychiatric illnesses (like BAD,<br />MDE, schizophrenia, and frontal lobe disease), neuroleptic use, and dehydration/malnutrition.