Psychiatry Clerkship - Review Questions

Front 1

Who is at increased risk for suicide?

Back 1

Male doctors 1.5x general population
Female doctors 3-4x general population

Medical students ~11% have SI in one year

Having a gun in the home increases risk of suicide by 5 times.

Front 2

What disorders carry the highest suicide rates?

Back 2

Mood disorders
Psychotic d/o (schizo)
Substance abuse
Personality disorder, cluster B

Front 3

What risk factors predict attempted and completed suicide?

Back 3

SADPERSONS

Sex (Male)
Age (<19 or <45)
Depression or hopelessness
Previous attempt
EtOH or substance abuse
Rational thought
Social support lacking
Organized plan
No spouse
Sickness

Front 4

SADPERSONAS + a few other risk factors

Back 4

S = Sex (M>F for completion)

A = Age (Caucasians from 74-84 have 2x the completion rate as those from 15-24)

D = Depression (15% suicide rate)

P = Previous attempts (Greatest risk within two years of first attempt, especially if attempt was of high lethality and circumstances have not changed.)

E = EtOH abuse

R = Rational thought (loss of, i.e. psychosis. Schizophrenia has a 10% suicide rate. Depression rather then command hallucinations are the cause for suicides in schizophrenia.)

S = Social supports lacking (Unemployment, fall in socioeconomic status, pregnancy in adolescents)

O = Organized plan

N = No spouse (Divorced widowed > Single > Married)

A = Access to means (i.e. firearms)

S = Sickness (AIDS 21-36x, Temporal lobe epilepsy 25x)

Also

1. Family history (9X more likely to commit suicide if a first degree relative completed suicide.)

2. Biological factors (dec 5-HIAA. High suicide rates seen in depression, schizophrenia, anxiety disorders, PTSD, substance abuse, delerium, and dementia

Front 5

Lifetime prevalence of MDD? Female to male ratio?
Is race a factor?
Socioeconomics?

Back 5

Lifetime prevalence is 5-20%
Female to male ratio is 2:1
Race and socioeconomics do not seem to be a factor in developing MDD.

Front 6

What percentage of pts with a depressive episode will go on to develop a second episode? What about those having had three episodes developing a fourth?

Back 6

~60%

90%

Front 7

What medical conditions increase the risk for depression?

Back 7

V

Infections: TB, CNS, syphilis, mono, HIV, hepatitis, encephalitis, post-encephalitis states.

Neoplastic: panc ca, primary cerebral tumor, cerebral mets.

Drugs: EtOH, amphetamines, cocaine, barbiturates, opiates, anti-HTN, sedatives, digitalis, steroids, OCP, lead poisoning and other heavy metals.

I

Congenital/Developmental: Parkinson’s, Huntington’s,
MS, primary degenerative dementia, chronic subdural hematoma


A

Trauma: Post-concussion syndromes

Endocrine: Hyper/hypothyroid, hyponatremia, hypokalemia, pernicious anemia, pellagra, hyperparathyroidism, uremia, Cushing’s disease, Addison’s disease, hepatic disease, Wernicke-Korsakoff syndrome

Front 8

What are the signs of alchol intoxication?

What are the main medical concerns?

Back 8

Slurred speech, uncoordiation, unsteady gait, nystagmus, memory/attention impairment, stupor or coma, maladaptive behavior or physiological changes.

Main medical concerns are autonomic depression resulting in coma, and aspiration

Front 9

What are some medical concerns with chronic alcholism?

Back 9

Cirrhosis, variceal bleeding, hepatocellular carcinoma, hepatic encephalopathy.

There is an increased risk of pneumonia, TB, cardiomyopathy, HTN, and GI cancers in chronic alcoholics.

Front 10

Treatment of chronic alcholism?

Back 10

Supportive -> IV fluid and electrolyte management, oral or parenteral thiamine administration before glucose administration to prevent Wernicke-Korsakoff syndrome.

It is thought that administration of glucose before thiamine will worsen the encephalopathy.

Front 11

Describe alchol withdrawal.
Time course?
Symptoms? Major symptoms?

What is DT?

Current preferred treatment for EtOH withdrawal?

Back 11

Time course: 12-18 hours after cessation of alcohol intake.

Tremors, nausea, vomiting, tachycardia, HTN. Major withdrawal symptoms may include seizures and delerium tremens.

Delerium tremens = delirium, autonomic hyperarousal, mild fever.

Benzodiazepines

Front 12

What hematologic finding will B12 deficiency cause?

Back 12

Increased MCV

Front 13

What is schizophreniform disorder?

Back 13

Schizophrenia, but lasts between 1 and 6 months.

Front 14

How does bereavement differ from major depression?

Back 14

The diagnosis of MDD is not given to a greiving person until at least 2 months after the event.

Things that can distinguish MDD from normal grief:
1) guilt about things other than actions taken or not taken by the survivor at the time of the death;
2) thoughts of death other than the survivor feeling that he or she would be better off dead or should have died with the deceased person;
3) morbid preoccupation with worthlessness;
4) marked psychomotor retardation;
5) prolonged and marked functional impairment; and
6) hallucinatory experiences

Transient hallucinatory experiences may occur with grief, but not more sustained psychotic symptoms indicative of a psychotic depression.

In grief, periods of crying and intense sadness occur as "pangs" as opposed to depression where the sadness is more continuous.

Self-reproach is experienced in both, but in grief, self-blame is focused on what could have been done differently, in depression, people are more negative about themselves.

Grief and depression respond differently to intervention. Those with grief welcome social support and feel better about venting their feelings. Those with depression tend to withdraw from reassurance and feel worse when encouraged to vent.

Antidepressants are not appropriate for grief. Benzos are often given to those with acute grief reaction with assocated sleep disturbance.

Front 15

6. What is the prognosis for dysthymic disorder? What treatments are available? What co-morbid psychiatric conditions should you look for?

Back 15

ACHEWS

Appetite disturbance
Concentration decrease
Hopelessness
Energy decrease
Worthlessness
Sleep disturbance

Significant DSM IV criteria:

A. Depressed mood is present for most of the day, for more days than it is not present, and depression has been present for at least 2 years.

C. Over the past year pt has never been without sx for more than two months consecutively.

Prognosis: Treatment is often refractory and the course may be more protracted than treatment of major depression. Dysthymia that occurs prior to the onset of major depression has a worse prognosis than major depression without dysthymia.

Treatment:
A. Hospitalization not required unless suicidality present
B. Antidepressants (SSRI’s are most often used)
C. Psychotherapy (Combined psychotherapy and pharmacotherapy produces the best outcome)

Co-morbid psychiatric conditions: Episodes of major depression may occur after the first two years of the disorder. The combination of dysthymia and major depression is known as “double depression.”

Front 16

Compare and contrast the management of opiate intoxication, opiate overdose, and opiate withdrawal.

Back 16

Opiate Intoxication:
Presentation: Behavioral or psychological changes such as euphoria, followed by dysphoria, psychomotor retardation, impaired judgment, or impaired social or occupational functioning. Pupillary constriction is always present. Other symptoms may include respiratory depression, drowsiness, coma, slurred speech, hypotension, bradycardia, hypothermia, nausea, vomiting, constipation and impaired attention / memory.
Management: For patients with respiratory compromise an airway should be established and naloxone (0.4 mg IV) should be given immediately.


Opiate overdose: Presentation: Same as intoxication but more often results is coma, respiratory depression, and death.
Management: Same as intoxication.

Opiate withdrawal: Presentation: Withdrawal symptoms usually begin within 10 hours after the last dose.

Management:
• Gradual withdrawal using methadone (20-80 mg/day) may be utilized or prolonged methadone maintenance may be instated. Methadone is a weak agonist of the  opiate receptor and has a longer half-life (15 hours) than heroin or morphine. Thus, it causes relatively few intoxicant or withdrawal effects.
• Clonidine, a centrally acting alpha-2 receptor agonist that decreases central noradrenergic output, can also be used for acute withdrawal symptoms. It is very effective at treating the autonomic symptoms of withdrawal but does little to curb the drug craving. Risks of sedation and hypotension limit clonidine’s usefulness for outpatients.

Front 17

What is schizoaffective disorder?

What elements of the history and MSE might lead you to consider changing a diagnosis of Bipolar I Disorder to Schizoaffective disorder, bipolar type? How would this impact your treatment planning?

Back 17

Schizoaffective Disorder is an illness which meets the criteria for schizophrenia and concurrently meets the criteria for MD episode, manic episode, or mixed episode. The illness must be assoc with delusions or hallucinations for two weeks, without significant mood symptoms.

If you are seeing a patient carrying a diagnosis of Bipolar I D/o, a two week period with psychotic sx and no mood d/o sx would lead you to consider changing the dx to Schizoaffective D/o, bipolar type. Bipolar I D/o is primarily treated with mood stabilizers while Schizoaffective D/o requires antipsychotics and mood stabilizers. ECT is a consideration for both disorders if pharmacotherapy fails.

Front 18

Name three clinical scenarios where ECT might be the treatment of choice.

Back 18

1. Depression:
- Response rate is 90%, higher than 70% response rate of antidepressants.
- In severe/refractory cases or high risk of suicide.
- In pts in which antidepressants are CI, e.g. the elderly
- In pregnant pts who wish to prevent long-term exposure of fetus to meds.

2. Bipolar
- For mania/depression, esp. when refractory to meds, medication intolerance, or when immediate improvement is critical.

3. Acute psychosis
- When immediate resolution of psychotic sx is required.

Front 19

What elements of the medical history and physical exam will you focus on when evaluating a patient being considered for ECT?

What are some CI to ECT?

Back 19

H&P:
- Neurologic hx
- Cardiovascular hx
- Physical exam

Labs/Studies:
- CBC, BMP, LFTs, UA, TFTs, EKG, CXR, spinal X-ray, and head CT.

CI to ECT and risks:
- Intracranial mass, recent stroke, recent MI.
- Risk of memory loss (anterograde and retrograde w respect to ECT txt). Most memory loss resolves within days to weeks. Small risk of persistent memory loss after several months.
- Headaches are common post-ECT. Give analgesics.

Remember that there are situations (e.g. in the case of a severely depressed pt w clear S plan w hx of stroke/MI) in which the benefits of having ECT outweigh the risks.

Front 20

For which anxiety disorders is BuSpar (buspirone) likely to be effective? Ineffective?

Back 20

Buspirone is a non-benzo anxiolytic agent. It is generally well-tolerated, non-addicting, and has no withdrawal syndrome or tolerance. It does not produce sedation or potentiate the effects of alcohol.

Buspirone works for:
GAD, OCD, augmentation of antidepressants in MDD.

Buspirone doesn't work for:
Panic disorder
Social phobia
PTSD
Acute stress disorder

Front 21

What are some of the uses of MOAIs?

Back 21

Major depresion with atypical features.
(social phobia, OCD, panic disorder with agoraphobia)

Front 22

What is the mechanism of action of MAOIs?

Back 22

Decreases the degredation of monoamines.

Front 23

How long after the discontinuation of an MAOI does the body require to replenish its normal amount of monoamines?

Back 23

2 weeks

Front 24

What affect do MAOIs have on the gut?

Back 24

The inhibition of MAO in the gut leads to an increase in the absorption of tyramine, which acts as a false NT and can elevate BP.

Front 25

What are some side effects of MAOIs? (14)

Back 25

1. Hypertensive crisis
2. HTN
3. Sedation
4. Weight gain
5. Orthostatic HTN
6. Pyroxidine deficiency
7. Liver toxicity
8. Agitation
9. Dry mouth
10. Constipation
11. Seizures
12. Sexual dysfunction
13. Insomnia
14. Edema

Dosage must be titrated over several weeks to minimize SE.

Front 26

What are some CI to MAOIs? (7)

Back 26

1. May ppt mania in bipolar pts.

2. Use w caution in pts with liver dz, CV dz, migraines, renal dz, hyperthyroidism, or Parkinson's.

3. Incompatible with OTC antihistamines.

4. Low tyramine diet to avoid hypertensive crisis

5. Dc before surgery to prevent hypertensive crisis from anesthetics.

6. Drug interaction with fluoxetine, leading to serotinergic syndrome (nausea, confusion, hyperthermia, autonomic instability, tremor, myoclonus, rigidity, seizures, coma, death.)

7. Antihypertensives can inc risk of hypotension. Major morbidity and mortality occurs upon use with phenelzine.

Front 27

What is the mechanism of action of TCA?

Back 27

It block the reuptake of NEPI, dopamine, and serotonin.

It interacts with muscarinic, cholinergic, alpha-1-adenergic, and histamine receptors

Front 28

What are the side effects of TCAs?

Back 28

1. Dry mouth
2. Blurry vision
3. Constipation
4. Urinary retention
5. Heat intolerance
6. Tachycardia
7. Exacerbation of narrow-angle glaucoma
8. Orthostatic hypotension.
9. Dizziness
10. Reflex tachycardia
11. Sedation
12. Weight gain
13. Intraventricular conduction delays
14. Long PR
15. AV block
16. Seizures
17. Neurotoxicity
18. Tremor
19. Ataxia
20. Sexual side effects

Front 29

What are the differences between the SE of primary and secondary TCAs?

Back 29

Secondary TCA are better tolerated and less likely to have anticholinergic and orthostatic side effects.

Dosage must be titrated over several weeks. Elderly pts are the most susceptible to SE.

Front 30

What are some CI of TCAs?

Back 30

1. May ppt mania in bipolar pts

2. Use caution in pts with liver or renal dz.

3. Do not use with MAOIs

4. Discontinuation syndrome: transient dizziness, nausea, headache, diaphoresis, insomnia, malaise.

5. TCAs can block the effects of antihypertensive medications

6. Don't use with other anticholinergics - can lead to delerium.

7. Avoid with class I antiarrhythmics due to additive effects on cardiac conduction

Front 31

What is the definition of panic disorder with agoraphobia?

Back 31

Recurrent anxiety attacks accompanied by somatic sx such as heart issues (palpitations, chest pains, paresthesias), breathlessness (choking sensation, SOB, chills/hot flashes), and fear (fear of dying, fear of going crazy, shaking, sweating, depersonalization/derealization)

Usually accompanied by agoraphobia.

Front 32

What are some pharmacologic interventions for panic disorder with agoraphobia?

What are some indications/CI with each med?

Back 32

SSRIS, benzos, TCAs, MAOIs.

SSRIs: start with low dose in first week to prevent exacerbation of anxiety. 20% will have a stimulant-like effect during initial tx. SSRIs can induce a manic episode (check FH).

Benzos: don't use if using alcohol. Usually used after other tx have failed. Avoid benzos during the first trimester.

Beta-blockers: can help with sx, but aren't good at preventing attacks.

Buspirone doesn't help with panic disorder.

Front 33

What is the medical workup for panic disorder with agoraphobia?

Back 33

PMH (CV dz, organic brain dz, asthma, colitis, sz d/o)

SH (drugs of abuse)

TFTs

EKG

glucose

Tox screen

Withdrawal from sedetives/hypnotics, benzos

Front 34

12. You are treating a frail 80-year-old woman for major depression. She has not responded to several adequate trials of SSRI medication with augmentation. Consider the risks/benefits of prescribing a tricyclic antidepressant or MAOI. How can you minimize these risks? She tells you she is on an antihypertensive, an antihistamine, and an anxiolytic medication. What drug interactions should you consider and what adverse outcomes might occur following your prescription of Fluoxetine? Amitriptyline? Phenelzine?

Back 34

Basically MAOIs and TCAs are bad choices for this poor woman. If she has failed SSRIs, she could try an atypical antidepressant (Wellbutrin, Remeron, Effexor, etc.) or consider ETC. She would otherwise have to get off all her other meds which would be BAD.

Front 35

New onset panic disorder with agoraphobia + EtOH abuse: which meds will you avoid?

Back 35

Avoid benzos.

Front 36

New onset panic disorder with agoraphobia + FH of bipolar d/o: which meds will you avoid?

Back 36

Caution with SSRIs. Up to 20% of pts will have a stimulant-like reaction with initial treatment.

Front 37

New onset panic disorder with agoraphobia + pregnancy: which meds will you avoid?

Back 37

Avoid benzos in first trimester.

Front 38

New onset panic disorder with agoraphobia: what medical disorders do you need to rule out?

Back 38

Medical work up:

PMH (looking for CV disease, colitis, asthma, organic brain d/o, seizure d/o),

SH looking for drugs of abuse

TFTs, EKG, glucose, tox screen,

withdrawal from sedatives/hypnotics, benzos

Front 39

14a. Your patient has a teenage son with Schizophrenia and asks you about Clozapine. What is clozapine?

Back 39

Clozapine: Acts as a Serotonin (5-HT2A) and Dopamine ([D1, D3, D4] > D2) receptor antagonist, also with some affinity for α1, H1, M1, 5-HT6-7 receptors. Clozapine has less affinity for D2 than typical antipsychotics; high affinity blockade of the D2 receptor is assoc w Parkinsonianism. Other atypicals include risperidone (Risperdal), olanzapine (Zyprexa), ziprasidone (Geodon), and quetiapine (Seroquel).

Front 40

14b. Your patient has a teenage son with Schizophrenia and asks you about Clozapine. What would you say its indications are?

Back 40

Indications:

- Only FDA-approved indication is for Txt-Resistant Schizophrenia (those who fail at least 3 trials of typical antipsychotics);

- Also used in patients with bothersome effects of typical antipsychotic drugs (e.g., EPS or effects of hyperprolactinemia);

Atypicals are becoming the drugs of first choice; clozapine has fewer EPS than risperidone, but has risk of agranulocytosis; therefore, other atypicals should be tried before clozapine, except in those with severe EPS symptoms.

Front 41

14c. Your patient has a teenage son with Schizophrenia and asks you about Clozapine. What would you say its risks are?

Back 41

1. Agranulocytosis:
- 1-2% of all pts txd with clozapine.
- Usually develops in first 6 months, but can happen anytime.
- Have to monitor with weekly CBC
- Only 7 day supply can be given

2. Seizures:
- 5% of those taking > 600 mg
- 3-4% taking 300-600 mg
- 1-2% taking <300 mg
will have clozapine induced seizures.
- txt is a) stopping clozapine, b) admin phenobarbital, c) clozapine restarted at 50%

3. CV effects:
- Tachcardia (due to antimuscarinic effect, can txt with beta-blockers, but may worsen hypotension)
- Hypotension --> syncope
- EKG changes


4. Paradoxical HTN is seen in 4% of pts.

5. Other SE:
- Sedation
- Sialorrhea
- Weight gain
- GI symptoms (constipation)
- Anticholinergic effects
- Fever

Front 42

Which of these drugs cause hyperprolactinemia? Clozapine, risperdone, olanzapine.

Back 42

Prolactin increases with risperdone and olanzepine, but not with clozapine.

Front 43

Which atypical antipsychotics cause the most wt gain?

Back 43

Clozapine, and olanzepine. Also risperidone.

Ziprasidone and aripiprazole not so much

Front 44

NMS is more likely when clozapine is administered with what mood stabilizer?

Back 44

lithium

Front 45

How long does lithium take to work?

Back 45

1 week

Front 46

what diuretic increases lithium levels?

Back 46

Thiazide diuretics

Front 47

What OTC meds are dangerous to take with lithium?

Back 47

NSAIDs

Front 48

14. Your patient has a teenage son with Schizophrenia and asks you about Clozapine. What would you say about its benefits?

Back 48

Benefits: Less EPS than with typical antipsychotics and other atypicals. Efficacy against some of the negative symptoms of schizophrenia. Less increase in prolactin levels.

Front 49

15. You are admitting a patient with pneumonia. He tells you he is prescribed clozapine 600 mg daily, but did not pick-up a refill and has not taken it for 8 days. The intern on your team writes an order to restart the medication at full dose. What concerns do you have?

Back 49

Initial dosage is usually 25 mg, daily or BID, although conservative initial dosage is 12.5 mg BID. Dosage then gradually raised (25 mg a day every 2 or 3 days). Gradual increase is necessitated by the potential development of hypotension, syncope and sedation; adverse effects for which the patient can usually develop tolerance if the dose titration is gradual enough. Usual effective treatment range is 400-500 mg per day, although doses up to 600 mg can be used. If Clozapine stopped for more than 36 hours, must be re-titrated to avoid the above effects. After the decision to terminate Clozapine treatment, the dosage should be tapered whenever possible to avoid cholinergic rebound symptoms (e.g., diaphoresis, flushing, diarrhea and hyperactivity).

Front 50

Name some high potency typical antipsychotics

Back 50

Dosing is in the 1-5 mg range

•Haloperidol (Haldol), “Gold standard”, available in depot form
•Trifluoperazine (Stelazine)
•Fluphenazine (Prolixin)
•Thiothixene (Navane)
•Pimozide (Orap)

Front 51

Name some mid potency typical antipsychotics

Back 51

Dosing is in the 10 mg range

•Perphenazine (Trilafon)
•Loxapine (Loxitane)
•Droperidol (Inapsine)
•Molindone (Moban)

Front 52

Name some low potency typical antipsychotics

Back 52

Dosing range is in 50-100s

•Chlorpromazine (CPZ; Thorazine)
•Thioridazine (Mellaril)
•Mesoridazine (Serentil)

Front 53

What is "atypical" about atypical antipsychotics?

Back 53

Atypical is variably meant to imply the following:
- less risk of adverse neurological effects,
- less potent increases in prolactin secretion,
- lacking dopamine antagonism as a primary mechanism of action,
- significant activity at specific, non-dopaminergic (e.g., 5-HT) receptors and
- greater efficacy in treating negative symptoms (e.g., withdrawal, flat affect and anhedonia).

Front 54

Which has more EPS sx: high or low potency typical antipsychotics?

Which has more anticholinergic SE: high or low potency typical antipsychotics?

Back 54

EPS = High

Anticholinergic = Low

Front 55

Which causes more hyperprolactinemia, typical or atypical antipsychotics?

Back 55

Typical antipsychotics cause more hyperprolactinemia

Front 56

What is considered an adequate trial of a typical antipsychotic?

What is considered an adequate trial of an atypical antipsychotic?

Back 56

Typical = 6-8 weeks

Atypical = 8-12 weeks

Front 57

Name three psychiatric medications from three different medication groups associated with an increased risk for seizures.

Back 57

Wellbutrin (bupropion):
Atypical antidepressant, seizure rate increases with dose (<450 mg/day: 0.4%, 450-600 mg/day:4%). Wellbutrin is contraindicated with a history of seizures, brain injury, EEG abnormality, and recent EtOH withdrawal.

Ritalin (methylphenidate):
Psychostimulant, toxicity can present with seizures.

Thorazine (chlorpromazine):
Low potency antipsychotic, higher risk of seizures than most other typical antipsychotics.

Front 58

How can you distinguish Generalized Anxiety Disorder, Panic Disorder, Social Phobia, Major Depression with Anxiety, and PTSD?

Back 58

Generalized Anxiety Disorder
• Intense pervasive worry over every aspect of life for at least 6 months
• Do not have panic attacks or phobias

Panic Disorder
• Recurrent unexpected panic attacks
• +/- agoraphobia

Social Phobia
• Intense fear of being scrutinized in social or public situations

Major Depression with Anxiety
• Depressed mood
• Neuro-vegetative signs

PTSD
• Persistent re-experience of a trauma via intrusive images, dreams, illusions, hallucinations, and flashbacks
• Hyperarousal
• Feelings of detachment
• Dissociation

Front 59

Define Delirium.

Back 59

Delirium: A reversible state of global cortical dysfunction characterized by alterations in attention and cognition. It is seen in 10% to 15% of general medical patients, and more frequently in the ICU. The onset of delirium is abrupt, and there is usually an identifiable precipitant, although it is often multifactorial. The course is variable, and often has a waxing/waning pattern. Delirium is associated with a one year mortality of > 40%.

Front 60

Define dementia

Back 60

Dementia: Memory loss in the presence of one or more cognitive deficits in the categories of aphasia, apraxia, agnosia, and disturbance in executive function. Onset is usually insidious, but can be abrupt (e.g. after head trauma). The two most common causes of dementia are Alzheimer’s disease and vascular disease. Dementia is usually permanent.

Front 61

Define psychosis

Back 61

Psychosis: Gross impairment of reality testing, can be either a primary disorder or secondary to another disorder (e.g. depression with psychotic features).

Front 62

Define pseudodementia

Back 62

Pseudodementia: Typically associated with depression, mood symptoms are prominent, memory is usually intact although patients will complain extensively of memory impairment and often answer “I don’t know,” to MSE questions.

Front 63

Describe behvioral psychotherapy

Back 63

1) Behavioral psychotherapy focuses on changing behavior without much consideration for the thought processes- either conscious or unconscious- that underlie them. This type of therapy is especially indicated for the treatment of phobias. Methods include systematic desensitization (the patient is gradually exposed to increasing amounts of spiders or dentists or whatever), flooding (lots of spiders all at once), and implosion (lots of imagined spiders all at once). Behavioral therapy is also used to modify behaviors in children or adults by conditioning them with positive or negative feedback. An example is using antabuse as aversive therapy for alcoholics.

Front 64

Describe cognitive psychotherapy

Back 64

Cognitive psychotherapy focuses on conscious thought processes. It sees psychiatric symptoms as being produced by inappropriate patterns of thought, or distortions. For example depressed people are said to automatically interpret situations in the most negative way possible. If they can be trained to recognize and change these illogical thought patterns their symptoms will improve. Cognitive psychotherapy is indicated for mild to moderately depressed patients without bipolar illness, psychosis, or ongoing substance abuse. It is time limited and generally occurs weekly over 15-25 weeks. Patients are taught to recognize and modify their automatic thoughts.

Front 65

Describe psychodynamic psychotherapy

Back 65

3) Psychodynamic psychotherapy focuses not on behaviors or conscious thoughts but on the unconscious processes underlying them. These therapies can vary from 6 years on the couch free-associating about early childhood experiences to brief interventions targeted at specific issues. In general these approaches require a high level of understanding on the part of the patient, the willingness to experience intense emotions, and high ego strength, whatever that is. In general this is not for the psychotic. Techniques include free association, interpretation of defenses, and a focus on understanding transference reactions.

Front 66

How is competency assessed regarding: medical decisions, financial affairs, use of anti-psychotic medications?

Back 66

Competency can only be considered with respect to a specific task. That is just because one is not competent to decide on medical treatment does not mean that one is not competent to manage one’s finances or to get married. Competency is a legal status and thus only a court can officially determine competency. A psychiatrist can give an opinion as to a patient’s psychological capacity, which opinion can be used in determining competency. Also competency can change with time and must be continuously reassessed. Capacity to consent to medical treatment can be broken down into the following requirements:

1) Ability to communicate a decision.
2) Ability to maintain a stable choice.
3) Understanding of relevant information.
4) Appreciation of the current circumstances and their potential consequences.
5) Ability to manipulate this information rationally, especially with respect to weighing the risks and benefits of treatment.

With respect to civil competencies, such as making out a will, or controlling finances, the same basic principles are applied. A person must understand the situation, be able to manipulate this information, and be able to communicate their decision. With respect to psychotropic medications the courts are stricter than with other medical issues. A person may refuse to take anti-psychotics until a court has heard the case, determined the patient to be incompetent with respect to this decision, and approved a specific treatment plan. If new medications need to be added later the court must hear the case again.

Front 67

What are the elements of “informed consent”?

Back 67

1) Competency

2) Disclosure: The pt must be given info concerning the nature of their illness, the proposed txt, its risks and benefits, the likelihood of success, and alternative txts available. Legal precedent dictates that the pt have any info that a reasonable person would find essential to making a decision.

3) Voluntariness: The pt may not be coerced into txt. According to one ruling this means that a pt’s discharge cannot depend on whether or not they comply with txt.

To treat a pt without obtaining informed consent is a tort (battery). Exceptions include the following:

a) Emergencies: If there is the imminent threat of danger to the patient or others.

b) Patient waivers: If the patient states that they do not wish to know all of the information.

c) Therapeutic privilege: The treating physician may withhold information that could harm the patient.