Psych 4 Exam

Front 1

How long must someone on antidepressants wait until symptoms improve?

Back 1

3-6 weeks

Front 2

What are the 5 different classes of antidepressants?

Back 2

TCAs, MAOIs, SSRIs, SNRIs, Novel antidepressants

Front 3

What are the three effects of tricyclic antidepressants?

Back 3

Antihistaminic, anticholinergic, antiadrenergic

Front 4

What dose of TCAs is lethal?

Back 4

One week supply

Front 5

What can TCAs cause at a therapeutic serum level?

Back 5

QT lengthening

Front 6

What is unique about tertiary TCAs?

Back 6

Tertiary amine side chains prone to cross react with other types of receptors leading to more side effects

Front 7

What are the side effects of tertiary TCAs?

Back 7

antihistaminic - sedation, weight gain
anticholinergic - dry mouth, dry eyes, constipation, memory deficits, delirium
antiadrenergic - orthostatic hypotension, sedation, sexual dysfunction

Front 8

What receptors do tertiary TCAs primarily act on?

Back 8

serotonin receptors

Front 9

What are the tertiary TCAs?

Back 9

imipramiine, amitriptyline, doxepin, clomipramine

Front 10

What are secondary TCAs? What are the two? Which receptors do they primarily act on?

Back 10

Metabolites of tertiary amines, less severe side effects
Despiramine, nortriptyline (despirate.... not)
Primarily block norepinephrine receptors

Front 11

What is the MOA of MAOIs?

Back 11

Bind irreversibly to monoamine oxidase, preventing inactivation of biogenic amines: norepinephrine, dopamine, serotonin, increasing synaptic levels
very effective for depression

Front 12

What are the general SE of MOAIs?

Back 12

Orthostatic hypertension, weight gain, dry mouth, sedation, sexual dysfunction, sleep disturbance

Front 13

What occurs when mixing MAOIs with tyramine rich foods or sympathomimetics?

Back 13

Hypertensive crisis

Front 14

What is serotonin syndrome? Sx?

Back 14

Occurs when meds like MAOIs and sympathomimetics are combined and increase serotonin too much
Sx: abdominal pain, diarrhea, sweats, tachycardia, HTN, myoclonus, irritability, delirium

Front 15

How long must you wait before switching from SSRI to an MAOI? Which SSRI must you wait longer for?

Back 15

2 weeks
Fluoxetine - wait 5 weeks because of long half life

Front 16

SSRIs are good to treat both...

Back 16

anxiety and depression symptoms

Front 17

What are the side effects of SSRIs?

Back 17

GI upset, sexual dysfunction (30%), anxiety, restlessness, insomnia, fatigue, sedation, dizziness

Front 18

What is a benefit of taking SSRIs?

Back 18

very little risk of cardiotoxicity in overdose

Front 19

What can develop if SSRI is stopped suddenly? How do you prevent this?

Back 19

Discontinuation syndrome can develop: agitation, nausea, disequilibrium, and dysphoria
Titrate up and down for atleast 2 wks

Front 20

What are SNRIs most similar to? how are they different?

Back 20

Similar to TCAs by inhibiting both serotonin and norepinephrine reuptake, but without all of the negative side effects.

Front 21

What can SNRIs beused for?

Back 21

depression, anxiety, NEUROPATHIC PAIN

Front 22

What pathway in the brain do antipsychotics target? What are the 4 pathways?

Back 22

Dopamine - Mesocortical, mesolimbic, nigrostriatal, tuberoinfundibular

Front 23

Important points about the mesocortical pathway?

Back 23

ventral tegmentum (brain stem) -> cerebral cortex
negative symptoms & cognitive disorders (lack of executive function) arise here
too little dopamine

Front 24

Important points about the mesolimbic pathway?

Back 24

dopaminergic cell bodies in ventral tegmentum -> limbic system
positive symptoms (hallucinations, delusions, thought disorders)
too much dopamine

Front 25

Important points about the nigrostriatal pathway?

Back 25

dopaminergic cell bodies in substantia nigra -> basal ganglia
movement regulation
dopamine suppresses acetylcholine activity
Dopamine hyperactivity causes Parkinsonian movements - rigidity, bradykinesia, tremors, akathisia, and dystonia

Front 26

Important points about the tuberoinfundibular pathway?

Back 26

hypothalamus -> ant. pituitary
dopamine release inhibits/regulates prolactin release
blocking this pathway = hyperprolactinemia (gynecomastia, galactorrhea, decreased libido, menstrual dysfunction)

Front 27

What are typical antipsychotics? Example of high & low potency drugs?

Back 27

D2 Dopamine Receptor Antagonist (DRAs)
HIGH: Fluphenazine, haloperidol*, pimozide (FHP)
LOW: Chlorpromazine and thioridazine

Front 28

What does HIGH potency typical antipsychotics mean? Examples?

Back 28

HIGH potency, bind to D2 receptor with HIGH affinity
HIGHER risk of extrapyramidal SE
Fluphenazine, haloperidol*, pimozide (FHP)

Front 29

What does LOW potency typical antipsychotics mean? Examples?

Back 29

LOW potency, LESS affinity for D2 receptors
Interact with nondopaminergic receptors: MORE cardiotoxic & anticholinergic adverse effects - sedation/hypotension

Chlorpromazine & thioridazine

Front 30

What are atypical antipsychotics?

Back 30

Serotonin-dopamine 2 antagonists (SDAs)
affected serotonin & dopamine neurotransmission in the 4 dopamine pathways

Front 31

What are the adverse SE of antipsychotics?

Back 31

tardive dyskinesia (TD), neuroleptic malignant syndrome (NMS), extrapyramidal side effects (EPS)

Front 32

Antipsychotic SE: tardive dyskinesia

Back 32

involuntary muscle movements, may not resolve after discontinuation, risk 5% per year

Front 33

Antipsychotic SE: neuroleptic malignant syndrome

Back 33

Severe muscle rigidity, fever, altered mental status, autonomic instability, elevated WBCs, CPK, LFTs
May be fatal

Front 34

Antipsychotic SE: extrapyramidal SE

Back 34

acute dystonia, Parkinson syndrome, akathisia

Front 35

What are some agents to treat EPS?

Back 35

anticholinergics: benztropine, trihexyphrnidyl, diphenhydramine
dopamine facilitators: amantadine
beta blockers: propranolol

Front 36

What are anxiolytics used to treat?

Back 36

panic disorder, GAD, withdrawal, insomias, parasomnias, with SSRIs/SNRIs for anxiety disorders

Front 37

What are some classes of anxiolytics?

Back 37

A2-adrenergic receptor agonist
Beta blockers
Benzos
Z drugs

Front 38

A2-adrenergic receptor agonists: absorbed? overdose SE? pregnancy?

Back 38

GI tract
Coma, constricted pupils, bradycardia
Should be avoided in pregnancy

Front 39

Which A2-adrenergic agonist has a longer half-life and less sedative effects, and less withdrawal symptoms?

Back 39

Guanfacine

Front 40

What is the most experienced A2-adrenergic agonist in psychiatry? What can occur with abrupt discontinuation? When does this happen? How do you fix it?

Back 40

Clonidine
Withdrawal can occur: anxiety, restlessness, perspiration, tremor, abdominal pain, palpitations, HA, HTN
Appear 20 hrs after last dose, must taper when d/c

Front 41

What are some pt precautions when taking A2-adrenergic agonists? 7

Back 41

BP below 90/60, cardiac arrhythmias (bradycardia), vascular dz, renal dz, Raynaud's syndrome, Hx of depression, Elderly pts

Front 42

What is propanolol useful for?

Back 42

social phobia (performance), PTSD, GAD

Front 43

What are Beta blockers used for? 5 As 1L

Back 43

Anxiety disorders (social phobia)
Acute akathisia (Neuroleptic-induced)
Aggression/violent behavior
Alcohol withdrawal
Antidepressant augmentation
Lithium induced postural tremor

Front 44

Beta blockers are contraindicated pts with...

Back 44

Asthma, insulin-dep diabetes, CHF, vascular dz, persistent angina, hyperthyroidism

Front 45

What are some adverse effects of beta blockers? If you need to use a beta blocker but you have heart risks which should you use?

Back 45

Can worsen AV conduction defects leading to HEART BLOCK & DEATH
Use selective Beta 1 blockers

Front 46

What are the MC SE of beta blockers (2)?

Back 46

Hypotension, bradycardia

Front 47

What plasma drug concentrations can propranolol increase?

Back 47

antipsychotics, anticonvulsants, theophylline, levothyroxine

Front 48

What are the benefits of benzos? CI?

Back 48

Absorbed in GI tract rapidly! rapid onset of action
Ideal for EPISODIC ISSUES
CI: narrow-angle glaucoma

Front 49

Which two benzos can be used IM?

Back 49

Lorazepam (Ativan) and Midazolam (Versed)

Front 50

What are the advantages and disadvantages of long half life benzos?

Back 50

Adv: Less frequent dosing, less variation in plasma conc, less severe withdrawal phenomenon

Disadv: Drug accumulation, risk of daytime psychomotor impairment, daytime sedation

Front 51

What are the advantages and disadvantages of short half life benzos

Back 51

Adv: No drug accumulation, less daytime sedation
Disadv: More frequent dosing, early/more severe withdrawal syndromes ("d/c syndrome"), rebound insomnia, anterograde amnesia

Front 52

What are Z drugs? Similar to? Work on? name the 3?

Back 52

Similar to benzos, Work on GABA, Rapid onset, Short half-life, No active metabolites

Zaleplon, zolpidem, eszopiclone

Front 53

What is Flumazenil? How does it works? Admin? Half life? Adverse effects?

Back 53

Reverse psychomotor, amnesic, sedative effects of benzos OD
Admin: IV
Half life: 7-15 min
SE: N/V, dizziness, agitation, emotional lability, cutaneous vasodilation, fatigue, HA, SEIZURES: if seizure disorder, physical dependence, large OD

Front 54

Benzos good during pregnancy?

Back 54

NO - possibly teratogenic, passes through breast milk

Front 55

What happens when SSRI is taken with zolpidem?

Back 55

prolong and exacerbated halluncinations

Front 56

What can increase the serum level of benzos and is CI with the use of benzos?

Back 56

Ketoconazole & itraconazole

Front 57

Benzos should be cautioned with?

Back 57

cimetidine, OCPs, valproic acid, azole antifungals

Front 58

Bupropion (Wellbutrin): use? benefit? formulations?

Back 58

Good as augmenting agent, second line ADHD agent (co-occuring diagnosis)

uses: SMOKING CESSATION, Cocaine detox, hypoactive SEXUAL DESIRE disorder, depression, SAD, bipolar

No weight gain, sexual SE, or cardiac interactions, low induction of mania

Immediate (TID), Sustained (BID), Extended (QD) release

Front 59

Bupropion cons? 3

Back 59

- Increased seizure risk at high doses (450 mg), avoid in pts with traumatic brain injury, bulimia, anorexia
- Does not treat anxiety - may CAUSE ANXIETY, agitation, insomnia
- Abuse potential - psychotic sx at high doses

Front 60

Bupropion SE & CI?

Back 60

HA, Insomnia, dry mouth, tremor, nausea

CI: SEVERE ANXIETY or PANIC DISORDER
(causes anxiety)

Front 61

Bupropion drug interactions?

Back 61

Venlafaxine - sign. interactions
Lithium - rarely causes CNS toxicity
MAOIs - never used with, hypertensive crisis, d/c MAOIs 2 wks before starting
Amphetamine - false neg on urinary screens
Herbs (kava kava, St. John's wort) - CNS depression
ETOH - increased seizure risk

Front 62

What is the half life of Busprione (BuSpar) and what does it act on? Most pronounced activity?

Back 62

Short half life (2-11 hrs) 2-3 times a day
Agonist, partial agonist, or antagonist of serotonin 5-HT1A receptors

Most pronounced as presynaptic agonist - inhibits release of serotonin = antianxiety effect

Front 63

What is the ONLY thing Busprione is indicated for? How is it better than benzos? worse?

Back 63

Generalized anxiety disorder
Better for sx of anger & hostility, effect for psychic sx of anxiety

Less effective for somatic sx

Front 64

What is the best advantage of Buspirone?

Back 64

NO LETHAL ODs EVER reported
LD50 is 160-550X recommended daily dose

Front 65

When do you use Buspirone with caution?

Back 65

Hepatic/renal impairment, pregnancy (B), nursing

Front 66

Drug interactions of Buspirone?

Back 66

Haloperidol - increases serum levels of haloperidol
MAOIs - hypertensive crisis, d/c 2 wks before initiating

Front 67

Which agents increase plasma levels of Buspirone?

Back 67

Erythromycin, itraconazole, nefazodone, grapefruit juice

Front 68

Which agents decrease plasma levels of Buspirone?

Back 68

Rifampin, phenytoin, phenobarbital, carbamazepine, fluoxetine

Front 69

Pros of buspirone?

Back 69

Good augmentation, works independently of endogenous release of serotonin, no sedation, wt gain, sex dysfxn, or d/c syndrome

Front 70

Cons of buspirone?

Back 70

takes 2 weeks for pts to notice results
will not reduce anxiety in pts used to taking benzos, no sedation to take the edge off

Front 71

Carbamazepine: absorption? half life? bound? metabolized?

Back 71

Absorp: slow, unpredictable, food enhances absorption
Half life: 15-84 hrs (decr with chronic admin - self metabolized/requires dose adjustment)
70-80% protein bound, metab. in liver

Front 72

Carbamazepine benefits

Back 72

Well tolerated, mild GI/CNS SE, does not cause wt gain

Front 73

Carbamazepine SE - serious/rare

Back 73

Serious: BLOOD DYSCRASIAS - need routine monitoring Q 3 months for 1st year - warn pts about petechiae/bruising, unusual bleeding
Hepatits & serious SKIN RXNs can occur early in use

Rare: Decr. cardiac conduction, SIADH

Front 74

Carbamazepine with pregnancy

Back 74

Not used unless absolutely necessary, can deplete available FOLIC ACID, secreted in breast milk

Front 75

Carbamazepine drug interactions

Back 75

Many!! med check before prescribing
OCPs - reduces serum conc.
MAOIs - Do not give, 2 wk wait
Grapefruit juice - inhibits hepatic metabolism of carbamazepine
Valproate - adjust dosing, decr. carbamazepine & incr. valproate

Front 76

Carbamazepine lab interference & labs to do before starting & during treatment

Back 76

increase T3 & T4 without increasing TSH
Cholesterol increased

Before: LFTs, CBC, EKG
During: Complete blood assessment Q 2 weeks for 2 months then every quarter (provider discretion)

Front 77

Dopamine receptor antagonists - Typical antipsychotics - half life? benefits of parenteral formulation?

Back 77

Half life: 24 hrs
Parenteral: rapid/reliable onset, greater bioavailability, long acting depot formulations available (haloperidol, fluphenazine)

Front 78

What is potency?

Back 78

Amount of drug required to achieve therapeutic effect?

Front 79

Dopamine receptor antagonists - Typical antipsychotics - difference btw low potency & high potency?

Back 79

Low potency - Chlorpromazine - more wt gain, sedation, given at higher amounts

High potency - Haloperidol - less wt gain, lower amounts, more likely to cause EPS

Front 80

Indications for Dopamine receptor antagonists - Typical antipsychotics? 5 What is Haloperidol uniquely used for? 2

Back 80

- Schizophrenia/schizoaffective disorder - more pronounced effect on positive symptoms
- Mania - acute stage
- Depression with psychotic sx (used in combo with antiDs)
- Delusional disorder
- Severe agitation/violent behavior
- Borderline Personality disorder

Haloperidol - Tourette's syndrome, dementia/delirium (low doses of high potency - Haloperidol)

Front 81

Adverse effects of Dopamine receptor antagonists - Typical antipsychotics? 9 Which ones are caused more by low potency? 2

Back 81

Lowers seizure threshold (low potency)
Orthostatic Hypotension (low potency)
Sedation
Anticholinergic effects
Prolonged QT/PR intervals
Hematologic - leukopenia, agranulocytosis
Increased prolactin secretion
Decr. libido
Jaundice

Front 82

Ci for Dopamine Receptor antagonist -Typical antipsychotics 7

Back 82

Serious allergic rxn
Ingestion of CNS depressant/interaction
Severe cardiac abnormality
High risk for seizures
Narrow-angle glaucoma
BPH + anticholinergic drug
Hx tardive dyskinesia

Front 83

Table: Haloperidol (Haldol) Chem class? Therapeutically equivalent oral dose (mg), Sedation? autonomic? EPS?

Back 83

Chem class: Butyrophenone
Therapeutically equivalent oral dose (mg): 2 mg
Sedation: +
Autonomic: +
EPS: +++

Front 84

Table: Compazine/Prochlorperazine Chem class? Therapeutically equivalent oral dose (mg), Sedation? autonomic? EPS?

Back 84

Chem class: Phenothiazine: piperazine compound
Therapeutically equivalent oral dose (mg): 15 mg
Sedation: ++
Autonomic: +
EPS: +++

Front 85

Table: Thorazine/Chlorpromazine Chem class? Therapeutically equivalent oral dose (mg), Sedation? autonomic? EPS?

Back 85

Chem class: Phenothiazine: aliphatic compound
Therapeutically equivalent oral dose (mg): 100 mg
Sedation: +++
Autonomic: +++
EPS: ++

Front 86

Name one of the two drugs used in psychiatry from this class, Α2-Adrenergic Receptor Agonists, of medications

Back 86

Clonidine (Catapres) and guanfacine (Tenex)

Front 87

What is the MOA? Α2-Adrenergic Receptor Agonists

Back 87

Stimulation of the presynaptic α2-adrenergic receptor reduces the firing rate of noradrenergic neurons and therefore the plasma concentration of norepinephrine – reduces sympathetic tone

Front 88

What psychiatric disorders can be treated with α2-adrenergic agonists?

Back 88

Has applications with ADHD, opioid withdrawal, Tourette’s disorder, and suppression of agitation in PTSD

Front 89

Name one psychiatric disorder treated with β-blockers

Back 89

Social phobia, lithium-induced tremor, control of aggressive behavior, neuroleptic-induced akathisia

Front 90

Name 2 β-blockers commonly used in psychiatry
What do the four first drugs have in common?

Back 90

Propranolol, nadolol, pindolol, labetalol,
They are equally selective for beta 1 and 2 receptors

atenolol, metoprolol, acebutolol

Front 91

What makes the underlined drugs, Propranolol, metoprolol, more advantageous in creating CNS effects?

Back 91

They are more lipophilic and more likely to cross the BBB

Front 92

Where do benzodiazepines exert their effects (receptor/neurotransmitter)?

Back 92

Benzodiazepine receptors/GABA

Front 93

What are the common psychiatric indications for use of benzodiazepines (and drugs acting on the benzo receptors)?

Back 93

Insomnia, anxiety disorders, agitation, social phobia, mania, alcohol withdrawal

Front 94

What is the most common risk associated with use of benzodiazepines?

Back 94

Psychological and physical dependence with long term use

Front 95

What neurotransmitters are affected by bupropion?

Back 95

Does not act on the serotonin system
Norepinephrine and dopamine reuptake inhibitor

Front 96

What is an advantage of bupropion over venlafaxine?

Back 96

No identified discontinuation syndrome

Front 97

What is the unique psychiatric indication for bupropion?

Back 97

Only medication approved by the FDA for SAD
Has indication for smoking cessation

Front 98

What is unique about Buspirone (BusPar) as compared to other anti-anxiety medications?

Back 98

1st non-sedating drug specifically indicated for the treatment of anxiety (1986)

Front 99

Why is Buspirone less commonly used than other treatment modalities?

Back 99

Gained less traction because not instantaneous (like benzodiazepine)
Came out only 2 years before fluoxetine (which has broader applications)

Front 100

Why is it difficult to switch patients from benzodiazepine to buspirone?

Back 100

Buspirone lacks the sedative-effect which some patients find desirable (euphoric) – easier to use in benzo naïve patients

Front 101

What is the indication for carbamazepine?

Back 101

Carbamazepine was approved in 2004 by the FDA in it’s extended release formulation for the treatment of bipolar I disorder (targets mania)

Front 102

What is the indication for oxcarbazepine?

Back 102

Oxcarbazepine has not been proven in large placebo-controlled studies to be efficacious as a mood-stabilizer

Front 103

What is the MOA of carbamazepine/oxcarbazepine?

Back 103

Structurally similar to TCAs, unclear as to the MOA for bipolar

Front 104

What was the first drug in this class? Dopamine Receptor Antagonists: Typical Antipsychotics

Back 104

Chlorpromazine (thorazine) was introduced in the mid-1950s – first drug that consistently reduced the symptoms of psychosis

Front 105

What is the MOA? Dopamine Receptor Antagonists: Typical Antipsychotics

Back 105

High-affinity antagonism of the dopamine D2 receptors – inhibits dopaminergic neurotransmission
Called DRAs – dopamine receptor antagonists
Also called first-generation, typical, traditional or conventional antipsychotics

Front 106

Why are the second-generation drugs preferred? Dopamine Receptor Antagonists: Typical Antipsychotics

Back 106

Fewer extrapyramidal side effects, better effects against negative symptoms – now first-line