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PRITE > Pharmacology PRITE Review (JB PPT) Part 2 > Flashcards

Pharmacology PRITE Review (JB PPT) Part 2 Flashcards

1
Q

Compare FGA and SGA.

A

FGA: more selective (dopamine blockade in all 4 dopamine pathways)
SGA: less selective (both dopamine and serotonergic activity)

FGA: acts mostly on positive symptoms via D2 antagonism
SGA: acts on both positive and negative symptoms via D2 and 5HT2A antagonism

FGA: side effects - motor symptoms (EPS/TD)
SGA: metabolic effects (DMII/HLD)

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2
Q

MOA - aripiprazole

A

Partial agonist at D2 and 5HT-1A

Antagonist at 5HT-2A receptor

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3
Q

MOA - cariprazine

A

Partial agonist at D2, 5HT1A

Antagonist at 5HT2A

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4
Q

What is the only antipsychotic primarily processed by the kidneys?

A

Paliperidone (good choice if compromised liver function)

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5
Q

List the fast-inactivated state sodium channel blockers.

A

Phenytoin
Carbamazepine, oxcarbazepine, eslicarbazepine
Lamotrigine

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6
Q

List the slow-inactivated state sodium channel blockers.

A

Lacosamide

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7
Q

List the low voltage activated calcium channel blockers.

A

Ethosuxmide

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8
Q

List the high voltage activated calcium channel blockers.

A

Gabapentin

Pregabalin

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9
Q

MOA - vigabatrin

A

Inhibits GABA-transaminase

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10
Q

MOA - tiagabine

A

Blocks synaptic GABA reuptake

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11
Q

MOA - levetiracetam

A

Synaptic vesicle protein 2A modulation

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12
Q

MOA - acetazolamide

A

Carbonic anhydrase ihibtion

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13
Q

Multiple MOA - valproate

A

GABA potentiation
Glutamate (NMDA) inhibition
Na+ channel blockade
T-type calcium channel blockade

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14
Q

Multiple MOA - topiramate

A

GABA potentiation
Glutamate (AMPA) inhibition
Sodium and calcium channel blockade

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15
Q

Suspected MOA of lithium (remains unclear)?

A

Inhibition of inositol phosphate metabolism

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16
Q

Key medications that are exclusively renally excreted?

A

Lithium
Acamprosate
Gabapentin

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17
Q

Discuss amoxapine and loxapine.

A

Loxapine is an antipsychotic with antidepressant properties (metabolized to amoxapine)

Amoxapine is an antideressant with antipsychotic properties (can cause EPS/TD, avoid in Parkinson’s)

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18
Q

Which cholinesterase inhibitor is NOT metabolized by liver CYP?

A

Rivastigmine

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19
Q

MOA - rivastigmine

A

Dual enzyme inhibition - AChE + BuChE

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20
Q

MOA - galantamine

A

AChE + modulates nicotinic acetylcholine receptors

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21
Q

Which cholinesterase inhibitor has a competitive MOA?

A

Galantamine

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22
Q

Less than 3% of levodopa would make it to the brain if it wasn’t combined with ___. How does this work?

A

Carbidopa; slows/decreases the peripheral conversion of L-Dopa to dopamine

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23
Q

MOA - carbidopa

A

Inhibits DOPA decarboxylase

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24
Q

MOA - Catechol-O-methyltransferase (COMT) inhibitors

A

Prevents both peripheral and central degradation of L-dopa

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25
Q

MOA - clonidine and guanfacine

A

Pre-synaptic alpha-2-receptor agonist

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26
Q

MOA - buprenorphine

A

Partial agonist at mu
Antagonist at delta
Antagonist at kappa

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27
Q

MOA - amphetamine

A

Increases dopamine release

Inhibits dopamine reuptake

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28
Q

MOA - triptans

A

Agonist at 5-HT1B and 5-HT1D - promotes vasoconstriction, blocks pain transmission

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29
Q

Notable CYP-4500 inducers (psych meds)

A 
Carbamazepine
Rifampin
Phenytoin
Primidone
Phenobarbital
St. John's wort
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30
Q

Notable CYP-4500 inhibitors (psych meds)

A 
Fluoxetine
Fluvoxamine
Sertraline
Other SSRIs
Isoniazid
Cimetidine
Grapefruit
Erythromycin
ETOH
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31
Q

Fluoxetine is an important ___ inhibitor.

A

2D6 (can increase toxicity)

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32
Q

African Americans have higher activity of CYP ___.

A

3A4

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33
Q

Higher risk of SJS in Asians is due to ___.

A

HLA B*1502 allele

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34
Q

Grapefruit is an important CYP ___ inhibitor.

A

3A4

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35
Q

Drug-drug interaction - depakote + lamotrigine

A

Depakote inhibits glucuronidation of lamotrigine -> risk of lamotrigine toxicity

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36
Q

Drug-drug interaction - carbamazepine + clozapine

A

Increased risk of marrow suppression

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37
Q

Drug-drug interaction - erythromycin + carbamazepine

A

Increased risk of side effects such as heart block

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38
Q

Which 5 antipsychotics are affected by smoking and why?

A

Haldol, chlorpromazine, clozapine, olanzapine, thioridazine; levels are decreased via CYP 1A2 induction

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39
Q

Typical impact of Depakote on other drugs? Exception?

A

Increases levels

Exception: increases epoxide metabolite of carbamazepine but overall there is a net decrease in carbamazepine

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40
Q

Typical impact of carbamazepine? Exception?

A

Decreases nearly everything; exception - it increases other inducers

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41
Q

List some non-SSRI/SNRIs that can increase the risk of serotonin syndrome when coadministered with MAOIs.

A 
Ziprasidone
Dextromethorphan, chlorpheniramine
Fentanyl, meperidine, tramadol
Linezolid
MDMA, LSD
Methylene blue
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42
Q

List 4 cardiovascular agents that can cause depression.

A
  1. Clonidine (reduces NE output via alpha-adrenergic receptor agonism)
  2. Guanethidine (depletes neuronal NE)
  3. Methyldopa (partial agonism of NE)
  4. Reserpine (depletes neuronal NE, 5HT, dopamine)
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43
Q

Proposed mechanism of depression caused by isotretinoin?

A

Alters dopaminergic, serotonin, possible NE systems

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44
Q

List 3 anticonvulsants that can cause depression.

A
  1. Phenobarbital (reduces unbound tryptophan -> influences plasma 5HT conentrations)
  2. Topiramate (increases amount of GABA available)
  3. Vigabatrin (ditto)
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45
Q

List 3 hormonal agents that can cause depression.

A
  1. Corticosteroids (elevates cortisol)
  2. GnRH agonists (reduces estrogen and androgen production)
  3. Tamoxifen (reduces estrogen function via antagonizing estrogen receptors)
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46
Q

MOA of depression caused by interfron?

A

Increases IL-6 production

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47
Q

Typical side effects caused by MOA - 5HT3 agonism

A

Nausea

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48
Q

Typical side effects caused by MOA - 5HT reuptake inhibition

A

GI disturbances

Activating effects

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49
Q

Typical side effects caused by MOA - 5HT2 agonism

A

Sexual dysfunction

Activing effects

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50
Q

Typical side effects caused by MOA - DA reuptake inhibition

A

Psychomotor activation

Psychosis

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51
Q

Typical side effects caused by MOA - H1 antagonism

A

Sedation/drowsiness

Weight gain

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52
Q

Typical side effects caused by MOA - AcH antagonism

A 
Blurred vision
Dry mouth
Constipation
Sinus tachycardia
Urinary retention
Memory dysfunction
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53
Q

Typical side effects caused by MOA - alpha1 antagonism

A

Priapism

54
Q

Typical side effects caused by MOA - Alpha2 antagonism

A

Postural hypotension
Dizziness
Reflex tachycardia

55
Q

Typical side effects caused by MOA - NE reuptake inhibition

A 
Dry mouth
Urinary retention
Activating effects
Tremor
CV troubles
56
Q

Which SSRI can have anticholinergic effects?

A

Paroxetine

57
Q

Antidepressants - high risk for orthostatic hypotension?

A

TCAs, trazodone, MAOIs

58
Q

Antidepressants - lower risk for orthostatic hypotension?

A

SSRIs, mirtazapine

59
Q

Antidepressants - “no” risk for orthostatic hypotension?

A

Bupropion

60
Q

Which antidepressant can increase LFTs and should be avoided in patients with liver disease and alcohol use disorder?

A

Duloxetine

61
Q

___ ?may cause amenorrhea, galactorrhea, and hyperprolactinemia.

A

Fluoxetine

62
Q

Notable side effects of lithium?

A

Weight gain (severe), lethargy (mild), ataxia (none or mild), nausea (moderate), tremor (severe); polyuria, nephrogenic DI, fatigue, reversible hypothyroidism, cognitive deficits, acne, headache, worsens psoriasis, benign leukocytosis, hyperparathyroidism (can lead to hypercalcemia)

63
Q

Notable side effects of lamotrigine?

A

Weight gain (mild), lethargy (moderate), ataxia (moderate), nausea (moderate), tremor (none or mild); dizziness, headache, insomnia, severe skin reactions

64
Q

Notable side effects of valproic acid?

A

Weight gain, lethargy, ataxia, nausea [all moderate], tremor (severe); headache ovarian cysts, rare hepatotoxicity, hyperammonemia, rare pancreatitis, alopecia, rare blood cell dyscrasias, teratogenicity

65
Q

Side effects of carbamazepine?

A

Rare blood cell dyscrasis (aplastic anemia, agranulocytosis, thrombocytopenia), hepatoxocitiy, rash (including SJS), SIADH, heart block, ataxia, hyponatremia, teratogenicity risk, hepatitis

66
Q

Monitoring needs - lithium

A 
TSH
RFP
Electrolytes
Pregnancy test
[EKG for patients over 40]
67
Q

Monitoring needs - valproic acid

A

LFTs
CBC (Plts)
Pregnancy test

68
Q

Monitoring needs - carbamazepine

A

LFTs
CBC
Electrolytes
Pregnancy test

69
Q

Monitoring needs - lamotrigine

A

Pregnancy test

70
Q

Management of lithium-associated polyuria?

A

Increase PO intake of salt-containing fluids
Lower dose
Once nightly dosing
Careful use of ameloride and potassium monitoring/supplementation

71
Q

Management of lithium-associated tremor?

A

Avoid caffeine
Assess use of catecholamines and antipsychotics
Treat worsening anxiety
Consider use of propranolol or primidone

72
Q

Management of lithium-associated diarrhea?

A 
Avoid slow-release preparation
Lower dose
Monitor levels (diarrhea may result in toxicity)
Consider switching to lithium citrate
73
Q

Management of lithium-associated thyroid abnormalities?

A

Monitor TSH, fT3, thyrotropin Q6 months

Thyroid supplementation for subclinical hypothyroidism

74
Q

Management of lithium-associated renal dysfunction?

A

Monitor serum Cr and BUN Q6 months
24-hour urine Cr Cl if there is a rise in serum Cr >1.5
Consider alternative treatment and nephrologist consultation

75
Q

Which drugs can decrease renal clearance of lithium and increase the risk of toxicity?

A

NSAIDs and diuretics

76
Q

Mechanism of lithium-induced nephrogenic DI?

A

Lithium competes with ADH -> increased urination -> volume depletion -> hyperNa

77
Q

Treat lithium-induced nephrogenic DI?

A

Amiloride (best) or thiazides

78
Q

Side effects of phenytoin?

A

Hirsutism
Fetal dysmorphism
Gingival hypertrophy
Cerebellar atrophy (long-term)

79
Q

Signs of phenytoin toxicity?

A

Unsteady gait
Slurred speech
Nystagmus

80
Q

True or false - VPA-induced hyperammonemia has been reported with acute and chronic use and can occur with therapeutic levels and in the absence of hepatotoxicity.

A

True

81
Q

Acute dose-related adverse effects of valproic acid?

A

Tremor

82
Q

Acute dose-related adverse effects of topiramate and zonidsamide?

A

Paresthesia

83
Q

Acute dose-related adverse effects of carbamazepine and lamotrigine?

A

Diplopia, blurred vision, visual distortion

84
Q

Acute dose-related adverse effects of topiramate?

A

Mental/motor slowing

85
Q

Acute dose-related adverse effects of levetiracetam, ezogabine, perampanel?

A

Mood or behavioral changes

86
Q

Acute dose-related adverse effects of carbamazepine, phenytoin, phenobarbital?

A

Changes in libido/sexual function

87
Q

List long-term adverse effects of AEDs.

A
  • Osteomalacia/osteoporosis: carbamazepine/oxcarbazepine, barbiturates, phenytoin, valproate
  • Altered connective tissue metabolism or growth (facial coarsening, hirsutism, gingival hyperplasia/contractures): phenytoin, phenobarbital
  • Neuropathy: phenytoin, carbamazepine
  • Cerebellar degeneration: phenytoin
  • Sexual dysfunction: phenytoin, carbamazepine, phenobarbital, primidone
88
Q

List teratogenic AEDs from lowest to highest risk.

A

Lowest: lamotrigine, levetiracetam
- Carbamazepine, oxcarbazepine
- Phenytoin, phenobarbital, topiramate
Highest: valproic acid

89
Q

List the 4 dopaminergic pathways.

A
  1. Mesolimbic (excess dopamine -> positive symptoms)
  2. Mesocortical (decreased dopamine -> negative symptoms)
  3. Nigrostriatal (dopamine antagonism > EPS/TD)
  4. Tuberoinfundibular (dopamine antagonism > hyperprolactinemia)
90
Q

Effect of D2-receptor antagonism?

A

+ symptom alleviation, EPS, endocrine effects

91
Q

Effect of 5-HT2A antagonism?

A

Negative symptom alleviation, less EPS

92
Q

Effect of high 5-HT2A/D2 binding affinity ratio?

A

Better antipsychotic activity and lower EPS than D2 antagonism alone

93
Q

Effect of 5-HT1A agonism?

A

Antidepressant and anxiolytic activity, improved cognition, reduced EPS, body weight changes

94
Q

Effect of 5-HT1D antagonism?

A

Antidepressant activity

95
Q

Effect of 5-HT2C antagonism?

A

+ symptom alleviation, weight gain (via satiety blockade)

96
Q

Effect of alpha-1 adrenoceptor antagonism?

A

Sedation, hypotension, weight gain

97
Q

Effect of H2-histamine antagonism?

A

Sedation, weight gain

98
Q

Effect of M1-muscarinic antagonism

A

Memory impairment, GI symptoms, dry mouth, blurry vision, less EPS

99
Q

Effect of mixed 5-HT/NE reuptake inhibition?

A

Antidepressant and anxiolytic activity, less weight gain

100
Q

Hypothesis to explain why typical antipsychotics cause more EPS than atypical?

A

More rapid dissociation from D2 receptors

101
Q

List the 3 most cholinergic and sedating antipsychotics.

A

Thioridazine
Chlorpromazine
Clozapine

102
Q

Antipsychotic with the highest EPS risk? Lowest EPS risk?

A

Haldol; clozapine

103
Q

Antipsychotics can cause poikilothermia - define this.

A

Inability to maintain constant body temperature

104
Q

Which antipsychotic can cause cataracts?

A

Quetiapin

105
Q

Which antipsychotics can cause retinal pigmentation?

A

Thioridazine; chlorpromazine

106
Q

Adding ___ to clozapine may increase the risk of developing NMS, seizures, and delirium.

A

Lithium

107
Q

When does clozapine-induced myocarditis typically occur?

A

Within the first month of use

108
Q

MOA of clozapine-induced myocarditis?

A

Acute IgE mediated hypersensitivity reaction

109
Q

True or false - agranulocytosis is not dose dependent with clozapine

A

True

110
Q

WBC and ANC levels needed to start clozapine?

A

WBC>3500 (if 3000-3500, need 2x weekly monitoring)

ANC>1500 (or >1000 benign ethnic neutropenia)

111
Q

Frequency of clozapine monitoring

A

First 6 months: weekly
6-12 months: Q2 week
12+ months: monthly

112
Q

How long do you need to continue weekly labs after stopping clozapine due to side effects?

A

1 month after achieving normal labs

113
Q

Why is clozapine thought to have lower than most risk of EPS/TD and hyperprolactinemia?

A

Weakest affinity for D2

114
Q

Response to mild neutropenia (1000-1499)?

A

BEN: no additional monitoring needed
General: monitor ANC 3x weekly until 1500+; return to last monitoring interval

115
Q

Response to moderate neutropenia (500-999)?

A

BEN: monitor ANC 3x weekly until 1000+ or patient’s baseline; then monitor weekly for 4 weeks; then return to last monitoring interval

General: interrupt clozapine; monitor ANC daily until 1000+, restart clozapine; then monitor 3x weekly until 1500+; then monitor weekly for 4 weeks; then return to last interval

116
Q

Response to severe neutropenia (<500)?

A

BEN: discontinue; daily ANC until 500+; 3x weekly until ANC is more than or equal to the patient’s established baseline

General: as above; [until ANC 1500+]

117
Q

Avoid concurrent use of clozapine and ___ due to agranulocytosis risk.

A

Carbamazepine

118
Q

What is metabolic syndrome?

A

3+ of the following:

Blood glucose 100+ (or on hypoglycemic)
HDL <40 (M) or <50 (F)
Triglycerides: 150+ (or on statins)
Weight circumference >40" (M) or >35" (F)
BP 130/85+ (or on antihypertensive)
119
Q

Frequency of A1C and lipid monitoring with atypical antipsychotics?

A

Baseline
3 months
Annually

120
Q

Rx akathisia?

A

1st line - propranolol (20 mg PO TID)

2nd line - benzodiazepine

121
Q

Rx dystonic reaction?

A

Anticholinergic (benztropine 1-2 mg PO BID or 2 mg IM, diphenhydramine 25-50 mg PO TID or 25 mg IM)

122
Q

Rx drug-induced parkinsonism?

A

1st line - anticholinergic

2nd line - dopaminergic agent (eg, amantadine 100 mg PO BID)

123
Q

Rx TD?

A

VMAT-2 inhibitor

124
Q

Key differentiating features of serotonin syndrome vs. NMS?

A 
SS: 
Reflex - hyperreflexia, clonus
Pupils - mydriasis
Bowel sounds - hyperactive
[Increased tone, particularly in lower extremities]
NMS:
Reflex - hypreflexia
Pupils - normal
Bowel sounds - normal to decreased
[Lead pipe rigidity in all muscle groups]
125
Q

Medication to treatment serotonin syndrome?

A

Cyproheptadine (serotonoin antagonist)

126
Q

Medication to treat NMS?

A

Bromocriptine (dopamine agonist)

127
Q

Which antidepressants can cause hyponatremia? MOA?

A 
Sertraline
Fluoxetine
Paroxetine
Citalopram
Venlafaxine

Increased secretion of ADH in hypothalamus
Potentiates the effect of ADH in the kidneys
Lowers threshold for release of ADH

128
Q

Which anticonvulsants can cause hyponatremia? MOA?

A

Carbamazepine, oxcarbazepine

Increased secretion of ADH by hypothalamus

129
Q

MOA of antipsychotics causing SIADH?

A

Serotonin effects on 5-HT2 and 5-HT1C lead to increased ADH

Psychogenic polydipsia leads to excessive consumption of water resulting in hyponatremia

130
Q

Symptoms of water intoxication?

A 
Polyuria
Restlessness, tremor
Diarrhea, vomiting
Ataxia
Stupor

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