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Human Disease Systems > Neuro+Psych Pharmacology > Flashcards

Neuro+Psych Pharmacology Flashcards

1
Q

sumatriptan

A

triptan used for acute migraine attack

MOA: 5HT1B/D agonist => block the release of vasoactive peptides from perivascular trigeminal neurons =? vasoconstriction

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2
Q

zolmitriptan

A

triptan used for acute migraine attack

MOA: 5HT1B/D agonist => block the release of vasoactive peptides from perivascular trigeminal neurons => vasoconstriction

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3
Q

triptan side effects

A

nausea, dizziness, parasthesias, somnolence, chest tightness

cerebral vasoconstriction and rebound headache with excessive dosing

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4
Q

triptan DDIs

A

MAOIs (serotonin syndrome), ergots (increased vasoconstriction)

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5
Q

lasmiditan

A

selective serotonin receptor agonist used for acute migraine attack

MOA: 5HT1F agonist => block release of vasoactive peptides from perivascular trigeminal neurons

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6
Q

lasmiditan side effects

A

nausea, dizziness, paresthesia, somnolence

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7
Q

ubrogepant

A

CGRP receptor antagonist to treat acute migraine attack

MOA: small molecule antagonist of CGRP receptors

CGRP receptor antagonists: ubrogepant, rimegepant

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8
Q

rimegepant

A

CGRP receptor antagonist to treat acute migraine attack

MOA: small molecule antagonist of CGRP receptors

CGRP receptor antagonists: ubrogepant, rimegepant

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9
Q

CGRP receptor antagonists

A

ubrogepant, rimegepant

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10
Q

CGRP receptor antagonist side effects

A

nausea, sedation

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11
Q

dihydroergotamine

A

ergot used to treat acute migraine attack

MOA: structurally similar to LSD; predominately 5HT1D agonist, but also 5HT-2A/B/C agonist, DA agonist, and a receptor agonist

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12
Q

dihydroergotamine DDIs

A

beta blockers (alpha vasoconstriction unopposed by B2 vasodilation => peripheral ischemia), protease inhibitors and macrolide antibiotics (excessive vasoconstriction and CYP450 interactions)

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13
Q

when dihydroergotamine is given parenterally, [drug] can help prevent vomiting

A

metoclopramide

dihydroergotamine is an ergot used in the treatment of acute migraine attack

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14
Q

galcanezumab

A

CGRP antibody used for migraine prophylaxis

MOA: prevents perivascular release of CGRP => prevents vasodilation

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15
Q

erenumab

A

CGRP receptor antibody used for migraine prophylaxis

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16
Q

beta blockers used for migraine prophylaxis

A

propranolol, timolol

MOA unknown in migraine

used in migraineurs with hypertension/angina, migraineurs with performance anxiety or aggressive behavior

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17
Q

beta blockers used for migraine prophylaxis - side effects

A

fatigue, exercise intolerance, cold extremities, diarrhea, constipation, dizziness, worsening depression

beta blockers used for migraine prophylaxis: propranolol, timolol

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18
Q

calcium channel blocker used for migraine prophylaxis

A

verapamil

MOA: blocks transmembrane influx of calcium across cells through their slow voltage-dependent channels => affects neurotransmission

used in migraineurs with hypertension, hemiplegic migraine

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19
Q

calcium channel blockers for migraine prophylaxis - side effects

A

constipation, hypotension, AV block, edema, nausea

CCB for migraine prophylaxis: verapamil

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20
Q

calcium channel blockers for migraine prophylaxis - contraindications

A

bradycardia, heart block, sick sinus syndrome

CCB for migraine prophylaxis: verapamil

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21
Q

tricyclic antidepressants used for migraine prophylaxis

A

amytriptyline, nortriptyline

MOA: central action via inhibition of 5HT and NE reuptake

used for headaches associated with premenstrual syndrome or premenstrual dysphoric disorder; migraineurs with depression, anxiety/panic disorders, or fibromyalgia

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22
Q

tricyclic antidepressants used for migraine prophylaxis - side effects

A

antimuscarinic effects (increased HR, blurred vision, difficulty urinating, dry mouth, constipation), weight loss/gain, orthostatic hypotension

tricyclic antidepressants used for migraine prophylaxis: amytriptyline, nortriptyline

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23
Q

TCA used for migraine prophylaxis - DDIs

A

MAOIs (serotonin syndrome)

tricyclic antidepressants used for migraine prophylaxis: amytriptyline, nortriptyline

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24
Q

tricyclic antidepressants used for migraine prophylaxis - contraindications

A

seizures, enlarged prostate, glaucoma

tricyclic antidepressants used for migraine prophylaxis: amytriptyline, nortriptyline

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25
Q

anti-epileptic medications used for migraine prophylaxis

A

topiramate, valproic acid

used in migraineurs that are overweight or have bipolar disorder

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26
Q

topiramate

A

anti-epileptic medication used for migraine prophylaxis in migraineurs that are overweight or have bipolar disorder

MOA: may antagonize AMPA receptors, inhibit sodium channels, or potentiate transmission at GABA-A receptors

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27
Q

valproic acid

A

anti-epileptic medication used for migraine prophylaxis in migraineurs that are overweight or have bipolar disorder

MOA: inhibits low threshold T-type calcium channels (use dependent block of sodium channels, increased GABA)

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28
Q

enfuviritide

A

fusion inhibitor to treat HIV patients that are resistant to other drugs

MOA: binds gp41 => interferes with entry into the cell

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29
Q

enfuviritide side effects

A

local injection site reactions (subcutaneous injection), increased rate of bacterial pneumonia, hypersensitivity reaction

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30
Q

maraviroc

A

CCR5 antagonist to treat HIV patients that are resistant to other drugs

MOA: blocks co-receptor => prevents entry

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31
Q

maraviroc side effects

A

cough, fever, rash, URT infection, musculoskeletal symptoms, abdominal pain, postural dizziness, hepatotoxicity, cardiovascular events

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32
Q

nucleoside reverse transcriptase inhibitors used to treat HIV

A

lamivudine, emtricitabine, abacavir, zidovudine, tenofovir

tenofovir is only one that does not need to be phosphorylated

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33
Q

lamivudine

A

nucleoside reverse transcriptase inhibitor (NRTI) used to treat HIV

MOA: nucleoside analogue phosphorylated to triphosphates => cause chain termination of DNA as it is being transcribed from RNA

NRTIs used to treat HIV: lamivudine, emtricitabine, abacavir, zidovudine, tenofovir

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34
Q

emtricitabine

A

nucleoside reverse transcriptase inhibitor (NRTI) used to treat HIV

MOA: nucleoside analogue phosphorylated to triphosphates => cause chain termination of DNA as it is being transcribed from RNA

NRTIs used to treat HIV: lamivudine, emtricitabine, abacavir, zidovudine, tenofovir

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35
Q

abacavir

A

nucleoside reverse transcriptase inhibitor (NRTI) used to treat HIV

MOA: nucleoside analogue phosphorylated to triphosphates => cause chain termination of DNA as it is being transcribed from RNA

NRTIs used to treat HIV: lamivudine, emtricitabine, abacavir, zidovudine, tenofovir

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36
Q

zidovudine

A

nucleoside reverse transcriptase inhibitor (NRTI) used to treat HIV

MOA: nucleoside analogue phosphorylated to triphosphates => cause chain termination of DNA as it is being transcribed from RNA

NRTIs used to treat HIV: lamivudine, emtricitabine, abacavir, zidovudine, tenofovir

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37
Q

tenofovir

A

nucleoside reverse transcriptase inhibitor (NRTI) used to treat HIV

MOA: nucleoside analogue that does not need to be phosphorylated => cause chain termination of DNA as it is being transcribed from RNA

NRTIs used to treat HIV: lamivudine, emtricitabine, abacavir, zidovudine, tenofovir

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38
Q

nucleoside reverse transcriptase inhibitors to treat HIV - side effects

A

mitochondrial toxicity (lactic acidosis, pancreatitis, peripheral neuropathy, myopathy, cardiomyopathy, hepatic steatosis, lipid dystrophy)

zidovudine-induced anemia and neutropenia, abacavir hypersensitivity reaction

NRTIs used to treat HIV: lamivudine, emtricitabine, abacavir, zidovudine, tenofovir

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39
Q

abacavir hypersensitivity reaction is related to what genetic variant?

A

HLA-B*5701

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40
Q

nucleoside reverse transcriptase inhibitors to treat HIV - DDIs

A

cytochrome p450 inhibitors (cimetidine) increase levels; probenecid increases levels; cytochrome p450 inducers (rifampin) decrease levels

NRTIs used to treat HIV: lamivudine, emtricitabine, abacavir, zidovudine, tenofovir

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41
Q

tenofovir side effects

A

weakness, headache, diarrhea

nucleoside reverse transcriptase inhibitor (NRTI) used to treat HIV

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42
Q

efavirenz

A

non-nucleoside reverse transcriptase inhibitor (NNRTI) used to treat HIV

MOA: inhibits reverse transcriptase

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43
Q

efavirenz side effects

A

rash, Steven-Johnson syndrome, hepatitis, CNS effects

a non-nucleoside reverse transcriptase inhibitor used to treat HIV

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44
Q

integrase inhibitors used to treat HIV

A

bictegravir, dolutegravir, elvitegravir, raltegravir, cabotegravir/rilpivirine

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45
Q

bictegravir

A

integrase inhibitor used to treat HIV

MOA: targets viral integrase

integrase inhibitors: bictegravir, dolutegravir, elvitegravir, raltegravir, cabotegravir/rilpivirine

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46
Q

dolutegravir

A

integrase inhibitor used to treat HIV

MOA: targets viral integrase

integrase inhibitors: bictegravir, dolutegravir, elvitegravir, raltegravir, cabotegravir/rilpivirine

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47
Q

elvitegravir

A

integrase inhibitor used to treat HIV

MOA: targets viral integrase

integrase inhibitors: bictegravir, dolutegravir, elvitegravir, raltegravir, cabotegravir/rilpivirine

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48
Q

raltegravir

A

integrase inhibitor used to treat HIV

MOA: targets viral integrase

integrase inhibitors: bictegravir, dolutegravir, elvitegravir, raltegravir, cabotegravir/rilpivirine

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49
Q

cabotegravir/rilpivirine

A

integrase inhibitor used to treat HIV

MOA: targets viral integrase

integrase inhibitors: bictegravir, dolutegravir, elvitegravir, raltegravir, cabotegravir/rilpivirine

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50
Q

integrase inhibitors for HIV - side effects

A

hypersensitivity reactions or serious dermatological reactions, rhabdomyolysis, diarrhea, headache

integrase inhibitors: bictegravir, dolutegravir, elvitegravir, raltegravir, cabotegravir/rilpivirine

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51
Q

integrase inhibitors for HIV - DDIs

A

rifampin enhances elimination; antacid may bind raltegravir and inhibit its action

integrase inhibitors: bictegravir, dolutegravir, elvitegravir, raltegravir, cabotegravir/rilpivirine

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52
Q

protease inhibitors used to treat HIV

A

darunavir, ritonavir

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53
Q

darunavir

A

protease inhibitor used to treat HIV

MOA: targets a dipeptide region in HIV aspartate protease that is not seen in other mammalian proteins

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54
Q

ritonavir

A

protease inhibitor used to treat HIV

MOA: targets a dipeptide region in HIV aspartate protease that is not seen in other mammalian proteins

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55
Q

protease inhibitors for HIV - side effects

A

nausea, vomiting, diarrhea, hyperglycemia, lipodystrophy, hyperlipidemia, hepatotoxicity

protease inhibitors: ritonavir, darunavir

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56
Q

fostemsavir

A

HIV attachment inhibitor

MOA: binds gp120 to prevent virus from attaching to CD4 receptor on T cells => prevents viral attachment

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57
Q

ibalizumab

A

monoclonal Ab used to treat HIV

MOA: recombinant mAb against domain 2 of CD4 T cells => prevents viral entry

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58
Q

preferred drug combinations for the treatment of HIV

A

bictegravir + tenofovir/emtricitabine

dolutegravir + abacavir/lamivudine (test for HLA-B*5701 first)

dolutegravir + tenofovir + emtricitabine or lamivudine

dolutegravir + lamivudine (in select individuals)

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59
Q

depolarizing neuromuscular blocker

A

succinylcholine

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60
Q

succinylcholine

A

depolarizing neuromuscular blocker

MOA: more stable agonist than ACh; initially causes persistent depolarization (=> fasciculations); with continuous exposure, desensitization of muscle nicotinic receptors => repolarization of the muscle but end plate is blocked (phase I); later, nicotinic receptors will inactivate (phase II)

used for brief procedures (mainly intubation)

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61
Q

succinylcholine side effects

A

apnea, hyperkalemia (precludes use in children), increased IOP, increased gastric pressure, malignant hyperthermia

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62
Q

genetic variability in [enzyme] affects duration of action of succinylcholine

A

plasma cholinesterase

homozygous individuals have greatly prolonged action; heterozygous individuals or those with severe liver disease have moderately prolonged action

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63
Q

non-depolarizing neuromuscular blockers

A

tubocurarine, pancuronium, cisatracurium, atracurium, vecuronium, rocuronium

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64
Q

tubocurarine

A

non-depolarizing neuromuscular blocker

long duration of action (kidney/liver metabolism); no longer available for use

MOA: basic competitive blocker of ACh at muscle nicotinic receptors; also blocks autonomic ganglia and causes histamine release

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65
Q

pancuronium

A

non-depolarizing neuromuscular blocker

long duration (kidney metabolism), moderate block of muscarinic receptors (cardiac)

MOA: basic competitive blocker of ACh at muscle nicotinic receptors

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66
Q

cistracurium, atracurium

A

non-depolarizing neuromuscular blocker

intermediate duration (spontaneous hydrolysis), widely used in surgery

MOA: basic competitive blocker of ACh at muscle nicotinic receptors

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67
Q

vercuronium

A

non-depolarizing neuromuscular blocker

intermediate duration (liver metabolism), widely used in surgery

MOA: basic competitive blocker of ACh at muscle nicotinic receptors

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68
Q

rocuronium

A

non-depolarizing neuromuscular blocker

rapid onset for brief procedures, shorter duration (lover metabolism)

MOA: basic competitive blocker of ACh at muscle nicotinic receptors

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69
Q

drugs used for reversal of non-depolarizing neuromuscular blockers

A

neostigmine (cholinesterase inhibitor)

atropine and glycopyrrolate (antimuscarinic given to prevent concomitant excess of ACh at muscarinic sites)

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70
Q

nitrous oxide

A

inhaled anesthetic

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71
Q

halogenated hydrocarbons

A

isoflurane, sevoflurane, desflurane, enflurane, halothane

inhaled anesthetics (* = used infrequently)

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72
Q

halogenated hydrocarbons side effects

A

renal toxicity (enflurane), hepatic toxicity (halothane), respiratory toxicity (sevoflurane)

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73
Q

intravenous anesthetics

A

thiopental, methohexital, etomidate, propofol, ketamine

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74
Q

inhaled anesthetics [increase/decrease] cerebral blood flow, while intravenous anesthetics [increase/decrease] cerebral blood flow

A

inhaled anesthetics increase cerebral blood flow, while intravenous anesthetics decrease cerebral blood flow

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75
Q

minimum alveolar concentration (MAC)

A

alveolar concentration at which 50% of healthy patients do not move (inhaled anesthetics)

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76
Q

the minimum alveolar concentration [increases/decreases] in elderly, pregnancy, and sickness

A

the MAC decreases in elderly, pregnancy, and sickness (need less inhaled anesthetics to achieve effect)

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77
Q

L-DOPA

A

dopamine precursor used to treat Parkinson’s

most effective at diminishing bradykinesia

MOA: taken up by neuron, converted to dopamine, stored in vesicle, and released

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78
Q

L-DOPA side effects

A

GI effects: anorexia, nausea, vomiting (decreased by giving drug with or after meals)

cardiovascular effects: orthostatic hypotension, tachycardia

dyskinesias (facial grimacing, restless feet syndrome, stereotyped behavior)

psychiatric and behavioral side effects: nightmares, anxiety, paranoia, hallucinations, mania

on-off phenomena

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79
Q

L-DOPA DDIs

A

MOAIs (hypertensive crisis)

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80
Q

L-DOPA contraindications

A

psychosis, closed angle glaucoma, melanoma

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81
Q

the presence of DOPA decarboxylase inhibitor [drug], much more L-DOPA enters the brain

A

carbidopa

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82
Q

sinemet

A

controlled release formulation of L-DOPA

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83
Q

bromocriptine

A

dopamine agonist used to treat Parkinson’s (also used at lower doses for hyperprolactinemia)

MOA: directly activate dopamine receptors (D2, D3); ergot alkaloid

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84
Q

bromocriptine side effects

A

cardiovascular effects: postural hypotension, erythromelalgia, digital vasospasm

GI effects: anorexia, nausea, vomiting, constipation, indigestion, peptic ulceration with bleeding, reflux esophagitis

dyskinesia (less than with L-DOPA)

mental disturbance (hallucinations, compulsive behaviors)

fibrosis

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85
Q

pramipexole

A

dopamine agonist used to treat Parkinson’s

MOA: D3>D2 agonist

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86
Q

ropinirole

A

dopamine agonist used to treat Parkinson’s

MOA: D2 and D3 agonist

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87
Q

pramipexole and ropinirole side effects

A

more likely to cause sudden sleep episodes; cardiovascular side effects are less common than bromocriptine; compulsive behavior; dyskinesia; hallucinations

dopamine agonists used to treat Parkinson’s

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88
Q

amantadine

A

dopamine releasing agent used in Parkinson’s to control for L-DOPA dyskinesias

MOA: antiviral drug that causes DA release in striatum; may also act at glutamate receptors

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89
Q

amantadine side effects

A

restlessness, agitation, hallucinations, livedo reticularis, peripheral edema

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90
Q

amantadine counterindications

A

seizures, CHF

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91
Q

selegiline

A

monoamine oxidase inhibitor used as an adjunctive therapy for Parkinson’s

MOA: MOA-B inhibitor => retards breakdown of dopamine, prolongs the effects of DOPA

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92
Q

anticholinergics used in Parkinson’s

A

benzotropine, trihezyphenidyl

MOA: restores dopamine and cholinergic balance within the striatum => improves rigidity/tremor, minor effect on bradykinesia

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93
Q

selegiline side effects

A

insomnia (metabolized to L-methamphetamine and L-amphetamine)

94
Q

benotropine, trihexyphenidyl side effects

A

restlessness, hallucinations, confusion, antimuscarinic effects

anticholinergics used for treatment of Parkinson’s

95
Q

benzotropine, trihexyphenidyl contraindications

A

prostatic hypertrophy, obstructive GI disease, glaucoma

96
Q

COMT inhibitors used in Parkinson’s

A

talcapone, entacapone

MOA: COMT converts DOPA to 3-O-methyldopa and DA to 3-methyoxytyramine => these agents enhance delivery of L-DOPA to the brain and stabilize DA

used to increase duration of effect of DOPA dose without increasing DOPA level (never used alone)

97
Q

tolcapone, entacapone side effects

A

dyskinesias

tolcapone requires frequent blood tests to measure liver function

98
Q

cholinesterase inhibitors used in Alzheimer’s

A

tacrine, donepezil, galantamine, rivastigmine

99
Q

tacrine

A

first centrally-acting cholinesterase inhibitor used for Alzheimer’s

still on the market but generally not used because of significant hepatotoxicity

100
Q

donepezil

A

cholinesterase inhibitor used in Alzheimer’s

MOA: reversible cholinesterase inhibitor that specifically and selectively inhibits cholinesterase in CNS and increases acetylcholine in the cortex*

*does also inhibit cholinesterase in periphery => side effects

101
Q

galantamine

A

cholinesterase inhibitor used to treat Alzheimer’s disease with a cerebrovascular component

MOA: inhibit acetylcholinesterase + positive allosteric modulator of nicotinic receptors => enhance activation of nicotinic receptors

102
Q

donepezil and galantamine side effects

A

nausea, diarrhea, headache, insomnia, anorexia, pain; urinary incontinence may also occur

cholinesterase inhibitors used to treat AD

103
Q

donepezil and galantamine DDIs

A

may accentuate effect of succinylcholine; cytochrome p450 interactions with cimetidine, ketoconazole, ritonavir, etc.

104
Q

donepezil and galantamine contraindications

A

cardiac conduction abnormalities, ulcers, seizures, asthma, COPD, older patients with low body weight

105
Q

rivastigmine

A

cholinesterase inhibitor used to treat Alzheimer’s

MOA: inhibits acetylcholinesterase and butyrl cholinesterase in glia => makes more ACh available for cholinergic neurons

106
Q

rivastigmine side effects

A

GI symptoms more severe than other drugs in this class (nausea, diarrhea, headache, insomnia, anorexia, pain; urinary incontinence may also occur)

cholinesterase inhibitor used to treat AD

107
Q

memantine

A

NMDAR antagonist used to treat Alzheimer’s, Huntington disease, AIDS-related dementia, vascular dementia

MOA: NMDAR antagonist that blocks “open” NMDA channels with low to moderate affinity => blocks effects of glutamate “leak” at NMDA receptors caused by amyloid plaques without blocking all glutamate transmission

108
Q

memantine side effects

A

dizziness, constipation, confusion, headache, hypertension

109
Q

memantine contraindications

A

renal impairment, cardiovascular disease, history of seizures

110
Q

raising urinary pH will [increase/decrease] elimination of memantine

A

decrease

111
Q

memantine DDIs

A

other NMDAR antagonists (amantadine, ketamine, dextromorphan)

112
Q

typical antipsychotics

A

high potency: haloperidol, fluphenazine

medium potency: periphenazine

low potency: chlorpromazine, thioridazine

MOA: D2 blockade

113
Q

haloperidol

A

high potency typical antipsychotic (D2 blockade, low anticholinergic effect)

114
Q

fluphenazine

A

high potency typical antipsychotic (D2 blockade, low anticholinergic effect)

115
Q

periphenazine

A

medium potency typical antipsychotic (D2 blockade, medium anticholinergic effect)

116
Q

chlorpromazine

A

low potency typical antipsychotic (D2 blockade, high anticholinergic effect)

117
Q

thioridazine

A

low potency typical antipsychotic (high anticholinergic effect)

118
Q

typical antipsychotics side effects

A

acute dystonia (treated with diphenhydramine), parkinsonism (treated with amantadine), akathisia (treated with propranolol), tardive dyskinesia (treated with valbenazine), orthostatic hypotension, male sexual dysfunction, constipation, dry mouth, urinary retention, visual problems, sedation, galactorrhea, amenorrhea, neuroleptic malignant syndrome (treated with dantrolene or bromocriptine)

119
Q

acute dystonia (typical antipsychotic side effect) is treated with [drug]

A

diphenhydramine

120
Q

parkinsonism (typical antipsychotic side effect) is treated with [drug]

A

amantadine

121
Q

akathisia (typical antipsychotic side effect) is treated with [drug]

A

propranolol

122
Q

tardive dyskinesia (typical antipsychotic side effect) is treated with [drug]

A

valbenazine

123
Q

neuroleptic malignant syndrome (rare side effect of typical antipsychotics) is treated with [drug]

A

dantrolene or bromocriptine

124
Q

atypical antipsychotics

A

clozapine, risperidone, olanzapine, quetiapine, ziprasidone, ariprazole

125
Q

clozapine

A

atypical antipsychotic

MOA: serotonin 5HT2A receptor antagonist; D2 antagonists with rapid dissociation (decreases EPS)

atypical antipsychotics: clozapine, risperidone, olanzapine, quetiapine, ziprasidone, ariprazole

126
Q

risperidone

A

atypical antipsychotic

MOA: serotonin 5HT2A receptor antagonist; D2 antagonists with rapid dissociation (decreases EPS)

atypical antipsychotics: clozapine, risperidone, olanzapine, quetiapine, ziprasidone, ariprazole

127
Q

olanzapine

A

atypical antipsychotic

MOA: serotonin 5HT2A receptor antagonist; D2 antagonists with rapid dissociation (decreases EPS)

atypical antipsychotics: clozapine, risperidone, olanzapine, quetiapine, ziprasidone, ariprazole

128
Q

quetiapine

A

atypical antipsychotic

MOA: serotonin 5HT2A receptor antagonist; D2 antagonists with rapid dissociation (decreases EPS)

atypical antipsychotics: clozapine, risperidone, olanzapine, quetiapine, ziprasidone, ariprazole

129
Q

ziprasidone

A

atypical antipsychotic

MOA: serotonin 5HT2A receptor antagonist; D2 antagonists with rapid dissociation (decreases EPS)

atypical antipsychotics: clozapine, risperidone, olanzapine, quetiapine, ziprasidone, ariprazole

130
Q

ariprazole

A

atypical antipsychotic

MOA: serotonin 5HT2A receptor antagonist; D2 antagonists with rapid dissociation (decreases EPS); dopamine D2 partial agonist (unique to ariprazole)

atypical antipsychotics: clozapine, risperidone, olanzapine, quetiapine, ziprasidone, ariprazole

131
Q

atypical antipsychotics side effects

A

increased appetite and weight gain (increased triglycerides, insulin resistance, diabetes, CV events); sedation, somnolence

+ agraunulocytosis, increased salivation, and seizures (clozapine)

+ cardiac arrhythmia (ziprasidone)

+ EPS at higher doses (risperidone)

atypical antipsychotics: clozapine, risperidone, olanzapine, quetiapine, ziprasidone, ariprazole

132
Q

selective serotonin reuptake inhibitors (SSRIs)

A

fluoxetine, sertraline, citalopram, fluvoxamine, paroxetine

used in major depression, generalized anxiety disorder, PTSD, OCD, panic disorder, and premenstrual dysphoric disorder

133
Q

fluoxetine

A

selective serotonin reuptake inhibitor

MOA: inhibit reuptake of serotonin

therapeutic effect occurs over 2-4 weeks; ultimately correlated with increased activation of postsynaptic 5HT1A receptors and decreased activation of 5HT2A receptors

SSRIs: fluoxetine, sertraline, citalopram, fluvoxamine, paroxetine

134
Q

sertraline

A

selective serotonin reuptake inhibitor

MOA: inhibit reuptake of serotonin

therapeutic effect occurs over 2-4 weeks; ultimately correlated with increased activation of postsynaptic 5HT1A receptors and decreased activation of 5HT2A receptors

SSRIs: fluoxetine, sertraline, citalopram, fluvoxamine, paroxetine

135
Q

citalopram

A

selective serotonin reuptake inhibitor

MOA: inhibit reuptake of serotonin

therapeutic effect occurs over 2-4 weeks; ultimately correlated with increased activation of postsynaptic 5HT1A receptors and decreased activation of 5HT2A receptors

SSRIs: fluoxetine, sertraline, citalopram, fluvoxamine, paroxetine

136
Q

fluvoxamine

A

selective serotonin reuptake inhibitor

MOA: inhibit reuptake of serotonin

therapeutic effect occurs over 2-4 weeks; ultimately correlated with increased activation of postsynaptic 5HT1A receptors and decreased activation of 5HT2A receptors

SSRIs: fluoxetine, sertraline, citalopram, fluvoxamine, paroxetine

137
Q

paroxetine

A

selective serotonin reuptake inhibitor

MOA: inhibit reuptake of serotonin

therapeutic effect occurs over 2-4 weeks; ultimately correlated with increased activation of postsynaptic 5HT1A receptors and decreased activation of 5HT2A receptors

SSRIs: fluoxetine, sertraline, citalopram, fluvoxamine, paroxetine

138
Q

selective serotonin reuptake inhibitor side effects

A

nausea, diarrhea, sexual dysfunction, discontinuation syndrome serotonin syndrome, reduced platelet aggregation, sweating, suicide

139
Q

[syndrome] is characterized by dizziness, tingling or numbness in skin

A

discontinuation syndrome

onset 1-2 days after stopping; continues for ~1 week

140
Q

[syndrome] is characterized by hyperthermia, muscle rigidity, cardiovascular collapse, flushing, diarrhea

A

serotonin syndrome

141
Q

[SSRI drug name] is relatively free of drug interactions, compared to other drugs in this class

A

citalopram

142
Q

[SSRI drug name] has the longest half-life of drugs in this class

A

fluoxetine

needs to be discontinued 4 weeks before switching to MAO inhibitor to avoid serotonin syndrome

143
Q

serotonin/ norepinephrine reuptake inhibitors

A

venlafaxine, duloxetine

used for major depression, atypical depression (venlafaxine), generalized anxiety, stress urinary incontinence, vasomotor symptoms of menopause, pain of diabetic neuropathy (duloxetine)

144
Q

venlafaxine

A

serotonin/ norepinephrine reuptake inhibitor

MOA: inhibits serotonin transporter; inhibits NE transporter at higher doses

can be used for atypical depression

145
Q

duloxetine

A

serotonin/ norepinephrine reuptake inhibitor

MOA: inhibits 5HT and NE transporter

can be used for diabetic neuropathy pain

146
Q

venlafaxine and duloxetine side effects

A

nausea, discontinuation syndrome, serotonin syndrome, NE effects (increased HR and BP), CNS activation (insomnia, anxiety, agitation); high doses of venlafaxine are more likely to have adverse cardiac effects

147
Q

tricyclic antidepressants

A

amitriptyline, nortriptyline, imipramine, desipramine, clomipramine

not commonly used; used in treatment resistant depression and for pain (at lower doses)

148
Q

amitriptyline

A

tricyclic antidepressant

MOA: inhibit NE and 5HT reuptake to varying degrees (clomipramine inhibits primarily 5HT reuptake, desipramine is more selective for NE)

149
Q

nortriptyline

A

tricyclic antidepressant

MOA: inhibit NE and 5HT reuptake to varying degrees (clomipramine inhibits primarily 5HT reuptake, desipramine is more selective for NE)

150
Q

imipramine

A

tricyclic antidepressant

MOA: inhibit NE and 5HT reuptake to varying degrees (clomipramine inhibits primarily 5HT reuptake, desipramine is more selective for NE)

151
Q

desipramine

A

tricyclic antidepressant

MOA: inhibit NE and 5HT reuptake to varying degrees (clomipramine inhibits primarily 5HT reuptake, desipramine is more selective for NE)

152
Q

clomipramine

A

tricyclic antidepressant

MOA: inhibit NE and 5HT reuptake to varying degrees (clomipramine inhibits primarily 5HT reuptake, desipramine is more selective for NE)

153
Q

tricyclic antidepressants side effects

A

anticholinergic (dry mouth, tachycardia, urinary retention, etc.), postural hypotension, weight gain, sedation, sexual side effects, discontinuation syndrome, serotonin syndrome

TCAs: amitriptyline, nortriptyline, imipramine, desipramine, clomipramine

154
Q

TCA toxicity is treated with [drug]

A

sodium bicarbonate

TCA toxicity: coma, convulsions, cardiotoxicity; caused by conduction delays

155
Q

5HT2A receptor antagonists

A

trazadone, mirtazapine

156
Q

trazadone

A

5HT2A receptor antagonist used to treat insomnia

MOA: 5HT2A antagonist => enhances 5HT transmission at postsynaptic 5HT1A receptors and other 5HT2 receptors

157
Q

trazadone side effects

A

sedation, GI upset, hypotension and priapism (rare); sexual side effects NOT common

trazadone = 5HT2A receptor antagonist used for insomnia

158
Q

mirtazapine

A

5HT2A receptor antagonist used to treat melancholic depression or depression with insomnia

blocks 5HT2A/2C and 5HT3 receptors and presynaptic a2 receptors => enhance release of 5HT and HE, enhance transmission at other 5HT receptors, especially 5HT1A

159
Q

mirtazapine side effects

A

increased appetite and weight gain, sedation; does NOT cause sexual side effects

mirtazapine = 5HT2A receptor antagonist used to treat melancholic depression or depression with insomnia

160
Q

bupropion

A

unicycle antidepressant used to treat atypical depression or for smoking cessation

MOA: resembles amphetamine => CNS activation properties; causes NE release and DA release to a lesser degree; moderate inhibitor of NE and DA reuptake

161
Q

bupropion side effects

A

agitation, insomnia, anorexia; NOT associated with sexual side effects

bupropion = unicycle antidepressant used to treat atypical depression or for smoking cessation

162
Q

monoamine oxidase inhibitors

A

phenelzine, tranylcypromine, isocarboxazid, selegiline

rarely used because of toxicity and potential for food interactions; used for treatment resistant depression or for Parkinson’s

163
Q

phenelzine

A

MOAI used to for treatment resistant depression or Parkinson’s

MOA: irreversibly inhibit both MOA isozymes => increase monoamine transmission

164
Q

tranylcypromine

A

MOAI used to for treatment resistant depression or Parkinson’s

MOA: irreversibly inhibit both MOA isozymes => increase monoamine transmission

165
Q

isocarboxazid

A

MOAI used to for treatment resistant depression or Parkinson’s

MOA: irreversibly inhibit both MOA isozymes => increase monoamine transmission

166
Q

selegiline

A

MOAI used to for treatment resistant depression or Parkinson’s

MOA: primarily inhibits MOA-B => protects DA from catabolism*

*at high doses to treat depression, probably loses isozyme selectivity

167
Q

monoamine oxidase inhibitor side effects

A

dramatic hypertension (because tyramine escapes normal enzymatic destruction and causes NE release from sympathetic neurons), serotonin syndrome, CNS stimulation in overdose, postural hypotension, weight gain

168
Q

MAOIs cause serotonin syndrome when combined with what drugs?

A

SSRIs, SNRIs, TCAs, and meperidine

169
Q

lithium

A

mood stabilizer used for acute mania, bipolar long-term treatment, severe recurrent depression with cyclic pattern, and psychosis

MOA: unknown

170
Q

lithium MOA is unknown; theories include:

A

(1) inhibition of inositol monophosphatase => depletion of brain inositol => inhibits receptor-activated phosphoinositide hydrolysis and formation of second messengers (IP3 and DAG)

(2) inhibits NE-stimulated adenylyl cyclase and some G-protein coupled receptors

(3) inhibition of growth factor pathways => neuroprotective effects and long-term plasticity

171
Q

lithium side effects

A

tremor (frequent), sedation, decreased cognition, incoordination

decreased thyroid function, polydipsia and polyuria (occasionally diabetes insipidus), tubulointerstital nephropathy

nausea, vomiting, diarrhea, weight gain

dermatitis, exacerbation of psoriasis, hair loss, acne

reversible increase in PMNs

172
Q

though considered safe in pregnancy, lithium use during the first trimester can cause [?]

A

cardiac malformations

173
Q

[drugs] reduce lithium clearance

A

diuretics, NSAIDs, and ACE inhibitors

174
Q

lithium overdose is characterized by [symptoms]

A

convulsions, coma, confusion, coarse hand tremor, muscle rigidity, fasciculations, ataxia

treated with fluids (mild) or hemodialysis (severe)

175
Q

lithium overdose is caused by Li accumulation due to decreased serum [?]

A

sodium

176
Q

benzodiazepines

A

diazepam, chlordiazepam, flurazepam, clonazepam, alprazolam, temazepam, triazolam, lorazepam, oxazepam

used for anxiety, insomnia, and alcohol detox

MOA: allosterically increase GABA-A receptor channel open frequency

177
Q

benzodiazepine receptors: BZ1 mediates [?] and BZ2 mediates [?]

A

BZ1 mediates sedation and anticonvulsant effects

BZ2 mediates anxiolytic effects and impairment of cognitive function

178
Q

diazepam, chlordiazepam, and flurazepam are metabolized by [?]

A

phase I and phase II metabolism in the liver => long-acting metabolites with a longer duration of action

179
Q

clonazepam, triazolam, lorazepam, and oxazepam are metabolized by [?]

A

phase II only (liver) => no active metabolites, shorter duration of action

180
Q

benzodiazepine side effects

A

sedation (may potentiate sedating effects of alcohol or barbiturates => cardiac and respiratory depression), physical dependence, psychological dependence, toxicity

181
Q

benzodiazepine toxicity is treated with [drug]

A

flumenazil

benzodiazepine toxicity is characterized by impaired judgement, slurred speech, incoordination, stupor, respiratory depression, and death

182
Q

buspirone

A

a non-benzodiazepine anxiolytic used for its relatively non-sedating properties

MOA: partial agonist at both presynaptic and postsynaptic 5HT1A receptors => inhibit normal inhibitory feedback of serotonin => increased 5HT release; also blocks DA D2 receptors

does NOT have problematic interactions with alcohol

183
Q

non-benzodiazepines used for insomnia

A

zolpidem, zaleplon, eszopiclone, suvorexant (orexin antagonist), rameltean (melatonin 1 and 2 receptor agonist)

184
Q

zolpidem, zaleplon, eszopiclone side effects

A

ataxia, nightmares, headache, confusion

185
Q

methylphenidate/ dexmethylphenidate

A

stimulants used for treatment of ADHD in children aged 6 and above

MOA: blocks reuptake of DA and NE

*dexmethylphenidate is a more active enantiomer of methylphenidate

186
Q

methylphenidate/ dexmethylphenidate side effects

A

anorexia, nervousness, growth suppression, GI distress, irritability/ increased crying, tachycardia, increased BP, tics

187
Q

dextroamphetamine, lisdextamfetamine, mixed amphetamine salts

A

amphetamines used for the treatment of ADHD in children aged 3 and above

MOA: enhances release and blocks reuptake of DA and NE

188
Q

dextroamphetamine, lisdextamfetamine, mixed amphetamine salts side effects

A

sudden death in children with cardiac abnormalities

+ same as methylphenidate (anorexia, nervousness, growth suppression, GI distress, irritability/ increased crying, tachycardia, increased BP, tics)

189
Q

atomoxetine

A

non-stimulant for treatment of ADHD (2nd line therapy)

MOA: NE reuptake inhibitor

190
Q

atomoxetine side effects

A

nausea, anorexia, increased HR and BP, constipation, hepatotoxicity

191
Q

clonidine, guanfacine

A

nonstimulants for treatment of ADHD (most effective for impulsivity and hyperactivity rather than inattentiveness)

MOA: central a2 agonist

192
Q

clonidine, guanfacine side effects

A

sedation, orthostatic hypotension, dry mouth

193
Q

what medication is used off-label for ADHD treatment?

A

bupropion

MOA: DA and NE reuptake inhibitor

194
Q

dissolution/absorption of drugs may be [?] in the elderly

A

slowed

due to decreased saliva production, decreased gastric fluid, decreased acidity, weaker peristalsis, decreased jejunal surface area

generally does NOT affect total amount of drug absorbed

195
Q

while the dissolution/ absorption of drugs may be slowed in the elderly, the total amount absorbed generally remains the same; a common exception to this is [?]

A

L-DOPA

more L-DOPA is absorbed with age because there is less DOPA decarboxylase to catabolize it

also, drugs that require active transport are less absorbed in old age

196
Q

the concentration of water soluble drugs [increases/decreases] with age

A

increases

decreased lean body mass means there is less volume of distribution and increased drug concentration

example: digoxin levels increase with age

197
Q

the duration of action of fat-soluble drugs [increases/decreases] with age

A

increases

more adipose tissue => increased volume of distribution and increased duration of action

example: diazepam duration of action increases with age

198
Q

phase [I/II] metabolism in the liver decreases with age

A

phase I metabolism decreases with age, while phase II metabolism does not decrease with age

metabolism of drugs metabolized by both phases (diazepam) decreases with age, while drugs metabolized by only phase II (lorazepam) are not as affected

199
Q

serum creatinine [increases/decreases] with age

A

trick question!!!

serum creatinine levels stay the same with age, despite decreasing GFR, due to simultaneous decreased creatinine production

200
Q

opioids use disorder is treated with [drugs]

A

clonidine, methadone, buprenorphine, naltrexone, and SSRIs

201
Q

nicotine MOA

A

activates nicotinic receptors in CNS, periphery, and NMJ; activation of receptors in the ventral tegmental area => DA release in nucleus accumbens

202
Q

nicotine effects

A

anxiolytic affects, increased arousal, decreased appetite

203
Q

nicotine withdrawal is characterized by [?]

A

irritability, anxiety, autonomic arousal, intense cravings

204
Q

nicotine use disorder is treated with [drugs]

A

varenicline, bupropion

205
Q

cocaine MOA

A

blocks reuptake of monoamines in presynaptic terminal; predominately DA but can also block NE and 5HT transporters at high concentrations

206
Q

amphetamine MOA

A

substrate for NE transporter; enters synaptic terminal and displaces NE => release of NE

207
Q

name the intoxication syndrome:

increased arousal and vigilance; profound sense of wellbeing, energy, and optimism that can progress to psychomotor agitation, paranoia, and psychosis; altered tactile sensation

A

cocaine/amphetamine

amphetamine effects last longer

208
Q

name the withdrawal syndrome:

listlessness, drowsiness, depressed mood, dysphoria, anhedonia

A

cocaine/amphetamine

209
Q

cocaine/amphetamine withdrawal is not typical of withdrawal syndromes because [?]

A

re-administration of the drug does not alleviate symptoms

withdrawal symptoms may occur in the presence of the drug (tachyphylaxis) when target becomes less responsive to the drug

210
Q

methamphetamine MOA

A

decreased DA reuptake and increased DA release via DA transporter

211
Q

caffeine MOA

A

blocks presynaptic adenosine receptors that normally inhibit the release of DA and NE => increased DA and NE release

212
Q

cannabis MOA

A

active metabolite (delta-9-THC) is a partial agonist at the cannabinoid receptor (CB1); stimulation of receptor leads to release of DA in the nucleus accumbens

213
Q

name the intoxication syndrome:

euphoria, laughter, giddiness, feeling of detachment, cognitive function deficits, trouble concentrating; high doses cause panic reactions, perceptual distortions, and changes in perception of reality

A

cannabis

214
Q

name the withdrawal syndrome:

insomnia, loss of appetite, irritability, anxiety

A

cannabis

215
Q

synthetic cannabinoids “spice” MOA

A

full agonist at CB1 receptor (more potent than cannabis)

216
Q

phencyclidine (PCP) MOA

A

NMDAR antagonist => disinhibition of pyramidal neurons

217
Q

name the intoxication syndrome:

euphoria, hallucinations, psychotic behavior, hostility, violent behavior; nystagmus, ataxia, seizures, coma; hypertension, tachycardia; reduced sensation to pain

A

PCP

218
Q

lysergic acid (LSD) MOA

A

synthetic ergot derivative; activation of 5-HT2 receptors in cortical layers => increased glutamate release (mesolimbic DA system is not targeted)

219
Q

name the intoxication syndrome:

perceptual changes, illusions, depersonalization, derealization, hallucinations, synesthesia, pupillary dilation, tachycardia, sweating, incoordination

A

hallucinogens

220
Q

ethosuximide (MOA, indication, AE)

A

MOA: T-type calcium channels (involved in absence seizures)

indication: absence seizures

AE: nausea, Steven-Johnson syndrome and aplastic anemia (rare)

221
Q

gabapentin (MOA, indication, AE)

A

MOA: binds to voltage-gated calcium channels => halts influx of calcium at presynaptic terminal, reducing the release of neurotransmitter into synapse during excitation

indication: focal seizures

AE: weight gain

222
Q

carbamazepine (MOA, indication, AE)

A

MOA: target sodium channels to inhibit depolarization selectively during period of hyperexcitability, but permit depolarization during normal neuronal transmission

indication: focal seizures

AE: hyponatremia, leukopenia (rare aplastic anemia), Steven-Johnson syndrome, hepatotoxicity, osteopenia

223
Q

oxcarbazine (MOA, indication, AE)

A

MOA: target sodium channels to inhibit depolarization selectively during period of hyperexcitability, but permit depolarization during normal neuronal transmission

indication: focal seizures

AE: hyponatremia

224
Q

lacosamide (MOA, indication, AE)

A

MOA: target sodium channels to inhibit depolarization selectively during period of hyperexcitability, but permit depolarization during normal neuronal transmission

indication: focal seizures

AE: dizziness/syncope, prolonged PR interval on EKG

225
Q

levetiracetam (MOA, indication, AE)

A

MOA: inhibit the release of excitatory neurotransmitters from the synapse by binding to synaptic vesicle 2A protein

indication: focal and generalized seizures

AE: mood changes including psychosis

226
Q

lamotrigone (MOA, indication, AE)

A

MOA: target sodium channels to inhibit depolarization selectively during period of hyperexcitability but permit depolarization during normal neuronal transmission

indication: focal and generalized seizures

AE: Steven-Johnson syndrome, commonly rase; levels increased by valproate

227
Q

phenytoin (MOA, indication, AE)

A

MOA: target sodium channels to inhibit depolarization selectively during period of hyperexcitability but permit depolarization during normal neuronal transmission

indication: focal and generalized seizures but NOT for absence or myoclonic seizures

AE: gingival hyperplasia, cerebellar atrophy, neuropathy, Steven-Johnson syndrome, osteopenia; phlebitis and rarely hand necrosis (purple glove syndrome) if given IV; several drug interactions (warfarin, valproic acid, some antibiotics)

228
Q

valproic acid (MOA, indication, AE)

A

MOA: enhance GABA transmission; inhibit T-type calcium channels; target sodium channels

indication: focal and generalized seizures

AE: liver toxicity, hyperammonemia, pancreatitis, tremor, thrombocytopenia, weight gain, PCOS, insulin resistance, hyperandrogenism; very teratogenic

229
Q

topiramate (MOA, indication, AE)

A

MOA: enhance GABA transmission; inhibit AMPA receptors; target sodium channels

indication: focal and generalized seizures

AE: weight loss, renal stones, acute angle-closure glaucoma, cognitive side effects, paresthesia

230
Q

zonisamide (MOA, indication, AE)

A

MOA: inhibit T-type calcium channels and sodium channels

indication: focal and generalized seizures

AE: weight loss, renal stones, cognitive side effects, oligohydrosis, sulfa allergy cross-reactivity, acute angle-closure glaucoma

231
Q

phenobarbital (MOA, indication, AE)

A

MOA: enhance GABA-A transmission

indication: focal and generalized seizures but NOT for absence seizures

AE: liver toxicity, sedation, cytopenias, osteopenia, contractures

Human Disease Systems (11 decks)

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