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Advanced Pharm > Exam 2 Drugs > Flashcards

Exam 2 Drugs Flashcards

1
Q

sypmathomimetic subclasses:

A

direct acting
indirect acting

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2
Q

midodrine

A

class: direct-acting (DA) sympathomimetic

receptor: alpha-1 agonist

indication: orthostatic hypotension

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3
Q

clonidine

A

class: DA sympathomimetic
receptor: CENTRAL alpha-2 agonist; considered a PARTIAL AGONIST
indication:
* HTN (off label: adjuvant drug for sedation)
* diarrhea
* hot flashes
* hemodynamic instability intraOP
* ADHD, Tourettes, withdrawal symptoms
* OFF LABEL: anxiety, PTSD, adjunct to anesthesia (prolongs anesthesia)

MOA:
CENTRAL Alpha-2-Rs:
* Rostro Ventrolateral Medulla (RVLM) stimulated > INHIBITION of sympathetic outflow leads to decreased vasoconstriction, HR, and contractility
* Nucleus of the Tractus Solitarius (NTS) stimulated > leads to INCREASED FIRING ON VAGUS NERVE (CN X) > leading to INCREASED PARASYMPATHETIC OUTFLOW leads to slower HR
* overall effects of decrased HR and decreased SV will decrease BP

SE:
* may see initial transient increase in BP prior to decrease in BP d/t peripheral alpha-2 stimulation via oral route prior to crossing BBB
* dry mouth
* also has effect to induce sedation

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4
Q

epinephrine

A

class: DA sympathomimetic
receptor: alpha + beta 1 + beta 2 agonist
indication: positive inotropic agent, positive chronotropic agent, dilation of skeletal muscles and bronchioles

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5
Q

norepi (NE)

A

class: DA sympathomimetic
receptor: alpha + beta 1 agonist
indication: hypotension
MOA: increase in SBP + DBP; vagal reflex overcomes chronotropic effects (does not stimulate HR as much)

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6
Q

isoproterenol

A

class: DA sympathomimetic
receptor: beta 1 + beta 2 agonist
indication: HTN
MOA:
* B1: will increase HR, CO, & contractility with a slight increase in SV; slight increase in pulse pressure but major effects will be to decrease DBP and a slight decrease in SBP
* B2: decrease vascular tone

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7
Q

dopamine

A

class: DA sympathomimetic
receptor: D + beta 1 agonist
indication: cardiac
MOA:
* decreases peripheral resistance at LOW DOSES (induces diuresis)
* mimics action of epinephrine at HIGH RATES OF INFUSION (increase in HR, increase in contractility, increase in peripheral resistance, could be arrythmogenic)

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8
Q

dobutamine (dobs)

A

class: DA sympathomimetic
receptor: beta 1 selective agonist
indication: cardiogenic shock, HF
MOA: positive inotropic/chronotropic effect

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9
Q

phenylephrine

A

class: DA sympathomimetic
receptor: pure alpha agonist
indication: decongestant, hypotension

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10
Q

midodrine

A

class: DA sympathomimetic
receptor: alpha-1 selective agonist
indication: postural/orthostatic hypotension

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11
Q

ephedrine

A

class: DA && INDIRECT ACTING sympathomimetic
receptor: alpha and beta agonist
indication: nasal decongestant (pseudoephedrine)
MOA: mimics epi (direct-acting); crosses the BBB

found in plants; can be used to make meth

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12
Q

dexmedetomidine

A

class: DA sympathomimetic
receptor: CENTRAL alpha-2-A selective agonist
indication: anxiolytic

MOA: induces anesthesia, analgesia, sympatholysis, sedation, anxiolysis, hypnosis, and increased congnition

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13
Q

amphetamines

A

class: INDIRECT-acting sympathomimetics
effects: mood elevator, appetite suppresant, increased attention
MOA: readily enter CNS

methamphetamines have a higher ratio of CNS to PNS actions

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14
Q

cocaine

A

class: indirect acting sympathomimetic
effects: amphetamine-like effects
MOA: inhibits dopamine reuptake into neurons in the “pleasure centers” of the brain

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15
Q

tyramine

A

class: indirect sympathomimetic
effects: releases stored catecholamines; metabolized by MAO

MAOIs (monoamine oxidase inhibitor) inhibit the breakdown of NTs and are often prescribed as antidepressants; MAOis may increase blood pressure after eating fermented foods

ex) cheese, chicken liver, sausage (fermented), red wine, yeast

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16
Q

phentolamine

A

class: reversible sympatholytic
receptor: competitive alpha-1, alpha-2 blocker
indication: HTN linked to pheochromocytoma, cardiac stimulant, ED (direct injection)
MOA:
* turns a pressor into a depressor
* if giving phentolamine BY ITSELF, very little effect
* if giving phentolamine AFTER pressor, will decrease some of the pressor agonists’ effects
* if giving phentolamine BEFORE pressor, GREATEST effect and decreases BP significantly

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17
Q

prazosin

A

class: reversible sympatholytic
receptor: alpha-1 selective blocker (low affinity for alpha-2)
indication: HTN, BPH
MOA: relaxes arterial and venous smooth muscle

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18
Q

labetalol

A

class: reversible sympatholytic
receptor: alpha & beta blocker
indication: HTN

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19
Q

phenoxybenzamine

A

class: IRREVERSIBLE sympatholytic
receptor: non-specific alpha antagonist & covalently bonds, blocks H1, ACh, and serotonin receptors
indication: HTN linked to
pheochromocytoma
MOA: inhihbits NE reuptake

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20
Q

-osin drug class

A

alpha-1 blockers

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21
Q

what is the drug Yohimbine?

A

an alpha-2 selective antagonist which has little use clinically

allegedly helps ED patients

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22
Q

propanolol

A

class: sympatholytic
receptor: non-specific beta blocker
indication: HTN
SE: bradycardia, rash, fever, CNS effects (sedation, sleep disturbances, depression), worsening of asthma (B2), hypoglyemia in diabetics (blocks glycogenolysis), must discontinue use gradually

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23
Q

metoprolol

A

class: sympatholytic
receptor: beta-1 blocker
indication: HTN (safer in COPD, asthma, and diabetic patients)

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24
Q

labetalol

A

class: sympatholytic
receptor: a1 **AND **b1, b2 blocker
indication: HTN, preeclampsia, pheochromocytoma

racemic mixture: 2 active forms and 2 inactive forms

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25
Q

esmolol

A

class: sympatholytic
receptor: beta-1 selective blocker
indication: tachycardia intraop, supraventricular arrythmia
other facts: ultra short acting, steady state infusion, terminated rapidly when discontinued, safer in critical care patients

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26
Q

ACh

A

class: DA parasympathomimetic// cholinomimetic
subclass: choline ester
indication: miosis (pupillary constriction)

insoluble in lipids

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27
Q

methacholine

A

class: DA parasympathomimetic // cholinomimetic
subclass: choline ester
indication: diagnostic drug for asthma

insoluble in lipids

28
Q

carbachol

A

class: DA parasympathomimetic// cholinomimetic
subclass: choline ester
indication: to decrease IOP

insoluble in lipids; resistant to hydrolysis

29
Q

bethanechol

A

class: DA parasympathomimetic// cholinomimetic
subclass: choline ester
indication: bladder dysfunction, reflux disease

insoluble in lipids; resistant to hydrolysis

30
Q

muscarine

A

class: DA parasympathomimetic// cholinomimetic
subclass: alkaloid
effects: mimics parasympathetic nerve discharge (saliva, bowel motility, urination, etc.)
MOA: takes place at effector cells, not in ganglia
toxicity: exaggeration of all symptoms of muscarinic agonism (MYCETISM); can occur with high consumption of wild mushrooms
reversal for toxicity: ATROPINE 1-2mg IM

31
Q

nicotine

A

class: DA parasympathomimetic// cholinomimetic
subclass: alkaloid
MOA: stimulates autonomic ganglia and skeletal muscle NMJ, not effector cells
release of dopamine, serotonin, GABA, and NE
SE: in larger doses – tremors, emesis, stimulates respiratory center, convulsions, fatal coma (OD ingestion), addiction

crosses BBB; lipid soluble
the antidote for nicotine OD is 2-PAM

32
Q

arecoline

A

class: DA parasympathomimetic// cholinomimetic
subclass: alkaloid
stimulant; from betel nut

33
Q

pilocarpine

A

class: DA parasympathomimetic// cholinomimetic
subclass: alkaloid
effects: N/V/D, salivation, sweating, bronchial constriction

34
Q

edrophonium

A

class: INDIRECT-acting parasympathomimetic// cholinomimetic
subclass: simple alcohol
indication: diagonist drug for myasthenia gravis
onset: 5-15 mins

35
Q

neostigmine

A

class: INDIRECT-acting parasympathomimetic// cholinomimetic
subclass: carbamate
indication: MG, surgical paralysis reversal agent
MOA: inhibits the effects of AChE

36
Q

pyridostigmine

A

class: INDIRECT-acting parasympathomimetic// cholinomimetic
subclass: carbamate
indication: MG
MOA: inhibits the effects of AChE

37
Q

echothiophate

A

class: INDIRECT-acting parasympathomimetic// cholinomimetic
subclass: organophosphate
indication: glaucoma
MOA: increases the drainage of intraocular fluid

38
Q

atropine

A

class: parasympatholytic // anticholinergic
subclass: antimuscarinic
indication: organophosphate poisoning (with pralidoxime), bradycardia

  • effects occur d/t racemix mixture
  • competitively inhibits muscarinic responses to ACh
39
Q

scopolamine

A

class: parasympatholytic // anticholinergic
subclass: antimuscarinic
indication: motion sickness, excessive salivation

40
Q

tropicamide

A

class: parasympatholytic // anticholinergic
subclass: antimuscarinic
indication: mydriasis and cycloplegia (diagnostic drug)

41
Q

ipratropium bromide

A

class: parasympatholytic // anticholinergic
subclass: antimuscarinic
indication: asthma

42
Q

succinylcholine

A

class: parasympatholytic // anticholinergic
subclass: antinicotinic && choline ester
indication: DEPOLARIZING muscle relaxant
MOA:
* resembles ACh; it is considered a n-ACh-R AGONIST
* blocks n-ACh-R on motor end plate of skeletal muscle
* depolarization PERSISTS
* continuous end-plate depolarization causes muscle relaxation (prolonged depol = delayed repolarization of cell)
* this depolarizing agent causes a PHASE I BLOCK (depol w/ lack of repolarization) which will then lead to a phase II block
SE:
* fasciculations
* muscle pain (when drug is bound for too long)
* hyperK+
* MH
* apnea

43
Q

curare derivatives (i.e. rocuronium)

A

class: parasympatholytic // anticholinergic
subclass: antinicotinic
indication: NON-depolarizing NMBA
**MOA: **
* competitive with ACh at n-ACh-Rs; acts as a COMPETITIVE ANTAGONIST
* does NOT depolarize motor end plate
* excessive [ ] = channel blockade

the reversal for ROCURONIUM & VECURONIUM is SUGGAMADEX

44
Q

suggamadex

A

reversal agent for NON-DEPOLARIZING NMBAs: ROCURONIUM & VECURONIUM

a cyclic molecule that cycles around the non-depolarizing blocking agent to prevent binding at the receptor site

45
Q

methyldopa

A

class: sympathoplegic
subclass: centrally acting alpha 2 agonist
indication: pregnancy induced HTN, (does NOT cross placental barrier); not first-line for normal HTN
MOA:
CENTRAL Alpha-2-Rs:
* Nucleus of the Tractus Solitarius (NTS) stimulated > leads to INCREASED FIRING ON VAGUS NERVE (CN X) > leading to INCREASED PARASYMPATHETIC OUTFLOW leads to slower HR

46
Q

hydralazine

A

class: oral vasodilator
indication: HTN
MOA:
* induces NO production in endothelium to relax smooth muscle of arterioles
* reduces peripheral vascular resistance
* reduces MAP
pharmacokinetics: well abosrbed, rapid first pass metab, tachyphylaxis
SE: HA, nausea, sweating, flushing, worse in slow ACETYLATORS (phase II metabolism); symptoms resemble LUPUS

47
Q

minoxidil

A

class: oral vasodilator
indication: HTN, hair growth (rogaine)
MOA:
* opens K+ channels in smooth muscles; stabilizes potential which will decrease likelihood to fire AP
* dilates arteries and arterioles
pharmacokinetics: well absorbed, typically rogaine
SE: HA, sweating, palpitations, tachycardia, angina, hypertrichosis (hair growth)

48
Q

nitroprusside

A

class: vasodilator
indication: HT emergency, cardiac failure
MOA:
* relaxes vascular smooth muscle
* breaks down in blood to release NO
* NO > increased cGMP > vasodilation of arteries and veins
SE:
* rapidly lowers BP
* higher rates cause toxicity: CN accumulation will occur (met acidosis, arrhythmias, death – worse in renal insufficiency patients)

**sodium thiosulfate **facilitates metabolism of cyanide

49
Q

fenoldopam

A

class: vasodilator
subclass: D1 agonist
indication: HTN emergencies, post-op HTN
MOA: peripheral arteriolar dilator; increases renal blood flow to promote diuresis

50
Q

calcium channel blockers

A

class: CCBs - vasodilators
indication: HTN, anti-anginal, anti-arrhythmic
MOA: blocks mostly L-type Ca2+ channels in the heart and inhibits Ca2+ influx in arterial smooth muscle

ex) verapamil, diltiazem, dihydropyridines (-dipines, i.e. nicardipine)

**class IV **vaughn-williams classification for arrythmia drugs

51
Q

ace inhibitors

A

class: anti-angiotensins
indication: HTN
MOA: inhibits the synthesis of angiotensin I to convert to angiotensin II by blocking the ACE enzyme
* decreaes PVR
* CO & HR are not significantly changed
* eliminated via kidneys
SE:
* severe hypotension
* teratogenic: contraindicated in pregnant women and especially those in their first trimester
* altereed sense of taste
* rashes
drug interactions:
* K+ supplements can lead to hyperK+
* NSAIDS block some effects
* DRY COUGH (d/t bradykinin build up; ACE converts bradykinin to its inactive metabolites, so inhibiting ACE would cause a build up of bradykinin

ex) -prils (i.e. captopril, lisinopril, enalapril)

52
Q

ARBs

A

class: anti-angiotensin
indication: HTN
MOA:
* ARBs block ATII from binding to receptor sites at sites where vasoconstriction would occur, as well as on the adrenal cortex where aldosterone gets secreted; by blocking vasoconstriction as well as aldosterone secretion, the overall effect is decreased PVR and decreased sodium/water retention, lowering overall BP

ex) -sartans (i.e. losartan, valsartan)

no effect on bradykinin, since ACE is not being inhibited, therefore NO cough symptoms associated

53
Q

bosentan (tracleer)

A

class: endothelin receptor antagonist
indication: PAHTN
MOA:
* blocks ET-1 from binding to ETa and ETb
* ET-1 is the active form of an endogenous product created in the lungs; normally ET-1 when bound to ETa receptors will cause vasoconstriction and increased cell proliferation
* when ET-1 is blocked from binding to ETa-Rs, there will be an increase in vasodilation in the pulmonary circulation as well as decreased cell proliferation to help with vascular remodeling
SE: HA, edema, rash, hepatotoxicity, teratogenic

54
Q

nitroglycerin

A

class: vasodilator
indication: angina, HTN
MOA:
* NO release in vascular smooth muscle
* increases guanylyl cyclase
* increases cGMP
* cGMP will dephosphorylate myosin-LC-PO4 and will be left with myosin-LC
* this will cause relaxation in the vascular smooth muscle
SE: orthostatic hypotension, syncope, HA, reflex tachycardia, hemoglobin interactions (NO2- reacts with Hgb to form methemoglobin > can cause pseudocyanosis at extremely high levels, but will ALSO have a high affinity for CN in the case of CN poisoning)

mononitrate form: isosorbide dinitrate

55
Q

digoxin

A

class: cardiac glycoside
indication: positive inotropic agent
MOA:
* blocks Na+/K+/ATPase pump
* leads to increased ICF [Na+] > lowers AP duration
* slows the NCX > increases ICF [Ca2+]
* increases more forcible contractility
SE:
* has a very low therapeutic index
* pro-arrythmogenic
* increases PR int & decreases QT int
* toxic doses = tachycardia, fibrillation, cardiac arrest
* hyperK+, hyperCa2+, and hypomg2+ can occur

56
Q

milrinone

A

class: PDE3 inhibitor
indication: HF
MOA:
* PDE3 is an enzyme that inactivates cAMP/cGMP
* when PDE3 is inhibited, increases cAMP/cGMP
* more cAMP = more foricble contraction (positive inotropic effect)
* more cGMP = more vasodilation
* also increases/prolongs Ca2+ effects

57
Q

levosimendan

A

class: calcium sensitizer
indication: positive inotropic agent; vasodilation
MOA:
* binds troponin
* stabilizes Ca2+ bound conformation
* opens K+ channels (vasodilation)
* not approved in US yet

58
Q

class I antiarrythmics

A

sodium channel blockers

works on phase 0 of the cardiac cycle

59
Q

class IA drugs (3)

A
  1. quinidine
  2. procainamide
  3. disopyramide
  • these drugs prolong AP duration
  • have an effective refractory period
  • depresses PM rate
  • lengthens QT int (2-8% Torsades de Pointes)
  • depresses conduction and excitability, especially in depolarized tissue
60
Q

class IB drug

A
  1. lidocaine
  • shortens AP duration
  • decreased ERP
  • low toxicity; high efficacy
  • acts exclusively on Na+ channel
  • suppresses abnormal cardiac activity
  • recovery from block between APs d/t rapid dissociation
  • no effect on conduction
61
Q

class IC drugs

A
  1. flecainide
  • minimnal effects on APD
  • slows dissociation; not enough sodium channels reset before next AP
  • suppresses abnormal firing channels
  • no effect on ERP (but sodium channels are still bklocked)
  • some beta blocking properties
62
Q

class II anti-arrythmics (2)

A

sympatholytics
(beta blockers)

  • suppresses ventricular ectopic depolarization
  • prevents infarction and sudden death in patients recovering from acute MI
  1. esmolol
  2. sotalol

works on phase 4 of the cardiac cycle

63
Q

class III anti-arrythmics

A

K+ channel blockers

  • prolongation of repolarization and refractoriness by increased AP duration
  1. amiodarone
    +has all V-W class effects; only categorized in class II d/t the nature of the receptors it works on
  2. dronedarone

these drugs work at phase 3 of the cardiac AP cycle

64
Q

amiodarone

A

class: potassium channel blocker
v-w class: class III antiarrythmic
indications: VT/Vfib/Afib/Aflutter
MOA:
* lengthens APs well in tachycardias
* weak CCB
* non-competitive inhibitor of beta receptors
* inhibits normal automaticity
SE:
* dilation in peripheral vasculature
* can precipitate HF; fatal in pulm fibrosis patients
* [ ] in tissues; found in almost every organ
* VERY LONG HALF LIFE

65
Q

class IV antiarrythmics

A

CCBs

  1. verapamil

MOA:
* blocks both activated/inactivated Ca2+ channels
* prolongs AV node conduction
* slows SA node
* useful in supRAventricular arrythmias
* (adenosine has become first line agent for SVT)
* can reduce ventricular rate in afib/flutters but rarely converts to NSR

these drugs work on phase 2 of the cardiac cycle

Advanced Pharm (8 decks)

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