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Pharmacology > Cardiology Drugs > Flashcards

Cardiology Drugs Flashcards

1
Q

Amlodipine

A

Dihydropyridine CCB. Block voltage dependent L-type ca channels in VSM. some cardiac effects
Arterial vasodilation, decreased chronotropy and inotropy
USE: HTN, angina (+prinzmetal), raynauds,
Adverse Effects: peripheral edema, flushing dizziness

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2
Q

Clevidipine

A

Dihydropyridine CCB. Block voltage dependent L-type ca channels in VSM. some cardiac effects
Arterial vasodilation, decreased chronotropy and inotropy
USE: HTN emergency, angina (+prinzmetal), raynauds,
Adverse Effects: peripheral edema, flushing dizziness

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3
Q

Nicardipine

A

Dihydropyridine. CCB. Block voltage dependent L-type ca channels in VSM. some cardiac effects
Arterial vasodilation, decreased chronotropy and inotropy
USE: HTN emergency, angina (+prinzmetal), raynauds,
Adverse Effects: peripheral edema, flushing dizziness

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4
Q

Nifedipine

A

DihydropyridineCCB. Block voltage dependent L-type ca channels in VSM. some cardiac effects
Arterial vasodilation, decreased chronotropy and inotropy
USE: HTN, angina (+prinzmetal), raynauds,
Adverse Effects: peripheral edema, flushing dizziness
Safe in pregnancy

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5
Q

nimodipine

A

Dihydropyridine CCB. Block voltage dependent L-type ca channels in VSM. some cardiac effects
Arterial vasodilation, decreased chronotropy and inotropy
USE: SAH
Adverse Effects: peripheral edema, flushing dizziness

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6
Q

Diltiazem

A

Non-dihydropyridine CCB. Block voltage dependent L-type ca channels in cardiac muscle and somewhat in periphery (VSM). Acts on SA node and AV node
Decreases HR, Conduction, and contractility
Use: HTN, stable angina,rate control in A fib and A flutter
Adverse effects: cardiac depression, AV block, hyperprolactinemia, constipation, gingival hyperplasia

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7
Q

Verapamil

A

Non-dihydropyridine CCB. Block voltage dependent L-type ca channels in cardiac muscle. Acts on SA and AV node. most selective for cardiac muscle
Decreases HR, Conduction, and contractility
Use: HTN, stable angina,rate control in A fib and A flutter, AVNRT, migraine prophylaxis
Adverse effects: cardiac depression, AV block, hyperprolactinemia, constipation, gingival hyperplasia
CI: AVRT (WPW) - especially when WPW presents with afib, AV block

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8
Q

Nitroprusside

A

direct NO release stimulated leads to increased cGMP and thus smooth muscle relaxation.
NO specificity. Arteriole AND venous dilation. rapid acting, short duration
Uses: HTN emergency
Adverse effects: cyandide toxicity, metabolic acidosis, cardiac arrhythmia
CI: hypotension, high ICP, HCM, diastolic HF
PDE5 inhibitors

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9
Q

Nitroglycerin

A

vasoditlate by increasing NO–> icnreased cGMP–>VSM relaxation
veins»»arteries - decreases preload + minimal coronaty steal
Uses: Angina, ACS, pulmonary edema
Adverse effects: Headache, reflex tachycardia, postural hypotension, flushing
CI: RV infarct (dont want to decrease preload), PDE5 inhibitors

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10
Q

Isosorbide di+mononitrate

A

vasoditlate by increasing NO–> icnreased cGMP–>VSM relaxation
veins»»arteries - decreases preload + minimal coronaty steal
Uses: Angina, ACS, pulmonary edema, in conjunction with hydralazine for HF in african americans
Adverse effects: Headache, reflex tachycardia, postural hypotension, flushing
CI: RV infarct (dont want to decrease preload), PDE5 inhibitors

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11
Q

Avanafil

A

PDE5 inhibitor. prevents breakdown of cGMP –> potentiates NO –> profound vasodilation
Use: ED
Adverse effects: headache, flushingh, hearling loss risk
CI: NO donors

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12
Q

Sildenafil

A

PDE5 inhibitor. prevents breakdown of cGMP –> potentiates NO –> profound vasodilation
Use: ED
Adverse effects: headache, flushingh, hearling loss risk
CI: NO donors

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13
Q

Dobutamine

A

B1 agonist, some B2 effects
increases contractility
USE: HF, cardiogenic shock with maintained BP, cardiac stress test
Adverse effects: tachyarrhythmias, PVCs, HTN

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14
Q

Dopamine

A

D1>D2>B>a
icnreased contractile force, diuresis, increased PVR, increased HR
low doses mainly effect kidneys
USES: stokes adams attack, cardiac arrest, heart block,
Adverse effects: tachycardia, HTN, dysrhythmia

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15
Q

Epinephrine

A

Beta>alpha agonist
Increased inotropy, bronchodilation, widened pulse pressure (SBP up - a1, DBP down - B2), vasodilation and K+ uptake, lipolysis, glycogenolysis, decreased ileal secreations, increased renin
Use: anaphylactic shock, asthma, open angle glaucoma
Adverse effects: palpitations, HTN, tremor, anxiety
CI: nonselective b blockers, hyperthyropidism

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16
Q

Isoproterenol

A

B1=B2 agonist
increased HR, contractility, conduction decreased PVR
Uses: stokes-adams attack, cardiac arrest, heart block (often used to maintain HR in bradyarrhythmias), tachyarrhythmia eval.
Adverse effects: tachycardia, HTN, dysrhythmia

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17
Q

Midodrine

A

A1 agonist - vasoconstriction
Use: postural hypotension, ANS insufficiency
Adverse effects: black box warning: supine HTN

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18
Q

Norepinephrine

A

A1 agonist effects with some B1
vaso+venoconstriction, (increased SBO + DBP), increased contractility (B1)
Use: septic shock, hypotnesion, cardiogenic shock
Adverse effects: loss of perfusion (NE=NEcrosis)

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19
Q

Phenylephrine

A

Alpha 1 agonist
Vasoconstriction and venoconstriction, so increased BP (SBP + DBP), also nasal decongestant
USE: hypotension –>septic shock, rhinitis, cause mydriasis for eye procedures, ischemic priapism
Adverse effects: reflex bradycardia

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20
Q

Clonidine

A

Alpha 2 agonist
Decreased SNS flow –> decreased HR, decreased arterial and venous tone
Uses: HTN urgency, ADHD, tourettes
Adverse effecs: Dry mouth, sedation, depression, bradycardia, rebound HTN

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21
Q

Guanfacine

A

Alpha 2 agonist
Decreased SNS flow –> decreased HR, decreased arterial and venous tone
Uses: HTN urgency, ADHD, tourettes
Adverse effecs: Dry mouth, sedation, depression, bradycardia, rebound HTN

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22
Q

alpha-methyl dopa

A

Alpha 2 agonist
-decreased SVR
USE: HTN in pregnancy
Adverse effects: drug induced lupus, direct coombs + hemolysis

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23
Q

Prazosin

A

Alpha 1 antagonist
Use: PTSD
Adverse effects: orthostatic hypotension, reflex tachycardia

24
Q

Terazosin

A

Alpha 1 antagonist

25
Q

Prazosin

A

Alpha 1 antagonist
arterial and venous vasodilation, prostate smooth muscle relaxation
Use: PTSD, BPH, HTN
Adverse effects: orthostatic hypotension, reflex tachycardia

26
Q

Terazosin

A

Alpha 1 antagonist
arterial and venous vasodilation, prostate smooth muscle relaxation
USE: BPH, HTN

27
Q

Doxazosin

A

Alpha 1 antagonist
arterial and venous vasodilation, prostate smooth muscle relaxation
USE: BPH, HTN

28
Q

Tamulosin

A

Alpha 1 antagonist
arterial and venous vasodilation, prostate smooth muscle relaxation
USE: BPH (best osin drug for this)

29
Q

Phenoxybenazamine

A

Irreversible A1+A2 antagonist
Decreased PVR and BP
USES: pheochromocytoma (preoperatively - so volume replenishes first)

30
Q

Phentolamine

A

Reversible A1 + A2 antagonist
Decreased PVR and BP
USES: Cocaine induced HTN (NO beta blockers), patients on MAOIs who ate tyramine containing foods, Pheochromocytoma intraoperatively if needed.

31
Q

*yohimbe

A

A2 antagonist
works in CNS to increase SNS outflow to periphery
USE: ED
CI: CVD

32
Q

Drugs used in HTN emergency

A

Carvedilol, labetolol (have alpha adrenergic antagonist activity), nicardipine, clevdipine, nitroprusside, fenoldopam

33
Q

*milirone + emoximone

A

PDE3 inhibitor. increases cAMP in cardiomyocytes by preventing degredation–> Ca influx–>increased inotropy and chronotropy. Also general vasodilation because Ca inhibits MLCK activty
Use: Short term in decompensated HF
Adverse effects: arrhythmias, hypotension

34
Q

*Ranolazine

A

Inhibits late phase of Na current –> decreased diastolic wall tension and O2 consumption. No affect on HR and contractility
USES: angina refractory to other therapy
Adverse Effects: constipation, dizziness, headache, nausea, QT prolongation

35
Q 
Lovastatin
Atorvastatin
Pravastatin
Simvastatin
Rosuvastatin
Pitvastatin
Fluvastatin
A

HMG CoA reductase inhibitors
inhibits HMG-CoA conversion to mevalonate (cholesterol precursor). Increases LDL-R due to increased SBREP activity
Decreases LDL a ton and TAGs slightly
USE: dyslipidemia, hypercholesterolemia
Adverse effects: Hepatotoxicty, myopthy, rhabdomyolysis, myoglobinuria
CI: pregnant, lactating, interaction with OAT inhibitors (gemfibrozil and cyclosporine) and red yeast rice
**atorvastatin and rosuvastin have longer half lives so typically used

36
Q

Alirocumab

A

PCSK9 Inhibitor
Monoclonal Abs target PCSK9 which prevents degredation of LDL-R
Decreases LDL a ton and TAGs slightly
Adverse effects: neurocognitive effects (dementia, delirium), myalgias

37
Q

Evolocumab

A

PCSK9 Inhibitor
Monoclonal Abs target PCSK9 which prevents degredation of LDL-R
Decreases LDL a ton and TAGs slightly
Adverse effects: neurocognitive effects (dementia, delirium), myalgias

38
Q

Ezetimibe

A

Prevent cholesterol absorption at SI brush border by blocking NPC1L1 transporter
LDL-R increases (SREBP activity increases), LDL decreases but more modest because HMG-CoA reductase upregulation via SREBP
*Synergistic with statins (prevent directy cholesterol and endogenous cholesterol)
Adverse effects: diarrhea, rare increase in LFTs

39
Q

Colestipol

A

Bile acid resin
+ charged so bind - charged bile acids. Prevent intestinal reabsorption of bile acids. Liver than uses cholesterol to make more. this also increases LDL-R production via SREBP and upregulates HMG-CoA reductase. LDL decreases but slightly attenuated by upregulated HMG-CoA R
USE: lower LDL, remov digitalis from GI tract, trt bile salt accumulation in cholestasis
Adverse effects: GI upset, decreased absorption of some drugs, fat soluble vitamins
CI: pts with hypertriglyceridemia - increased bile acid production leads to icnreased hepatic TAG synthesis

40
Q

Cholestyramine

A

Bile acid resin
+ charged so bind - charged bile acids. Prevent intestinal reabsorption of bile acids. Liver than uses cholesterol to make more. this also increases LDL-R production via SREBP and upregulates HMG-CoA reductase. LDL decreases but slightly attenuated by upregulated HMG-CoA R
USE: lower LDL, remov digitalis from GI tract, trt bile salt accumulation in cholestasis
Adverse effects: GI upset, decreased absorption of some drugs, fat soluble vitamins
CI: pts with hypertriglyceridemia - increased bile acid production leads to icnreased hepatic TAG synthesis

41
Q

Colesevelam

A

Bile acid resin
+ charged so bind - charged bile acids. Prevent intestinal reabsorption of bile acids. Liver than uses cholesterol to make more. this also increases LDL-R production via SREBP and upregulates HMG-CoA reductase. LDL decreases but slightly attenuated by upregulated HMG-CoA R
USE: lower LDL, remov digitalis from GI tract, trt bile salt accumulation in cholestasis
Adverse effects: GI upset, decreased absorption of some drugs, fat soluble vitamins
CI: pts with hypertriglyceridemia - increased bile acid production leads to icnreased hepatic TAG synthesis

42
Q

Gemfibrozil

A

Fibric Acid Derivatives
Upregulates LPL, which results in icnreased TAG clearance. Also activates PPAR-alpha to induce HDL synthesis
USE: hypertriglyceridemia
Adverse effects: cholesterol gallstones (cholesterol alpha hydroxylase inhibition), oral anticoagulant potentiation, GI symptoms, myopathy
CI: renal failure, pregnancy, hepatic dysfunciton, children

43
Q

Fenofibrate

A

Fibric Acid Derivatives
Upregulates LPL, which results in icnreased TAG clearance. Also activates PPAR-alpha to induce HDL synthesis
USE: hypertriglyceridemia
Adverse effects: cholesterol gallstones (cholesterol alpha hydroxylase inhibition), oral anticoagulant potentiation, GI symptoms, myopathy
CI: renal failure, pregnancy, hepatic dysfunciton, children

44
Q

Bezafibrate

A

Fibric Acid Derivatives
Upregulates LPL, which results in icnreased TAG clearance. Also activates PPAR-alpha to induce HDL synthesis
USE: hypertriglyceridemia
Adverse effects: cholesterol gallstones (cholesterol alpha hydroxylase inhibition), oral anticoagulant potentiation, GI symptoms, myopathy
CI: renal failure, pregnancy, hepatic dysfunciton, children

45
Q

Niacin (nicotinic acid, B3)

A

inhibits lipolysios (Hormone sensitive lipase) in adipose tissue which decreases VLDL synthesis and thus decreases LDL. Also decreases TAGs because decreased transport of FFAs to liver. LPL enhanced. HDL icnreases
Adverse effects: Red flushed face (tr this with NSAIDs), pruritus, rashes, dry skin, hyperglycemia, hyperuricemia, hepatotoxicity
Not really used anymore due to side effects

46
Q

Class 1A antiarrhythmics

A

Drugs: Procainamide, Quinidine, Disopyramide
Mech: sodium channel block, some K+ block
AP change: slow upstroke, prolonged AP, QT prolongation, prolonged ERP (why its good for reentry)
Use: Artia and ventricualr arrhythmias. reentrant/ectopic SVT + VT. can terminate a Fib given IV
CI: Long QT syndrome
Adverse effects: ALL: torsades, thrombocytopenia
-Qunidine: cinchonism (headache, tinnitus)
-Procainamide: decreased PVR, reversible SLE syndrome, torsades de pointe (NAPA accumulation
-Disopyramide: HF, atropine like - urinary retention, dry mouth, blurred vision, constipation

47
Q

Class 1B antiarrhythmics

A

Drugs: Lidocaine, Mexetiline - phenytoin can fall into this category
Mech: sodium channel block. preferentially effect ischemic or depolarized ventricular tissue (because bind channels in open or inactive state -ventricles have longer AP so more likely depolarized and ischemic tissue have higher RMP that prevent transition from inactive to resting as quick)
AP change: decreased slope ) upstroke (but most modest of Class 1). shortened AP duration
Use: Post MI ventricualr arrhythmias, VT termination, prevention of V fib following cardioversion in ischemia setting, digitalis induced arrhythmias
mexelitine also used for diabetic neuropathy pain + nerve injury
NOT affective for SVT, or anything atrial
CI:
Adverse effects: CNS stimualiton/depression –>PARESTHESIA, tremor, slurred speech, convulsions

48
Q

Class 1C antiarrhythmics

A

Drugs: Flecanide, Propafenone
Mech: sodium channel block. tightest bind. prolong ERP in AV node and bypass tracts. No effect on ERP in purkinje and ventricular tissue
AP change: Largest decrease in slope of phase 0. minimal effect on duration
Use: Supraventricualr arrhythmias, A fib + flutter cardioversion
CI: post MI, in structural heart disease
Adverse effects: proarrhythmatic - especially post MI - ventricular arrhythmias

49
Q

Sotalol

A

Class 3 antiarrhythmatic
Mech: phase 2 K+ block
AP change: increase AP duration, increase ERP, increase QT interval
Use: a fib, a flutter, VT
CI:
Adverse effects: torsades, excessive beta blockade (asthma, bradycardia

50
Q

Amiodarone

A

Class 3 antiarrhythmatic
Mech: phase 2 K+ block. also some Na blocking - has effects of all the classes
AP change: prolongs AP duration, decreases slope of phase 0
Use: A fib, A flutter, VT
CI:
Adverse effects: pulmonary fibrosis, hypo/hyperthyroidism (drug is 40% iodine), acts as a hapten resulting in corneal deposits and blue/gray skin deposits - results in photodermatitis, neuro effects, constipation

51
Q

Ibutilide, Dofetilide

A

Class 3 antiarrhythmatic
Mech: phase 2 K+ block. so effect ability to respond to tachyarrhythmias, but DO NOT effect conduction velocity. reverse use dependence (so AP prolongation is most marked at slower rates rather than fast which is what is wanted)
AP change: increas AP duration, increase ERP, increase QT interval
Use: A fib, A flutter
CI: long QT syndrome
Adverse effects: Torsades de pointe (drug action is most potent at slower rates, which is when this is more likely to happen to begin with)

52
Q

Class 2 antiarrhythmatics

A

Beta blockers - metoprolol, propranolol, esmolol, atenolol, timolol, carvedilol
Mech: sympatholytic. decrease cAMP and calcium current –> decreased SA and AV node activity. AV node is particularly sensitive (increased PR interval).
AP change: decreased phase 4 slope
Use: SVT (terminate as well as prevent by suppressing pvcs), rate control in A fib and flutter
CI: WPW (uncontrolled firing in accessory path)
Adverse effects: bradycardia, AV block, HF, unopposed alpha in cocaine overdose or pheochromocytoma (except nonselective ones with some alpha effects -labetolol, carvedilol)
Overdose: trt with saline, atropine, glucagon

53
Q

Class 4 antiarrhythmatics

A

CCB: verapamil, diltiazem
Mech: calcium current blockade, slowed AP rise, and prolonged repoalrization. slows conduction in the AV (mainly) and SA node. drugs also peripheral dilate
AP change: slows conduction, increases ERP, increases PR
Use: AVNRT (SVT) rate control in A fib + flutter,
CI:WPW
Adverse effects:

54
Q

Adenosine

A

Mech:increases K+ exit out of cell (IKr), and inhibits Ca2+ and funny current. causes hyperpolarization and suppresion of Ca dependent APs. MAJORLY effects AV node specifically. Very short acting
Use: #1 for terminating SVTs.
CI:
Adverse effects:

55
Q

Magnesium

A

Cofactor for Na/K ATPase. antagonist of Ca channels.
hypomagnesia contributes to many arrhythmias.
treats torsades de pointe

56
Q

Digoxin

A

Mech: inhibits Na/K ATPase, which indirectly inhibits NCX and allows Ca to stay in the cell. ALso stimulates the vagus N
End effect: increased inotropy (Ca), decrased HR (vagus)
Use: HF, A fib (decrease conduction at AV node)
CI: renal failure, hypokalemia (allows extra drug binding), verapamil, quinidine, amiodarone
Adverse effects: cholinergic (nausea, vomiting, diarrhea, blurry yellow vision- van Gogh , arrhythmias, AV block. can cause hyperkalemia,

57
Q

Ivabradine

A

use dependent. blocks funny current in SA node and reduces HR without affecting myocardial contractility, ventricular repolarization, or intracardiac conduction. so may be good for patients with low EF

Pharmacology (7 decks)

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