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USLME Pharmacology > Cardiovascular Pharm > Flashcards

Cardiovascular Pharm Flashcards

1
Q

Anti-arrhythmics (Na+ channel blockers) (class I) have class IA (3) class IB (2), class IC (2). List the respective drugs.

A

Class IA: Quinidine, Procainamide, Disopyramide
Class IB: Lidocaine, Mexiletine,
Class IC: Flecainide, Propafenone

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2
Q

Anti-arrhythmics class I slow or block conduction, esp in depolarized cells. It decreases slope of phase 0 depolarization and are state dependent. What does state dependent mean?

A

selectively depress tissue that is frequently depolarized, such as arrhythmic tissues since they spend more time in depolarized state.

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3
Q

List the 3 Class IA drugs, mech and clinical use.

A

Quinidine, disopyramide, procainamide

Mech: increases AP duration, increases effective refractory period, increases QT interval

Clinical use: Both atrial & ventricular arrhythmias, especially re-entrant and ectopic SVT and VT.

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4
Q

List the 3 Class IA drugs and their side effects.

A

Quinidine: cinchonism (headache, tinnitus)
Procainamide: reversible SLE-like syndrome
Disopyramide: heart failure

  • thrombocytopenia
  • torsades de pointes due to increase QT interval
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5
Q

List the 2 Class IB agents, mech of action and clinical use, and side effects

A

lidocaine, mexiletine (side note: PHENYTOIN falls under here -increases inactivation of Na+ channels for seizures)

Mech: decreases AP duration, preferentially affect ischemic or depolarized purkinje and ventricular tissue

Uses: Acute ventricular arrhythmias, digitalis-induced arryhthmias ***Best for arrhythmias post-MI

side effects: CNS stimulation/depression, cardiovascular depression

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6
Q

List the 2 Class IC agents, mech of action, and clinical use and toxicity

A

Flecainamide
Propafenone

mech: significantly prolongs ERP in AV node & accessory bypass tracts. No effect on ERP in purkinje and ventricular tissue. Minimal effect on AP duration

Clinical use: SVTs, including AF.

Toxicity: proarrhythmic, esp post-MI. “IC is contraindicated in structural and ischemic heart disease”

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7
Q

Which class of anti-arrhytmics (IB vs IC) is best post-MI and contraindicated post-MI

A

Best post-MI = IB = lidocaine, mexiletine

Contraindicated post-MI = IC = Flecainamide, Propafenone

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8
Q

List the 6 class II anti-arrhythmics and mech of activity.

A
  • metoprolol, propranolol, esmolol (very short-acting), atenolol, timolol, carvedilol
    mech: decrease SA and AV nodal activity by decreasing cAMP, decreasing Ca2+ currents. Suppress abnormal pacemakers by decreasing slope of phase 4 (funny channels/INa -affected by ANS)

AV node particularly sensitive –> increase PR interval (time from start of atrial depolarization to start of ventricular depolarization)

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9
Q

List the 6 class II anti-arryhtmics and their clinical uses

A

metoprolol, propranolol, esmolol (very short acting), atenolol, timolol, carvedilol

uses: SVT, ventricular rate control for AF and atrial flutter

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10
Q

List all the toxicities assoc with using class II anti-arrhytmics

A

metoprolol, propranolol, esmolol, atenolol, timolol, carvedilol

  • impotence
  • exacerbation of COPD and asthma (b/c antagonizes B2)
  • cardiovascular effects (bradycardia, AV block, HF)
  • CNS effects (sedation, sleep alterations)
  • dyslipidemia (METOPROLOL)
  • propranolol can exacerbate vasopasm in Prinzmetal
  • b-blockers can cause unopposed a1-agonism so don’t use alone in pheo or cocaine
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11
Q

How can glucagon treat b-blocker toxicity?

A

stimulates Gs –> increases cAMP –> Ca2+ release –> increases SA node firing

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12
Q

List the 4 class III anti-arrhythmics (K+ channel blockers) and mech of action.

A

AIDS = Amiodarone, Ibutilide, Dofetilide, Sotalol

Mech: increase AP duration, increase ERP, increase QT interval (by prolonging repolarization by blocking outward K+ conductance)

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13
Q

What are the clinical uses of class III anti-arrhytmics

A

amiodarone, ibutilide, dofetilide, sotalol

uses: AF, atrial flutter; ventricular tachycardia (amiodarone, sotalol

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14
Q

List the side effects assoc with the class III anti-arrhythmics

A

Amiodarone -pulmonary fibrosis hepatotoxicity, hypothyroidism/hyperthyroidism (b/c amiodarone is 40% iodine by weight), act as hapten (corneal deposits, blue/gray skin deposits –> photodermatitis), neuro effects, constipation, cardiovascular effects (bradycardia, heart block, HF); NO TORSADES

Ibutilide, Dofetilide - torsades de pointes

Sotalol -torsades de pointes, excessive beta blockade

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15
Q

Which anti-arrhythmic is lipophilic and has class I, II, III, IV effects?

A

amiodarone

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16
Q

List the 2 class IV anti-arrhythmics (Ca2+ channel blockers) and mech of action, side effects?

A

Verapamil, dilitazem

mech: prevention of nodal arrhythmias (SVT), and rate control in AF

side effects: constipation, flushing, edema, cardiovascular effects (HF, AV block, sinus node depression)

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17
Q

Adenosine is drug of choice for diagnosing/abolishing paroxymal supraventricular tachycardia. What is the mech of action?

A

increase K+ out of cells –> hyperpolarizing the cell and decrease ICa.

Very short acting (15 sec)

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18
Q

Which 2 drugs blunt the effects of adenosine?

A

effects blunted by theophylline (PDEI –> increases cAMP) and caffeine b/c both are adenosine receptor antagonists.

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19
Q

What are the side effects of adenosine

A

flushing, hypotension, chest pain, sense of impending doom, bronchospasm

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20
Q

What are 2 uses of Mg2+?

A

torsades de pointes

digoxin toxicity

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21
Q

Digoxin is a cardiac glycoside. What is its mech of action? Clinical use?

A
  • direct inhibition of Na+/K+ ATPase but binding K+’s spot –> ruining the out to in Na2+ [ ] graident so then the Na+/Ca2+ pump doesnt work so less Ca2+ is pumped out; more Ca2+ is in the cell –> POSITIVE INOTROPY
  • stimulates vagus nerve –> decrease HR (NEGATIVE CHRONOTROPY)

Uses: HF (increase inotropy), AF (decrease conduction at AV node & depression of SA node)

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22
Q

List toxicity of digoxin

A
  • cholinergic: N/V, diarrhea
  • blurry yellow vision
  • arrhythmias
  • AV block
  • hyperkalemia *indication of prognosis
23
Q

What are some factors that predispose to digoxin toxicity?

A
  • renal failure (decreased excretion of digoxin)
  • hypokalemia (permissive for digoxin binding at K+ binding site on Na+/K+ ATPase) ***therefore, be careful with loop and thiazides
  • verapamil, amiodarone, quinidine = displace digoxin clearance; and displace digoxin from tissue binding site increasing free digoxin)
24
Q

How to correct digoxin toxicity?

A
  • slowly normalize K+ is 1st step
  • cardiac pacer
  • digibind
  • Mg2+
25
Q

Lipid lowering agents include HMG-CoA reductase inhibitors, Bile Acid resins, Ezetimibe, Fibrates, and Niacin. Which one decreases LDL the most?

A

HMG-CoA reductase inhibitors

26
Q

Lipid lowering agents include HMG-CoA reductase inhibitors, Bile Acid resins, Ezetimibe, Fibrates, and Niacin. Which one decreases triglycerides the most?

A

fibrates (gemfibrozil, clofibrate, bezafibrate, fenofibrate)

27
Q

Lipid lowering agents include HMG-CoA reductase inhibitors, Bile Acid resins, Ezetimibe, Fibrates, and Niacin. Which one increases HDL the most?

A

Niacin

28
Q

Lipid lowering agents include HMG-CoA reductase, Bile Acid resins, Ezetimibe, Fibrates, and Niacin.

Explain MOA of HMG-CoA reductase inhibitors, its effects on LDL, HDL, triglycerides.

A

HMG-CoA reductase inhibitors are statins (lovastatin, pravastatin, -statin). They work by inhibiting conversion of HMG-CoA to mevalonate (a cholesterol precursor). Known to decrease mortality in CAD patients.

  • liver will upregulate LDL receptors to compensate for decreased endogenous cholesterol synthesis.
  • decrease LDL, slightly increase HDL, slightly decrease TGs
29
Q

What are some impt side effects of statins?

A
  • hepatotoxicity
  • myopathy (esp when used with fibrates or niacin, macrolides b/c they inhibit CYP3A4 that is used to metabolize statins)
30
Q

List the 3 bile acid resins. How do they work? TOxicity? And effects on LDL, HDL, TGs

A

cholestyramine, colestipol, colesevelam

  • prevent intestinal reabsorption of bile acids; liver must use cholesterol to make more (cholesterol –> bile acids in liver)
  • decrease LDL, slightly INCREASES both HDL and TGs

side effects: GI upset, decrease absorption of other drugs and fat-soluble vitamins

31
Q

Which is the only lipid lowering agent that causes a slight increase in TGs?

A

bile acid resins (cholestyramine, colestipol, colesevelam)

32
Q

Ezetimibe is a lipid lowering agent. How does it work? What does it do to LDL, HDL, triglycerides? List side effects

A

Ezetimibe decreases LDL, but has no effect on HDL or trigylcerides. It prevents cholesterol reabsorption at small intestine brush border.

side effects: Rare elevations in LFTs, diarrhea

33
Q

Which is the only lipid lowering agent that doesn’t affect HDL or TG levels?

A

Ezetimibe, which prevents cholesterol reabsorption at small intestine brush border.

34
Q

List the fibrates used as lipid lowering agents. MOA? Side effects? Effects on LDL, HDL, and TGs levels

A

Gemfibrozil, clofibrate, bezafibrate, fenofibrate

upregulate LPL on endothelial cells –> increase TG clearance
activates PPAR-alpha to induce HDL synthesis

It slightly decreases LDL, slighly increases HDL, and drastically reduces triglycerides

35
Q

What are some side effects of fibrates?

A
  • myopathy (increase risk with statins)

- cholesterol gallstones

36
Q

Niacin, like HMG-COA reductase inhibitors, are 2 of the 5 classes of lipid-lowering agents that work on hepatocytes. What does niacin do? What does it do to LDL, HDL, and TG levels.

A

Niacin inhibits lipolysis in adipose tissues and reduces hepatic VLDL and LDL synthesis by inhibiting conversion of cholesterol to VLDL –> IDL –> LDL

It decreases LDL, increases HDL, and decreases TGs

37
Q

What are the side effects of niacin?

A
  • red, flushed face which is decreased by giving NSAIDs therefore (prostaglandins might play a role in side effect)
  • hyperglycemia
  • hyperuricemia
38
Q

If patient is diabetic and has to be on niacin, what should one do?

A

niacin can cause hyperglycemia, so you can increase diabetic drug dosages.

39
Q

If ppl can’t tolerate statins to reduce lipids, what is 2nd choice?

A

bile acid resins (cholestyramine, colestipol, colesevelam)

40
Q

Calcium channel blockers can be separated into dihydropyridines and non-dihydropyridines. List them

A

dihydropyridines (act on vascular smooth muscle): amlodipine, clevidipine, nicardipine, nifedipine, nimodipine

non-dihydropyridines (act on heart): diltazem, verapamil

41
Q

Ca2+ channel blockers block voltage-dependent L-type calcium channels of cardiac and smooth muscle –> decrease muscle contractility.

Of the four drugs: nefidipine, amlodipine, dilitazem, verampil; rank them in terms of effect on vascular smooth muscle and then on heart

A

vascular smooth muscle:
amlodipine = nefidipine > diltizem > verapamil

heart:
verapamil > diltiazem > amlodipine = nifedipine

42
Q

What are the clinical uses of dihydropyridines?

A

Dihydropyridines (except nimodipine): HTN, angina (including Prinzmetal), Raynaud

Nimodipine: subarachnoid hemorrhage (prevents cerebral vasospasm

Clevidipine: hypertensive urgency or emergency

43
Q

Which dihydropyridine can be used for hypertensive urgency or emergency?

A

clevidipine

44
Q

Which dihydropyridine can be used for subarachnoid hemorrhage?

A

Nimodipine

45
Q

What are the 3 conditions that non-dihydropyridines can be used for?

A

HTN, angina, AF/atrial flutter

46
Q

What are some side effects assoc with Ca2+ channel blockers (both non-dihydro and dihydropyridines)?

A

-cardiac depression, peripheral edema, flushing, dizziness, constipation, gingival hyperplasia

  • AV block (non-dihydropyridines)
  • hyperprolactinemia (verapamil)
47
Q

List the 4 drugs that can be used for HTN during pregnancy

A
  • hydralazine
  • labetalol
  • methyldopa
  • nifedipine
48
Q

How does hydralazine work? Clinical use? Toxicity?

A

Hydralazine increases cGMP –> smooth muscle relaxation. It vasodilates ARTERIOLES more so than veins = afterload reduction

Uses: severe HTN (acute), HF (w/ nitrates). Frequently co-administered with beta blockers to prevent reflux tachycardia.

Toxicity: compensatory tachy (contraindicated in angina/CAD), fluid retention, headache, angina, LUPUS-LIKE syndrome

49
Q

Should you administer hydralazine on its own?

A

No, vasodilation of arterioles will decrease BP, but will have compensatory increase in HR resulting in very significant tachycardia. Co-administer with beta blockers.

50
Q

List the 5 drugs that can be used in hypertensive emergency

A 
clevidipine
fenoldopam
labetalol
nicardipine
nitroprusside
51
Q

How does nitroprusside work? What should you worry about?

A

It is short-acting, that increases cGMP via direct release of NO that will vasodilate arterioles more so than venules leading to decrease afterload. It also decreases preload by decreasing TPR. THIS IS WHY IT’S FIRST LINE TREATMENT for cardiogenic shock because it can decrease both preload and afterload.

It releases CN so be aware of cyanide toxicity. This is why nitroprusside can be co-administered with sodium thiosulfate to prevent CN toxicity.

52
Q

What is fenoldopam

A

D1 receptor agonist that can lead to coronary, peripheral, renal, and splanchnic vasodilation. Can decrease BP and increase naturiesis good in times of hypertensive emergency.

53
Q

List the 3 nitrates and mech of action, uses

A

nitroglycerin, isosorbide dinitrate, isosorbide mononitrate

MOA: vasodilate by increasing NO in vascular SM –> increase cGMP and smooth muscle relaxation
DILATE VEINS&raquo_space;> ARTERIOLES –> decrease preload

uses: angina, acute coronary syndrome, pulmonary edema

54
Q

What are some toxicities assoc with nitrate?

A
  • reflex tachy (treat w/ b blockers)
  • hypotension
  • flushing
  • headache
  • “Monday disease” due to industrial exposure to nitrates causing tolerance during the workdays, loss of tolerance over weekend, and then Monday -re-exposure –> tachycardia, dizziness, headache
  • to prevent tolerance, physicians plan nitroglycerin holidays

USLME Pharmacology (15 decks)

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