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Pharmacology > Cardio drugs > Flashcards

Cardio drugs Flashcards

1
Q

What is the antihypertensive therapy for primary (essential) HTN?

A

thiazide diuretics
ACE inhibitors
ARBs
dihydropyridine Ca2+ channel blockers

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2
Q

What is the treatment therapy for HTN with HF?

A

Diuretics, ACE inhibitors/ARBs, beta-blockers (compensated HF only), aldosterone antagonists

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3
Q

What is the treatment therapy for HTN with diabetes mellitus?

A

ACE inhibitors/ARBs (protective against diabetic nephropathy), Ca2+ channel blockers, thiazide diuretics, beta-blockers

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4
Q

What is the treatment therapy for HTN in pregnancy?

A

Hydralazine, labetalol, methyldopa, nifedipine

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5
Q

What is the mechanism of Ca2+ channel blockers?

A

block voltage-dependent L-type calcium channels of cardiac and smooth muscle -> decreased muscle contractility

dihydropyridines act on smooth muscle preferentially and non-dihydropyridines act on cardiac muscle preferentially

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6
Q

Dihydropyridine Ca2+ channel blockers - examples, mechanism, clinical use and toxicity

A

Amlodipine, clevidipine, nicardipine, nifedipine, nimodipine

Mechanism: block voltage-dependent L-type calcium channels of smooth muscle preferentially (minor cardiac muscle effects)

Clinical use:
all except nimodipine - HTN, angina, Raynaud phenomenon

Nimodipine - subarachnoid hemorrhage (prevents cerebral vasospasm)

Clevidipine and nicardipine: HTN urgency or emergency (BP>180/120)

Toxicity: cardiac depression, peripheral edema, flushing, dizziness, gingival hyperplasia, reflex tachycardia

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7
Q

Non-Dihydropyridine Ca2+ channel blockers - examples, mechanism, clinical use and toxicity

A

Diltiazem, verapamil

Mechanism: block voltage-dependent L-type calcium channels of cardiac muscle preferentially

Clinical use: HTN, angina, atrial fibrillation/flutter

Toxicity: cardiac depression, AV block, peripheral edema, flushing, dizziness, hyperprolactinemia (verapamil), constipation, gingival hyperplasia

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8
Q

Hydralazine

A

Mechanism: increases cGMP -> smooth muscle relaxation. Vasodilates arterioles > veins; afterload reduction

Use: HTN (especially acute), HF (with organic nitrate). Safe to use in pregnancy. Coadministered with beta-blocker to prevent reflex tachycardia

Toxicity: reflex tachycardia (contraindicated in angina/CAD), fluid retention, HA, angina, SLE-like syndrome

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9
Q

HTN emergency drug therapy

A
  • Clevidipine (dihydropyridine Ca2+ channel blocker)
  • Fenoldopam (D1 agonist)
  • Labetalol (beta-blocker)
  • Nicardipine (dihydropyridine Ca2+ channel blocker)
  • Nitroprusside(increase NO release)
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10
Q

Nitroprusside

A

Mech: short acting; increases cGMP via direct release of NO

Use: HTN emergency

Toxicity: can cause cyanide toxicity

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11
Q

Fenoldopam

A

specific D1 receptor agonist-> increase cAMP -> coronary, peripheral, renal and splanchnic vasodilation

Use: HTN emergency

Only IV agent that decreases BP and IMPROVES renal function Decreases BP and increases natriuresis

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12
Q

nitrates

A

Nitroglycerin, isosorbide dinitrate, isosorbide mononitrate

Mechanism: increase NO in vascular smooth muscle -> increases cGMP and smooth muscle relaxation *dilates veins&raquo_space; arteries –> decreases preload

Use: angina, acute coronary syndrome, pulmonary edema

Toxicity: reflex tachycardia (treat with beta-blocker), hypotension, flushing, HA, “Monday disease” in industrial exposure

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13
Q

Beta1-selective blockers (beta1>beta2): examples, mechanism and uses

A

acebutolol (partial agonist), atenolol, betaxolol, bisoprolol, esmolol, metoprolol

Mechanism: selectively block beta1 receptors -> good for patients with co-morbid pulmonary disease since beta2 blockage causes bronchoconstriction

Use:
angina -> decreases O2 consumption bu decreasing HR and contractility (acebutolol contraindicated in angina)
MI (bisoprolol, metoprolol) -> decreases mortality
SVT (esmolol, metoprolol) -> class II antiarrhythmic, decreases AV conduction velocity
HTN -> decreases CO and renin secretion
HF

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14
Q

Beta blockers toxicity

A

Impotence
cardiovascular effects (bradycardia, AV block, HF)
CNS effects (seizures, sedation, sleep alteration)
dyslipidemia (metoprolol)
asthma/COPD exacerbations (more in nonselective beta blockers)

CONTRAINDICATED in cocaine users -> can cause unopposed alpha receptor agonist activity

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15
Q

Nonselective alpha and beta blockers

A

carvedilol, labetalol

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16
Q

Nebivolol

A

cardiac selective beta1 blockage and stimulation of beta3 which activates NO in vasculature -> vasodilation

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17
Q

HMG-CoA reductase inhibitors

A

‘statins’

Mechanism: inhibit conversion of HMG-CoA to mevalonate (cholesterol precursor)
-This causes lower LDL and increased LDL receptor expression on hepatocytes -> increased LDL-receptor-mediated endocytosis of LDL -> decreased circulating LDL

Effect: decreases LDL the most, increases HDL and decreases TGs; decreases mortality in CAD patients

Toxicity: Hepatotoxicity (increases LFTs), myopathy (especially when used with fibrates or niacin)

18
Q

Bile acid resins

A

Cholestyramine, colestipol, colesevelam

Mechanism: prevent reabsorption of bile acids -> liver uses cholesterol to make more

Effect: significantly decreases LDL, slightly increases HDL and slightly increases TGs

Toxicity: GI upset, decreased absorption of other drugs and fat-soluble vitamins

19
Q

Ezetimibe

A

Mechanism: prevents cholesterol absorption at small intestine brush border

Effect: significant reduction in LDL, no effect on HDL or TGs

Toxicity: Rare increase in LFTs, diarrhea

20
Q

Fibrates

A

Gemfibrozil, clofibrate, bezafibrate, fenofibrate

Mechanism: stimulates lipoprotein lipase -> upregulates LDL -> increased TG clearance; Activates PPAR-alpha to induce HDL synthesis

Effect: modest reduction in LDL, modest increase in HDL and huge decrease in TGs

Toxicity: myopathy (increased risk with statins), cholesterol gallstones

21
Q

Niacin (vitamin B3)

A

Mechanism:

  1. inhibits lipolysis (hormone-sensitive lipase) in adipose tissue -> reduces TGs
  2. reduces hepatic VLDL synthesis -> decreased LDL
  3. inhibits TG synthesis in liver
  4. Increases HDL levels by limiting cholesterol transfer from HDL to VLDL and slowing HDL clearance

Effect: significant reduction in LDL and increase in HDL, modest reduction in TGs

Toxicity: *Red, flushed face (decreases when used with NSAID or long-term use) from release of PGD2 -> vasodilation of skin
Hyperglycemia, hyperuricemia

22
Q

Digoxin - mechanism and uses

A

Cardiac glycoside

Mechanism: inhibits Na+/K+ ATPase -> indirectly inhibits Na+/Ca+ exchanger -> increased intracellular Ca2+-> positive inotropy. Stimulates vagus nerve (CN X) -> decreases HR

Use: HF (increases contractility), Atrial fibrillation (decreases conduction at AV node and depression of SA node)

23
Q

Digoxin toxicity, factors predisposing to toxicity and antidote

A

Toxicity:

  • Cholinergic - nausea, vomiting, diarrhea, blurry yellow vision, arrhythmias, AV block
  • Can cause hyperkalemia - poor prognosis

Factors predisposing toxicity:

  • Renal failure (decreased excretion)
  • Hypokalemia (digoxin has more ability to bind K+ site on Na+/K+ ATPase)
  • verapamil, amiodarone and quinidine decrease digoxin clearance as it displaces digoxin from binding sites

Antidote: slowly normalize K+, cardiac pacer, anti-digoxin Fab fragments, Mg2+

24
Q

Angiotensin II receptor blockers (ARBs)

A

Losartan, candesartan, valsartan

Mechanism: selectively block binding of ATII to AT1 receptor. Similar effects to ACE inhibitors but do NOT increase bradykinin

Use: HTN, HF, proteinuria or diabetic nephropathy with intolerance to ACE inhibitors (cough, angioedema)

Toxicity: hyperkalemia, decrease renal fxn, hypotension, teratogen CONTRAINDICATED in pregnancy

25
Q

What drug can provoke Prinzmetal angina and aid in its diagnosis?

A

Ergonovine (ergot alkaloid) stimulates alpha and serotonin receptors -> vasoconstriction of vascular smooth muscle

26
Q

What are the anti-arrhythmic classes?

A

Class IA-C - Na+ channel blockers
Class II - Beta blockers
Class III - K+ channel blockers
Class IV - Ca2+ channel blockers

27
Q

Class IA Antiarrhythmics

A

Quinidine, Procainamide, Disopyramide

Mechanism: Na+ channel blocker. Slows the conduction preferentially in depolarized cells State dependent -> Decreases slope of phase 0 depolarization

Increases AP duration, increases effective refractory period (ERP) in ventricular AP (also blocks K+ channels) –> increases QT interval

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

Toxicity: Torsades de pointes (increased QT interval), thrombocytopenia

28
Q

Quinidine

A

Class IA antiarrhythmetic - Na+ channel blocker; increases AP duration (decreased slope of phase 0) and increases QT interval

Use: atrial and ventricular arrhythmias, especially re-entrant and ectopic SVT and VT

Toxicity: Cinchonism**- HA, vision changes, tinnitus;
thrombocytopenia, Torsades de pointes (increased QT interval)

29
Q

Procainamide

A

Class IA antiarrhythmetic - Na+ channel blocker; increases AP duration (decreased slope of phase 0) and increases QT interval

Use: atrial and ventricular arrhythmias, especially re-entrant and ectopic SVT and VT

Toxicity: SLE-like syndrome**, thrombocytopenia, Torsades de pointes (increased QT interval)

30
Q

Disopyramide

A

Class IA antiarrhythmetic - Na+ channel blocker; increases AP duration (decreased slope of phase 0) and increases QT interval

Use: atrial and ventricular arrhythmias, especially re-entrant and ectopic SVT and VT

Toxicity: HF**, thrombocytopenia, Torsades de pointes (increased QT interval)

31
Q

Class IB Antiarrhythmics

A

Lidocaine, Mexiletine, (phenytoin)

Mechanism: Na+ channel blocker. Least strength in binding Na+ channel out of Class I antiarrhythmics. Decreases slope of phase 0 depolarization. Decreases AP duration**

Clinical use: acute ventricular tachycardias (especially post-MI since state dependent), digitalis-induced arrhythmias

Toxicity: CNS stimulation/depression, cardiovascular depression

32
Q

Class IC Antiarrhythmics

A

Flecainide, Propafenone

Mechanism: Na+ channel blocker. Strongest binding in class IC! Significantly prolongs ERP in AV node and accessory bypass tracts-> prolongs QRS at increasing HR. No effect on ERP in Purkinje and ventricular tissue. No change in AP duration.

Clinical use: Rarely used; SVTs and as last resort in refractory VT

Toxicity: NEVER GIVE IN MI-> proarrhythmic, especially post-MI; Contraindicated in structural and ischemic heart disease

33
Q

Class II Antiarrhythmics - mechanism and uses

A

Beta-blockers

Metoprolol, propranolol, esmolol, atenolol, timolol, carvedilol

Mechanism: Decreases SA and AV nodal activity by decreasing cAMP-> decreases Ca2+ current. Decreases slope of phase 4 (funny channel). –> increases PR interval (time between atrial and ventricular depolarization)

Uses: SVT, Ventricular rate control for A fib and atrial flutter

34
Q

Class II Antiarrhythmics - Toxicity

A

Toxicity: Impotence, exacerbation of COPD and asthma, cardiovascular effects, CNS effects,

  • *May mask the signs of hypoglycemia,
  • *Can cause unopposed alpha1-agonism if given alone for pheochromocytoma or cocaine toxicity

Propranolol (via beta2 blocking) can exacerbate vasospasm in Prinzmetal angina

Metoprolol - dyslipidemia (metabolized in liver)

Treat OD with saline, atropine, glucagon

35
Q

Class III Antiarrhythmics

A

Amiodarone, Ibutilide, Dofetilide, Sotalol

Mechanism: K+ channel blockers; *very prolonged repolarization * increase AP duration, increase ERP and increases QT interval with decreasing HR

Use: A fib, atrial flutter, ventricular tachycardia (amiodarone, sotalol) use as a last resort

Toxicity: risk of torsades de pointes, less risk with amiodarone

36
Q

Sotalol toxicity

A

Class III antiarrythmic

toxicity: torsades de pointes, excessive beta blockade -> bradycardia

37
Q

Amiodarone

A

Class III antiarrythmic; lipophilic –> CNS effects, has class I, II, III and IV effects

Toxicity: (less risk for torsades de pointes than other class III)

  • pulmonary fibrosis (check PFTs)
  • hepatotoxicity (check LFTs)
  • hypo/hyperthyroidism (check thyroid fxn test)
  • acts as hapten (corneal deposits, blue/gray skin deposits causing photodermititis)
  • Neruo effects
  • Constipation
  • Cardiovascular effects (bradycardia, HF, heart block)
38
Q

Class IV Antiarrhythmics

A

Verapamil, diltiazem (less potency as antiarrhythmic than verapamil bc more effect on vascular smooth muscle)

Mechanism: Ca2+ channel blocker decreases slope of phase 0 of AV node, decreases conduction velocity, increases ERP and increases PR interval (delay of AV node)

Use: prevention of nodal arrhythmias, rate control in atrial fibrillation

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

39
Q

Adenosine

A

Antiarrhythmic

Mechanism: increases K+ flux out of cells -> hyperpolarization and decreased Ca2+ current.
Decreases contractility and HR via A1 receptor, relaxes vascular smooth muscle via A2 receptor

Use: drug of choice in diagnosing/abolishing supraventricular tachycardia; very short acting

Toxicity: flushing, hypotension, chest pain* (sense of impending doom), bronchospasm

effects blunted by theophylline and caffeine

40
Q

alpha-methyldopa - mechanism, use and toxicity

A

mechanism: alpha2 agonist -> vasodilation
use: HTN in pregnancy
toxicity: Direct Coombs (+), SLE-like syndrome

41
Q

Cyanide toxicity antidote

A

Usually caused by nitroprusside infusion- rapid vasodilator for use in HTN emergency

Sodium nitrite- Promotes methemoglobin formation which combines with CN to form cyanmethemoglobin

Sodium thiosulfate- Sulfur donor to prommote hepatic rhodanese-mediated conversion of cyanide to thiocyanate -> excreted in urine

Hydroxocobalamin - Cobalt binds to intracellular CN ions and forms cyanocobalamin -> excreted in urine

Pharmacology (19 decks)

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