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Drugs > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

Primary (essential) hypertension

A

Thiazide diuretics
ACE inhibitors
ARBs
Dihydropyridine Ca2+ channel blockers

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2
Q

Hypertension w/ HF

A

ACE inhibitors/ARBs
Beta blockers (only in compensated HF, contra in cardiogenic shock)
Diuretics
Aldosterone antagonists

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3
Q

Hypertension w/ diabetes mellitus

A

ACE inhibitors/ARBs (protective against diabetic nephropathy)
Ca2+ channel clockers
Thiazide diuretics
Beta-blockers

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4
Q

Hypertension w/ pregnancy

A

Hydralazine
Labetalol
Methyldopa
Nidedipine (causes peripheral vasodilation which may cause reflex tachycardia —> useful in ptns w/ bradycardia)

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5
Q

Dihydropyridine Ca2+ channel blockers

A

Amlodipine, Clevedipine. Nicardipine, Nefedipine, Nimodipine

MOA:
Block voltage-gated L-type calcium channels of cardiac and smooth muscle —> dec. muscle contractility
Vascular smooth muscle > Heart

Use:
All except Nimodipine - Hypertension, Angina (including Prinzmetal), Raynaud phenomenon
Nimodipine - Subarachnoid hemorrhage
Clevidipine - hypertensive emergency

Adv. effects: 
Peripheral edema
Flushing
Dizziness
Gingival hyperplasia

Increased mortality and risk of MI with short acting DHPs

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6
Q

Non-dihydropyridine Ca2+ channel blockers

A

Verapamil, Diltiazem

MOA:
Block voltage-gated L-type calcium channels of cardiac and smooth muscle —> dec. muscle contractility
Slow SA and AV nodes
Heart > Vascular smooth muscle

Use:
Hypertension
Angina
Atrial fibrillation/flutter (SVT)

Adv. effects:
Cardiac depression
AV block
Hyperprolactinemia
Constipation
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7
Q

Hydrallazine

A

MOA:
Inc. cGMP —> smooth muscle relaxation
Vasodilates arterioles > veins
Afterload reduction

Use:
Severe HTN (acute) - emergency
HF (w/ organic nitrate for mortality benefit)

Safe to use during pregnancy
Co-admin with beta blocker to prevent reflex tachycardia

Adv. effects:
Compensatory tachycardia (contra in angina/CAD)
Lupus-like syndrome
Fluid retention
Headache
Angina
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8
Q

Nitroprusside

A

MOA:
Increase cGMP via direct release of NO
Short acting arterial and venous dilator

Use: Hypertensive emergency

Can cause cyanide toxicity (releases cyanide), modest tachycardia and Na- and H20 retention

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9
Q

Fenoldopam

A 
MOA: 
Dopamine D1 receptor agonist
Coronary , peripheral, RENAL, and splanchnic vasodilation
Decrease BP
Increase natriuresis

Use: Hypertensive emergency, postoperative antihypertensive

Can cause hypotension and tachycardia

Exceptionally beneficial in hypertensive patients with renal insufficiency

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10
Q

Nitrates

Nitroglycerin, Isosorbide dinitrate, isosorbide mononitrate

A

MOA:
Vasodilate by increasing NO in vascular smooth muscle —> inc. in cGMP and smooth muscle relaxation
Dilate veins&raquo_space; arteries
Decrease preload, increase peripheral venous capacitance, decrease LVEDP

Use:
Angina
Acute coronary syndrome
Pulmonary edema

Adv. effects:
Reflex tachycardia (treat w/ beta blockers)
Hypotension
Flusing
Headaches
"Monday disease"

Patients taking daily maintenance nitrates need to have a nitrate free period every day to avoid tolerance of the drug

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11
Q

Ranolazine

A

MOA:
Inhibits late phase of sodium current –> reducing diastolic wall tension and oxygen consumption
Does not affect HR or contractility

Use:
Angina refractory to other medical therapies

Adv. effects:
Constipation
Dizziness
Headache
Nausea
QT prolongation
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12
Q

HMG-CoA reductase inhibitors

statins

A

MOA:
Inhibit conversion of HMG-CoA to mevalonate (a cholesterol precursor)
Causes hepatocytes to increase their LDL receptor density

Lower LDL, Increase HDL, Slightly lower TG

Adv. effects:
Hepatotoxicty (rise in LFTs)
Myopathy (esp. when used with fibrates or niacin)

Do liver function test before starting on a statin

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13
Q

Bile acid resins

Cholestyramine, Colestipol, Colesevelam

A

MOA:
Prevent intestinal reabsorption of bile acids
Liver must use cholesterol to make more

Lower LDL, Slightly increase HDL, Slightly increase TG

Adv. effects:
GI upset
Decrease absorption of other drugs and fat-soluble vitamins

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14
Q

Ezetimibe

A

MOA:
Prevent cholesterol absorption at small intestine brush border

Lower LDL

Adv. effects:
Rare increase in LFTs (with statins)
Diarrhea

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15
Q

Fibrates

Gemfibrozil, Bezafibrate, Fenofibrate

A

MOA:
Upregulate LPL —> Inc. TG clearance
Activates PPAR-a to induce HDL synthesis –> dec. hepatic VLDL production

Lower TG, Slightly increase HDL, Slightly lower LDL

Adv. effects:
Myopathy (inc. risk with statins)
Cholesterol gallstones

mainly used to prevent pancreatitis in patients with very high TG levels

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16
Q

Niacin (vitamin B3)

A

MOA:
Inhibits lipolysis (hormone sensitive lipase) in adipose tissue
Reduces hepatic VLDL synthesis

Lower LDL, Increase HDL, Slightly lower TG

Adv. effects:
Red, flushed face (decreased by NSAIDs or long term use)
Hyperglycemia
Hyperuricemia

Used in patients who have failed other lipid lowering drugs

17
Q

Digoxin

A

MOA:
Direct inhibition of Na+/K+ ATPase –> indirect inhibition of Na+/Ca2+ exchanger.
Increase in intracellular Ca2+ —> positive inotropy
Stimulates vagus nerve —> decrease HR

Use:
HF (increase contractility)
Atrial fibrillation (decrease conduction at AV node, depression of SA node)

Adv. effects:
Cholinergic - nausea, vomiting, diarrhea, blurry yellow vision, arrhythmias, AV block, fatigue, abdominal pain, confusion and delirium
Hyperkalemia (poor prognosis)

Toxicity due to renal failure (dec. excretion), hypokalemia, drugs that displace digoxin from tissue binding sites and dec. clearance (verapamil, amiodarone, quinidine)

Antidote:
Slowly normalize K+, cardiac pacer, anto-digoxin Fab fragments, Mg2+

18
Q

Antiarrhythmics (Class IA)

Quinidine, Procainamide, Disopyramide

A

Na+ channel blockers - state dependent; modest dissoc.
Moderate K+ channel blocking activity*

MOA:
Increase AP duration
Increase effective refractory period in ventricular AP (ERP)
Increase QT interval

Use:
Both atrial and ventricular arrhythmias (esp. re-entrant and ectopic SVT and VT)

Adv. effects:
Torsades de pointes* (due to inc. QT interval)
Thrombocytopenia
HF (disopyramide)
Reversible SLE-like syndrome (procainamide)
Cinchonism (headache, tinnitus) (quinidine)

19
Q

Antiarrhythmics (Class IB)

Lidocaine, Mexiletime, Phenytoin

A

Na+ channel blockers - state dependent; fast dissoc.

MOA:
Decrease AP duration
Preferentially affect ischemic or depolarize Purkinje & ventricular tissue.

Use:
Acute ventricular arrhythmias (esp post MI*)
Digitalis-induced arrhythmias

Adv. effects:
CNS stimulation/depression
Cardio depression

20
Q

Antiarrhythmics (Class IC)

Flecainide, Propafenone

A

Na+ channel blockers - state dependent; slow dissoc.

MOA:
Sig. prolongs ERP in AV node & accessory bypass tracts
No effect - ERP in purkinje and ventricular tissue
Min. effect on AP duration

Prolong QRS duration to a greater extent at higher heart rates

Use:
SVTs -esp atrial fibrillation
Last resort in refractory VT

Adv. effects:
Proarrhythmic esp post MI

Contraindicated in structural and ischemic heart disease

21
Q

Antiarrhythmics (Class II)

metoprolol, propranolol, esmolol, atenolol, timolol, carvedilol

A

Beta-blockers

MOA:
Decrease SA and AV nodal activity (decrease cAMP. decrease Ca2+)
Decrease slope of phase 4 (suppress abnormal pacemakers)
Prolonged repolarization (at AV node)
Esmolol very short acting

Use:
SVT
Atrial fibrillation & atrial flutter ventricle rate control

Adv. effects:
Impotence
Exacerbation of COPD / asthma
Cardio effects - bradycardia, AV block, HF
Dyslipidemia (Metoprolol)
Exacerbate vasospasm in Prinzmetal (Propranolol)
Unopposed alpha agonism in pheochromocytoma or cocaine toxicity if given alone (except carvedilol & labetalol)

Treat overdose w/ saline, atropine, glucagon

22
Q

Antiarrhythmics (Class III)

Amiodarone, Ibutilide, Dofetilide, Sotalol

A

K+ channel blockers - markedly prolonged repolarization

MOA:
Increase AP duration
Increase ERP
Increase QT interval

demonstrate reverse use dependence (slower HR, more QT interval is prolonged)

Use:
Atrial fibrillation
Atrial flutter
Ventricular tachycardia (amiodarone, sotalol)

Adv. effects:
Sotalol - torsades de pointes, excessive Beta blockade
Ibutilide - torsades de pointes
Amiodarone - pulmonary fibrosis*, hepatotoxicity, hypo/hyperthyroidism, acts as a hapten (corneal blue/grey deposits resulting in photodermatitis), neurologic effects, constipation, cardio effects (bradycardia, heart block, HF)

Check PFTs, LFTs, and TFTs when using amiodarone

Amiodarone is lipophilic has class I, II, III, IV effects

23
Q

Antiarrhythmics (class IV)

Verapamil, Diltiazem

A

Ca2+ channel blockers

MOA:
Decrease conduction velocity
Increase ERP
Increase PR interval

slow rise of action potential
prolonged repolarization (at AV node)

Use:
Prevention of nodal arrhythmias (SVT)
Rate control in atrial fibrillation

Adv. effects:
Constipation
Flushing
Edema
Cardio effects (HF, AV block, sinus node depression)
24
Q

Adenosine

A

MOA:
Increased K+ out of cells —> hyperpolarizing the cell and decreasing Ica

Very short acting

DOC in diagnosing/terminating certain forms of SVT
Used for chemical stress test

Effects blunted by theophylline and caffeine (antagonists)

Adv, effects:
flushing, hypotension, chest pain, sense of impending doom, bronchospasm

25
Q

Mg2+

A

Effective in torsades de pointes & digoxin toxicity

Drugs (15 decks)

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