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USMLE Pharmacology > Cardiovascular > Flashcards

Cardiovascular Flashcards

1
Q

Tx primary (essential) HTN

A

Diuretics
ACEI
ARBs
CCBs

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2
Q

Tx HTN with CHF

A

Diuretics
ACEI/ARBs
B-blockers (compensated CHF)
Aldosterone antagonists (spironolactone)

B-blockers contraindicated in cardiogenic shock

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3
Q

Tx HTN with DM

A 
ACEI/ARBs = protective against diabetic neuropathy
CCBs
Diuretics
B-blockers
a-blockers
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4
Q

Dihydropyridine CCBs (3)

A

Amlodipine
Nimodipine
Nifedipine

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5
Q

Non-dihydropyridine CCBs (2)

A

Diltiazem

Verapamil

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6
Q

CCBs

A

Block voltage-dependent L-type Ca channels of cardiac and smooth muscle = reduce muscle contractility

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7
Q

CCB effect on vascular smooth muscle

___ = ___ > ___ > ___

A

amlodipine = nifedipine > diltiazem > verapamil

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8
Q

CCB effect on heart

___ > ___ > ___ =

A

verapamil > diltiazem > amlodipine = nifedipine

verapamil = ventricle

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9
Q

Dihydropyridine use (except nimodipine)

A

HTN
Angina (including Prinzmetal)
Raynaud phenomenon

Nimodipine = subarachnoid hemorrhage (prevents cerebral vasospasm)

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10
Q

Non-dihydropyridine use

A

HTN
Angina
Atrial fibrillation/flutter

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11
Q

Hydralazine

A

Increases cGMP = smooth muscle relaxation
Vasodilates arterioles > veins
AFTERLOAD reduction

Severy HTN, CHF
First line HTN in pregnancy (with methyldopa)
Coadmin with B-blocker to prevent reflex tachycardia

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12
Q

Hydralazine toxicity

A

Compensatory tachycardia (contraindicated in angina/CAD)
Fluid retention
Nausea, headache, angina
Lupus-like syndrome

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13
Q

Tx hypertensive emergency

A 
Nitroprusside
Nicardipine
Clevidipine
Labetalol
Fenoldopam
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14
Q

Nitroprusside

A

Short acting
Increases cGMP via direct release of NO
Cyanide toxicity (releases cyanide)

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15
Q

Fenoldopam

A

Dopamine D1 receptor agonist = coronary, peripheral, renal, and splanchnic vasodilation
Decreases BP and increases natriuresis

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16
Q

Nitroglycerin, isosorbide dinitrate

A

Vasodilate by increasing NO in vascular smooth muscle = increase in cGMP and smooth muscle relaxation
Dilates veins&raquo_space; arteries
Decreases PRELOAD

Tx angina, acute coronary syndrome, pulmonary edema

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17
Q

Nitroglycerin, isosorbide dinitrate toxicity

A

Reflex tachycardia (treat with B-blockers)
Hypotension, flushing, headach
“Monday disease” = industrial exposure; tolerance for vasodilating action during work week and loss of tolerance over weekend leads to tachycardia, dizziness, and headache upon reexposure

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18
Q

What are 4 determinants of myocardial O2 consumption (MVO2)?

A

End-diastolic volume
Blood pressure
Heart rate
Contractility

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19
Q

Lipid lowering drug classes (5)

A

HMG-CoA reductase inhibitors (statins)
Niacin (vitamin B3)
Bile acid resins (cholestyramine, colestipol, colesevelam)
Cholesterol absorption blockers (ezetimibe)
Fibrates (gemfibrozil, clofibrate, bezafibrate, fenofibrate)

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20
Q

Lovastatin, pravastatin, simvastatin, atorvastatin, rosuvastatin
MOA
SE (3)

A

HMG-CoA reductase inhibitors
Inhibit conversion of HMG-CoA to mevalonate (cholesterol precursor)

Hepatotoxicity (increased LFTs)
Rhabdomyolysis (esp when used with FIBRATES and NIACIN)
Myalgias

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21
Q

Niacin
MOA
SE (3)

A

Vitamin B3
Inhibits lipolysis in adipose tissue; reduces hepatic VLDL synthesis

Red, flushed face (decreased by ASA)
Hyperglycemia (acanthosis nigricans)
Hyperuricemia (exacerbates gout)

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22
Q

Cholestyramine, colestipol, colesevelam
MOA
SE (4)

A

Bile acid resins
Prevent intestinal reabsorption of bile acids; liver must use cholesterol to make more

Bad taste
GI discomfort
Decreased absorption of fat-soluble vitamins
Cholesterol gallstones

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23
Q

Ezetimibe
MOA
SE (2)

A

Cholesterol absorption blocker
Prevents cholesterol absorption at small intestine brush border

Rare increase in LFTs
Diarrhea

24
Q

Gemfibrozil, clofibrate, bezafibrate, fenofibrate
“fib”
MOA
SE (3)

A

Fibrates
Upregulate LPL = increased TG clearance
Activates PPAR-a to induce HDL synthesis

Myositis (increased risk with concurrent STATINS)
Hepatotoxicity (increased LFTs)
Cholesterol gallstones (esp with concurrent BILE ACID RESINS)

25
Q

Statin effects

A

Decrease (3) LDL
Increase (1) HDL
Decrease (1) triglycerides

26
Q

Niacin effects

A

Decrease (2) LDL
Increase (2) HDL
Decrease triglycerides

27
Q

Bile acid resin effects

A

Decrease (2) LDL
Slightly increase HDL
Slightly INCREASE TRIGLYCERIDES

28
Q

Cholesterol absorption blocker effects

A

Decrease (2) LDL

No effect on HDL or triglycerides

29
Q

Fibrate effects

A

Decrease (1) LDL
Increase (1) HDL
DECREASE (3) TRIGLYCERIDES

30
Q

Digoxin

A

Cardiac glycoside
Direct inhibition of Na/K ATPase = indirect inhibition of Na/Ca exchanger/antiport
Increased Ca concentration = positive inotropy
Stimulates vagus nerve to decrease HR

31
Q

Digoxin toxicity

A 
Cholinergic = n/v/d, blurry yellow vision
ECG = increased PR, decreased QT, ST scooping, T wave inversion, arrhythmia, AV block
Hyperkalemia = poor prognosis
32
Q

Factors predisposing to digoxin toxicity

A

Renal failure (decreased excretion)
Hypokalemia (permissive for digoxin binding at K binding site on Na/K ATPase)
Verapamil, amiodarone, quinidine (decrease clearance; displace digoxin from tissue binding sites)

33
Q

Digoxin antidote

A

Normalize K, cardiac pacer, anti-digoxin Fab fragments, Mg

34
Q

Class I antiarrhythmics

A

Na channel blockers
Slow or block conduction
Decrease slope of phase 0 depolarization and increase threshold for firing in abnormal pacemaker cells
Hyperkalemia causes increased toxicity

35
Q

Class IA

Na blockers

A

Quinidine
Procainamide
Disopyramide

INCREASE AP duration, effective refractory period, and QT interval (risk torsades)

36
Q

Quinidine, Procainamide, Disopyramide

Class and Toxicity

A

Class IA = Na channel blockers
CINCHONISM (headache, tinnitus with quinidine)
Reversible SLE like syndrome (procainamide)
Heart failure (disopyramide)
Thrombocytopenia
Torsades de pointes due to increase QT interval

37
Q

Class IB

Na blockers

A 
Lidocaine
Mexiletine
(Phenytoin can also fall into category)

DECREASE AP duration
Preferentially affect ischemic or depolarized Purkinje and ventricular tissue
Best for post-MI

38
Q

Lidocaine, Mexiletine

Class and toxicity

A

Class IB = Na channel blockers
CNS stimulation/depression
Cardiovascular depression

39
Q

Class IC

A

Flecainide
Propafenone

Significantly prolongs refractory period in AV node
Minimal effect on AP duration

40
Q

Flecainide, Propafenone

Class and toxicity

A

Class IC

Proarrhythmic, especially post-MI (contraindicated in structural and ischemic heart disease)

41
Q

Class II antiarrhythmics

A

Beta-blockers
Decrease SA and AV nodal activity by decreasing cAMP and Ca currents
Suppress abnormal pacemakers by decreasing slope of phase 4 (nodal tissue)
AV node particularly sensitive

42
Q

Class II B-blockers

A 
Metoprolol
Propranolol
Esmolol
Atenolol
Timolol
Carvedilol
43
Q

B-blocker toxicity

A

Impotence
Exacerbation of COPD and asthma
Cardiovascular effects (bradycardia, AV block, CHF)
CNS effects (sedation, sleep alterations)
May MASK SIGNS of HYPOGLYCEMIA
Metoprolol = dyslipidemia
Propranolol = exacerbate vasospasm in Prinzmetal angina
Contraindicated in COCAINE users (risk of unopposed a-adrenergic receptor agonist activity)

44
Q

B-blocker antidote

45
Q

Class III antiarrhythmics

A

K channel blockers
Increase AP duration and effective refractory period
Used when other antiarrhythmics fail
Increase QT interval (risk torsades)

46
Q

Class III K channel blockers

A

Amiodarone
Ibutilide
Dofetilide
Sotalol

47
Q

Amiodarone, Ibutilide, Dofetilide, Sotalol

Class and toxicity

A

Class III K channel blockers
Sotalol = torsades de pointes, excessive B blockade
Ibutilide = torsades de pointes
Amiodarone = pulmonary fibrosis, hepatotoxicity, hypothyroidism/hyperthyroidism (amiodarone is 40% iodine), corneal deposits, skin deposits (blue/gray) resulting in photodermatitis, neurologic effects, constipation, cardiovascular effects (bradycardia, heart block, CHF)

48
Q

What tests should you always check when using amiodarone?

A

PFTs
LFTs
TFTs

Amiodarone has class I, II, III, and IV effects and alters the lipid membrane

49
Q

Class IV antiarrhythmics

A

Ca channel blockers
Decrease conduction velocity
Increase effective refractory period and PR interval

Slow rise of action potential (phase 0 nodal)
Prolonged repolarization (at AV node)
50
Q

Class IV Ca channel blockers

A

Verapamil
Diltiazem

Non-dihydropyridine

51
Q

Verapamil, Diltiazem

Class and toxicity

A

Class IV non-dihydropyridine CCBs

Constipation, flushing, edema, CV effects (CHF, AV block, sinus node depression)

52
Q

Adenosine

A

Increase K out of cells = hyperpolarize cell and decrease Ca current
Drug of choice = supraventricular tachycardia dx/tx
Short acting = 15 seconds

53
Q

Adenosine adverse effects

A

Flushing
Hypotension
Chest pain

Effects blocked by theophylline and caffeine

54
Q

Magnesium is effective in the treatment of which two conditions?

A

Torsades de pointes

Digoxin toxicity

55
Q

Drugs prolonging QT interval

“Some Risky Meds Can Prolong QT”

A 
Sotalol
Risperidone (antipsychotics)
Macrolides
Chloroquine
Protease inhibitors (-navir)
Quinidine (class Ia; also class III)
Thiazides
56
Q

Treatment for torsades de pointes

A

Magnesium sulfate

USMLE Pharmacology (15 decks)

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