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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
Statin effects
Decrease (3) LDL Increase (1) HDL Decrease (1) triglycerides
26
Niacin effects
Decrease (2) LDL Increase (2) HDL Decrease triglycerides
27
Bile acid resin effects
Decrease (2) LDL Slightly increase HDL Slightly INCREASE TRIGLYCERIDES
28
Cholesterol absorption blocker effects
Decrease (2) LDL | No effect on HDL or triglycerides
29
Fibrate effects
Decrease (1) LDL Increase (1) HDL DECREASE (3) TRIGLYCERIDES
30
Digoxin
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
Digoxin toxicity
``` Cholinergic = n/v/d, blurry yellow vision ECG = increased PR, decreased QT, ST scooping, T wave inversion, arrhythmia, AV block Hyperkalemia = poor prognosis ```
32
Factors predisposing to digoxin toxicity
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
Digoxin antidote
Normalize K, cardiac pacer, anti-digoxin Fab fragments, Mg
34
Class I antiarrhythmics
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
Class IA | Na blockers
Quinidine Procainamide Disopyramide INCREASE AP duration, effective refractory period, and QT interval (risk torsades)
36
Quinidine, Procainamide, Disopyramide | Class and Toxicity
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
Class IB | Na blockers
``` 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
Lidocaine, Mexiletine | Class and toxicity
Class IB = Na channel blockers CNS stimulation/depression Cardiovascular depression
39
Class IC
Flecainide Propafenone Significantly prolongs refractory period in AV node Minimal effect on AP duration
40
Flecainide, Propafenone | Class and toxicity
Class IC | Proarrhythmic, especially post-MI (contraindicated in structural and ischemic heart disease)
41
Class II antiarrhythmics
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
Class II B-blockers
``` Metoprolol Propranolol Esmolol Atenolol Timolol Carvedilol ```
43
B-blocker toxicity
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
B-blocker antidote
Glucagon
45
Class III antiarrhythmics
K channel blockers Increase AP duration and effective refractory period Used when other antiarrhythmics fail Increase QT interval (risk torsades)
46
Class III K channel blockers
Amiodarone Ibutilide Dofetilide Sotalol
47
Amiodarone, Ibutilide, Dofetilide, Sotalol | Class and toxicity
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
What tests should you always check when using amiodarone?
PFTs LFTs TFTs Amiodarone has class I, II, III, and IV effects and alters the lipid membrane
49
Class IV antiarrhythmics
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
Class IV Ca channel blockers
Verapamil Diltiazem Non-dihydropyridine
51
Verapamil, Diltiazem | Class and toxicity
Class IV non-dihydropyridine CCBs | Constipation, flushing, edema, CV effects (CHF, AV block, sinus node depression)
52
Adenosine
Increase K out of cells = hyperpolarize cell and decrease Ca current Drug of choice = supraventricular tachycardia dx/tx Short acting = 15 seconds
53
Adenosine adverse effects
Flushing Hypotension Chest pain Effects blocked by theophylline and caffeine
54
Magnesium is effective in the treatment of which two conditions?
Torsades de pointes | Digoxin toxicity
55
Drugs prolonging QT interval | "Some Risky Meds Can Prolong QT"
``` Sotalol Risperidone (antipsychotics) Macrolides Chloroquine Protease inhibitors (-navir) Quinidine (class Ia; also class III) Thiazides ```
56
Treatment for torsades de pointes
Magnesium sulfate

USMLE Pharmacology (15 decks)

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