Cardiovascular Pharmacology

Front 1

Diuretics, ACE inhibitor, angiotensin II receptor blockers, CCBs

Back 1

Primary (essential hypertension)

Front 2

Diuretics, ACE/ARBs, B-blockers (compensated), aldosterone antagonists

Back 2

Hypertension with CHF

Front 3

ACE/ARBs, CCBs, diuretics, B-blockers, alpha-blockers

Back 3

Hypertension with DM

ACE/ARBs protective against diabetic nephropathy

Front 4

Amlodipine

Nimodipine

Nifedipine (dihydropyridines)

Diltiazem

Verapamil (non-dihydropyridines)

Give drug class and mechanism

Which act on vascular? Which act on cardiac?

Back 4

CCBs

Block voltage dependent L-type calcium channels of cardiac and smooth muscle => decrease muscle contractibility

Vascular = amlodipine = nifedipine > diltiazem > verapamil

Heart = verapamil > diltiazem > amlodipine = nifedipine

Front 5

Which CCB class?

1. Hypertension, angina (including Prinzmetal), Raynaud

2. Hypertension, angina, atrial fibrillation/flutter

3. Subarachnoid hemorrhage (prevents cerebral vasospasm)

Back 5

1. Dihydropryidine (except nimodipine)

2. Non-dihydropyridine

3. Nimodipine

Front 6

Cardiac depression, AV block, peripheral edema, FLUSHING, dizziness, hyperprolactinemia, and constipation

Toxicity of which class?

Back 6

CCBs

Front 7

Increases cGMP => smooth muscle relaxation

Vasodilates arterioles > veins; after load reduction

Which drug?

Back 7

Hydralazine

Front 8

What is hydralazine used for?

Back 8

Severe hypertension, CHF.

First line therapy in pregnancy, with methyldopa.

Frequently coadministered with beta blocker to prevent reflex tachycardia

Front 9

Compensatory tachycardia (contraindicated in angina/CAD), fluid retention, nausea, headache, angina. Lupus-like syndrome

Which drug?

Back 9

Hydralazine

Front 10

Nitroprusside, nicardapine, clevidipine, labetalol, and fenoldopam. When would you use these drugs?

Back 10

Hypertensive emergency!

Front 11

Short acting; increased cGMP via DIRECT release of NO. Can cause cyanide toxicity.

Back 11

Nitroprusside

Front 12

Dopamine D1 receptor agonist => coronary, peripheral, renal, and splanchnic vasodilation => decreased BP and increased natriuresis.

Back 12

Fenoldopam

Front 13

Vasodilate by increasing NO in vascular smooth muscle => increased cGMP and smooth muscle relaxation

Dilates veins >>>> arteries. Decrease preload.

Used in angina, acute coronary syndrome, pulmonary edema

Back 13

Nitroglycerin, isosorbide dinitrate

Front 14

Reflex tachycardia (treat with B-blockers), hypotension, flushing, headache, "Monday disease" in industrial exposure: development of tolerance for vasodilating action during the work week and loss of tolerance over the weekend results in tachycardia, dizziness, and headache upon re-exposure.

Which drugs?

Back 14

Nitroglycerin, isosorbide dinitrate

Front 15

Inhibit conversion of HMG-CoA to mevalonate, a cholesterol precursor

Back 15

HMG-CoA reductase inhibitors ("statins")

Front 16

Inhibits lipolysis in adipose tissue; reduces hepatic VLDL synthesis

Back 16

Niacin (vitamin B3)

Front 17

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

Back 17

Bile acid resins (cholestyramine, colestipol, colesevelam)

Front 18

Prevent cholesterol absorption at small intestine brush border

Back 18

Cholesterol absorption blockers (ezetimibe)

Front 19

Upregulate LPL => increased TG clearance

Activates PPAR-alpha to induce HDL synthesis

Back 19

Fibrates (gemfibrozil, clofibrate, bezafibrate, fenofibrate)

Front 20

Red, flushed face, which is decreased by aspirin or long term use

Hyperglycemia (acanthosis nigricans)

Hyperuricemia (exacerbates gout)

Back 20

Niacin (B3)

Front 21

Hepatotoxicity (increased LFTs), rhabdomyolysis (esp. when used with fibrates and niacin)

Back 21

HMG-CoA reductase inhibitors ("statins")

Front 22

Rare increase in LTS, diarrhea

Back 22

Cholesterol absorption blockers (ezetimibe)

Front 23

Patient hates it--tastes bad and causes GI discomfort, decreased absorption of fat-soluble vitamins, cholesterol gallstones

Back 23

Bile acid resins (cholestyramine, colestipol, colesevelam)

Front 24

Myositis (increased risk with current statins), hepatotoxicity (increased LFTs), cholesterol gallstones (esp. with concurrent bile acid resins)

Back 24

Fibrates (gemfibrozil, clofibrate, bezafibrate, fenofibrate)

Front 25

Direct inhibition of Na+/K+ ATPase leads to direct inhibition of Na+/Ca2+ exchanger/antiport. Increased calcium concentration => positive entropy. Stimulates vagus nerve => decreases heart rate

Back 25

Cardiac glyosides

Digoxin

75% bioavailability, 20-40% protein bound, half-life = 40 hours, urinary excretion

Front 26

What drug would you use to increase contractibility in CHF? Decreased conduction at AV node and depression of SA node in atrial fibrillation?

Back 26

Digoxin

Front 27

Blurry yellow vision

Increased PR, decreased QT, ST scooping, T-wave inversion, arrhythmia, AV block

Hyper or hypokalemia

What is antidote?

Back 27

Digoxin toxicity

Digibind (anti-digoxin Fab fragments), Mg2+, normalize K+, cardiac pacer

Front 28

Slow or block (decrease) conduction (especially in depolarized cells). Decrease the slope of phase 0 depolarization and increase threshold for firing in abnormal pacemaker cells. Are state dependent (selectively depress tissue that is frequently depolarized) [tachycardia]

Back 28

Na+ channel blockers (class I)

Front 29

Quinidine, procainamide, disopyramide

Back 29

Class IA

Front 30

Increase AP duration, increase effective refractory period, increase QT interval (have effect on K+)

Back 30

Class IA drugs

Front 31

Used for both atrial and ventricular arrhythmias, especially re-entrant and ectopic SVT and VT.

Back 31

Class IA

Front 32

Cinchonism (headache, tinnitus), reversible SLE-like syndrome, heart failure, thrombocytopenia, torsades des points due to increased QT interval

Back 32

Quinidine = cinchonism

Procainamide = SLE

Front 33

What are the two class IB drugs?

Back 33

Lidocaine, mexiletine

Front 34

Decreased AP duration, preferentially affect ischemic or depolarized Purkinje and ventricular tissue. Phenytoin can also fall into this category.

Back 34

Class IB

Front 35

Used for acute ventricular arrhythmias (especially post MI), digitalis-induced arrhythmias.

Back 35

Class IB

Front 36

CNS stimulation/depression, cardiovascular depression

Back 36

Class IB

Front 37

Flecainide, propafenone. Which class?

Back 37

Class IC

Can I have Fries Please?

Front 38

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

Back 38

Class IC

Front 39

Used to treat SVTs, including atrial fibrillation. Only as last resort in refractory VT.

Back 39

Class IC

Front 40

Proarrhythmic, especially post MI (contraindicated).

Back 40

Class IC

IC is CONTRAINDICATED in structural and ischemic heart disease

Front 41

Metoprolol, propranolol, esmolol, atenolol, timolol, carvedilol. Which class?

Back 41

Class II

Beta blockers

ESMOLOL VERY SHORT ACTING

Front 42

Decrease SA and AV nodal activity by decreasing cAMP, decreasing Ca2+ currents. Suppress abnormal pacemakers by decreasing slope of phase 4.

AV node particularly sensitive, PR interval increased

Back 42

Class II

Beta blockers

Front 43

Used for SVT, slowing ventricular rate during atrial fibrillation and atrial flutter.

Back 43

Class II

Beta blockers

Front 44

Impotence, exacerbation of COPD and asthma, cardiovascular effects (bradycardia, AV block, CHF), CNS effects (sedation, sleep alterations). May mask the signs of hypoglycemia.

Back 44

Class II

Beta blockers

Front 45

What are the class III drugs?

Back 45

K+ channel blockers:

AIDS = Amiodarone, Ibutilide, Dofetilide, Sotalol

Front 46

Increase AP duration, increase ERP, used when other antiarrhythmics fail. Increased QT interval.

Back 46

Class III

Front 47

Used for atrial fibrillation, atrial flutter, ventricular tachycardia (amiodarone, sotalol)

Back 47

Class III

Front 48

Which class III causes torsades de points and excessive B blockade?

Which causes torsades de pointes?

Which causes everything... especially associated with iodine!

Back 48

Sotalol

Ibutilide

Amiodarone => check PFTs, LFTs, and TFTs, effects from all classes and alters the lipid membrane

Front 49

What are the two class IV antiarrhythmics?

Effects on conduction velocity, ERP, and PR interval?

Back 49

Verapamil, diltiazem

Decreased conduction velocity, increased ERP, increased PR interval

Front 50

What class is used for prevention of nodal arrhythmias (SVT) and rate control in atrial fibrillation?

Back 50

Class IV

Front 51

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

Back 51

Class IV toxicities

Front 52

Increased K+ out of cells => hyper polarizing the cell and decreased Ica. Drug of choice in diagnosing/abolishing supra ventricular tachycardia. Very short acting (15 seconds). Adverse effects include hypotension, chest pain, sense of impending doom. Effects blocked by theophylline and caffeine (receptor antagonists).

Back 52

Adenosine

Front 53

Effective in torsades de points and digoxin toxicity.

Back 53

Mg2+

Front 54

What beta blocker can cause dyslipidemia?

Which can cause vasospasm in Prinzmetal angina?

Can you use beta blockers with cocaine users?

What do you treat overdose with?

Back 54

Metoprolol

Propranolol

No => too much unopposed alpha-adrenergic

Glucagon