Cardiology Pharm - First Aid

Question 1

Hypertension in pregnancy

Answer 1

hydralazine, labetalol, methyldopa, nifedipine

Question 2

Calcium channel blockers, mechanism

Answer 2

block voltage dependent L-type calcium channels of cardiac smooth muscle, decreasing muscle contractility.

Question 3

calcium channel blockers working on vascular smooth muscle

Answer 3

amlodipine, nifedipine (class called dihydropyridines)

Question 4

calcium channel blockers acting on heart

Answer 4

diltiazem, verapamil (non-dihydropyridines)

Question 5

specific clinical uses nimodipine

Answer 5

subarachnoid hemorrhage

Question 6

dihydropiridines

Answer 6

hypertension, angina (including prinzmetal), raynauds

Question 7

Hydralazine mechanism of action

Answer 7

increases cGMP leading to smooth muscle relaxation. vasodilates arterioles > venules. reduces afterload.

Question 8

Hydralazine clinical uses

Answer 8

severe hypertension, particularly acute. safe to use in pregnancy.

Question 9

Hydralazine adverse effects

Answer 9

compensatory tachycardia (treat with beta blocker), fluid retention, headache

Question 10

Treatment of hypertensive emergency

Answer 10

nitroprusside - increases cGMP via direct release of NO. can causes cyanide toxicity

fenoldopam - dopamine D1 receptor agonist. coronary, peripheral, renal, splanchnic vasodilation. decrease BP, increases naturiesis.

nitrates - vasodilate by increasing NO in vascular smooth muscle. increase cyclic GMP leading to smooth muscle relaxation in veins&raquo_space; arteries. decrease in preload.
–> adverse effects, reflex tachycardia, treat with beta blocker.

Question 11

HMG-CoA reductase inhibitors mechanism of action

lovastatin, pravastatin

Answer 11

decrease LDL, increase HDL, decrease triglycerides. They inhibit the conversion of HMG COA to mevalonate a cholesterol precursor.

Question 12

HMG-CoA reductase inhibitors adverse effects

Answer 12

hepatotoxicity (increase LFTs), myopathy (especially when used with fibrates or niacin)

Question 13

bile acid resins mechanism of action

cholestyramine, colestipol, colesevelam

Answer 13

decrease LDL, slightly increase HDL, slightly increase triglycerides. prevent intestinal reabsorption of bile acids. liver must use cholesterol to make more bile acids.

Question 14

bile acid resins adverse effects

Answer 14

GI upset. decreased absorption of other drugs and fat soluble vitamins

Question 15

Ezetimibe mechanism of action

Answer 15

decrease cholesterol reabsorption. prevent cholesterol absorption at the brush border.

Question 16

Ezetimibe adverse effects

Answer 16

rare increas in LFTs, diarrhea

Question 17

Fibrates mechanism of action

gemfibrozil, bezafibrate, fenofibrate

Answer 17

DECREASE triglycerides. increase HDL. slight decrease in LDL. upregulate LPL to TG clearance. activates PPAR-alpha to induce HDL synthesis.

Question 18

Fibrates adverse effects

Answer 18

myopathy (increased risk with statin), cholesterol gall stones

Question 19

Niacin (Vitamin B3) mechanism of action

Answer 19

decrease LDL, increase HDL, decrease triglycerides. Inhibits lipolysis (hormone sensitive lipase) in adipose tissue, reduces hepatic VLDL synthesis.

Question 20

Niacin (Vitamin B3) adverse effects

Answer 20

red, flushed face, which can be improved with NSAIDs or long term use,
hyperglycemia
hyperuricemia

Question 21

image page 300 for lipid lowering agents

Answer 21

first aid page 300

Question 22

Digoxin mechanism of action

Answer 22

direct inhibition of Na/K ATPase –> indirect inhibition of Na/Ca exchanger. Increase Ca –> positive inotropy. Stimulates vagus nerve, decrease HR

Question 23

Digoxin adverse effects

Answer 23

cholinergic - nausea, vomiting, afib, blurry yellow vision, arrhythmias, AV block,
–> can lead to hyperkalemia, poor prognosis.
factors predisposing to toxicity: renal failure leading to decreased excretion, hypokalemia

Question 24

Antiarrhythmics - class I mechanism of action

Answer 24

sodium channel blockers. they slow or block conduction especially in depolarized cells. they decrease slope of phase 0.

Question 25

Class IA drugs

Answer 25

Quinidine, procainamide, disopyramide

Question 26

Class IA mechanism of action

Answer 26

Increase AP duration, increase effective refractory period in ventricular action potential, increase QT interval.

Question 27

Class IB drugs

Answer 27

lidocaine, mexiletine

Question 28

Class IB mechanism of action

Answer 28

decrease AP duration, preferentially affect ischemic or depolarized purkinje and ventricular tissue.

Question 29

Class IC drugs

Answer 29

flecainide, propafenone

Question 30

Class IC mechanism of action

Answer 30

significantly prolongs effective refractory period in AV and accessory bypass tracts. No effect on ERP in purkinje and ventricular tissue. Minimal effect on action potential duration.

Question 31

Antiarrhythmics - class II beta blocker - mechanism of action

Answer 31

decrease SA and AV nodal activity by decreasing cyclic AMP, decreasing Ca currents.

Question 32

Antiarrhythmics - class II beta blocker - clinical use

Answer 32

SVT, ventricular rate control for afib, atrial flutter

Question 33

Antiarrhythmics - class II beta blocker - adverse effects

Answer 33

impotence, exacerbation of COPD and asthma, cardiovascular effects (Av block, bradycardia, heart failure), CNS effects (sedation, sleep alterations), unopposed alpha antagonism if given with pheo or cocaine toxicity, Tx of beta blocker overdose with saline, atropine, glucagon.

Question 34

Antiarrhythmics - class III potassium channel blockers - mechanism of action

Answer 34

amiodarone, ibutiide, dofetilide, sotalol | --> increase AP duration, increased effective refractory period, increased QT interval.

Question 35

Antiarrhythmics - class III potassium channel blockers - clinical use

Answer 35

afib, a flutter, ventricular tachycardia

Question 36

Antiarrhythmics - class III potassium channel blockers - amiodarone adverse effects

Answer 36

pulmonary fibrosis, hepatotoxicity, hypothyroidism/hyperthyroidism, acts as hapten leading to corneal deposits. --> check PFTs, LFTs, TFTs.

Question 37

Antiarrhythmics - class IV calcium channel blockers - mechanism of action

Answer 37

verapamil, diltiazem | --> decrease conduction velocity, increase effective refractory period, increase PR interval.

Question 38

Antiarrhythmics - class IV calcium channel blockers - clinical use

Answer 38

prevention of nodal arrhythmias (SVT), rate control for afib.

Question 39

Antiarrhythmics - class IV calcium channel blockers - adverse effects

Answer 39

constipation, flushing, edema