Cardiology--Pharmacology

Question 1

What are some dihydropyridine CCBs?

Answer 1

amlodipine, nimodipine, nifedipine

Question 2

What are some non-DHPR CCBs?

Answer 2

diltiazem, verapamil

Question 3

greater effects on vascular smooth muscle?

Answer 3

amlodipine =nifedipine

Question 4

greater effects on heart?

Answer 4

verapamil > diltiazem > amlodipine

Question 5

subarachnoid hemorrhage

Answer 5

use nimodipine to prevent vasospasm

Question 6

CCBs side effects?

Answer 6

cardiac depression, AV block, peripheral edema, flushing, dizziness, hyperprolactinemia, constipation

Question 7

hydralazine moA?

Answer 7

increases cGMP–>smooth muscle relaxation, vasodilates arterioles > veins, afterload reduction

Question 8

first line use for HTN in pregancy

Answer 8

hydralazine with methyldopa

Question 9

what should be co-administered with hydralazine?

Answer 9

a beta blocker to prevent reflex tachycardia

Question 10

hydralazine SEs?

Answer 10

reflex tachy, fluid retention, lupus like syndrome

Question 11

nitroprusside moa?

Answer 11

short acting, increases cGMP via direct release of NO, can cause cyanid toxicity

Question 12

fenoldopam moa?

Answer 12

D1 receptor agonist–>coronary, peripheral, renal, splanchnic vasodilation, decreases BP and increases natriuresis

Question 13

nitroglycerin, isosorbide dinitrate moa

Answer 13

vasodilates by increasing NO in vascular smooth muscle, increase in cGMP and smooth muscle relaxation–>Dilates veins&raquo_space;> arteries, decrease preload

Question 14

b blockers contraindicated in angina?

Answer 14

pindolol and acebutolol–partial B agonists

Question 15

statin effects on lipids?

Answer 15

— LDL, + HDL, - TGs

Question 16

Niacin (B3) effects on lipids?

Answer 16

– LDL, ++HDL, - TGs

Question 17

Bile acid resins lipid effect?

Answer 17

– LDL, slightly increase HDL/TGs

Question 18

ezetimibe lipid effect?

Answer 18

– LDL, no effect on other lipids,

Question 19

Fibrates lipid effect?

Answer 19

• LDL, + HDL, —TGs

Question 20

lipid lowering agent combos that cause rhabdomyolysis?

Answer 20

statin + fibrate; statin + niacin

Question 21

hepatotoxic lipid lowering agents?

Answer 21

statains and fibrates, ezetimibe

Question 22

red flushed face, hyperglycemia, hyperuricemia

Answer 22

Niacin, decrease flushing by aspirin, possibly a prostaglandin mediated effect

Question 23

decrease absorbtion of fat soluble vitamins, lipid lowering agent

Answer 23

bile acid resins

Question 24

lipid lowering agent that causes cholesterol gall stones

Answer 24

fibrates, esp in conjunction with bile acid resins

Question 25

niacin moa?

Answer 25

inhibits lipolysis in adipose tissue; reduces hepatic VLDL synthess

Question 26

fibrate moa?

Answer 26

upregulate LPL–>increase TG clearance, activates PPAR-alpha to induce HDL synthesis

Question 27

digoxin toxicity?

Answer 27

cholinergic, eKG: increased PR, decreased QT, ST scooping, T wave inversion, arrhythmia, AV block; hyperkalemia–poor prognosis;

Question 28

factors predisposing to digoxin tox?

Answer 28

renal failure, hypokalemia (permissive for digoxin binding to Na/K ATPase K+ binding site); verapamil, amiodarone, quinidine (decreases clearance)

Question 29

Class IA antiarrythmics? Moa?

Answer 29

quinidine, procainable, disopyramide; block Na channels, affects phase 0 depolarization and phase 3 repolarization–>increased AP duration, increased effective refractory period, increases QT interval

Question 30

Class IA use?

Answer 30

both atrial and ventricular arrythmias esp re-entrant and ectopic SVT and VT (like WPW)

Question 31

Class IA sideeffects?

Answer 31

cinchonism (headache, tinnitus) with quinidine, reversible SLE like syndrome with procainamide, heart failure with disopyramide, thrombocytopenia, torsades de pointes due to prolonged QT

Question 32

General rules for Class I antiarrhythmics?

Answer 32

All are Na channel blockers. all decrease slope of phase 0 depolarization and increased firing threshold in abnormal pacemaker cells. State dependent. Hyperkalemia increases tox for all class I drugs.

Question 33

class IB antiarrythmics? moa?

Answer 33

lidocaine, mexiletine; decrease AP duration, blocks Na in very rapidly depolarizing cells, preferentially affects ischemic/depolarized purkinje and ventricular tissue

Question 34

Class IC antiarrhthymics? moa?

Answer 34

Flecainide, Propafenone; significant prolongs refractory period in AV node, no effect on AP duration

Question 35

Class IC use?

Answer 35

SVTs including afib

Question 36

Class IC tox?

Answer 36

pro-arrhythmic, contraindicated post MI or structural heart disease

Question 37

Class II antiarrhthymics? moa?

Answer 37

B blockers, decrease SA/AV nodal activity by decreasing cAMP/Ca currents. Suppresses abnormal pacemakers by decreasing slope of phase 4; AV node particularly sensitive

Question 38

Class II use?

Answer 38

SVT, slowing ventricular rate in afib/flutter

Question 39

B-blocker tox?

Answer 39

exacerbate COPD/asthma, sedation/sleep alteration, may mask signs of hypoglycemia, metoprolol can cause dyslipidemia, propanolol can exacerbate prinzmetals angina, tx overdose w/ glucagon

Question 40

Class III? moa?

Answer 40

amiodarone, ibutilide, dofetilide, sotalol; blocks K efflux, increases AP length w/out affects Na or Ca–>increases AP duration, prolonged QT; used when other drugs fail

Question 41

class III use?

Answer 41

afib/flutter; VT (amiodarone, sotalol)

Question 42

SEs of sotalol?

Answer 42

torsades de points, excessive B blockade

Question 43

SE of amiodarone? what to always check?

Answer 43

PFTS, LFTs, TFTs; pulmonary fibrosis, liver tox, hyper/po thyroidism, corneal deposits, blue gray skin deposits–>photodermatitis; neurologic effects, constipation, CV effects

Question 44

amiodarone can be in what classes?

Answer 44

class I, 2, 3, and 4 and affects lipid membrane.

Question 45

Class IV antiarrthmics? moa?

Answer 45

CCBs, verapamil, diltiazem; decrease conduction velocity, increase ERP/PR interal

Question 46

Class IV use?

Answer 46

prevention of nodal arrythmias, rate control in afib

Question 47

Class IV SEs?

Answer 47

constipation, flushing, edema

Question 48

adenosine MOA?

Answer 48

increases K flux out of cells–>hyperpolarizing cell and decreaseing Ica

Question 49

adenosine use?

Answer 49

drug of choice in diagnosing/abolishing SVTs, very short half life (15 sec)–can cause hypotension/chest pain

Question 50

Mg2+ use?

Answer 50

torsades de pointes and digoxin tox

Question 51

which classes are nodal blockers?

Answer 51

class II (beta blockers), class IV (CCBs)