Cardiology--Pharmacology Flashcards Preview

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Flashcards in Cardiology--Pharmacology Deck (51)
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1
Q

What are some dihydropyridine CCBs?

A

amlodipine, nimodipine, nifedipine

2
Q

What are some non-DHPR CCBs?

A

diltiazem, verapamil

3
Q

greater effects on vascular smooth muscle?

A

amlodipine =nifedipine

4
Q

greater effects on heart?

A

verapamil > diltiazem > amlodipine

5
Q

subarachnoid hemorrhage

A

use nimodipine to prevent vasospasm

6
Q

CCBs side effects?

A

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

7
Q

hydralazine moA?

A

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

8
Q

first line use for HTN in pregancy

A

hydralazine with methyldopa

9
Q

what should be co-administered with hydralazine?

A

a beta blocker to prevent reflex tachycardia

10
Q

hydralazine SEs?

A

reflex tachy, fluid retention, lupus like syndrome

11
Q

nitroprusside moa?

A

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

12
Q

fenoldopam moa?

A

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

13
Q

nitroglycerin, isosorbide dinitrate moa

A

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

14
Q

b blockers contraindicated in angina?

A

pindolol and acebutolol–partial B agonists

15
Q

statin effects on lipids?

A

— LDL, + HDL, - TGs

16
Q

Niacin (B3) effects on lipids?

A

– LDL, ++HDL, - TGs

17
Q

Bile acid resins lipid effect?

A

– LDL, slightly increase HDL/TGs

18
Q

ezetimibe lipid effect?

A

– LDL, no effect on other lipids,

19
Q

Fibrates lipid effect?

A
  • LDL, + HDL, —TGs
20
Q

lipid lowering agent combos that cause rhabdomyolysis?

A

statin + fibrate; statin + niacin

21
Q

hepatotoxic lipid lowering agents?

A

statains and fibrates, ezetimibe

22
Q

red flushed face, hyperglycemia, hyperuricemia

A

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

23
Q

decrease absorbtion of fat soluble vitamins, lipid lowering agent

A

bile acid resins

24
Q

lipid lowering agent that causes cholesterol gall stones

A

fibrates, esp in conjunction with bile acid resins

25
Q

niacin moa?

A

inhibits lipolysis in adipose tissue; reduces hepatic VLDL synthess

26
Q

fibrate moa?

A

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

27
Q

digoxin toxicity?

A

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

28
Q

factors predisposing to digoxin tox?

A

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

29
Q

Class IA antiarrythmics? Moa?

A

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

30
Q

Class IA use?

A

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

31
Q

Class IA sideeffects?

A

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

32
Q

General rules for Class I antiarrhythmics?

A

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.

33
Q

class IB antiarrythmics? moa?

A

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

34
Q

Class IC antiarrhthymics? moa?

A

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

35
Q

Class IC use?

A

SVTs including afib

36
Q

Class IC tox?

A

pro-arrhythmic, contraindicated post MI or structural heart disease

37
Q

Class II antiarrhthymics? moa?

A

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

38
Q

Class II use?

A

SVT, slowing ventricular rate in afib/flutter

39
Q

B-blocker tox?

A

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

40
Q

Class III? moa?

A

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

41
Q

class III use?

A

afib/flutter; VT (amiodarone, sotalol)

42
Q

SEs of sotalol?

A

torsades de points, excessive B blockade

43
Q

SE of amiodarone? what to always check?

A

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

44
Q

amiodarone can be in what classes?

A

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

45
Q

Class IV antiarrthmics? moa?

A

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

46
Q

Class IV use?

A

prevention of nodal arrythmias, rate control in afib

47
Q

Class IV SEs?

A

constipation, flushing, edema

48
Q

adenosine MOA?

A

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

49
Q

adenosine use?

A

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

50
Q

Mg2+ use?

A

torsades de pointes and digoxin tox

51
Q

which classes are nodal blockers?

A

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