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

What are some dihydropyridine CCBs?

amlodipine, nimodipine, nifedipine

2

What are some non-DHPR CCBs?

diltiazem, verapamil

3

greater effects on vascular smooth muscle?

amlodipine =nifedipine

4

greater effects on heart?

verapamil > diltiazem > amlodipine

5

subarachnoid hemorrhage

use nimodipine to prevent vasospasm

6

CCBs side effects?

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

7

hydralazine moA?

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

8

first line use for HTN in pregancy

hydralazine with methyldopa

9

what should be co-administered with hydralazine?

a beta blocker to prevent reflex tachycardia

10

hydralazine SEs?

reflex tachy, fluid retention, lupus like syndrome

11

nitroprusside moa?

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

12

fenoldopam moa?

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

13

nitroglycerin, isosorbide dinitrate moa

vasodilates by increasing NO in vascular smooth muscle, increase in cGMP and smooth muscle relaxation-->Dilates veins >>> arteries, decrease preload

14

b blockers contraindicated in angina?

pindolol and acebutolol--partial B agonists

15

statin effects on lipids?

--- LDL, + HDL, - TGs

16

Niacin (B3) effects on lipids?

-- LDL, ++HDL, - TGs

17

Bile acid resins lipid effect?

-- LDL, slightly increase HDL/TGs

18

ezetimibe lipid effect?

-- LDL, no effect on other lipids,

19

Fibrates lipid effect?

- LDL, + HDL, ---TGs

20

lipid lowering agent combos that cause rhabdomyolysis?

statin + fibrate; statin + niacin

21

hepatotoxic lipid lowering agents?

statains and fibrates, ezetimibe

22

red flushed face, hyperglycemia, hyperuricemia

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

23

decrease absorbtion of fat soluble vitamins, lipid lowering agent

bile acid resins

24

lipid lowering agent that causes cholesterol gall stones

fibrates, esp in conjunction with bile acid resins

25

niacin moa?

inhibits lipolysis in adipose tissue; reduces hepatic VLDL synthess

26

fibrate moa?

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

27

digoxin toxicity?

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

28

factors predisposing to digoxin tox?

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

29

Class IA antiarrythmics? Moa?

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

Class IA use?

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

31

Class IA sideeffects?

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

32

General rules for Class I antiarrhythmics?

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

class IB antiarrythmics? moa?

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

34

Class IC antiarrhthymics? moa?

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

35

Class IC use?

SVTs including afib

36

Class IC tox?

pro-arrhythmic, contraindicated post MI or structural heart disease

37

Class II antiarrhthymics? moa?

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

Class II use?

SVT, slowing ventricular rate in afib/flutter

39

B-blocker tox?

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

Class III? moa?

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

class III use?

afib/flutter; VT (amiodarone, sotalol)

42

SEs of sotalol?

torsades de points, excessive B blockade

43

SE of amiodarone? what to always check?

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

44

amiodarone can be in what classes?

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

45

Class IV antiarrthmics? moa?

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

46

Class IV use?

prevention of nodal arrythmias, rate control in afib

47

Class IV SEs?

constipation, flushing, edema

48

adenosine MOA?

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

49

adenosine use?

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

50

Mg2+ use?

torsades de pointes and digoxin tox

51

which classes are nodal blockers?

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