Cardiac Flashcards Preview

First Aid Drugs > Cardiac > Flashcards

Flashcards in Cardiac Deck (77)
Loading flashcards...
1
Q

how to treat primary hypertension

A

diuretics, ACE inhibitors, ARBs, calclium channel blockers

2
Q

should you use beta blockers in CHF

A

only if it is compensated. it is not good to use in decompensated CHF.

3
Q

drug for hypertension and diabetes

A

ACE inhibitors/ARBs- protective against diabetic nephropathy

4
Q

amlodipine, nimodipine and nifedipine

A

dihyropyridine calcium channel blocker. all end in dipine

5
Q

diltiazam and verapamil

A

non dihydropyridine calcium channel blockers

6
Q

mechanism of calcium channel blockers

A

block L type calclium channels in cardiac and smooth muscle. no issue in skeletal muscle because not dependent on calcium inflow from the outside.

7
Q

which calcium channel is best for cardiac use

A

Verapamil>diltiazam > dihydropyridine types

8
Q

uses of non dihydropyridine calcium channel blockers

A

hypertension, angina, atrial fib/flutter

9
Q

use of nimodipine specifically

A

subarachnoid hemorrage (prevents cerebral vasospasm)

10
Q

hydralazine mechanism

A

increases cGMP which leads to smooth muscle relaxation. preferentially vasodilates the arterioles >veins so it is good for afterload reduction.

11
Q

first line therapy for hypertension in pregnancy

A

hydralazine with methyldopa

12
Q

other uses of hydralazine

A

severe hypertension, CHF, give with a beta blocker to prevent reflex tachycardia

13
Q

strange toxicity to know of hydralazine

A

drug induced lupus, headache, nausea

14
Q

nitroprusside

A

used in a hypertensive emergency. short acting, increases cGMP, via direct release of NO.

15
Q

important side effect of nitroprusside

A

can cause cyanide toxicity by releasing the cyanide

16
Q

fenoldopam mechanism

A

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

17
Q

nitroglycerin mechanism

A

vasodilates- by increasing NO in vascular smooth muscle, get increased cGMP, and smooth muscle relaxation. veins> arteries so it reduces preload mostly

18
Q

uses of nitroglycerine

A

angina, pulmonary edema, acute coronary syndrome

19
Q

Monday disease

A

this is in response to exposure to nitroglycerine and other veno dilating agents. this leads to tachycardia, dizziness and headaches upon return to work on Monday with renewed exposure

20
Q

two partial beta agonists contra-indicated in angina

A

pindolol and aceutolol

21
Q

best drug to decrease LDL

A

HMG coa reductase inhibitors

22
Q

statins mechanism

A

inhibit conversion of HMG CoA to mevalonate, a cholesterol precursor

23
Q

side effects of statins

A

hepatoxociticity (increased LFTs), rhabdomyalasis when used with fibrates and niacin

24
Q

use of niacin

A

this is used to reduce LDL and it is really the only drug to effectively increase HDL.

25
Q

mechanism of niacin

A

inhibits lipolysis in adipose tissue, reducing hepatic VLDL production

26
Q

classic side effect of niacin

A

flushed face. this can be decreased by taking an aspirin or just with time

27
Q

other side effects of niacin

A

hyperglycemia and hyperuricemia (makes gout worse)

28
Q

which anti choelsterol agent actually increases triglycerides

A

bile acid resins

29
Q

effect of bile acid resins

A

decreases LDL

30
Q

mechanism of bile acid resins like choelstyramine, colestipol, colesevelam

A

decreases LDL by preventing intestinal re-absorption of bile acids. the liver must then use cholesterol to make more.

31
Q

side effects of bile acid resins

A

tastes bad, GI issues, reduced absorption of fat soluble vitamins, cholesterol gallstones

32
Q

ezetimibe

A

this is a choelsterol absorption blocker.

33
Q

mechanism of ezetimibe

A

this prevents cholesterol absorption at small intestine brush border.

34
Q

side effects of ezetimibe

A

can cause a rare increase in LFTs, and can cause dairrhea

35
Q

patient with high triglycerides, what drug to use

A

fibrates.

36
Q

mechanism of fibrates

A

increases Lipoprotein lipase to increase triglyceride clearance. also activates PPAR alpha to induce HDL synthesis.

37
Q

side effects of fibrates

A

myositis (increased risk with use of statins too), hepatotoxicit, and cholesterol gall stones

38
Q

digoxin mechanism

A

inhibits the Na/K pump which leads to inhibiton of the Na/Ca pump so there is more calclium in the cell- positive inoptrope. also stimulates the vagus nerve- decreases HR.

39
Q

clinical use of dogoxin

A

used in CHF to increase contractility and in atrial fibrilation to decrease conduction at the AV node and depress the SA node

40
Q

whats is an important factor leading to dig toxicity

A

hypokalemia. also renal failure and co-adminstration with verapamil, amiodarone and quinidine (decrease dig clearance by displacig it from tissue binding sites)

41
Q

side effects of dig

A

nausea, vomiting, yellow blurry vision, AV block, low QT, hyperkalemia

42
Q

class 1 anti arrythmics

A

block Na

43
Q

class 1a drugs

A

quinidine, procainamide and disopyramide

44
Q

side effect of quinidine

A

cinchonism (headache, tinnitus)

45
Q

side effect of procainamide

A

drug induced lupus

46
Q

side effect of disopyramide

A

heart failure

47
Q

side effects common to all 1a

A

thrombocytopenia, torsades de pointes due to QT prolongation

48
Q

class 1b drugs

A

lidocaine, mexiletine

49
Q

what is special about 1b drugs

A

preferentially affect depolarized myocytes which are those that have been damaged by an MI. they like ischemic or depolarized perkinje cells and ventricular tissue. phenytoin can also fall into this category.

50
Q

clinical use of 1b

A

ventricular arrythmias (post MI) and digitalis induced arrythmias

51
Q

class 1c drugs

A

Can I have Fries Please

1C: Flecainide and Propafenone

52
Q

mechanism of 1c

A

prolongs the refractory period but has minimal effect on action potential (unlike Class 1a and 1b)

53
Q

clinical use of 1c

A

SVTs and atrial fibrilation

54
Q

important to know about 1c

A

contraindicated in ischemic heart disease or post MI

55
Q

class 2 antiarrythmics

A

beta blockers

56
Q

beta blocker mechanism as an anti arrythmic

A

decrease SA and AV node acivitiy by decreasing cAMP and decreasing Ca current. decreases the slope of phase 4.

57
Q

when are beta blockers used

A

to slow the rate during a fib or a flutter

58
Q

beta blocker used with lipid issues

A

metoprolol

59
Q

when should you never use a beta blocker

A

in a cocaine user- can get unapposed alpha adrenergic and get serious hypertension crisis

60
Q

how to treat an overdose of beta blockers

A

glucagon

61
Q

Class III anti arrythmics

A
potassium channel blockers. AIDS
Amoiodarone
Ibutilide
Dofetilide
Solatol
62
Q

mechanism of class III

A

like class Ia, they increase the AP duration, increase effective refractory period but the slope of the Na first up part is NORMAL. also increase the QT interval

63
Q

clinical use of Class 3

A
a fib and a flutter
ventricular tachycardia (amiodarone, sotalol)
64
Q

solatol toxicity

A

torsades de pointes, excessive beta blockade

65
Q

side effect of Ibutilide

A

torsades de pointes

66
Q

side effect of amiodarone

A

pulmonary fibrosis, hepatoxocit, hypo and hyper thryoidism, corneal deposits, skin deposits (blue/gray) resulting in photodermatitis, neurologic effects, constipation, bradycardia, CHF, heart block.

67
Q

what labs do you need for amiodarone

A

PFTs, LFTs and thyroid function

68
Q

what is special about amiodarone

A

has class I, II and III and IV effects and alters the lipid membrane

69
Q

class IV anti arrythmics

A

these are calcium channel blockers

70
Q

class IV

A

verapamil, diltiazem

71
Q

mechanism of class IV

A

decrease conduction velocity, increase the effective refractory period, increase the PR interval.

72
Q

clinical use of class IV

A

prvention of nodal arrythmias (SVT) and rate control in a fib

73
Q

side effects of class IV

A

constipation, flushing, edema, CV effects

74
Q

adenosine mechanism

A

increases K+ out of the cells. hyper-polarizes the cell and decreases Ica. very short acting.

75
Q

use of adenosine

A

diagnosing and abolishing supraventricular tachycardia. very shot acting- about 15 secs. can cause flushing.

76
Q

what blocks the effect of adenosine

A

theophylline and caffeine

77
Q

clinical use of Mg2+

A

used to treat torsades de pointes and digoxin toxicity