Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

STEP 1 (2) > Cardiovascular Pharm > Flashcards

Cardiovascular Pharm Flashcards

1
Q

How should HTN in pregnancy be tx?

A

-hydralazine, labetalol, methyldopa, nifedipine

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the dihydropyridine CCBs (act on peripheral smooth muscle)?

A

-ipines (e.g. amlodipine, nifedipine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the non-dihydropyridine CCBs (act on heart)?

A

verapamil and diltiazem

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How do CCBs work?

A

they block voltage-dependent L-type Ca2+ channels of muscle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How does hydralazine work?

A

it increases cGMP to cause smooth muscle relaxation and vasodilates arterioles to reduce afterload for tx of HTN

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

T or F. Hydralazine is safe in pregnancy

A

T.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is hydralazine usually given with?

A

a BB to prevent reflex tachycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How does nitroprusside work?

A

it is short acting and increases cGMP via direct release of NO

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

The main toxicity of nitroprusside is _____

A

cyanide poisoning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How does fenoldopam help in HTN crises?

A

it is a dopamine D1 agonist that causes coronary, peripheral, renal, and splanchnic vasodilation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are some common nitrates?

A

-nitroglycerin, isosorbide dinitrate, isosorbide mononitrate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How do nitrates work?

A

vsaodilate by increasing NO in vascular SM increasing cGMP and predominantly working in VEINS (over arteries) to decrease preload

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What are the main uses of nitrates?

A

angina, pulmonary edema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the AEs of nitrates?

A
  • reflex tachycardia (give with a BB)
  • hypotension
  • flushing, HA
  • tachyphlyaxis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the goal of antianginal therapy?

A

reduction of myocardial O2 consumption by decreasing either end-diastolic volume, BP, HR, or contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What determinants of angina do nitrates affect?

A

decrease end-diastolic volume, BP, ejection time, and MVO2

increase HR

dont affect contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What determinants of angina do BBs affect?

A

decrease end-diastolic volume, BP, Contractility, HR, and MVO2

increase ejection time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What determinants of angina do BBs AND Nitrates affect?

A

no effect on end-diastolic volume, contractility, HR, or ejection time

decreased BP

**drastically decrease MVO2**

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What are some HMG-CoA reductase inhibitors?

A
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

How do statins affect LDL, HDL, and triglycerides?

A

LDL- reduced

HDL- increased

TAGs- decreased

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How do statins work?

A

they inhibit conversion of HMG-CoA ro mevalonate, a cholesterol precursor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What are the AEs of STATINs?

A

elevated LFTs

myopathy when used with fibrates or niacin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are some bile acid resins used to decrease cholesterol uptake?

A

cholestyramine, colestipol

colesevelam

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How do bile acid resins affect LDL, HDL, and triglycerides?

A

LDL- decrease

HDL and TAGs- slightly increase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How does Ezetimibe work?

A

it prevents cholesterol absorption at the small intestine brush border (only affects LDL- decreases)

26
Q

What are the fibrates?

A

gemfibrozil

clofibrate, bezafibrate, fenofibrate

27
Q

How do fibrates affect LDL, HDL, and TAGs?

A

LDL- decrease

HDL- increase

TAGs- greatly decrease

28
Q

How do fibrates work?

A

they upregulate LPL to increase TAG clearance and

activate PPARa to induce HDL synthesis

29
Q

How does niacin work?

A

inhibits lipolysis in adipose tissue and reduces hepatic VLDL synthesis to decrease LDL and increase HDL

30
Q

What are the AEs of niacin?

A
  • niacin flush
  • hyperglycemia
  • hyperuricemia
31
Q

How does digoxin work?

A

it directly inhibits Na/K ATPase to indirectly inhibit the Na/Ca exchanger in myocytes to prevent efflux of calcium and thus act as a positive inotrope

it also stimulates the vagus nerve to decrease HR

32
Q

What are the uses of digoxin?

A

HR (increases contractility) and a. fib (decreases conduction at AV and SA node)

33
Q

What are the AEs of digoxin?

A
  • cholinergic- N/V, diarrhea, blurry ision, AV block
  • hyperkalemia
34
Q

What things predispose to digoxin toxicity?

A

renal failure, verapamil, amiodarone, and quinidine all decrease clearance

35
Q

How do Class I Antiarrhythmics work?

A

slow conduction by decreasing the slope of phase 0 depolarization by acting as Na+ channel blockers

36
Q

What are the Class IA AAs?

A

Quinidine, Procainamide, Disopyramide

‘the Queen Proclaims Diso’s pyramid”

37
Q

How do Class IAs work?

A
  • increase AP duration
  • elongate effective refractory period (ERP) in ventricular action potential
  • increase QT interval
38
Q

What are the uses of Class IAs?

A

both atrial and ventricular arryhthmias, especially re-entrant and ectopic SVT and VT

39
Q

AEs of Class IAs?

A
  • cinchonism (headache, tinnitus with quinidine)
  • SLE like syndrome (procainamide)
  • HF (Disopyramide)
  • torsades de pointes

-thrombocytopenia

40
Q

What are the Class IBs?

A

Lidocaine, Mexiletine

41
Q

How do Class IBs work?

A

decrease the AP duration, preferrably affecting ischemic or depolarized Purkinje and ventricular tissue.

42
Q

What are the uses of Class IBs?

A

acute ventricular arrythmias (especially post-MI)

digitalis-induced arryhthmias

43
Q

AEs of Class IBs?

A

CNS modulation

CV depression

44
Q

What are the Class ICs?

A

Flecainide, Propafenone

45
Q

How do Class ICs work?

A

significantly prolongs ERP in AV node and accessory bypss tracts (no effect on ERP in Purkinje and ventricular tissue)

minmal effect on AP duration

46
Q

What are the uses of Class ICs?

A

SVTs, including a fib.

47
Q

AEs of Class ICs?

A

porarryhthmic in ischemic (post-MI) and structural heart disease

48
Q

What are the Class II AAs?

A

BBs (metoprolol, propranolol, etc.)

49
Q

How do BBs work?

A

decrease SA and AV nodal activity by decreasing cAMP and Ca2+ currents and decrease the slope of phase 4 depolarization

50
Q

What are the AEs of beta blockers?

A

impotence, exacerbation of COPD and asthma, bradycardia, AV block, etc.

may mask the signs of hypoglycemia

51
Q

What are the Class III AAs?

A

Amiodarone, Ibutilide, Dofetilide, Sotalol

AIDS

52
Q

What are the AEs of amiodarone?

A

pulmonary fibrosis,

hepatotoxicity,

hypo/hyperthyroidism (40% iodine by weight)

  • can act as a hapten
  • bradycardia, heart block
53
Q

What does amiodarone do if it acts as a hapten?

A

contributes to corneal deposits, blue/gray skin depositis resulting in photodermatitis

54
Q

What are the uses of Class III AAs?

A

a. fib, a. flutter,

ventricular tachycardia (amiodarone, sotalol)

55
Q

T or F. Class III can cause TDP

A

TRUE. Prolong the QT interval

56
Q

What are the Class IV AAs?

A

CCBs - verapamil and diltiazem

57
Q

What is the DOC for abolishing supraventicular tachycardia?

58
Q

How does adenosine work?

A

it increases K+ efflux to hyperpolarize the cell and decrease Ica activity

59
Q

Adenosine

A

-very short acting (15 sec)

effects blunted by theophylline and caffeine (both are adenosine receptor antagonists)

60
Q

What are the AEs of adenosine?

A

flushing, hypotension,

chest pain, sense of impending doom

bronchospasm

STEP 1 (2) (16 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions