Brainscape's Knowledge GenomeTM

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


See full index

NP Adv Pharm_S21 > Cardiovascular Pharmacology > Flashcards

Cardiovascular Pharmacology Flashcards

1
Q

Treatment of Primary (Essential) Hypertension by drug type

A
  1. thiazide diuretics
  2. ACE inhibitors
  3. angiotensin II receptor blockers (ARBs)
  4. dihydropyridine Ca2+ channel blockers
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Treatment of HTN in Heart Failure by drug type

A
  • diuretics
  • ACE inhibitors/ARBs
  • beta blockers (for compensated HF)–must use cautiously with decompensated HF and are contraindicated in cardiogenic shock
  • aldosterone antagonists
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Treatment of HTN with diabetes mellitus by drug type

A

ACE inhibitors/ARBs

Ca2+ channel blockers

thiazide diuretics

beta blockers

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

why are ACE I inhibitors used for HTN with diabetes mellitus?

A

they are protective against diabetic neuropathy

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

name the Calcium channel blockers

A

amlodipine

clevidipine

nicardipine

nifedipine

nimodipine

verapamil

diltiazem

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

Calcium channel blockers–mechanism

A

block voltage dependent L type calcium channels of cardiac and smooth muscle–>reduce muscle contractility

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

which calcium channel blockers act more on vascular smooth muscle?

A

amlodipine = nifedipine > diltiazem > verapamil

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

which calcium channel blockers act more on the heart?

A

verapamil > diltizem > amlodipine = nifedipine

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

Calcium channel blockers Dihydropyridines (except nimodipine)–clinical use

A

HTN

angina (including Prinzmetal/variant angina)

Raynaud phenomenon

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

Calcium channel blockers Nimodipine–clinical use

A

subarachnoid hemorrhage–prevents cerebral vasospasm

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

Calcium channel blockers Clevidipine–clinical use

A

hypertensive urgency or emergency

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

Calcium channel blockers Non-dihydropyridines–clinical use

A

HTN

angina

atrial fibrillation/flutter

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

Calcium channel blockers non dihydropyridine–toxicity

A

cardiac depression

AV block

hyperprolactinemia

constipation

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

Calcium channel blockers dihydropyridine–toxicity

A

peripheral edema

flushing

dizziness

gingival hyperplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Hydralazine–mechanism

A

increase cGMP–smooth muscle relaxation

vasodilates arterioles more than veins, so afterload reduces

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

hydralazine–clinical use

A

severe HTN (particularly acute)

HF (with organic nitrate)

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

what is hydralazine often coadministered with?

why?

A

beta blocker

to prevent reflex tachycardia

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

hydralazine–toxicity

A

compensatory tachycardia–so contraindicated in angina/CAD

fluid retention

headache

angina

Lupus like syndrome

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

drugs used for treatment of hypertensive emergency

A

clevidipine

fenoldopam

labetalol

nicardipine

nitroprusside

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

nitroprusside–mechanism

A

short acting

increases cGMP via direct release of NO

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

nitroprusside–toxicity

A

releases cyanide, so can lead to cyanide toxicity

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

fenoldopam–mechanism

A
  • dopamine D1 receptor agonist–coronary, peripheral, renal, and splanchnic vasodilation
  • decreases BP, inc natriuresis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

fenoldopam–toxicity

A

HTN

tachycardia

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

name the nitrate drugs

A

nitroglycerin

isosorbide dinitrate

isosorbide mononitrate

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

nitrates–mechanism

A
  • vasodilate by increasing NO in vascular smooth muscle –> inc in cGMP and smooth muscle relaxation
  • dilate veins >> arteries, so dec preload
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

nitrates–use

A

angina

acute coronary syndrome

pulmonary edema

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

nitrates–toxicity

A

reflex tachycardia (treat with beta blockers)

orthostatic hypotension

flushing headache

“Monday disease” in industrial exposure–development of tolerance for vasodilating action during the work week and loss of tolerance over the weekend –> results in tahcycardia, dizziness, headache upon reexposure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

antianginal therapy–use

A

reduce myocardial O2 consumption by decreasing 1 or more of the determinants of myocardial O2 consumption; end diastolic volume, BP, HR, contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

ranolazine–mechanism

A

inhibits the late phase of sodium current thereby reducing diastolic wall tension and oxygen consumption

does not affect heart rate or contractility

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

ranolazine–use

A

angina refractory to other medical therapies

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

ranolazine–toxicity

A

constipation

dizziness

headache

nausea

QT prolongation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

name lipid lowering agents

A

HMG CoA reductase inhibitors

bile acid resins

ezetimibe

fibrates

niacin (B3)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what type of Lipid lowering agent decreases LDL the most?

A

HMG CoA reductase inhibitor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what type of lipid lowering agent increases HDL the most?

A

niacin (B3)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what type of lipid lowering agent decreases triglycerides the most?

A

fibrates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

what type of lipid lowering agent has NO effect on HDL and triglycerides?

A

ezetimibe

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

what type of lipid lowering agent has the smallest effect on lowering LDL?

A

fibrates

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

what type of lipid lowering agent only slightly elevates triglycerides?

A

bile acid resins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

HMG CoA reductase inhibitors–mechanism

A

inhibit conversion of HMG CoA to mevalonate (a cholesterol precursor)

dec mortality in CAD patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

name 5 HMG CoA reductase inhibitors

A

(-vastatins)

atorvastatin

lovastatin

pravastatin

simvastatin

rosuvastatin

41
Q

HMG CoA reductase inhibitors–toxicity

A
  • hepatotoxicity (inc LFTs)
  • myopathy (especially when used with fibrates or niacin)
42
Q

name 3 bile acid resins

A
  • cholestyramine
  • colestipol
  • colesevelam
43
Q

bile acid resins–use

A

prevent intestinal reabsorption of bile acids

liver must use cholesterol to make more

44
Q

bile acid resins–toxicity

A

GI upset

decrease absorption of other drugs and fat soluble vitamins

45
Q

ezetimibe–mechanism

A

prevent cholesterol absorption at small intestine brush borders

46
Q

ezetimibe–toxicity

A

rare inc LFTs; diarrhea

47
Q

name fibrate drugs

A

gemfibrozil

bezafibrate

fenofibrate

48
Q

fibrates–mechanism

A

upregulate LDL –> inc triglyceride clearance

activates PPAR alpha to induce HDL synthesis

49
Q

fibrates–toxicity

A

myopathy–inc risk with statins

cholesterol gallstones

50
Q

name a cardiac glycoside

A

digoxin

51
Q

cardiac glycosides–mechanism

A
  • direct inhibition of Na/K ATPase –> indirect inhibition of Na/Ca exchanger
  • increase concentration of Ca –> positive intropy
  • stimulates vagus nerve –> dec HR
52
Q

cardiac glycosides–use

A

HF (inc contractility)

atrial fibrillation (dec conduction at AV node and depression of SA node)

53
Q

cardiac glycosides–toxicity

A

cholinergic–nausea, vomiting, diarrhea, blurry yellow vision (think van Gogh), arrhythmia, AV block

can lead to hyperkalemia, which indicates poor prognosis

54
Q

factors that predispose to toxicity with cardiac glycosides

A

renal failure–dec excretion

hypokalemia–permissive for digoxin binding to K+ binding site on Na/K ATPase

drugs that replace digxin from tissue binding sites

decreased clearance (eg. verapamil, amiodarine, quinidine)

55
Q

cardiac glycosides–antidote

A

slowly normalize K+

cardiac pacer

anti digoxin Fab fragments

Mg2+

56
Q

what are class I antiarrhythmics, and how do they work?

A
  • sodium channel blockers
  • slow or block (dec) conduction especially in depolarized cells
  • dec slope of phase 0 depolarization
  • are state dependent (selectively depress tissue that is frequently depolarized, ie. tachycardia)
57
Q

what causes toxicity in all class I antiarrhythmics?

A

hyperkalemia

58
Q

what are the class IA antiarrhythmic drugs?

A

Quinifine, Procainamide, Disopyramide

“The Queen Proclaims Diso’s pyramid.”

59
Q

what are the class IB antiarrhythmic drugs?

A

Lidocaine

MexileTine

“I‘d Buy Liddy’s Mexican Tacos”

60
Q

class IB antiarrhythmics–mechanism

A
  • dec AP duration
  • preferentially affect ischemic or depolarized Purkinje and ventricular tissue
  • Phenytoin can also fall into the IB category
61
Q

class IB antiarrhythmics–use

A

acute ventricular arrhythmias (especially post MI)

digitalis-induced arrhythmias

“IB is Best post MI”

62
Q

class IB antiarrhythmics–toxicity

A

CNS stimulation/depression

cardiovascular depression

63
Q

what is the best antiarrhythmic drug to use for a post MI patient?

A

class IB

64
Q

what are the class IC antiarrhythmic drugs?

A

Flecainide

Propafenone

“Can I have Fries, Please?”

65
Q

class IC antiarrhythmics–mechanism

A

significantly prolongs ERP in AV node and accessory bypass tracts

no effect on ERP in purkinje and ventricular tissue

minimal effect on AP duration

66
Q

class IC antiarrhythmics–toxicity

A

proarrhythmics, especially post-MI (contraindicated)

IC is Contraindicated in structural and ischemic heart disease

67
Q

which class IA antiarrhythmic drug may cause digoxin toxicity?

A

Quinidine–decreases digoxin clearance and displaces digoxin from tissue binding sites

68
Q

class IC antiarrhythmics–use

A

SVTs, including atrial fibrillation

only as a last resort in refractory VT

do not affect AP duration

69
Q

when are class IC antiarrhythmics contraindicated?

A

structural heart diseases and post MI

70
Q

what are class II antiarrhythmics?

name 5

A

beta blockers

metoprolol

propranolol

esmolol

atenolol

timolol

71
Q

class II antiarrhythmics–mechanism

A

decrease SA and AV nodal activity by decreasing cAMP, dec Ca currents

suppress abnormal pacemakers by dec slope of phase 4

72
Q

what node is most sensitive to class II antiarrhythmics? and what is the effect of class II antiarrhythmics on the node?

A

AV node

inc PR interval

73
Q

which class II antiarrhythmic is most short acting?

A

esmolol

74
Q

class II antiarrhythmics–use

A

SVT

ventricular rate control for atrial fibrillation and atrial flutter

75
Q

class II antiarrhythmics–toxicity

A

impotence

exacerbation of COPD and asthma

cardiovascular effects (bradycardia, AV block, HF)

CNS effects (sedation, sleep alterations)

may mask signs of hypoglycemia

beta blockers (except non selective alpha and beta antagonists carvedilol and labetalol) cause unopposed alpha 1 agonism if given alone for pheochromocytoma or cocaine toxicity

76
Q

metoprolol toxicity and how to treat

A

(classII antiarrhythmic)

can cause dyslipidemia

treat with glucagon

77
Q

propranolol toxicity

A

(class II antiarrhythmic)

can exacerbate vasospasm in Prinzmetal angina

78
Q

how to treat beta blocker overdose

A

saline

atropine

glucagon

79
Q

what are class III antiarrhythmics and name 4

A

potassium channel blockers

Amiodarone

Ibutilide

Dofetilide

Sotalol

“AIDS”

80
Q

class III antiarrhythmics–mechanism

A

inc AP duration

inc ERP

inc QT interval

81
Q

class III antiarrhythmics–use

A

atrial fibrillaiton

atrial flutter

ventricular tachycardia (amiodarone, sotalol)

82
Q

what is the indication for class III antiarrhythmics?

A

when all other antiarrhythmics fail

83
Q

sotalol toxicity

A

(class III antiarrhythmic)

torsades de pointes

excessive beta blockade

84
Q

ibutilide–toxicity

A

(class III antiarrhythmic)

torsades de pointes

85
Q

amiodarone–toxicity

A

(class III antiarrhythmic)

pulmonary fibrosis

hepatotoxicity

hypothyroidism/hyperthyroidism (amiodarone is 40% iodine by weight)

acts as hapten–corneal deposits, blue/gray skin deposits causing photodermatitis

neurologic effects

constipation

cardiovascular effects–bradycardia, heart block, HF

86
Q

what should you always check when using amiodarone?

A

pulmonary function tests

liver function tests

thyroid function tests

87
Q

amiodarone has effects of which classes and why?

A

I, II, III, IV

b/c lipophilic–alters lipid membrane

88
Q

what are class IV antiarrhythmics and name 2?

A

calcium channel blockers

verapail

diltiazem

89
Q

class IV antiarrhythmic–mechanism

A

dec conduction velocity

inc ERP

inc PR interval

90
Q

class IV antiarrhythmic–use

A

prevention of nodal arrhythmias (eg. SVT)

rate control in atrial fibrillation

91
Q

class IV antiarrhythmic–toxicity

A

flushing

constipation

edema

cardiovascular effects–HF, AV block, sinus node depression

92
Q

name 2 antiarrhythmics other than those in classes

A

adenosine

Mg2+

93
Q

what is the antiarrhythmic mechanism of adenosine?

A

inc K+ out of cells –> hyperpolarizes the cell and dec intracellular Ca

94
Q

adenosine–use as a antiarrhythmic

A

diagnosing/terminating certain forms of SVT

95
Q

how long does adenosine last?

A

~15 seconds

96
Q

what are 2 things that block the effects of adenosine?

A

theophylline and caffeine–adenosine receptor antagonists

97
Q

adenosine as a antiarrhythmic–toxicity

A

flushing, hypotension, chest pain, sense of impending doom, bronchospasm

98
Q

when would you use Mg as an antiarrhythmic?

A

torsades de pointes

digoxin toxicity

NP Adv Pharm_S21 (25 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions