Brainscape's Knowledge GenomeTM

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


See full index

LECOM pharmacology notecards > chapter 21- pharmacology of vascular tone > Flashcards

chapter 21- pharmacology of vascular tone Flashcards

1
Q

what is the mechanism of action of nitrates and nitroprusside

A

donate NO, which activates guanylyl cyclase and increases dephosphorylation of myosin light chain in vascular smooth muscle, causing vasodilation

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

how is the short acting isosorbide denigrate administered

A

sublingually

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

what it is the clinical application of short acting isosorbide dinitrate

A

prophylaxis and treatment of acute anginal attacks

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

how is the long-acting isosorbide dinitrate administered

A

oral, extended-release

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

what is the clinical application of long-acting isosorbide dinitrate

A

prophylaxis of angina, treatment of chronic ischemic heart disease, diffuse esophageal spasm

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

what are the common adverse effects of isosorbide dinitrate

A

refractory hypotension, angina from reflex tachycardia, palpitations, syncope, flushing, headache

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

what are the contraindications for isosorbide dinitrate

A

severe hypotension, shock or acute MI with low ventricular filling pressure, increased intracranial pressure, angle-closure glaucoma, co-admin with phosphodiesterase type V inhibitors (slidenafil, vardenafil, tadalafil)

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

what can continued therapy with isosorbide denigrate lead to

A

tolerance

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

what is the clinical application of isosorbide 5-mononitrate

A

prophylaxis angina, treatment of chronic ischemic heart disease

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

why is isosorbide 5-mononitrate preferred over isosorbide dinitrate

A

it has longer half-life, better absorption from GI tract, non-susceptibility to extensive first-pass metabolism in liver, less rebound angina, greater efficacy at equivalent dose

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

what is the clinical application of short-acting nitroglycerin

A

short term treatment of acute anginal attachs

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

what is the clinical application of long-acting nitroglycerin

A

prophylaxis of angina, treatment of chronic ischemic heart disease

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

what is the clinical application of IV nitroglycerin

A

unstable angina, acute heart failure

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

what dilation predominates at therapeutic doses of nitroglycerin

A

venous

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

what is the mechanism of action of inhaled NO

A

selectively dilates the pulmonary vasculature

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

who is the transdermal form of nitroglycerin contraindicated in

A

its with allergy to skin tape

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

who is the IV form of nitroglycerin contraindicated in

A

its with cardiac tamponade, restrictive cardiomyopathy or constrictive pericarditis

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

what drug may oppose the coronary vasodilation of nitrates

A

ergotamine

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

what is the clinical application of sodium nitroprusside

A

hypertensive emergencies, severe cardiac failure, ergot alkaloid toxicity

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

how does sodium nitroprusside primarily liberate NO

A

through non-enzymatic prices

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

what are the important therapeutic considerations of sodium nitroprusside

A

non-selective in venous vs arterial dilation; thiocyanate toxicity becomes life-threatening at serum concentrations of 200mg/mL

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

what are the contraindications of sodium nitroprusside use

A

pre-existing hypotension, obstructive valvular disease, heart failure associated with reduced peripheral vascular resistance

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

what are the adverse effects of sodium nitroprusside

A

cyanide toxicity, cardiac arrhythmia, excessive bleeding, hypotension, metabolic acidosis, bowel obstruction, methemoglobinemia, increased intracranial pressure, flushing, headache, renal azotemia

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

what can the ability of NTG to relieve angina-like chest pain of esophageal spasm lead to the misdiagnosis of

A

CAD

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

what drug can be co-administered with sodium nitroprusside to possible reduce the risk of cyanide toxicity

A

sodium thiosulfate

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what are the clinical applications of inhaled NO gas

A

neonatal respiratory failure, perinatal hypoxia, pulmonary HTN

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

what are the common adverse effects of inhaled NO gas

A

hypotension, withdrawal syndrome

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

what are the contraindications for inhaled NO gas use

A

neonates with dependence on right-to-left shunting

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

how is NO gas rapidly inactivated

A

because it is in the blood, it is rapidly inactivated by binding to hemoglobin

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

what is the mechanism of action of sildenafil, vardenafil, tadalafil

A

inhibit PDE5, an enzyme that converts cGMP to GMP, leading to cGMP accumulation in target tissues

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

what are the clinical applications of sildenafil, vardenafil, tadalafil

A

erectile dysfunction

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

what is an additional clinical application of slidenafil besides ED

A

pulmonary HTN

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

what are the common adverse effects of sildenafil, vardenafil, tadalafil

A

MI, nonarteritic ischemic optic neuropathy, priapism

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

what is the contraindication of sildenafil, vardenafil, tadalafil

A

concomitant use of organic nitrate vasodilators

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

what is the mechanism of action of calcium channel blockers

A

block voltage-gated L-type calcium channels and prevent the influx of calcium that promotes actin-myosin cross-brindleformation.

36
Q

what are the dihydropyridines

A

nifedipine, amiodipine, felodipine, clevidipine

37
Q

what are the clinical applications of dihydropyridines

A

external and unstable angina, coronary spasm, HTN, raynauds phenomenon, pre-eclampsia

38
Q

what are the contraindications for dihydropyridines

A

preexisting hypotension

39
Q

what are the adverse effects of dihydropyridines

A

increased angina, rare MI, flushing, heartburn

40
Q

what calcium channel blocker has the least effects on SA node automaticity and AV node conduction velocity

A

nifedipine ( dihydropyridines)

41
Q

what dihydropyridines can trigger severe reflex tachycardia

A

nifedipine

42
Q

what is clevidipine administered via IV for the management of

A

hypertensive urgency and emergency

43
Q

what excretes dihydropyridines

A

the kidney

44
Q

what calcium binding sites overlap

A

D and V

45
Q

how do nifedipine and diltiazem interact

A

synergistically

46
Q

how do nifedipine and verapamil interact

A

reciprocally inhibit each other’s binding

47
Q

what excretes dilitiazem

A

liver

48
Q

what are the clinical applications of dilitiazem

A

prenzmetals or variant or chronic stable angina, HTN, atrial fibrillation or flutter, paroxysmal supra ventricular tachycardia

49
Q

what are the common adverse effects with dilitiazem

A

AV block, bradyarrhythmia, exacerbation of heart failure, peripheral edema, gingival hyperplasia

50
Q

what are the contraindications of dilitiazem

A

sick sinus syndrome or 2nd or 3rd degree AV block, supra ventricular tachycardia associated with a bypass tract, left ventricular failure, hypotension

51
Q

how does dilitiazem effect carbamazepine levels

A

raises them, possibly leading to toxicity

52
Q

what calcium channel blocker should not be used concomitantly with beta-adrenergic blockers

A

dilitiazem

53
Q

what excretes verapamil

A

kidney

54
Q

who is IV verapamil contraindicated in

A

patients with ventricular tachycardia and patients receiving IV beta-blockers

55
Q

what calcium channel blocker should not be used with alcohol because it may result in higher serum alcohol concentrations

A

chronic verapamil therapy

56
Q

what might happen with co-administration of pimozide with verapamil do

A

may result in higher pimozide concentrations and cardiac arrhythmias

57
Q

what does coadministration of verapamil with simvastatin do

A

markedly increases simvastatin concentrations

58
Q

what is the mechanism of action of minoxidil, pinacidil, nicorandil, cromakalim

A

potassium channel openers

59
Q

what are the clinical applications of minoxidil, pinacidil, nicorandil, cromakalim

A

severe or refractory HTN

60
Q

what is the clinical application of topical mioxidil

A

male pattern alopecia

61
Q

what are the common adverse effects of minoxidil, pinacidil, nicorandil, cromakalim

A

reflex tachycardia, sterens-johnson syndrome, leukopenia, thrombocytopenia, headache, hirsutism, hypertrichosis

62
Q

what are the contraindications of minoxidil, pinacidil, nicorandil, cromakalim

A

pheochromocytoma

63
Q

what do minoxidil, pinacidil, nicorandil, cromakalim effect more: veins or arterioles

A

arterioles

64
Q

who should minoxidil, pinacidil, nicorandil, cromakalim be used with caution in

A

patients with impaired renal function or dissecting aortic aneurysm or after acute MI

65
Q

what is the mechanism of action of bosentan and ambrisentan

A

endothelia receptor antagonists

66
Q

what is the clinical application of bosentan and ambrisentan

A

severe pulmonary HTN

67
Q

what are the adverse effects of bosentan and ambrisentan

A

hepatotoxicity, anemia, hypotension, fluid retention, headache, flushing

68
Q

what are the contraindications of bosentan and ambrisentan

A

pregnancy, concomitant use of cyclosporin A or glyburide

69
Q

why must LFTs be monitored with bosentan and ambrisentan use

A

may increase serum transaminase levels

70
Q

what is the mechanism of action of hydralazine

A

arteriolar vasodilator; mechanism of action unclear

71
Q

what is the clinical application of hydralazine

A

moderate to severe HTN, severe heart failure

72
Q

what are the adverse effects of hydralazine

A

agranulocytosis, leukopenia, hepatotoxicity, SLE

73
Q

what are the contraindications of hydrazine use

A

dissecting aortic aneurysm, CAD, mitral valvular rheumatic heart disease

74
Q

what is hydralazine usually used in combination with when treating HTN

A

beta blocker and diuretic in treatment of HTN

75
Q

what is hydrazine used in combination with when treating heart failure

A

isosorbide denitrate

76
Q

what are the contraindications of propranolol and atenolol, metaprolol

A

bronchial asthma or COPD; cariogenic shock, decompensated cardiac failure; 2nd or 3rd AV block; severe since bradycardia

77
Q

what is the systolic ventricular wall stress

A

afterload

78
Q

what is the after load equivalent to

A

resistance that the ventricle must overcome to eject its contents

79
Q

what is the end-diastolic volume of the heart (definition)

A

preload

80
Q

what is the preload equivalent to

A

stretch on the ventricular fibers just before contraction, which is approximated by end-diastolic volume or pressure

81
Q

when does ischemia occur

A

when decreased perfusion leads to an O2 deficit

82
Q

what does the Ca++ CaM complex bind to and activate

A

myosin light chain kinase

83
Q

what is the parameter of cardiovascular physiology of the coronary arteries

A

myocardial O2 supply

84
Q

what is the parameter of cardiovascular physiology of the arerioles

A

after load, myocardial O2 demand, regional myocardial perfusion

85
Q

what is the parameter of cardiovascular physiology of the capacitance veins

A

venous pooling, preload, myocardial O2 demand

86
Q

what is the most potent endogenous vasoconstrictor

A

endothelin

87
Q

what endothelia form is most associated with cardiovascular actions

A

ET-1

LECOM pharmacology notecards (22 decks)

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