chapter 21- pharmacology of vascular tone Flashcards

(87 cards)

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

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2
Q

how is the short acting isosorbide denigrate administered

A

sublingually

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3
Q

what it is the clinical application of short acting isosorbide dinitrate

A

prophylaxis and treatment of acute anginal attacks

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4
Q

how is the long-acting isosorbide dinitrate administered

A

oral, extended-release

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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

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6
Q

what are the common adverse effects of isosorbide dinitrate

A

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

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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)

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8
Q

what can continued therapy with isosorbide denigrate lead to

A

tolerance

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9
Q

what is the clinical application of isosorbide 5-mononitrate

A

prophylaxis angina, treatment of chronic ischemic heart disease

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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

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11
Q

what is the clinical application of short-acting nitroglycerin

A

short term treatment of acute anginal attachs

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12
Q

what is the clinical application of long-acting nitroglycerin

A

prophylaxis of angina, treatment of chronic ischemic heart disease

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13
Q

what is the clinical application of IV nitroglycerin

A

unstable angina, acute heart failure

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14
Q

what dilation predominates at therapeutic doses of nitroglycerin

A

venous

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15
Q

what is the mechanism of action of inhaled NO

A

selectively dilates the pulmonary vasculature

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16
Q

who is the transdermal form of nitroglycerin contraindicated in

A

its with allergy to skin tape

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17
Q

who is the IV form of nitroglycerin contraindicated in

A

its with cardiac tamponade, restrictive cardiomyopathy or constrictive pericarditis

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18
Q

what drug may oppose the coronary vasodilation of nitrates

A

ergotamine

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19
Q

what is the clinical application of sodium nitroprusside

A

hypertensive emergencies, severe cardiac failure, ergot alkaloid toxicity

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20
Q

how does sodium nitroprusside primarily liberate NO

A

through non-enzymatic prices

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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

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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

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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

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24
Q

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

A

CAD

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25
what drug can be co-administered with sodium nitroprusside to possible reduce the risk of cyanide toxicity
sodium thiosulfate
26
what are the clinical applications of inhaled NO gas
neonatal respiratory failure, perinatal hypoxia, pulmonary HTN
27
what are the common adverse effects of inhaled NO gas
hypotension, withdrawal syndrome
28
what are the contraindications for inhaled NO gas use
neonates with dependence on right-to-left shunting
29
how is NO gas rapidly inactivated
because it is in the blood, it is rapidly inactivated by binding to hemoglobin
30
what is the mechanism of action of sildenafil, vardenafil, tadalafil
inhibit PDE5, an enzyme that converts cGMP to GMP, leading to cGMP accumulation in target tissues
31
what are the clinical applications of sildenafil, vardenafil, tadalafil
erectile dysfunction
32
what is an additional clinical application of slidenafil besides ED
pulmonary HTN
33
what are the common adverse effects of sildenafil, vardenafil, tadalafil
MI, nonarteritic ischemic optic neuropathy, priapism
34
what is the contraindication of sildenafil, vardenafil, tadalafil
concomitant use of organic nitrate vasodilators
35
what is the mechanism of action of calcium channel blockers
block voltage-gated L-type calcium channels and prevent the influx of calcium that promotes actin-myosin cross-brindleformation.
36
what are the dihydropyridines
nifedipine, amiodipine, felodipine, clevidipine
37
what are the clinical applications of dihydropyridines
external and unstable angina, coronary spasm, HTN, raynauds phenomenon, pre-eclampsia
38
what are the contraindications for dihydropyridines
preexisting hypotension
39
what are the adverse effects of dihydropyridines
increased angina, rare MI, flushing, heartburn
40
what calcium channel blocker has the least effects on SA node automaticity and AV node conduction velocity
nifedipine ( dihydropyridines)
41
what dihydropyridines can trigger severe reflex tachycardia
nifedipine
42
what is clevidipine administered via IV for the management of
hypertensive urgency and emergency
43
what excretes dihydropyridines
the kidney
44
what calcium binding sites overlap
D and V
45
how do nifedipine and diltiazem interact
synergistically
46
how do nifedipine and verapamil interact
reciprocally inhibit each other's binding
47
what excretes dilitiazem
liver
48
what are the clinical applications of dilitiazem
prenzmetals or variant or chronic stable angina, HTN, atrial fibrillation or flutter, paroxysmal supra ventricular tachycardia
49
what are the common adverse effects with dilitiazem
AV block, bradyarrhythmia, exacerbation of heart failure, peripheral edema, gingival hyperplasia
50
what are the contraindications of dilitiazem
sick sinus syndrome or 2nd or 3rd degree AV block, supra ventricular tachycardia associated with a bypass tract, left ventricular failure, hypotension
51
how does dilitiazem effect carbamazepine levels
raises them, possibly leading to toxicity
52
what calcium channel blocker should not be used concomitantly with beta-adrenergic blockers
dilitiazem
53
what excretes verapamil
kidney
54
who is IV verapamil contraindicated in
patients with ventricular tachycardia and patients receiving IV beta-blockers
55
what calcium channel blocker should not be used with alcohol because it may result in higher serum alcohol concentrations
chronic verapamil therapy
56
what might happen with co-administration of pimozide with verapamil do
may result in higher pimozide concentrations and cardiac arrhythmias
57
what does coadministration of verapamil with simvastatin do
markedly increases simvastatin concentrations
58
what is the mechanism of action of minoxidil, pinacidil, nicorandil, cromakalim
potassium channel openers
59
what are the clinical applications of minoxidil, pinacidil, nicorandil, cromakalim
severe or refractory HTN
60
what is the clinical application of topical mioxidil
male pattern alopecia
61
what are the common adverse effects of minoxidil, pinacidil, nicorandil, cromakalim
reflex tachycardia, sterens-johnson syndrome, leukopenia, thrombocytopenia, headache, hirsutism, hypertrichosis
62
what are the contraindications of minoxidil, pinacidil, nicorandil, cromakalim
pheochromocytoma
63
what do minoxidil, pinacidil, nicorandil, cromakalim effect more: veins or arterioles
arterioles
64
who should minoxidil, pinacidil, nicorandil, cromakalim be used with caution in
patients with impaired renal function or dissecting aortic aneurysm or after acute MI
65
what is the mechanism of action of bosentan and ambrisentan
endothelia receptor antagonists
66
what is the clinical application of bosentan and ambrisentan
severe pulmonary HTN
67
what are the adverse effects of bosentan and ambrisentan
hepatotoxicity, anemia, hypotension, fluid retention, headache, flushing
68
what are the contraindications of bosentan and ambrisentan
pregnancy, concomitant use of cyclosporin A or glyburide
69
why must LFTs be monitored with bosentan and ambrisentan use
may increase serum transaminase levels
70
what is the mechanism of action of hydralazine
arteriolar vasodilator; mechanism of action unclear
71
what is the clinical application of hydralazine
moderate to severe HTN, severe heart failure
72
what are the adverse effects of hydralazine
agranulocytosis, leukopenia, hepatotoxicity, SLE
73
what are the contraindications of hydrazine use
dissecting aortic aneurysm, CAD, mitral valvular rheumatic heart disease
74
what is hydralazine usually used in combination with when treating HTN
beta blocker and diuretic in treatment of HTN
75
what is hydrazine used in combination with when treating heart failure
isosorbide denitrate
76
what are the contraindications of propranolol and atenolol, metaprolol
bronchial asthma or COPD; cariogenic shock, decompensated cardiac failure; 2nd or 3rd AV block; severe since bradycardia
77
what is the systolic ventricular wall stress
afterload
78
what is the after load equivalent to
resistance that the ventricle must overcome to eject its contents
79
what is the end-diastolic volume of the heart (definition)
preload
80
what is the preload equivalent to
stretch on the ventricular fibers just before contraction, which is approximated by end-diastolic volume or pressure
81
when does ischemia occur
when decreased perfusion leads to an O2 deficit
82
what does the Ca++ CaM complex bind to and activate
myosin light chain kinase
83
what is the parameter of cardiovascular physiology of the coronary arteries
myocardial O2 supply
84
what is the parameter of cardiovascular physiology of the arerioles
after load, myocardial O2 demand, regional myocardial perfusion
85
what is the parameter of cardiovascular physiology of the capacitance veins
venous pooling, preload, myocardial O2 demand
86
what is the most potent endogenous vasoconstrictor
endothelin
87
what endothelia form is most associated with cardiovascular actions
ET-1