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Cardio > Directly acting vasodilators > Flashcards

Directly acting vasodilators Flashcards

1
Q

what are the different types of vasodilators

A

calcium channel blockers (dihydropyridine and non-dihydropyridine), hydralazine, potassium channel agonists (minoxidil), nitrates

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2
Q

what is the GENERAL mechanism of all vasodilators

A

they act directly on vascular smooth muscle cells and reduce the magnitude of smooth muscle contraction—> reducing the myogenic tone of the cells, resulting in vasodilation

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3
Q

the major difference between DHP and nDHP is _____

A

nDHP’s also decrease heart rate

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4
Q

what are the dihydropyridines

A

amlodipine, felodipine, isradipine, nicardipine, cifedipine, nimodipine, clevidipine

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5
Q

what are the non-dihydropyridines

A

diltiazem, verapamil

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6
Q

diltiazem is a _____

A

benzothiazepine

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7
Q

verapamil is a ______

A

phenylalkylamine

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8
Q

calcium channel blockers bind to ______ calcium channels

A

voltage-sensitive, L-type

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9
Q

which subunit of the calcium channel do CCBs bind to

A

the alpha 1 subunit (part that forms the pore thru which calcium passes)

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10
Q

CCBs binding to the L-type calcium channel causes it to _____

A

stay in the closed inactivated conformation

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11
Q

what is the result of CCBs inactivating channels

A

less calcium can enter smooth muscle cells, which decreases contraction

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12
Q

contractions depend on ____

A

availability of calcium

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13
Q

CCBs relax the vascular smooth muscle of _______, which reduces ___

A

arteries and arterioles, TPR

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14
Q

the vascular smooth muscle of ____ is NOT significantly affected by CCBs

A

veins

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15
Q

CCBs are especially useful for patients with _____

A

LOW renin

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16
Q

clinical uses of CCB

A

use alone or in combo, effective in reducing BP, also useful in the treatment of coronary artery disease

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17
Q

why are CCBs useful in coronary artery disease

A

since they are able to relax coronary arteries and increase blood flow to the heart muscle. since they lower BP, they reduce the work that the heart must do to provide the energy to move blood through the blood vessels

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18
Q

when are CCBs a great alternative to BBs

A

for patients with asthma

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19
Q

which CCB should you NOT combine w/ a BB and why?

A

nDHP–> because they both lower heart rate

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20
Q

diltiazem and verapamil are also used to treat _____

A

arrhythmias

21
Q

dihydropyridines do not have a major effect on ________, so they are not used as antiarrhythmics

A

AV node conduction

22
Q

what is a side effect with CCBs

A

peripheral edema (ankles in particular)

23
Q

how would CCBs cause peripheral edema

A

they relax the small arterioles leading into capillaries but not the veins leading out of the capillary bed–> which elevates the hydrostatic pressure within the capillary and favors leakage of fluid into interstitial space

24
Q

which patients should not take CCBs

A

in heart failure patients, the decrease in contractility could depress cardiac function. in patients with cardiac disease that is associated with AV node conduction, they are a bad choice as they can further reduce AV node conduction

25
Q

what is the mechanism of hydralazine

A

it enters vascular smooth muscle cells–> keeps Ca channels closed–> blocks release of Ca from sarcoplasmic reticulum–> reduces cytoplasmic Ca concentration–> reduces contraction

26
Q

hydralazine has an affect on ____ smooth muscle which decreases ____

A

arterial; TPR

27
Q

hydralazine has no effect on ____ smooth muscle

A

venous

28
Q

what is an adverse effect of hydralazine

A

systemic lupus erythematosus-like syndrome (an antibody response causing rash and muscle pain)

29
Q

what are the clinical uses of hydralazine in HTN

A

reserved for pts whose HTN is refractory to treatment with other agents

30
Q

hydralazine can be combined with ______ to prevent sympathetic reflex activation

A

beta blockers

31
Q

hydralazine can be combined with a _____ to prevent sodium retention

A

diuretic

32
Q

hydralazine can be combined with ______ for heart failure

A

isosorbide dinitrate

33
Q

what is the mechanism of minoxidil

A

potassium channel agonist–> K channel opens–> more negative membrane potential–> more voltage gated L-type calcium channels will be closed—> less Ca will enter the cells—> smooth muscle relaxed

34
Q

minoxidil is a potent _____ vasodilator that decreases ____

A

arterial, TPR

35
Q

minoxidil has no significant effect on ____ smooth muscle

A

venous

36
Q

how does sympathetic reflex activation work against the vasodilators

A

baroreceptors detect the decrease in blood pressure and compensate

37
Q

use of minoxidil in HTN

A

reserved for complicated patients

38
Q

adverse effect of minoxidil

A

hypertrichosis (hair growth)–> rogaine

39
Q

what are the nitrates

A

nitroglycerin, isosorbide dinitrate, isosorbide mononitrate, sodium nitroprusside

40
Q

use of sodium nitroprusside

A

hypertensive emergencies

41
Q

use of nitroglycerin

A

coronary artery disease (chronic stable angina and acute MI)

42
Q

use of isosorbide mononitrate & dinitrate

A

chronic stable angina

43
Q

the metabolism of nitrates and sodium nitroprusside leads to intracellular production of _____ in vascular smooth muscle

A

nitric oxide

44
Q

nitric oxide stimulates _____

A

guanylate cyclase

45
Q

the increased production of ______ by guanylate cyclase causes cytoplasmic Ca to decrease

A

cyclic GMP

46
Q

it has been hypothesized that impaired formation of _____ may be a cause of hypertension

A

nitric oxide

47
Q

what are symptoms of sodium nitroprusside toxicity

A

metabolic acidosis, decreased oxygen saturation, bradycardia, confusion, convulsions

48
Q

when does toxicity occur with sodium nitroprusside

A

high doses, long term administration, poor liver/kidney function

49
Q

what is the mechanism of sodium nitroprusside toxicity

A

it is made up of ferric cyanide and nitric oxide–> cyanide is released into the bloodstream, then further metabolized by the liver to thiocyanate which is then slowly cleared by the kidneys

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