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Pharmacology Exam 3 > 3-Vasodilators > Flashcards

3-Vasodilators Flashcards

1
Q

Primary autonomic mechanism for blood pressure homeostasis; involves sensory input from carotid sinus and aorta to the vasomotor center and output via the parasympathetic and sympathetic motor nerves

A

Baroreceptor reflex

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2
Q

Vascular damage in heart, kidney, retina or brain

A

End-organ damage

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3
Q

Hypertension of unknown etiology; primary hypertension

A

Essential hypertension

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4
Q

An accelerated form of severe hypertension associated with rising blood pressure and rapidly progressing damage to vessels and end organs. Often signaled by renal damage, encephalopathy, and retinal hemorrhages or by angina, stroke, or myocardial infarction

A

Hypertensive emergency/malignant hypertension

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5
Q

Hypotension on assuming upright posture; postural hypotension

A

Orthostatic hypotension

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6
Q

Elevated BP resulting from loss of antihypertensive drug effect

A

Rebound hypertension

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7
Q

Tachycardia resulting from lowering of BP; mediated by the baroreceptor reflex

A

Reflex tachycardia

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8
Q

Hypertension caused by a diagnosable abnormality (exp. aortic coarctation, renal artery stenosis, adrenal tumor,)

A

Secondary hypertension

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9
Q

Drug that reduces effects of the SNS

A

Sympatholytic, Sympathoplegic

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10
Q

Chest discomfort caused by insufficient cardiac blood flow resulting in cardiac ischemia

A

Angina

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11
Q

Drugs that decrease peripheral vascular resistance or cardiac output

A

Vasodilators

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12
Q

Blockade of calcium channels, release of nitric oxide, opening of K+ channels (hyperpolarization), activation of D1 receptors

A

Mechanisms of vasodilators

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13
Q

Verapamil, Amlodipine, Clevidipine, Felodipine, Isradipine, Nisoldipine, Nicardipine, Nifedipine, Diltiazem

A

Calcium channel blockers

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14
Q

MOA of Verapamil, Diltiazem, Nifedipine

A

Reduction of calcium influx

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15
Q

Primary hyperaldosteronism

A

Conn’s Syndrome

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16
Q

Hypertensive urgency with end-organ damage

A

Hypertensive Emergency

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17
Q

Severely elevated BP with no evidence of end-organ damage

A

Hypertensive Urgency

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18
Q

Excessive hair growth

A

Hypertrichosis

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19
Q

Catecholamine-secreting tumor of the adrenal gland

A

Pheochromocytoma

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20
Q

A rare syndrome of encephalitis and hepatic dysfunction seen in children recovering from a viral illness linked to aspirin

A

Reye’s Syndrome

21
Q

Repeated administration of medication leads to decreased effectiveness

A

Tolerance

22
Q

T/F: Calcium combines with calmodulin to convert myosin light-chain kinase to its active form

A

True

23
Q

What does active form of MLCK (MLCK*) do?

A

Phosphorylates myosin light chains, initiating interaction of myosin with actin

24
Q

What other proteins inhibit ATPase activity of myosin during relaxation of smooth muscle?

A

Calponin & Caldesmon

25
Q

Where are Type L channels (Cav1.1-Cav1.4) found?

A

Cardiac, skeletal, & smooth muscle, neurons, endocrine cells, bone

26
Q

Verapamil, DHPs, Cd2+, omega 3-A block this type of Ca2+ channel?

A

L type

27
Q

What is the MOA of CCBs?

A

Bind to L type Ca2+ channels & block inward movement of Ca2+, causing vasodilation

28
Q

Where do CCBs bind?

A

L-type Ca2+ channels in heart & smooth muscle of coronary & peripheral vasculature

29
Q

What are contraindications & indications for CCBs?

A

Contraindications: Bradycardia, HF
Indications: Hypertension, angina, arrhythmias

30
Q

Peripheral edema, nausea, & flushing are adverse effects for what?

A

CCBs

31
Q

Amlodipine, Felodipine, Isradipine, Nicardpine

A

Dihydropyridine (DHP) CCBs

32
Q

Nifedipine is the prototype for?

A

DHP CCBs

33
Q

What is the MOA of Non-DHP CCBs?

A

Decrease HR & Contractility; more cardioselective

34
Q

Verapamil, Diltiazem

A

Non-DHP CCBs

35
Q

Constipation is a common adverse effect for what drug?

A

Verapamil

36
Q

Constipation, Vertigo, Headache, Fatigue, & Hypotension are common adverse effects for what kind of drugs?

A

CCBs

37
Q

MOA for Nitroprusside, Hydrolazine, Nitrates, Histamine & Acetylcholine?

A

Release of nitric oxide from drug or endothelium

38
Q

MOA for Minoxidil & Diazoxide?

A

Hyperpolarization of cell membranes through opening of potassium channels

39
Q

MOA for Fenoldopam?

A

Activation of dopamine receptors

40
Q

Nitroglycerin, Isosorbide mononitrate, & Isosorbide dinitrate are what kind of nitrates?

A

Oral

41
Q

Nitroprusside is what kind of nitrate?

A

Parenteral

42
Q

What are indirect acting organic nitrates and what enzyme do they require to release NO?

A

Nitroglycerin, Isosorbide mononitrate, & Isosorbide dinitrate
Enzyme: Aldehyde dehydrogenase

43
Q

MOA of Nitrates?

A

Conversion to NO -> NO increases cGMP -> smooth muscle relaxation
-at higher conc’s, nitrates decrease afterload

44
Q

Most commonly used antianginal agent & drug of choice for relieving acute coronary spasm

A

Nitroglycerin

45
Q

How is Nitroglycerin administered?

A

Sublingually (for rapid onset), can be transdermal for longer duration of action

46
Q

Orally active nitrate with relatively long half-life

A

Isosorbide dinitrate

47
Q

Given by continuous IV infusion, rapidly metabolized to cyanide

A

Nitroprusside

48
Q

Used for hypertensive emergencies

A

Nitroprusside

49
Q

Throbbing headache & postural hypotension are adverse effects for this type of drug?

A

Nitrates

Pharmacology Exam 3 (4 decks)

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