3-Vasodilators

Question 1

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

Answer 1

Baroreceptor reflex

Question 2

Vascular damage in heart, kidney, retina or brain

Answer 2

End-organ damage

Question 3

Hypertension of unknown etiology; primary hypertension

Answer 3

Essential hypertension

Question 4

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

Answer 4

Hypertensive emergency/malignant hypertension

Question 5

Hypotension on assuming upright posture; postural hypotension

Answer 5

Orthostatic hypotension

Question 6

Elevated BP resulting from loss of antihypertensive drug effect

Answer 6

Rebound hypertension

Question 7

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

Answer 7

Reflex tachycardia

Question 8

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

Answer 8

Secondary hypertension

Question 9

Drug that reduces effects of the SNS

Answer 9

Sympatholytic, Sympathoplegic

Question 10

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

Answer 10

Angina

Question 11

Drugs that decrease peripheral vascular resistance or cardiac output

Answer 11

Vasodilators

Question 12

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

Answer 12

Mechanisms of vasodilators

Question 13

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

Answer 13

Calcium channel blockers

Question 14

MOA of Verapamil, Diltiazem, Nifedipine

Answer 14

Reduction of calcium influx

Question 15

Primary hyperaldosteronism

Answer 15

Conn’s Syndrome

Question 16

Hypertensive urgency with end-organ damage

Answer 16

Hypertensive Emergency

Question 17

Severely elevated BP with no evidence of end-organ damage

Answer 17

Hypertensive Urgency

Question 18

Excessive hair growth

Answer 18

Hypertrichosis

Question 19

Catecholamine-secreting tumor of the adrenal gland

Answer 19

Pheochromocytoma

Question 20

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

Answer 20

Reye’s Syndrome

Question 21

Repeated administration of medication leads to decreased effectiveness

Answer 21

Tolerance

Question 22

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

Answer 22

True

Question 23

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

Answer 23

Phosphorylates myosin light chains, initiating interaction of myosin with actin

Question 24

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

Answer 24

Calponin & Caldesmon

Question 25

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

Answer 25

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

Question 26

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

Answer 26

L type

Question 27

What is the MOA of CCBs?

Answer 27

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

Question 28

Where do CCBs bind?

Answer 28

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

Question 29

What are contraindications & indications for CCBs?

Answer 29

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

Question 30

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

Answer 30

CCBs

Question 31

Amlodipine, Felodipine, Isradipine, Nicardpine

Answer 31

Dihydropyridine (DHP) CCBs

Question 32

Nifedipine is the prototype for?

Answer 32

DHP CCBs

Question 33

What is the MOA of Non-DHP CCBs?

Answer 33

Decrease HR & Contractility; more cardioselective

Question 34

Verapamil, Diltiazem

Answer 34

Non-DHP CCBs

Question 35

Constipation is a common adverse effect for what drug?

Answer 35

Verapamil

Question 36

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

Answer 36

CCBs

Question 37

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

Answer 37

Release of nitric oxide from drug or endothelium

Question 38

MOA for Minoxidil & Diazoxide?

Answer 38

Hyperpolarization of cell membranes through opening of potassium channels

Question 39

MOA for Fenoldopam?

Answer 39

Activation of dopamine receptors

Question 40

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

Answer 40

Oral

Question 41

Nitroprusside is what kind of nitrate?

Answer 41

Parenteral

Question 42

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

Answer 42

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

Question 43

MOA of Nitrates?

Answer 43

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

Question 44

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

Answer 44

Nitroglycerin

Question 45

How is Nitroglycerin administered?

Answer 45

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

Question 46

Orally active nitrate with relatively long half-life

Answer 46

Isosorbide dinitrate

Question 47

Given by continuous IV infusion, rapidly metabolized to cyanide

Answer 47

Nitroprusside

Question 48

Used for hypertensive emergencies

Answer 48

Nitroprusside

Question 49

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

Answer 49

Nitrates