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Pharmacology Exam 3 > Vasodilators > Flashcards

Vasodilators Flashcards

1
Q

Specific cause for HTN is identified in what % of the population?

A

10-15%

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2
Q

What is essential HTN?

A

HTN with no cause found, aka primary HTN

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3
Q

What are some specific causes of HTN?

A

pheo, thyroid, parathyroid, cushings, aldosterone issues, renal artery stenosis, genetics, gestational, steroids, oral contraceptives, long term NSAIDS

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4
Q

What is the treatment for stage I HTN?

A

usually diet/exercise, decrease salt

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5
Q

What is the treatment for stage 2 HTN?

A

prescribe: 1st thiazide diuretics. cheap, minimal s/e, dosed once daily

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6
Q

What are the 4 anatomic sites at the body that control blood pressure moment to moment?

A

arterioles(resistance), postcapillary venules (capacitance vessels), heart (altering pump output), kidney (regulating intravascular volume)

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7
Q

What are the 4 types of antihypertensive agents?

A

sympathoplegic agents, direct vasodilators, angiotensin blocking agents, diuretics

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8
Q

How do sympathoplegic agents decrease BP?

A

decrease SVR, inhibit cardiac function, increase venous pooling

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9
Q

How do direct vasodilators decrease BP?

A

relaxing vascular smooth muscle therefore dilating resistance vessels and increasing capacitance a bit as well

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10
Q

How do angiotensin blockers decrease BP?

A

decreased PVR

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11
Q

How do diuretics decrease BP?

A

depleting the body of sodium and reducing blood volume. used mild/moderate HTN and in conjunction with other drugs for more severe HTN.

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12
Q

What 3 ways does Calcium affect peripheral vessel diameter?

A

Stimulate beta-2, block alpha-1, nitric oxide

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13
Q

What does stimulating beta-2 do?

A

g-protein-adenylate cyclase-increase cAMP: vasodilation because decreased intracellular Ca

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14
Q

What does blocking alpha-1 do?

A

g-protein-phospholipase C, decrease Calcium, decrease IP3, decrease DAG: decreased intracellular Ca causes vasodilation

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15
Q

What does nitric oxide do?

A

chemical messenger in many biologic systems, modulator of CV tone (smooth muscle relaxant), platelet regulation/aggregation, NT function in CNS

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16
Q

Where is nitric oxide formed?

A

endothelium

17
Q

What is the effector for nitric oxide?

A

guanylate cyclase: increases cGMP

18
Q

What does increased cGMP do?

A

decreases intracellular calcium and causes vasodilation

19
Q

How is intracellular calcium decreased with Nitric oxide?

A

decreased calcium entry into the cell and increased uptake by sarcoplasmic reticulum

20
Q

What is nitric oxide dependent on?

A

calcium and calmodulin

21
Q

What type NOS is flow dependent or receptor dependent?

A

type 3, cNOS

22
Q

What type NOS is produced by inflammation?

A

type 2, iNOS

23
Q

What are the NT that cause receptor stimulated NOS?

A

ACh, substance P, serotonin, bradykinin, thrombin, stress

24
Q

Does nitric have long or short half life?

A

short, binds to heme-based proteins

25
Q

What is NO approved for in US?

A

only pediatric lung injury

26
Q

What are the off label uses of NO?

A

severe PHTN, transplant, ARDS

27
Q

True/false, inhaled NO only affects pulmonary circulation.

A

True, not diffused systemically

28
Q

What is increased as NO combines with Hgb?

A

methemoglobin levels, can change proportion of iron in Hgb

29
Q

How many cyanide molecules are released by Nipride?

A

5

30
Q

What limits the conversion of cyanide to thiocyanate?

A

temperature. hypothermia delays conversion.

31
Q

What is hypoxic pulmonary vasoconstriction (HPV)?

A

local reaction in response to reduction in alveolar oxygen tension, selectively increases pulmonary vascular resistance in poorly vent areas to minimize shunt flow, protective mechanism during atelectasis or one-lung ventilation. Nipride inhibits HPV.

32
Q

What’s the major side effect of Nipride and its s/s?

A

cyanide toxicity: increased mixed venous O2, metabolic acidosis, CNS dysfunction, tachyphylaxis, cardiac arrhythmia

33
Q

What is the treatment for cyanide toxicity?

A

shut off nipride drip and use 100% O2, sodium bicarb, thiosulfate 150mg/kg to help convert to thiocyanate, sodium nitrate, B12

34
Q

What are the signs of thiocyanate toxicity?

A

slow clearance…3-7 days. fatigue, nausea, vomiting, CNS, hypothyroid, vague.

35
Q

What is the treatment of thiocyanate toxicity?

A

dialysis

36
Q

Is isosorbide dinitrate subject to first pass?

A

No

37
Q

What is isosorbide dinitrate used for?

A

angina, post CABG

38
Q

What is the metabolite of isosorbide dinitrate?

A

isosorbide mononitrate (more active)

39
Q

What happens with acute admin of isosorbide dinitrate?

A

orthostatic hypotension

Pharmacology Exam 3 (5 decks)

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