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
What is NO approved for in US?
only pediatric lung injury
26
What are the off label uses of NO?
severe PHTN, transplant, ARDS
27
True/false, inhaled NO only affects pulmonary circulation.
True, not diffused systemically
28
What is increased as NO combines with Hgb?
methemoglobin levels, can change proportion of iron in Hgb
29
How many cyanide molecules are released by Nipride?
5
30
What limits the conversion of cyanide to thiocyanate?
temperature. hypothermia delays conversion.
31
What is hypoxic pulmonary vasoconstriction (HPV)?
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
What's the major side effect of Nipride and its s/s?
cyanide toxicity: increased mixed venous O2, metabolic acidosis, CNS dysfunction, tachyphylaxis, cardiac arrhythmia
33
What is the treatment for cyanide toxicity?
shut off nipride drip and use 100% O2, sodium bicarb, thiosulfate 150mg/kg to help convert to thiocyanate, sodium nitrate, B12
34
What are the signs of thiocyanate toxicity?
slow clearance...3-7 days. fatigue, nausea, vomiting, CNS, hypothyroid, vague.
35
What is the treatment of thiocyanate toxicity?
dialysis
36
Is isosorbide dinitrate subject to first pass?
No
37
What is isosorbide dinitrate used for?
angina, post CABG
38
What is the metabolite of isosorbide dinitrate?
isosorbide mononitrate (more active)
39
What happens with acute admin of isosorbide dinitrate?
orthostatic hypotension