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Pharmacology Exam 3 > Antihypertensives > Flashcards

Antihypertensives Flashcards

1
Q

Define BP

A

The force/tension of blood pressing against arterial walls

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2
Q

What is the equation for BP?

A

CO x SVR

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3
Q

What is essential HTN?

A

no identifiable cause, likely d/t environment and genetics. 95% of cases.

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4
Q

What is secondary HTN?

A

CKD, Cushings, pheos, OSA

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5
Q

What are the limits for Stage 1 HTN?

A

130/80

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6
Q

What are the limits for Stage 2 HTN?

A

140+/90+

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7
Q

What constitutes HTN crisis?

A

180+/120+

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8
Q

What regulates BP?

A

Pressure sensitive neurons called baroreceptors in the aortic arch and carotid sinuses–they form the vagus nerve at the aortic arch

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9
Q

Explain mechanism of BP regulation.

A

If BP falls too low baroreceptors send signals to adrenal medulla causing release of catecholamines and increasing sympathetic activity through activation of beta and alpha receptors.

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10
Q

What do beta 1 receptors do?

A

increase HR and SV, thus increasing CO and BP

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11
Q

What do alpha 1 receptors do?

A

on smooth muscles, vasoconstrict, increasing vascular resistance and increasing BP

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12
Q

What are the classifications of antihypertensives?

A

sympatholytics, calcium channel blockers, angiotensin converting enzyme inhibitors, angiotensin II receptor inhibitors, centrally acting drugs, diuretics

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13
Q

What’s another name for sympatholytics?

A

adrenergic antagonists

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14
Q

What do sympatholytics do?

A

inhibit activity of SNS mediated by epi/NE, bind to adrenergic receptors of smooth muscle causing vasodilation and decreased SVR, prevent their activations.

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15
Q

What are the groups of sympatholytics?

A

alpha blocker and beta blocker

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16
Q

What are examples of non-selective alpha blockers?

A

phentolamine, phenoxybenzamine

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17
Q

How can non-selective alpha blockers cause tachycardia and arrhythmias?

A

non-selective bind to alpha-1 and 2, NE acts on alpha-2 so blocking this results in more NE release which can then stimulate beta-1 receptors on the heart

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18
Q

What’s the difference between phentolamine and phenoxybenzamine?

A

phentolamine is reversible, phenoxybenzamine is not.

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19
Q

What do alpha-1 antagonists end in? examples?

A

-osin, prazosin, terazosin, doxazosin, alfuzosin, tamulosin

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20
Q

How do alpha-1 antagonists work?

A

selectively and reversibly block alpha-1 receptors from vascular smooth muscle which reduces PVR and BP

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21
Q

Is there still baroreceptor involvement with alpha-1 antagonists?

A

yes, cause hypotension and tachycardia

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22
Q

Do alpha-1 antagonists have more or less side effects that non-selective alpha blockers?

A

less, since negative feedback inhibition through alpha-2 receptors is still working

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23
Q

What’s different about the alpha-1 antagonists: alfuzosin, silodosin, and tamulosin?

A

little effect on BP but more so for relieving enlarged prostate, increased activity of alpha-1 receptors in prostate, less alpha-1 in blood vessels.

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24
Q

What are side effects of alpha-1 antagonists?

A

orthostatic hypotension, headaches, nasal congestion, reflex tachy unlikely because selective antagonist doesn’t impact NE regulating effect of alpha-2 receptor

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25
Q

What is yohimbine?

A

selective alpha-2 blocker. found in dietary supplements for ED, used to reverse sedation in vet medicine.

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26
Q

What is phenoxybenzamine’s MOA?

A

irreversible, noncompetitive nonselective alpha antagonist: binds irreversibly to different site on receptor and changes the shape of the receptor so it can’t bind to catecholamines anymore. Only way out is to synthesize new adrenergic receptors (takes 24 hours)

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27
Q

What is phenoxybenzamine used for?

A

treat pheo, symptoms HTN, tachy, arrhythmias, start 7-10 days preop, slow onset

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28
Q

What is the MOA for phentolamine?

A

REVERSIBLE, competitive nonselective alpha antagonist: competes with catecholamines for the exact same binding site. lasts about 4 hours

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29
Q

What is phentolamine used for?

A

used to treat pheos, also prevents dermal necrosis after inadvertent extravasation of alpha receptor agonist, ED, HTN crisis

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30
Q

What are the classifications for beta blockers?

A

first gen: nonselective, 2nd gen: b-1 selective, 3rd gen: vasodilatory (non-selective and b-1 selective)

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31
Q

Which beta blockers have additional alpha blocking activity?

A

carvedilol, labetalol

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32
Q

Discuss beta-1 receptors (not blockers).

A

located in heart, increases HR and contractility, in kidneys: stimulate juxtaglomerular cells- to release renin–renin-angiotensin-aldosterone system increases sodium and water retention which increases BP.

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33
Q

Discuss beta-2 receptors

A

in smooth muscle cells, lungs (causes bronchodilation), GI (decreases motility), eye (maintains shape), liver (promotes glucagon release)

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34
Q

What’s the MOA of beta blockers?

A

competitive inhibitors of beta-adrenergic receptors that counter the effects of catecholamines which leads to decreased sympathetic effects on cardiac system

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35
Q

What are beta blockers used to treat?

A

HTN, HF, heart attacks, angina, glaucoma, keep ICP down

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36
Q

What are examples of first generation, non-selective beta blockers?

A

propranolol, pindolol, nadolol, sotalol, timolol, oxprendolol, penbotalol

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37
Q

What happens when 1st gen beta blockers are given?

A

primarily hit beta-1’s, decreased HR, delayed AV node conduction, reduced contractility, decreased CO and O2 demand of the heart

38
Q

Which 1st gen beta blocker can be given for migraine prophylaxis?

A

propranolol, due to its liphophilicity and ability to penetrate CNS

39
Q

What 1st gen beta blocker can be used in the eye?

A

timolol, found to decrease intraocular pressure, used for glaucoma

40
Q

What are cautions with 1st gen beta blockers?

A

can lead to bronchoconstriction and not recommended for COPD/Asthma, beta-2 receptors found in lungs

41
Q

Describe 2nd gen beta blockers.

A

selective for beta-1, called cardio-selective beta blockers, better for chronic lung disease,

42
Q

What is esmolol commonly used for?

A

blunt the effects of intubation

43
Q

What do 3rd generation beta blockers do?

A

act on blood vessels causing vasodilation

44
Q

What are example of non-selective 3rd generation beta blockers?

A

carvedilol, labetalol

45
Q

What are examples of 2nd gen beta blockers?

A

atenolol, acebutolol, bisoprolol, esmolol, metoprolol

46
Q

What do non-selective 3rd generation beta blockers do?

A

produce peripheral vasodilation by blocking beta and alpha-1 receptors

47
Q

What do 3rd gen non-selective beta blockers do at beta 1 receptors on the kidneys?

A

on kidneys, suppress release of renin, formation of angiotensin II and secretion of aldosterone which causes decreased SVR and BP

48
Q

What do 3rd gen selective beta blockers do?

A

selective for beta-1, produce vasodilation by introducing release of nitric oxide from endothelial cells which relaxes smooth muscle and dilates blood vessels

49
Q

What are examples of 3rd gen selective beta blockers?

A

nebivolol, betaxolol

50
Q

What does betaxolol do?

A

3rd gen selective beta-1 blocker, produces vasodilation by additionally blocking Ca channels. (used for glaucoma because decreases intraocular pressure.

51
Q

Which beta blockers have intrinsic sympathomimetic activity?

A

pindolol and acebutolol, block but also weakly stimulate beta 1 and 2 receptors leading to diminished effect on cardiac rate and CO so beneficial in pts with pre-existing brady and heart block.

52
Q

Should patients continue beta blockers preop?

A

YES, to avoid SNS hyperactivity

53
Q

What is the commonly used beta blocker that depends on the kidneys as its primary route of elimination?

A

atenolol (others are combo of liver/kidney)

54
Q

What is the only beta blocker metabolized by RBC esterase?

A

esmolol

55
Q

What are the common side effects of beta blockers?

A

Bradycardia, hypotension, fatigue, cold hands/feet, dry mouth/skin/eyes, headache, stomach upset, diarrhea/constipation.

56
Q

What is the MOA of calcium channel blockers?

A

work on voltage gated ion channels to block the inward movement of Ca across myocardial and vascular smooth muscle causing arterial vasodilation

57
Q

What do calcium channel blockers do?

A

decrease myocardial contractility, decreases myocardial O2 requirement, decrease arteriole tone and SVR–decreased intraventricular pressure and decreased left wall stress, reduce/block impulse generation in SA node and conduction in AV node

58
Q

What are the clinical uses of Calcium Channel Blockers?

A

HTN, SVT, preventricular cerebral vasospasm, decrease chest pain

59
Q

What are the 2 types of calcium channel blockers?

A

dihydropyridines and nondihydropyridines

60
Q

What do dihydropyridines do?

A

selectively inhibit L-type Ca channels in vascular smooth muscle which decreases vascular resistance=vasodilation, decrease SVR

61
Q

What are examples of dihydropyridines?

A

nifedipine, nicardipine, nimodipine, clevidipine

62
Q

What are side effects of dihydropyridines?

A

related to systemic vasodilation, dizziness, HA, flushing, peripheral edema, gingival hypertorphy

63
Q

Describe Nondihydropyridines?

A

Non-selective inhibitors of l-type ca channels, block Ca channels on vascular muscle but also Ca channels on cardiac cells like AV/SA node which decreases contractility, HR, and conduction.

64
Q

Which type of calcium channel blocker has significant antiarrhythmic properties?

A

Nondihydropyridines

65
Q

What are the side effects of nondihydropyridines?

A

excessive bradycardia, conduction delay/abnormalities, hypotension, HA, ab discomfort, peripheral edema

66
Q

What’s the MOA of ACE inhibitors?

A

inhibits conversion of angiotensin I to angiotensin II in the lungs, part of the RAAS, causes relaxation of blood vessels and decrease in blood volume which decreases BP and O2 demand for heart

67
Q

Discuss RAAS.

A

Renin released from juxtaglomerular cells of afferent arteriole, converts angiotensinogen to angiotensin I–> converted to angiotensin II by angiotensin converting enzymes in lungs–>angiotensin II promotes vasoconstriction and aldosterone release.

68
Q

What are the clinical uses of ACE inhibitors?

A

treat HTN, acute MI, cardiac failure, kidney complications associated with DM

69
Q

What’s the suffix for ACE inhibitors?

A

-pril

70
Q

What are the side effects of ACE inhibitors?

A

CAPTOPRIL: Cough, Allergic reactions, Potassium elevation, Taste changes, Oedema(angioedema), Photosensitivity, Renal failure, Indigestion, Low bp

71
Q

When are ACE inhibitors contraindicated?

A

Renal artery stenosis/impairment (decrease GFR and excreted by kidneys), Insulin dependent DM (causes insulin resistance), Hyperkalemia (suppression of angio II leads to decreased aldosterone levels–aldosterone needed to increase excretion of K so more K absorbed), Pregnancy (fetal hypotension), Cough (increase bradykinin levels)

72
Q

What’s special about captopril?

A

rapidly absorbed, eliminated by kidneys

73
Q

What’s special about enalapril?

A

incidence of side effects is lower

74
Q

What’s special about lisinopril?

A

limit salt substitutes or K supplements d/t potential for hyperK

75
Q

What’s the suffix for Angiotensin II Receptor Blockers (ARBs)?

A

-sartan

76
Q

What’s the MOA of ARBs?

A

interfere with binding of angiotensin II with its receptor so inhibits ATII mediated vasoconstriction by inhibiting aldosterone

77
Q

Which has more side effects? ACE-Is or ARBs

A

ACE-Is

78
Q

What are the side effects of losartan?

A

hyperK(from decreased aldosterone), increases lithium reabsorption by kidneys (toxicity)

79
Q

How do centrally acting adrenergic drugs work? and what are examples?

A

by blocking sympathetic activity in brain, clonidine and methyldopa

80
Q

What’s the MOA of clonidine?

A

centrally acting selective partial alpha-2 agonist:
selectively stimulates pre-synaptic alpha-2 receptors thus providing negative feedback to reduce catecholamine production and release–causing decreased SVR, CO, and BP.

81
Q

What are the clinical uses of clonidine?

A

HTN, ADHD, anxiety, ETOH withdrawal

82
Q

What are the side effects of clonidine?

A

bradycardia (increases signaling through vagus nerve)

83
Q

When should you take caution with clonidine?

A

withdrawal after long term use causes HTN crisis d/t increased sympathetic activity

84
Q

How does methyldopa work?

A

lowers BP same way as clonidine (stimulates pre-synaptic alpha-2 receptors providing negative feedback to reduce catecholamine production and release) but not an agonist, needs to be converted to active metabolite: Methylnorepinephrine

85
Q

What’s the most frequently prescribed med for HTN?

A

diuretics

86
Q

What’s the clinical uses of diuretics?

A

fluid overload, edema, CHF, HTN, promote excretion of urine

87
Q

How are diuretics classified?

A

according to site of action on renal tubules and mechanism they alter the solute

88
Q

What are the types of diuretics?

A

3 common: loop, thiazide, K-sparing; Less common: carbonic anhydrase inhibitors, osmotics

89
Q

Where do each type of diuretics act?

A

Carbonic Anhydrase inhibitors: proximal tubule
Osmotics: proximal tubule and descending limb LoH
Loop: thick ascending limb LoH
Thiazide: early distal tubule
K-sparing diuretics: late distal tubule

90
Q

Where in the nephron do mineral corticoids exert their effects?

A

collecting tubule/late distal tubule

91
Q

What is the only site in the nephron that membrane water permeability can be regulated?

A

late DT/collecting tubule. It’s impermeable to H2O in the absence of ADH so dilute urine is produced.

Pharmacology Exam 3 (5 decks)

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