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Pharmacology Test 2 > Anti-hypertensive Meds > Flashcards

Anti-hypertensive Meds Flashcards

1
Q

General MOAs for antiHTN meds

A

affect variables in CO and MAP to alter BP

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2
Q

AntiHTN meds effect on variables of CO and MAP

A

1) . reduce HR –> decrease CO and AP
2) . decrease contractility –> decrease SV –> decrease BP
3) . increase vasodilation –> lower peripheral vascular resistance –> decrease BP
4) . reduce plasma volume –> decrease SV –> decrease bP

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3
Q

Classes of AntiHTN meds

A

1) . diuretics
2) . direct vasodilators
3) . calcium-channel blocking vasodilators
4) . beta-blockers
5) . α1-Adrenoceptor Blockers
6) . Dual α- & β- blockers
7) . alpha agonists
8) . RAAS inhibitors

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4
Q

what is the recommended initial therapy for all HTN patients?

A

Diuretics

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5
Q

Types of Diuretics

A

1) . Loop
2) . Thiazide
3) . K+ sparring

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6
Q

which diuretic is the most frequently used?

A

Thiazide

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7
Q

MOA of loop diuretics

A

inhibits reabsorption of Na+, K+, chlorine – prevents reabsorption of water

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8
Q

AE of Loop Diuretics

A

dehydration, hypokalemia, hyponatremia, hypocalcemia, ototoxicity, hyperglycemia, increased LDLs

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9
Q

PK/PD considerations for Loop Diuretics

A

may be taken along with supplemental K+ or K+ sparing diuretics to reduce risk of hypokalemia and metabolic alkalosis

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10
Q

Loop diuretics suffix

A

-ide

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11
Q

MOA for Thiazide diuretics

A

inhibits mechanism that favors Na+ reabsorption –> result in Na+ and K+ excretion and reabsorption of Ca2+

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12
Q

AE of Thiazide diuretics

A

similar to loop diuretics, may cause hypercalcemia and significant loss of K+

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13
Q

PK/PD considerations for Thiazide Diuretics

A

1) . may be given along w/loop diuretics in cases of CHF, severe edema
2) . favored for older adults to reduce Ca+ loss and maintain bone loss

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14
Q

which Diuretic is better choice for individuals prone to renal calculi?

A

Thiazide Diuretics

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15
Q

Thiazide Diuretic suffix

A

-azide

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16
Q

MOA for K+ sparring diuretics

A

inhibits the Na+/K+ exchange mechanism and limits the reabsorption of Na+ and excretion of K+. Limits osmotic gradient which drives reabsorption of water from tubule

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17
Q

AE of K+ sparring diuretics

A

hyperkalemia, nausea, lethargy, mental confusion

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18
Q

PK/PD considerations for K+ sparring diuretics

A

1) . less effective at producing diuresis but are K+ sparring
2) . Prevents hypokalemia (good for arrythmias)

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19
Q

Therapeutic Concerns with Diuretics

A

1) . look for signs of hypokalemia or hyperkalemia
2) . hyperglycemia and abnormal lipid levels
3) . dehydration
4) . DDIs with NSAIDs

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20
Q

T/F: there is a fall risk with diuretics

A

True: mental status can change due to hypo/hyperkalemia, dehydration

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21
Q

T/F: risk of orthostatic hypotension with diuretics

A

True, increased TPR

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22
Q

effect of NSAIDs in DDIs with diuretics

A

NSAIDs cause Na+ retention and decreases in renal perfusion –> cause diuretics to be less effective

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23
Q

MOA of direct vasodilators

A

inhibit smooth muscle contraction in arterioles to directly vasodilate the peripheral vasculature

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24
Q

AE of direct vasodilators

A

dizziness, orthostatic hypotension (reflex tachycardia - to compensate for fall in BP)

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25
Q

examples of direct vasodilators

A

apresoline and Loniten

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26
Q

T/F: direct vasodilators are commonly used

A

FALSE

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27
Q

MOA of Calcium-channel blocking vasodilators

A

block Ca2+ entrance into vascular smooth muscle, reducing smooth muscle tone and allowing for vasodilation

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28
Q

Classes of Ca-channel blocking vasodilators

A

1) . dihydropyridines
2) . phenylakylamines
3) . benzothiazepines

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29
Q

effect of dihydropyridines

A

reduce arteriole tone

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30
Q

effect of phenylalkylamines

A

affect the heart

31
Q

effect of benzothiazepines

A

affect heart and vasculature

32
Q

AE of Ca-channel blocking vasodilators

A

HA, dizziness, hypotension, bradycardia, reflex tachycardia, sweating, tremor, flushing, constipation

33
Q

PK/PD considerations for Ca-Channel blocking vasodilators

A

1) . useful when beta-blockers are contraindicated (asthma, DM, PVD)
2) . originally developed for treating cardiac disease

34
Q

MOA for beta-blockers

A

competitive antagonist, binds to beta receptors and prevents NE from binding, results in decrease HR, contractility and conduction

35
Q

types of beta-blockers

A

1) . non-selective

2) . cardioselective

36
Q

AE of Non-selective beta-blockers

A

contribution to peripheral vasoconstriction, bronchoconstriction, bradycardia, reduced exercise tolerance, dizziness, OH, depression, fatigue, sexual dysfunction

37
Q

abrupt withdrawl of Non-selective Beta-blockers results in ______

A

arrhythmia, angina, MI

38
Q

Non-selective beta-blockers suffix

A

-lol

39
Q

MOA of cardioselective beta-blockers

A

selectively block beta-1 receptors without causing bronchoconstriction

40
Q

AE of cardioselective beta-blockers

A

same as non-selective but no pulmonary effects

41
Q

therapeutic concerns for beta-blockers

A

1) . depresses HR and CO during exercise
2) . may contribute to orthostatic hypotension
3) . may cause CHF
4) . masks symptoms of hypoglycemia in diabetic pts.

42
Q

MOA of alpha-1 adrenoceptor blockers

A

reduces sympathetic tone of blood vessels causing VD and decreased peripheral vascular resistance

43
Q

AE of alpha-1 adrenoceptor blockers

A

orthostatic hypotension, nasal stuffiness, reflex tachycardia, arrhythmia

44
Q

seletive alpha-1 blockers suffix

A

-azosin

45
Q

therapeutic concerns for alpha-1 adrenoceptor blockers

A

fall risk

increased risk of CHF

46
Q

types of alpha agonists

A

alpha-1 receptor agonists

alpha-2 receptor agonists

47
Q

alpha-2 receptor agonists indications

A

HTN, anxiety/PTSD, spasticity

48
Q

central-acting alpha-2 agonist for HTN MOA

A

decrease sympathetic output from CNS (decrease NE) by binding to presynaptic

49
Q

AE of central-acting alpha-2 agonists

A

dizziness, drowsiness, fatigue, headache

50
Q

PT concerns for central-acting alpha-2 agonists

A

orthostatic hypotension, rebound hypertension

51
Q

central-acting alpha-2 agonist that is in the form of a weekly patch

A

clonidine

52
Q

clonidine indication

A

reserved for resistance HTN, ADHD, adjunct pain control

53
Q

AE of clonidine

A

dry mouth, rash

54
Q

what centrally acting alpha-2 agonist will be used with pregnant women w/HTN?

A

methyldopa

55
Q

AE of methyldopa

A

sexual dysfunction, sodium/water retention with long-term use

56
Q

Types of RAAS inhibitors

A

1) . Direct renin inhibitor (DRI)
2) . Angiotension 1 converting inhibitor (ACEi)
3) . Angiotensin II receptor blocker (ARB)

57
Q

DRI MOA

A

block conversion of angiotensinogen to angiotensin I

58
Q

AE of DRI

A

similar to ACEi and ARB

59
Q

ACEi MOA

A

blocks conversion of angiotensin I and angiotensin II

60
Q

downstream effects of ACEi

A

1) . increases blood vessel VD, bradykinin&raquo_space; increases VD

2) . decreases aldosterone secretion&raquo_space; decreases Na+ and H20 retention

61
Q

ACEi indications

A

HTN, reduced ejection fraction heart failure, post-MI, post-stroke, kidney disease

62
Q

Common ACEi AE

A

dry cough, hypotension/dizziness, hyperkalemia

63
Q

rare ACEi AE

A

acute renal failure, angioedmea

64
Q

PT concerns with ACEi

A

coughing, DDI with NSAIDs

65
Q

ACEi suffix

A

-pril

66
Q

ARB MOA

A

antagonist at receptor which blocks the binding of angiotensin II from the RAAS and other pathways

67
Q

ARB indications

A

alternative if ACEi intolerant in HTN, kidney disease, HF

68
Q

Common AE of ARB

A

hypotension/dizziness, hyperkalemia

69
Q

Rare AE of ARB

A

acute renal failure, angioedema

70
Q

ARB suffix

A

-sartan

71
Q

which RAAS inhibitor is the best tolerated?

A

ARB

72
Q

Therapeutic concerns about ACEi

A

cough (instant referral), NSAIDs are contraindicated

73
Q

General therapeutic concerns for hypertensive agents

A

1) . orthostatic hypotension
2) . dehydration
3) . caution w/heat
4) . cannot use HR as exercise tolerance determinant
5) . depletion of electrolytes
6) . poly pharmacy

Pharmacology Test 2 (9 decks)

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