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
examples of direct vasodilators
apresoline and Loniten
26
T/F: direct vasodilators are commonly used
FALSE
27
MOA of Calcium-channel blocking vasodilators
block Ca2+ entrance into vascular smooth muscle, reducing smooth muscle tone and allowing for vasodilation
28
Classes of Ca-channel blocking vasodilators
1) . dihydropyridines 2) . phenylakylamines 3) . benzothiazepines
29
effect of dihydropyridines
reduce arteriole tone
30
effect of phenylalkylamines
affect the heart
31
effect of benzothiazepines
affect heart and vasculature
32
AE of Ca-channel blocking vasodilators
HA, dizziness, hypotension, bradycardia, reflex tachycardia, sweating, tremor, flushing, constipation
33
PK/PD considerations for Ca-Channel blocking vasodilators
1) . useful when beta-blockers are contraindicated (asthma, DM, PVD) 2) . originally developed for treating cardiac disease
34
MOA for beta-blockers
competitive antagonist, binds to beta receptors and prevents NE from binding, results in decrease HR, contractility and conduction
35
types of beta-blockers
1) . non-selective | 2) . cardioselective
36
AE of Non-selective beta-blockers
contribution to peripheral vasoconstriction, bronchoconstriction, bradycardia, reduced exercise tolerance, dizziness, OH, depression, fatigue, sexual dysfunction
37
abrupt withdrawl of Non-selective Beta-blockers results in ______
arrhythmia, angina, MI
38
Non-selective beta-blockers suffix
-lol
39
MOA of cardioselective beta-blockers
selectively block beta-1 receptors without causing bronchoconstriction
40
AE of cardioselective beta-blockers
same as non-selective but no pulmonary effects
41
therapeutic concerns for beta-blockers
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
MOA of alpha-1 adrenoceptor blockers
reduces sympathetic tone of blood vessels causing VD and decreased peripheral vascular resistance
43
AE of alpha-1 adrenoceptor blockers
orthostatic hypotension, nasal stuffiness, reflex tachycardia, arrhythmia
44
seletive alpha-1 blockers suffix
-azosin
45
therapeutic concerns for alpha-1 adrenoceptor blockers
fall risk | increased risk of CHF
46
types of alpha agonists
alpha-1 receptor agonists | alpha-2 receptor agonists
47
alpha-2 receptor agonists indications
HTN, anxiety/PTSD, spasticity
48
central-acting alpha-2 agonist for HTN MOA
decrease sympathetic output from CNS (decrease NE) by binding to presynaptic
49
AE of central-acting alpha-2 agonists
dizziness, drowsiness, fatigue, headache
50
PT concerns for central-acting alpha-2 agonists
orthostatic hypotension, rebound hypertension
51
central-acting alpha-2 agonist that is in the form of a weekly patch
clonidine
52
clonidine indication
reserved for resistance HTN, ADHD, adjunct pain control
53
AE of clonidine
dry mouth, rash
54
what centrally acting alpha-2 agonist will be used with pregnant women w/HTN?
methyldopa
55
AE of methyldopa
sexual dysfunction, sodium/water retention with long-term use
56
Types of RAAS inhibitors
1) . Direct renin inhibitor (DRI) 2) . Angiotension 1 converting inhibitor (ACEi) 3) . Angiotensin II receptor blocker (ARB)
57
DRI MOA
block conversion of angiotensinogen to angiotensin I
58
AE of DRI
similar to ACEi and ARB
59
ACEi MOA
blocks conversion of angiotensin I and angiotensin II
60
downstream effects of ACEi
1) . increases blood vessel VD, bradykinin >> increases VD | 2) . decreases aldosterone secretion >> decreases Na+ and H20 retention
61
ACEi indications
HTN, reduced ejection fraction heart failure, post-MI, post-stroke, kidney disease
62
Common ACEi AE
dry cough, hypotension/dizziness, hyperkalemia
63
rare ACEi AE
acute renal failure, angioedmea
64
PT concerns with ACEi
coughing, DDI with NSAIDs
65
ACEi suffix
-pril
66
ARB MOA
antagonist at receptor which blocks the binding of angiotensin II from the RAAS and other pathways
67
ARB indications
alternative if ACEi intolerant in HTN, kidney disease, HF
68
Common AE of ARB
hypotension/dizziness, hyperkalemia
69
Rare AE of ARB
acute renal failure, angioedema
70
ARB suffix
-sartan
71
which RAAS inhibitor is the best tolerated?
ARB
72
Therapeutic concerns about ACEi
cough (instant referral), NSAIDs are contraindicated
73
General therapeutic concerns for hypertensive agents
1) . orthostatic hypotension 2) . dehydration 3) . caution w/heat 4) . cannot use HR as exercise tolerance determinant 5) . depletion of electrolytes 6) . poly pharmacy