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RC Test 3 > B4.043 Pharmacology of Drugs to Treat HTN > Flashcards

B4.043 Pharmacology of Drugs to Treat HTN Flashcards

1
Q

risk of end organ damage is…

A

proportional to BP elevation

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2
Q

why does systolic BP increase with age

A

progressive stiffening of arterial circulation

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3
Q

discuss the differences between black and white patients with respect to HTN risk

A

HTN common in black people and occurs at a younger age
higher proportion of black people sensitive to salt in the diet
black patients 3-5x more likely to have renal complications and end stage kidney disease

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4
Q

which treatments work best for black patients

A

CCBs
diuretics
combination therapies work similarly in white and black patients

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5
Q

mechanism of action of diuretics

A

deplete body of sodium and reduce blood volume

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6
Q

mechanism of actions of agents that interact with angiotensin

A

reduce peripheral vascular resistance

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7
Q

mechanism of action of direct vasodilators

A

relax vascular smooth muscle and dilate resistance vessels

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8
Q

mechanism of action of sympatholytic agents

A

reduce peripheral vascular resistance, inhibit cardiac function, and increase venous pooling

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9
Q

starting point for antihypertensive treatment

A

lifestyle modifications

  • exercise
  • weight reduction
  • reduction of dietary fats, salt, alcohol
  • avoid or reduce smoking
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10
Q

why do lifestyle modifications help?

A

reduce risks

reduce number and doses of antihypertensive meds required for treatment

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11
Q

why can drug treatment be a hard sell

A

high BP not normally felt

need to take drugs despite feeling healthy

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12
Q

most common cause of treatment failure

A

noncompliance

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13
Q

in HTN meds there are wide variations in:

A

responsiveness to individual drugs

toxicity or frequency and nature of adverse effects

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14
Q

first line agents used in HTN

A

thiazide diuretics
ACE inhibitors
angiotensin receptor blockers (ARBs)
calcium channel blockers (CCBs)

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15
Q

mechanism of action of thiazides

A

inhibit NaCl reabsorption in distal convoluted tubule

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16
Q

2 main clinical uses for thiazide diuretics

A
  1. at low dose lower BP

2. at high dose second to loop diuretics in CHF

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17
Q

examples of thiazide/ thiazide like diuretics

A

names ending in -thiazide

chlorthalidone, indapamide, metolazone

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18
Q

preferred thiazide

A

cholorothalidone

long half life and proven reduction of CVD

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19
Q

what groups respond particularly well to thiazides

A

black and eldery

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20
Q

this drug class is composed of sulfonamides

A

thiazide/thiazide like diuretics

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21
Q

2 non heart related uses of thiazides

A

nephrolithiasis: reduce urinary Ca concentration

nephrogenic diabetes insipidus: reduce polyuria and polydipsia, paradoxical effect due to plasma volume reduction

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22
Q

primary adverse effects of thiazides

A

hypokalemia metabolic alkalosis
hyponatremia

hyperglycemia
hyperlipidemia
hyperuricemia
hypercalcemia

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23
Q

other thiazide toxicities

A

weakness, fatigability, paresthesias, erectile dysfunction

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24
Q

why does erectile dysfunction occur with thiazides

A

probably related to volume depletion

can add a PDE5 inhibitor like sildenafil to combat this

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25
Q

3 types of drugs that interact with the renin-angiotensin system

A
  1. direct renin inhibitor
  2. angiotensin converting enzyme inhibitors
  3. angiotensin receptor blockers
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26
Q

examples of ACE inhibitors

A

end in -pril

benazepril, captopril, enalapril, fosinopril, Lisinopril, moexipril, perindopril, quinapril, Ramipril, or trandolapril

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27
Q

captopril

A

active drug

all others are prodrugs

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28
Q

mechanism of action of ACE inhibitors

A

inhibits conversion of angiotensin I to angiotensin II

BP lowering mostly due to decrease in peripheral vascular resistance

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29
Q

why is there vasodilation with ACE inhibitors?

A

reduced angiotensin induced vasoconstriction

increased bradykinin levels

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30
Q

effects of increased bradykinin levels due to ACE inhibitors

A
  1. contribute to the antihypertensive effect

2. causes adverse effects of coughing and angioneurotic edema

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31
Q

how can you get rid of a cough with with ACE inhibs

A

switch to an ARB

gets rid of bradykinin effects

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32
Q

therapeutic characteristics of ACE inhibitors

A

lower BP without compromising blood supply to heart, brain, or kidneys
few, mild adverse effects
do not cause reflex sympathetic activation because of concurrent baroreceptor resetting/vagal activation

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33
Q

effectiveness of ACE inhibitors in different population

A

effective orally for monotherapy
lower BP in 50% of patients
most effective in young/middle ages Caucasians
less effective in elderly and African americans

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34
Q

what populations of patients are ACE inhibitors first choice treatments for

A

diabetics
chronic renal disease
LVH

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35
Q

adverse effects of ACE inhibitors

A

dry, hacking, nonproductive cough in 5-20% of patients
hyperkalemia
angioedema and anaphylaxis
acute renal failure in patients with bilateral renal artery stenosis
taste disturbances
pruritic maculopapular rash

36
Q

when should you not use ACE inhibitors

A 
in combo with ARBs or direct renin inhibitor
in pregnancy (2nd and 3rd trimester)
37
Q

examples of ARBs

A

end in -sartan

38
Q

2 important differences between ARBs and ACEI

A
  1. ARBs more specific than ACEI: do not affect bradykinin metabolism (less angioedema and cough)
  2. more complete inhibition of angiotensin action bc other enzymes can also generate angiotensin II
39
Q

examples of calcium channel blockers

A

verapamil, diltiazem (act on SA and AV nodes)

dihydropyridines (act in periphery): amlodipine and all others that end in -dipine

40
Q

mechanism of action of CCBs

A

blocking slow calcium channels will reduce intracellular Ca2+ > relax arteriolar smooth muscles > vasodilation and lower BP

41
Q

strongest CCB vasodilator

A

dihydropyridines like nifedipine

42
Q

CCB w strongest cardiac effects

A

verapamil

43
Q

diltiazem

A

action somewhere between nifedipine and verapamil

44
Q

most likely CCB to produce reflex tachycardia

A

dihydropyridines

cause pronounced vasodilation without inhibition of AV conduction

45
Q

CCBs that DO NOT cause reflex tachycardia

A

verapamil and diltiazem

depress SA and AV node conduction

46
Q

potential harmful cardiac effect of verapamil and diltiazem

A

bradycardia due to myocardial depression in the presence of SA node dysfunction
contraindicated in patients with SA or AV node abnormalities or CHF

47
Q

most common side effects of dhydropyridines

A

vascular side effects

headache, flushing, dizziness, and peripheral edema

48
Q

most common side effect fo verapamil

A

constipation

49
Q

mechanism of action of sympatholytic drugs

A

lower BP by acting on adrenergic receptors to reduce sympathetic vasomotor tone either as:
-peripheral antagonists that block receptors at nerve endings
OR
-central agonists that stimulate medullary receptors

50
Q

why are sympatholytic drugs not recommended for monotherapy

A

produce postural hypotension and sodium retention

add a diuretic

51
Q

cardioselective (B1 specific) B blockers

A

atenolol
betaxolol
bisoprolol
metoprolol

52
Q

cardioselective and vasodilatory B blockers

A

nebivolol

NO production

53
Q

noncardioselective B blockers

A

nadolol
propranolol
be careful w asthmatics (B2 blocker too)

54
Q

B blockers with intrinsic sypathomimetic activity

A

acebutolol
penbutolol
pindolol (B2 agonist)
carteolol (NO production)

55
Q

B blockers with combined a activity

A

carvedilol (a1 antagonist, blocks Ca2+ entry)

labetalol (a1 antagonist)

56
Q

mechanism of action of B blockers

A

lower BP by blocking B adrenergic receptors in:

  • heart to reduce CO (slow HR)
  • kidneys to reduce renin recreation
  • CNS to reduce sympathetic vasomotor tone
57
Q

efficacy in different populations

A

genetic and age efficacy opposite to diuretics

more effective in Caucasians and young hypertensives

58
Q

why are B blockers combined with other drugs?

A

counteract reflex tachycardia caused by vasodilation and increased renin secretion caused by thiazide and loop diuretics

59
Q

adverse effects of B blockers

A 
may worsen symptoms in patients with:
-reduced myocardial reserve
-asthma
-peripheral vascular insufficiency
-diabetes
may decrease exercise tolerance in patients with HF (usually increases exercise tolerance in most people, however)
60
Q

how do B blockers predispose to atherosclerosis

A

increase plasma triglycerides

decrease HDL cholesterol

61
Q

how do B blockers pose a risk of new onset diabetes

A

delay recovery of normoglycemia because they inhibit hyperglycemia responses mediated by epinephrine
this is why they are no longer 1st line treatment

62
Q

risk of abrupt cessation of B blockers

A

tachycardia, HTN, angina, MI

63
Q

renin inhibitor drug

A

aliskiren

64
Q

discuss the mechanism of action of aliskiren

A

orally active
dose dependent reduction of plasma renin
dose dependent reduction of BP
safety and tolerability similar to ACEI

65
Q

when should you avoid aliskiren

A

pregnancy

when taking ACEI or ARBs

66
Q

drugs that blocks renin secretion

A

clonidine

B blockers

67
Q

mechanism of action of clonidine

A

reduce renal sympathetic nerve activity

may also exert direct renal activity

68
Q

a1 antagonists

A

doxazosin, prazosin, terazosin

69
Q

mechanism of action of a1 antagonists

A

reduce NE induced vasoconstriction to dilate both arteries and veins
BP falls bc of decreased peripheral resistance

70
Q

when are a1 antagonists considered second line agents

A

in pts with benign prostatic hyperplasia

71
Q

common adverse effects of a1 antagonists

A

orthostatic hypotension, esp in older adults

drowsiness, dizziness, palpitations, headache, easy fatigability

72
Q

central acting sympatholytic drugs (a2 agonists)

A

clonidine
methyldopa
guanfacine

73
Q

why are a2 agonists last line drugs

A

significant CNS adverse effects, especially in older adults

74
Q

mechanism of action of a2 agonists

A

at in CNS as agonist on presynaptic a2 receptors in brainstem and reduce peripheral vascular resistance

75
Q

how can a2 agonists be given

A

orally- clonidine

transdermal patch- 2 hrs (methydopa) or 8-12 hrs (clonidine)

76
Q

which drug is limited to pregnancy?

A

methyldopa

77
Q

oral direct vasodilator

A 
hydralazine
minoxidil (K+ channel opener)
78
Q

IV direct vasodilators

A 
sodium nitroprusside (NO)
diazoxide (hyperpolarization by activating K+ channels)
fenoldopam (dopamine agonist)
enalaprilat (ACEI)
nicardipine (CCB)
hydralazine (preeclampsia/eclampsia)
79
Q

mechanism of direct vasodilators

A

act directly on vascular smooth muscle to cause relaxation and reduce vascular resistance

80
Q

which drugs dilate arteries selectively without affecting venous smooth muscle

A

hydralazine
minoxidil
diazoxide
fenoldopam

81
Q

which drug dilates both arteries and veins

A

sodium nitroprusside

82
Q

adverse effects of vasodilators

A

hypotension accompanied by:

  • reflex tachy
  • increased myocardial contractions
  • increased renin secretion
  • fluid retention
  • headaches
  • flushing
  • palpitations
  • dizziness
83
Q

distinct adverse effect of hydralazine

A

lupus like syndrome

84
Q

distinct adverse effect of minoxidil

A

hypertrichosis

topical ointment used to treat baldness

85
Q

what is resistant hypertension

A

hypertensive even with 2 drugs

86
Q

example of compensatory mechanisms evoked by one drug being treated with addition of other drugs

A

hydralazine decreases vascular resistance
compensatory reflex tachy (add B blocker)
compensatory salt and water retention (treat with diuretic)

87
Q

recommendations for treatment in pregnancy

A 
B blocker (labetalol)
CCB (nifedipine)
methyldopa and hydralazine may be used

RC Test 3 (22 decks)

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