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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

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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
3 types of drugs that interact with the renin-angiotensin system
1. direct renin inhibitor 2. angiotensin converting enzyme inhibitors 3. angiotensin receptor blockers
26
examples of ACE inhibitors
end in -pril | benazepril, captopril, enalapril, fosinopril, Lisinopril, moexipril, perindopril, quinapril, Ramipril, or trandolapril
27
captopril
active drug | all others are prodrugs
28
mechanism of action of ACE inhibitors
inhibits conversion of angiotensin I to angiotensin II | BP lowering mostly due to decrease in peripheral vascular resistance
29
why is there vasodilation with ACE inhibitors?
reduced angiotensin induced vasoconstriction | increased bradykinin levels
30
effects of increased bradykinin levels due to ACE inhibitors
1. contribute to the antihypertensive effect | 2. causes adverse effects of coughing and angioneurotic edema
31
how can you get rid of a cough with with ACE inhibs
switch to an ARB | gets rid of bradykinin effects
32
therapeutic characteristics of ACE inhibitors
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
33
effectiveness of ACE inhibitors in different population
effective orally for monotherapy lower BP in 50% of patients most effective in young/middle ages Caucasians less effective in elderly and African americans
34
what populations of patients are ACE inhibitors first choice treatments for
diabetics chronic renal disease LVH
35
adverse effects of ACE inhibitors
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
when should you not use ACE inhibitors
``` in combo with ARBs or direct renin inhibitor in pregnancy (2nd and 3rd trimester) ```
37
examples of ARBs
end in -sartan
38
2 important differences between ARBs and ACEI
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
examples of calcium channel blockers
verapamil, diltiazem (act on SA and AV nodes) | dihydropyridines (act in periphery): amlodipine and all others that end in -dipine
40
mechanism of action of CCBs
blocking slow calcium channels will reduce intracellular Ca2+ > relax arteriolar smooth muscles > vasodilation and lower BP
41
strongest CCB vasodilator
dihydropyridines like nifedipine
42
CCB w strongest cardiac effects
verapamil
43
diltiazem
action somewhere between nifedipine and verapamil
44
most likely CCB to produce reflex tachycardia
dihydropyridines | cause pronounced vasodilation without inhibition of AV conduction
45
CCBs that DO NOT cause reflex tachycardia
verapamil and diltiazem | depress SA and AV node conduction
46
potential harmful cardiac effect of verapamil and diltiazem
bradycardia due to myocardial depression in the presence of SA node dysfunction contraindicated in patients with SA or AV node abnormalities or CHF
47
most common side effects of dhydropyridines
vascular side effects | headache, flushing, dizziness, and peripheral edema
48
most common side effect fo verapamil
constipation
49
mechanism of action of sympatholytic drugs
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
why are sympatholytic drugs not recommended for monotherapy
produce postural hypotension and sodium retention | add a diuretic
51
cardioselective (B1 specific) B blockers
atenolol betaxolol bisoprolol metoprolol
52
cardioselective and vasodilatory B blockers
nebivolol | NO production
53
noncardioselective B blockers
nadolol propranolol be careful w asthmatics (B2 blocker too)
54
B blockers with intrinsic sypathomimetic activity
acebutolol penbutolol pindolol (B2 agonist) carteolol (NO production)
55
B blockers with combined a activity
carvedilol (a1 antagonist, blocks Ca2+ entry) | labetalol (a1 antagonist)
56
mechanism of action of B blockers
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
efficacy in different populations
genetic and age efficacy opposite to diuretics | more effective in Caucasians and young hypertensives
58
why are B blockers combined with other drugs?
counteract reflex tachycardia caused by vasodilation and increased renin secretion caused by thiazide and loop diuretics
59
adverse effects of B blockers
``` 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
how do B blockers predispose to atherosclerosis
increase plasma triglycerides | decrease HDL cholesterol
61
how do B blockers pose a risk of new onset diabetes
delay recovery of normoglycemia because they inhibit hyperglycemia responses mediated by epinephrine this is why they are no longer 1st line treatment
62
risk of abrupt cessation of B blockers
tachycardia, HTN, angina, MI
63
renin inhibitor drug
aliskiren
64
discuss the mechanism of action of aliskiren
orally active dose dependent reduction of plasma renin dose dependent reduction of BP safety and tolerability similar to ACEI
65
when should you avoid aliskiren
pregnancy | when taking ACEI or ARBs
66
drugs that blocks renin secretion
clonidine | B blockers
67
mechanism of action of clonidine
reduce renal sympathetic nerve activity | may also exert direct renal activity
68
a1 antagonists
doxazosin, prazosin, terazosin
69
mechanism of action of a1 antagonists
reduce NE induced vasoconstriction to dilate both arteries and veins BP falls bc of decreased peripheral resistance
70
when are a1 antagonists considered second line agents
in pts with benign prostatic hyperplasia
71
common adverse effects of a1 antagonists
orthostatic hypotension, esp in older adults | drowsiness, dizziness, palpitations, headache, easy fatigability
72
central acting sympatholytic drugs (a2 agonists)
clonidine methyldopa guanfacine
73
why are a2 agonists last line drugs
significant CNS adverse effects, especially in older adults
74
mechanism of action of a2 agonists
at in CNS as agonist on presynaptic a2 receptors in brainstem and reduce peripheral vascular resistance
75
how can a2 agonists be given
orally- clonidine | transdermal patch- 2 hrs (methydopa) or 8-12 hrs (clonidine)
76
which drug is limited to pregnancy?
methyldopa
77
oral direct vasodilator
``` hydralazine minoxidil (K+ channel opener) ```
78
IV direct vasodilators
``` sodium nitroprusside (NO) diazoxide (hyperpolarization by activating K+ channels) fenoldopam (dopamine agonist) enalaprilat (ACEI) nicardipine (CCB) hydralazine (preeclampsia/eclampsia) ```
79
mechanism of direct vasodilators
act directly on vascular smooth muscle to cause relaxation and reduce vascular resistance
80
which drugs dilate arteries selectively without affecting venous smooth muscle
hydralazine minoxidil diazoxide fenoldopam
81
which drug dilates both arteries and veins
sodium nitroprusside
82
adverse effects of vasodilators
hypotension accompanied by: - reflex tachy - increased myocardial contractions - increased renin secretion - fluid retention - headaches - flushing - palpitations - dizziness
83
distinct adverse effect of hydralazine
lupus like syndrome
84
distinct adverse effect of minoxidil
hypertrichosis | topical ointment used to treat baldness
85
what is resistant hypertension
hypertensive even with 2 drugs
86
example of compensatory mechanisms evoked by one drug being treated with addition of other drugs
hydralazine decreases vascular resistance compensatory reflex tachy (add B blocker) compensatory salt and water retention (treat with diuretic)
87
recommendations for treatment in pregnancy
``` B blocker (labetalol) CCB (nifedipine) methyldopa and hydralazine may be used ```

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