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Renal Exam III > Clinical Pharm of Antihypertensives > Flashcards

Clinical Pharm of Antihypertensives Flashcards

1
Q

Choice of therapy in Primary hypertension

General classes typically employed as initial monotherapy:

A

i) ACE Inhibitors/ARBs
ii) Calcium channel blockers (long-acting)
iii) Thiazide diuretics
iv) Beta-blockers are NOT typically used in the absence of a specific indication

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2
Q

Choice of therapy in primary hypertension

Exhibit roughly equal efficacy, but some patients will respond to one drug and not to another

A

i) Some predictable differences, e.g., black patients respond better to thiazide diuretics and CCBs, and respond poorly to ACE inhibitors and beta-blockers
ii) ACE inhibitors and ARBs are recommended in mild-to-moderate chronic kidney disease with or without diabetes because these agents are renoprotective
iii) See also table below from UpToDate, will make cards for those

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3
Q

Generally, the magnitude of BP reduction, not choice of drug predicts reduction of what?

A

Cardiovascular risk

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4
Q

Why is monotherapy of hypertension advantageous?

A

increase in patient compliance, a decrease in cost, and less adverse effects

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5
Q

Rationale behind polypharmacy

A

1) each of the drugs acts on one of a set of interacting, mutually compensatory regulatory mechanisms for maintaining blood pressure
2) minimal toxicity: Two or three drugs at half standard doses might have greater efficacy and less toxicity than one drug at standard or twice standard dose

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6
Q

When do you add a second drug for hypertension

A

when hypertension does not respond adequately to a regimen of one drug, a second drug from a different class with a different MOA and different pattern of toxicity is added

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7
Q

Combination of hypertension drugs

A

i) ACEIs and calcium channel blockers (trandolapril/verapamil)
ii) ACEIs and diuretics (benazepril/hydrochlorothiazide)
iii) ARBs and diuretics (valsartan/hydrochlorothiazide)
iv) β-blockers and diuretics (propranolol/hydrochlorothiazide)
v) Centrally acting agent and diuretic (reserpine/chlorothiazide)
vi) Diuretic and diuretic (spironolactone/hydrochlorothiazide)
vii) Triple drug regimens are also common and typically include a thiazide diuretic, a dihydropyridine CCB, and either an ACE inhibitor, an angiotensin receptor blocker, or a renin inhibitor

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8
Q

Loop and thiazide diuretics in combination

A

(1) Can be combined if patients fail or become refractory to the usual dose of loop diuretics

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9
Q

Systolic Heart Failure Drug indication

A

ACE inhibitor or ARB blocker, beta blocker, diuretic, aldosterone antagonist

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10
Q

Post-myocardial infarction indication

A

ACE inhibitor, beta blocker, ARB, aldosterone antagonist

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11
Q

Proteinuric chronic kidney disease indication

A

ACE inhibitor or ARB

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12
Q

Angina Pectoris indication

A

Beta Blocker, Calcium channel blocker

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13
Q

Atrial fibrillation rate control indication

A

Beta blocker, nondihydropyridine calcium channel blocker

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14
Q

Atrial flutter rate control indication

A

Beta blocker, nondihydropyridine calcium channel blocker

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15
Q

BPH with htn indication

A

alpha blocker

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16
Q

essential tremor with htn indication

A

beta blocker (noncardioselective)

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17
Q

hyperthyroidism with htn indication

A

beta blocker

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18
Q

migraine with htn indication

A

beta blocker or calcium channel blocker

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19
Q

Osteoporosis with htn indication

A

thiazide diuretic

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20
Q

Raynauds with htn indication

A

dihydropyridine calcium channel blocker

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21
Q

Andgioedema contraindication

A

ACE inhibitor

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22
Q

Bronchospastic disease contraindication

A

beta blocker

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23
Q

depression contraindication

A

reserpine

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24
Q

liver disease contraindication

A

methyldopa

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25
Q

pregnancy contraindication

A

ACE inhibitor, ARB, renin inhibitor

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26
Q

Second or third degree heart block contraindication

A

beta blocker, nondihydropyridne

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27
Q

Adverse effect on comorbid conditions depression

A

Beta blocker, central alpha-2-agonist

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28
Q

adverse effect on comorbid condition gout

A

diuretic

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29
Q

adverse effect of comorbid condition hyperkalemia

A

aldosterone antagonist, ACE inhibitor, ARB, renin inhibitor

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30
Q

Adverse effect on comorbid condistion renovascular disease

A

ACE inhibitor, ARB, or renin inhibitor

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31
Q

Loop agents and thiazides in combination will often produce diuresis when either agent acting alone is minimally effective (2 reasons)

A

(a) Salt and water reabsorption in either the thick ascending loop (blocked by loop diuretics) or DCT (blocked by thiazides) can increase when the other is blocked; inhibition of both can produce more than an additive diuretic response
(b) Thiazides often produce mild natriuresis (sodium excretion) in the PCT that is usually masked by increased absorption in the thick ascending loop; this combination can therefore block Na+ reabsorption from all three segments (PCT, ascending loop, and DCT)

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32
Q

Metolazone (thiazide) is a popular choice for combination with?

A

loop agents

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33
Q

Combination can cause profuse diuresis and therefore

A

routine outpatient use is not recommended (K+ wasting is extremely common)

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34
Q

Potassium-sparing diuretics and loop agents or thiazides

A

(1) Hypokalemia is a common side effect of loop agents and thiazide diuretics, which can initially be managed with dietary NaCl restriction (decreases Na+ delivery to the K+-secreting CCT, thus reducing K+ secretion; has also been shown to potentiate the effects of diuretics in essential HTN) or KCl supplementation
(2) Alternatively, the addition of K+-sparing diuretics can lower K+ secretion
(3) This combination is generally safe but should be avoided in patients with renal insufficiency and in those receiving angiotensin antagonists

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35
Q

COMBINATIONS TO AVOID

A

i) ACE inhibitors, ARBs, and renin inhibitors (only one at a time)
ii) Beta-blockers and non-dihydropyridine CCBs
iii) Potassium-sparing diuretics and ACE inhibitors/ARBs/renin inhibitors

36
Q

Hypertensive Urgency

A

Severe hypertension (> 180/120 mmHg) without acute end-organ damage

37
Q

Hypertensive Emergency

A

Severe hypertension (> 180/120 mmHg) with acute end-organ damage

38
Q

controlled and gradual BP reduction (10-20% in the first hour and by a further 5-15% over the next 23 hr) may prevent

A

excessive hypotension that could lead to MI, stroke, or loss of vision

39
Q

Vasodilators (IV)

A 
Sodium nitropursside
nitroglycerin
nicardipine
clevidipine
enalaprilat
Fenoldopam
hydralazine
40
Q

Sodium nitroprusside

A

considered the most effective parenteral drug for hypertensive emergencies; potential for cyanide toxicity limits prolonged use

41
Q

nitroglycerin

A

less antihypertensive efficacy than other agents for HTN emergencies; useful adjunct in patients with cardiac ischemia or after coronary bypass surgery

42
Q

nicardipine

A

DHP-CCB with longer onset of action and longer elimination half-life, but good safety profile

43
Q

Clevidipine

A

ultra short-acting DHP-CCB is approved only for hypertensive emergencies

44
Q

Enalaprilat

A

rarely used due to slow onset and long duration of action; hypotensive response is unpredictable and dependent on plasma volume and plasma renin activity

45
Q

Fenoldopam

A

maintains or increases renal perfusion by dilating renal arteries; possibly a good choice for patients with renal dysfunction; avoid in glaucoma

46
Q

Hydralazine

A

use of parenteral form limited by prolonged and unpredictable hypotensive effect; considered safe in pregnant patients

47
Q

Adrenergic agonists (IV)

A

Phentolamine
Esmolol
labetolol

48
Q

Phentolamine

A

nonselective α-blocker used to treat patients with hypertension due to elevated catecholamines (cocaine intoxication, pheochromocytoma)

49
Q

Esmolol

A

rapid but short-acting β1-blocker used to treat aortic dissection or postoperative hypertension

50
Q

Labetolol

A

combined α- and β-blocker that may be safe in patients with active coronary disease

51
Q

Considerations for pharmacotherapy with htn in pregnancy

A

i) Consider risks and benefits for both mother and fetus
ii) Maternal benefit is well-established for treatment of severe hypertension (systolic pressure ≥ 160 mmHg and/or diastolic pressure ≥ 110) in reduction of stroke risk
(1) Timing of delivery: if cesarean delivery is imminent, pharmacotherapy may not be necessary
iii) Maternal or fetal benefits have not been shown for treatment of mild to moderate hypertension
iv) All anti-hypertensives cross the placenta; some may inhibit fetal growth

52
Q

Acute management for severe hypertension in pregnancy drug choices

A

labetalol (IV)
Hydralazine (IV)
Calcium channel blockers
Nitroglycerin (IV)

53
Q

Acute management for severe hypertension in pregnancy labetalol

A

effective, rapid onset of action, good safety profile

54
Q

Acute management for severe hypertension in pregnancy hydralazine

A

has been used extensively in the setting of preeclampsia

55
Q

Acute management for severe hypertension in pregnancy calcium channel blockers

A

sustained release nifedipine or immediate release nicardipine; nicardipine can also be given IV; data is more limited for use in pregnancy compared to labetalol and hydralazine

56
Q

Acute management for severe hypertension in pregnancy nitroglycerin

A

is a good option for HTN associated with pulmonary edema

57
Q

Long-term oral therapy for htn in pregnancy drug options

A 
methyldopa
labetalol
nifedipine (ER)
hydralazine
thiazide diuretics
58
Q

Long-term oral therapy for htn in pregnancy methyldopa

A

long-term safety for the fetus has been demonstrated; mild antihypertensive of limited efficacy; sedative effect is bothersome to already fatigued patients; clonidine is another centrally acting sympatholytic that is considered safe in pregnant women

59
Q

Long-term oral therapy for htn in pregnancy labetolol

A

more rapid onset of action than methyldopa; alternatives in this category include pindolol and long-acting metoprolol; safety is controversial

60
Q

Long-term oral therapy for htn in pregnancy nifedipine

A

other CCBs , including non-DHPs, have been used in pregnant patients, but only small numbers of patients are reported in the literature

61
Q

Long-term oral therapy for htn in pregnancy hydralazine

A

Due to reflex tachycardia, monotherapy with oral hydralazine is not recommended; hydralazine may be combined with methyldopa or labetalol if needed as add-on therapy

62
Q

Long-term oral therapy for htn in pregnancy thiazides

A

use is controversial due to potential fluid loss; some guidelines suggest they are safe to continue in patients who began taking them prior to pregnancy; generally only introduced during pregnancy if pulmonary edema has developed

63
Q

Agents contraindicated during pregnancy

A

ACE inhibitors, ARBs, direct renin inhibitors and nitroprusside

64
Q

contraindicated during pregnancy ACE inhibitors, ARBs, direct renin inhibitors

A

these drugs are associated with significant fetal renal and cardiac abnormalities

65
Q

contraindicated during pregnancy Nitroprusside

A

possible fetal cyanide poisoning if used for more than a few hours; last resort for urgent control of severe refractory HTN

66
Q

Clinical pharmacology of diuretic agents

A

a) A common use for diuretics is for the reduction of peripheral or pulmonary edema that has accumulated as a result of cardiac, renal, or vascular diseases that reduce blood delivery to the kidney
b) Physiologically, this reduction is sensed as a lack of effective arterial blood volume and leads to salt and water retention, followed by edema formation

67
Q

edematous states treated with diuretics

A

Heart failure
kidney disease
hepatic cirrhosis

68
Q

Heart failure diuretics use

A

(1) Heart failure reduces cardiac output, which results in a decrease in blood pressure and blood flow to the kidney
(2) Decreases in BP and blood flow is sensed as hypovolemia and leads to renal retention of salt and water
(3) Pulmonary or interstitial edema occur when the plasma volume increases and the kidney continues to retain salt and water, which then leaks from the vasculature

69
Q

Kidney disease diuretic use

A

(1) Most kidney diseases cause retention of salt and water
(2) When loss of renal function is severe, there is insufficient glomerular filtration to sustain a natriuretic response and diuretic agents are of little benefit
(3) Patients with mild cases of renal disease can be effectively treated with diuretics when they retain sodium
(4) Diuretics are beneficial in glomerular diseases, such as systemic lupus erythematosus or diabetes mellitus, that exhibit renal retention of salt and water
(5) Loop and thiazide diuretics are beneficial in individuals that develop hyperkalemia associated with early stage renal failure

70
Q

Hepatic cirrhosis diuretic use

A

(1) Diuretics are useful when edema and ascites (accumulation of fluid in the abdominal cavity) become severe due to liver disease
(2) Aggressive use of diuretics can be disastrous in patients with liver disease (more so than heart failure)

71
Q

Nonedematous states treated with diuretics

A

Htn
Nephrolithiasis
Hypercalcemia
Diabetes insipidus

72
Q

Htn diuretic use

A

(1) Thiazides are often used because of their diuretic and mild vasodilator activities
(2) Loop diuretics are often reserved for patients with mild renal insufficiency or heart failure
(3) Diuretics are often used in combination with vasodilators (hydralazine, minoxidil) because vasodilators cause significant salt and water retention

73
Q

nephrolithiasis diuretic use

A

(1) 2/3 of kidney stones contain calcium phosphate or calcium oxalate
(2) Thiazide diuretics enhance Ca2+ reabsorption in the DCT and reduce urinary Ca2+ concentration, making them appropriate agents in the treatment of kidney stones

74
Q

hypercalcemia diuretic use

A

(1) Loop diuretics reduce Ca2+ reabsorption and promote Ca2+ diuresis, but can also cause marked volume contraction when used alone (counterproductive)
(2) Saline can be administered simultaneously with loop diuretics to maintain effective Ca2+ diuresis

75
Q

Dibetes insipidus diuretic use

A

(1) Can be due to either deficient production of ADH (neurogenic or central diabetes insipidus) or inadequate responsiveness to ADH (nephrogenic diabetes insipidus)
(2) Supplementary ADH or one of its analogs is only effective in central diabetes insipidus
(3) Thiazide diuretics can reduce polyuria and polydipsia in both types of diabetes insipidus

76
Q

Centrally acting sympatholytic agents hemodynamic effects

A

decrease - heart rate, co, tpr, and plasma renin activity

increase - plasma volume

77
Q

alpha receptor antagonists hemodynamic effects

A

decrease - tpr

increase - heart rate, co, plasma volume

same - plasma renin activity

78
Q

Diuretics effect on hemodynamics

A

same - heart rate, co

decrease - tpr and plasma volume

increase plasma renin activity

79
Q

no ISA beta receptor antagonists hemodynamic effect

A

decrease - heart rate, cardiac output, tpr and plasma renin activity

increase - plasma volume

80
Q

ISA beta receptor antagonist hemodynamic effects

A

same - heart rate, co

increase - plasma volume

decrease - tpr and plasma renin activity

81
Q

Arteriolar vasodilators hemodynamic effect

A

increase - heart rate, co, plasma volume and palamsa renin activity

decrease - tpr

82
Q

Calcium channel blockers hemodynamic effect

A

increase or decrease - heart rate and co

increase - plasma volume and plasma renin activity

decrease - tpr

83
Q

ACE inhibitors hemodynamic effect

A

same - heart rate, co and plasma volume

increase - plasma renin activity

decrease - tpr

84
Q

renin inhibitor hemodynamic effect

A

same - heart rat, co and plasma volume

decrease - tpr, plasma renin activity (but renin levels increase)

85
Q

AT1 receptor antagonists hemodynamic effect

A

same - heart rat, co and plasma volume

decrease - tpr, plasma renin activity

Renal Exam III (17 decks)

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