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Renal Exam > Pharmacology of HTN > Flashcards

Pharmacology of HTN Flashcards

1
Q

hypertension - general treatment concepts

A
  1. reducing cardiac output: decrease blood volume/stroke volume, heart rate, and contractility
  2. reducing systemic vascular resistance: vasodilation

recall: MAP = CO x SVR

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2
Q

pharmacologic treatment of HTN - classes

A

ABCDs:
1. ACE inhibitors / ARBs
2. beta blockers (BBs)
3. calcium channel blockers (CCBs)
4. diuretics

other:
-direct acting vasodilators
-alpha1 receptor blockers
-centrally acting alpha2 agonists

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3
Q

angiotensin converting enzyme inhibitors (ACEi) - MOA

A

*inhibit ACE (in the lungs; inhibits conversion of Ang I to Ang II) → decreased Ang II → decreased GFR by dilating (preventing constriction of) efferent arterioles
*note - ACEi dilate both afferent and efferent arterioles, but predominantly the efferent arteriole
*increased renin due to loss of negative feedback
*prevents inactivation of bradykinin → buildup of bradykinin → vasodilation

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4
Q

angiotensin converting enzyme inhibitors (ACEi) - cardiorenal effects

A

*vasodilation that results in reduced arterial and venous pressure and a reduction in ventricular afterload & preload
*natriuretic and diuretic
*depresses sympathetic activity
*inhibit cardiac and vascular hypertrophy

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5
Q

angiotensin converting enzyme inhibitors (ACEi) - uses

A

*HYPERTENSION
*HEART FAILURE
*proteinuria
*diabetic nephropathy

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6
Q

angiotensin converting enzyme inhibitors (ACEi) - examples

A

“-prils”:
*lisinopril
*captopril
*enalapril
*ramipril

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7
Q

angiotensin converting enzyme inhibitors (ACEi) - ADEs

A

*COUGH
*ANGIOEDEMA
*HYPERKALEMIA
*renal injury / increased serum creatinine
*contraindicated in pregnancy

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8
Q

angiotensin II receptor blockers (ARBs) - MOA

A

*selectively block binding of Ang II to AT1 receptor → inhibits vasoconstriction and prevents release of aldosterone
*net effect: decrease in fluid volume + peripheral vasodilation

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9
Q

angiotensin II receptor blockers (ARBs) - examples

A

“-sartans”
*losartan
*candesartan
*valsartan

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10
Q

angiotensin II receptor blockers (ARBs) - ADEs

A

*HYPERKALEMIA
*ANGIOEDEMA
*increased serum creatinine

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11
Q

beta blockers - MOA in HTN tx

A

*block beta 1 adrenergic receptors to lower BP via several mechanisms:
-blockade of cardiac beta1 receptors → decreased HR and decreased contractility → decreased cardiac output
-blockade of beta1 receptors in juxtaglomerular cells → blocks renin secretion

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12
Q

beta blockers - uses

A

*hypertension
*heart failure

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13
Q

metoprolol - receptor selectivity

A

beta1 selective beta blocker (cardioselective)

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14
Q

labetalol - receptor selectivity

A

blocks alpha1, beta1, and beta2

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15
Q

carvedilol - receptor selectivity

A

blocks alpha1, beta1, and beta2

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16
Q

beta blockers - ADEs

A

*drowsiness
*lethargy
*erectile dysfunction
*confusion
*AV nodal blockade → bradycardia → shock
*CAN MASK HYPOGLYCEMIA SYMPTOMS
*beta blockers that block beta2 (labetalol, carvedilol) can cause bronchoreactive events (exacerbate asthma & COPD)

17
Q

calcium channel blockers - MOA

A

*inhibit L-type calcium channels on vascular smooth muscle, cardiac myocytes, and nodal cells (SA and AV), inhibiting influx of calcium and resulting in:
1. reduced peripheral vascular resistance & reduced BP (vasodilation)
2. decreased contractility (negative inotropy) and decreased HR (negative chronotropy)

18
Q

dihydropyridine calcium channel blockers (DHP CCBs) - MOA

A

*inhibit L-type calcium channels, mainly in vascular smooth muscle
*predominantly vasodilators → main effect is to lower SVR

examples: amlodipine, nifedipine

19
Q

non-dihydropyridine calcium channel blockers (NDHP CCBs) - MOA

A

*inhibit L-type calcium channels, mainly in SA & AV nodes
*predominantly slow cardiac contractility & conduction → main effect is to lower HR

examples: verapamil, diltiazem

20
Q

dihydropyridine calcium channel blockers - examples

A

*amlodipine
*nifedipine

21
Q

dihydropyridine calcium channel blockers - uses

A

*more selective as vasodilators
*used for HTN

examples: amlodipine, nifedipine

22
Q

dihydropyridine calcium channel blockers - ADEs

A

*flushing
*headache
*EDEMA
*gingival hyperplasia

examples: amlodipine, nifedipine

23
Q

what causes the edema ADE associated with DHP CCBs?

A

*edema is due to increased capillary hydrostatic pressure from preferential pre-capillary arteriolar vasodilation

24
Q

non-dihydropyridine calcium channel blockers - examples

A

*verapamil
*diltiazem

25
Q

non-dihydropyridine calcium channel blockers - uses

A

*predominantly used for lowering heart rate and contractility
*AV nodal blocking activity → used for tachyarrhythmias and stable angina

examples: verapamil, diltiazem

26
Q

non-dihydropyridine calcium channel blockers - ADEs

A

*bradycardia
*can precipitate heart failure (avoid starting if in acute heart failure)
*gingival hyperplasia
*constipation

examples: verapamil, diltiazem

27
Q

hydralazine - drug class & MOA

A

*direct-acting vasodilator
*relaxes arterioles → decreased systemic vascular resistance → decreased BP

compensatory changes: tachycardia

28
Q

hydralazine - ADEs

A

*headaches
*flushing
*tachycardia
*LUPUS-LIKE SYNDROME (erythematous rash)

note - tachycardia may precipitate angina in pts with coronary artery disease

29
Q

minoxidil - drug class & MOA

A

*direct-acting vasodilator
*relaxes arterioles → decreased systemic vascular resistance → decreased BP

30
Q

minoxidil - ADEs

A

*fluid retention

31
Q

peripheral alpha1 receptor blockers - examples

A

“-zosins”
*prazosin
*doxazosin
*terazosin

32
Q

peripheral alpha1 receptor blockers (“-zosins”) - MOA

A

*stimulation of alpha1 receptors in periphery → vasoconstriction
*BLOCK ALPHA1 RECEPTORS (with this drugs) → VASODILATION → decreased SVR → decreased BP

33
Q

peripheral alpha1 receptor blockers (“-zosins”) - ADEs

A

*postural hypotension
*watch for first-dose syncope, dizziness, lethargy

34
Q

alpha2 receptor agonists - examples

A

*clonidine
*methyldopa

35
Q

alpha2 receptor agonists - MOA

A

*alpha2 are presynaptic receptors located on neurons that release NE
*NE activates alpha2 receptors → DECREASED NE RELEASE BY THE NEURON
*alpha2 receptor agonists → lower NE release → less smooth muscle contraction → lower BP

36
Q

clonidine - drug class, MOA, ADEs

A

*drug class: alpha2 receptor agonist
*MOA: act within the CNS on alpha2 receptors to decrease sympathetic outflow to CV system → decreased BP
*ADEs: sedation, dry mouth, decreased HR
*rebound hypertension if abrupt cessation

37
Q

methyldopa - drug class, MOA, ADEs

A

*alpha2 receptor agonist → less NE release → less smooth muscle contraction → decreased BP
*ADE: hemolytic anemia
*note - often used for HTN in pregnancy

38
Q

what medication should you give to a patient with CKD (chronic kidney disease) or proteinuria?

A

ACEi or ARB

Renal Exam (44 decks)

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