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Renal II Final > ACE inhibitors and ARBs > Flashcards

ACE inhibitors and ARBs Flashcards

1
Q

ACE inhibitors

A 
Benazepril
Captopril
Enalapril
Enalaprilat
Fosinopril
Lisinopril
Moexipril
Perindopril
Quinapril
Ramipril
Trandolapril
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2
Q

Angiotensin receptor blockers

A 
Azilsartan
Candesartan
Eprosartan
Irbesartan
Losartan
Olmesartan
Telmisartan
Valsartan
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3
Q

Drugs that block renin secretion

A

Clonidine

propranolol

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4
Q

Renin inhibitor

A

Aliskiren

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5
Q

Renin

A
  • Aspartyl protease
  • Catalyzes conversion of angiotensinogen to angiotensin 1
  • Synthesized and stored in the juxtaglomerular apparatus of the nephron
  • Sympathetic stimulation activates B1 adrenergic receptors on juxtaglomerular cells, stimulates the release of renin
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6
Q

Angiotensinogen

A
  • Synthesized in the liver
  • Cleaved by renin into angiotensin 1
  • Angiotensinogen increased by corticosteroids, estrogens, thyroid hormones, and angiotensin II
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7
Q

Angiotensin I

A
  • Cleaved to angiotensin II by angiotensin converting enzyme (ACE)
  • Pharmacological responses to these peptides are indistinguishable due to the rapid conversion
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8
Q

Angiotensin II

A
  • Exerts actions at vascular smooth muscle (contraction), adrenal cortex (aldosterone synthesis), kidney (renin secretion inhibition), heart (hypertrophy), and brain (reset baroreceptor)
  • Angiotensin II 40x more potent vasoconstrictor than epi
  • Most active angiotensin peptide
  • Activates GPCR angiotensin II receptor
  • Rate determined by renin
  • Removed rapidly by angiotensinase
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9
Q

Converting Enzyme (ACE)

A
  • Converts angiotensin I to angiotensin II
  • Bradykinin (vasodilator) is inactivated by ACE
  • Widely distributed and on luminal surface of vascular endothelial cells
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10
Q

Angiotensin II receptors

A
  • AT1 is the major receptor in adults. AT2 is also a receptor. Both GPCR
  • AT1 is Gq activating IP3 and DAG causing smooth muscle contraction
  • AT2 activates bradykinin and NO causing vasodilation
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11
Q

Aldosterone

A
  • Promotes reabsorption of Na from distal convoluted tubule
  • Increases ENaC and Na/K ATPase to increase Na reabsorption and K secretion
  • Causes increased H2O retention, increased blood volume, increased BP and hypokalemia
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12
Q

What drugs inhibit the RAAS system?

A

Ace inhibitors and ARBs

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13
Q

ACEIs MOA

A
  • Inhibition of ACE to conversion to angiotensin II
  • Lower BP by decreasing peripheral vascular resistance
  • They don’t impact cardiac output or HR
  • Approved for HTN, nephropathy, heart failure, left ventricular dysfunction, AMI, prophylaxis of cardiovascular events
  • Dosing based on half life
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14
Q

Angiotensin receptor blockers (ARBs) MOA

A
  • Selective blockade of AT1-type receptors
  • No effect on bradykinin metabolism
  • Tx for HTN, diabetic nephropathy, HF, left ventricular dysfunction, prophylaxis of cardiovascular events
  • Blockade of angiotensin II induced contraction of vascular smooth muscle, pressor responses, aldosterone secretion, changes in renal function, cellular hypertrophy and hyperplasia
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15
Q

Differences between ARBs and ACEIs

A
  • ARBs reduce activation of AT1 receptors more effectively than do ACEIs
  • ARBs permit activation of AT2 receptors
  • ACEIs increase the levels of number of ACE substrates including bradykinin
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16
Q

ARB toxicities and adverse effects

A
  • Cough and angioedema occur at lower rates
  • Not recommended in patients with non diabetic renal disease or pregnancy
  • Avoid use with potassium supplements or potassium sparing diuretics
17
Q

Clonidine MOA

A
  • Agonist of a2-receptors in the brainstem
  • a2-receptors cause inhibition of sympathetic vasomotor centers resulting in a centrally mediated reduction in renal sympathetic nerve activity
  • Ultimate effect is reduction in renin secretion
18
Q

Propranolol MOA

A
  • Nonspecific antagonist of adrenergic B-receptors
  • Block B1-receptors on juxtaglomerular cells which release renin and thereby decrease BP
  • Also decreases cardiac output and decreases sympathetic outflow from CNS
19
Q

Aliskiren

A
  • Renin inhibitor
  • Dose-dependent reduction in plasma renin activity, decreased angiotensin I and II and aldosterone concentrations
  • *Decrease in baseline renin is in contrast to the rise seen from ACEIs, ARBs, and diuretics
  • 85-90% of the effect is in 2 weeks of therapy starting
  • Possible fetal and neonatal morbidity and mortality when used during pregnancy
  • Use caution in patients with kidney insufficiency
20
Q

Polypharmacy

A

-When HTN doesn’t respond to a regimen enough from one drug, a second is added with a different MOA in order to try and lower it more

21
Q

ACEI adverse effects and contraindications

A
  • Adverse effects: hypotension, acute renal failure, renal stenosis, hyperkalemia, dry cough, angioedema
  • Common side effect: cough
  • Contraindicated in pregnancy: fetal hypotension, anuria, renal failure in 2-3 trimesters; malformations, death 2-3 trimesters; teratogenicity 1st trimester
  • Avoid K supplements or K sparing diuretics and NSAIDs

Renal II Final (5 decks)

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