RAAS antagonists Flashcards

1
Q

Angiotensin converting enzyme inhibitors example

A

Lisinopril

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2
Q

ACEI MOA in HF

A

Inhibits ACE conversion of Ang I to Ang II, blocking Ang II-induced vasoconstriction and decreasing preload/afterload. Other mechanism is decrease of Ang II-induced release of aldosterone which moderates the myocardial hypertrophy and remodeling response to aldosterone. Decreases Bradykinin, reduces SNS

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3
Q

ACEI pharmacokinetics

A

All are well absorbed orally. All ACEIs, except lisinopril and captopril, are prodrugs that are converted to the active metabolite in the liver. • The active metabolites are primarily eliminated by the kidneys (except moexipril and fosinopril). Once daily dosing

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4
Q

Describe dosing for ACEI

A

start at low dose then titrate to goal

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5
Q

ACEI side effects

A

Contraindicated in pregnancy. Dry cough, Hyperkalemia, hypotension, acute renal failure

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6
Q

Angiotensin II receptor (AT1) Antagonists examples

A

Valsartan, Losartan

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7
Q

ARBs MOA in HF

A

Prevent remodeling and reduce SNS. Similar to ACEI

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8
Q

Compare and contrast ACEI and ARBs

A

ARBs have more complete block of angiotensin action since ACEI do not block alternative pathways. ARBs do not affect bradykinins so NO cough. ARBs only block actions at AT1 receptors while ACEIs will block actions mediated by both AT1 and AT2

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9
Q

ARBs pharmacokinetics

A

Oral

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10
Q

ARBs side effects

A

contraindicated in pregnancy, NO cough or angioedema.

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11
Q

Should ACEI and ARBs be used together?

A

No apparent benefit from dual therapy

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