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8 Cards in this Set
- Front
- Back
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What is the normal pathway to activation and effect of the RAAS? |
Hypotension leads to renal secretion of renin which cleaves hepatically released angiotensinogen to A-1 which is converted by ACE to A-2 which stimulates renal release of aldo which leads to sodium conservation and volume retention.
BOTTOM LINE: RAAS INCREASES BP |
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What is the mechanism of ACE-I? |
Prevent conversion of angiotensin-1 to angiotensin-2, thus prevention of: vasoconstriction hyperfiltration through kidneys vascular and cardiac remodeling
Also prevents the inactivation of bradykinin, thus concentration stays high leading to vasodilation |
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What are the therapeutic uses of RAAS inhibitors?
Are there any differences between ACE-I and ARBs? |
Anti-hypertensive (can prevent LVH) Secondary prevention of vascular disease Improve survival and hemodynamics in patients with CHF Protection against hypertensive nephropathy
Similar effects of ACE-I to ARBs in monotherapy for reduction of blood pressure |
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What are the side effects of ACE-I?
Which are seen especially with captopril? |
Hypotension Renal insufficiency Hyperkalemia Angioedema Cough Captopril: neutropenia, nephrotic syndrome, skin rash, dysguesia
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What are the major contraindications for ACE-I? |
Intolerance (pt. gets angioedema, allergy, anuric renal failure) Bilateral renal artery stenosis (bc then not enough pressure to perfuse kidneys --> failure) Pregnancy Renal insufficiency Hyperkalemia Severe hypotension |
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What is the mechanism for ARBs? |
Prevent the binding of A-2 to the AT1 receptor (which normally causes vasoconstriction)
Allows binding to the AT2 receptor which promotes vasodilation
Lack of bradykinin effect |
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How are the side effects of ARBs different than ACE-I? |
No cough, less angioedema, less rash |
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What are the secondary benefits of ACE-I? |
Prevention of arterial disease Slow pathogenic remodeling of the heart Reduces post MI mortality Reduce the progression of renal disease (esp. in patients with DM) |
