ACEI (amboss and UW) Flashcards
ACEI agents?
captopril, enalapril, lisinopril, ramipril, benazepril
ACEI indicatons?
Arterial hypertension
Diabetes mellitus (type I and type II)
HF with reduced ejection fraction
History of MI
Nondiabetic chronic kidney disease with proteinuria
Scleroderma-associated hypertensive crisis (even if creatinine is elevated)
Why ACEI used in DM?
Nephroprotective indications, such as: Arterial hypertension, Microalbuminuria and proteinuria (especially ≥ 300 mg/g)
Coronary heart disease
ACE inhibitors and ARBs are generally recommended in hypertensive diabetic patients to reduce the risk of cardiovascular events, but they are strongly recommended in diabetic patients with concurrent hypertension and an elevated urinary albumin-to-creatinine ratio (as an indicator for microalbuminuria).
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Why ACEI used in CHD?
To reduce the risk of cardiovascular events.
There is minimal evidence to support primary prevention of moderately increased albuminuria in normotensive and normoalbuminuric type I and type II diabetes. Annual screening to identify persistently increased albuminuria is recommended instead. Treatment with a RAAS inhibitor may be considered if albuminuria persists to delay progression towards severely increased albuminuria, especially in patients with type I diabetes, and cardiovascular events
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ACEI has similar effect of what drug?
Amyl nitrite is a vasodilator that mimics the effects of ACE inhibitors on the heart.
Why ACEI used in MI?
The ability of ACE inhibitors to attenuate ventricular dilatation (remodeling) after an MI is responsible for its survival benefit. Patients will still derive benefit from ACE inhibitors or ARBs if they are not administered immediately after the event.
ACEI mechanism?
Mechanism of action: inhibition of ACE → ↓ conversion of angiotensin I to angiotensin II
ACEI effect on GFR?
Dilation of efferent arteriole → ↑ renal plasma flow → ↓ GFR → ↓ filtration fraction
ACEI effect on blood pressure? 2
↓ Vasoconstriction → ↓ blood pressure
↓ Secretion of aldosterone → ↓ reabsorption of Na+ and water → ↓ blood pressure
ACEI on renin secretion?
↑ Renin secretion (due to lack of feedback inhibition) → ↑ angiotensin I
ACEI and bradykinin?
↓ Breakdown of bradykinin → ↑ production of arachidonic acid metabolites → ↑ vasodilation → ↓ blood pressure
ACEI on proteinuria and proteinuric CKD?
↓ Proteinuria and ↓ progression of proteinuric chronic kidney disease: ↓ intraglomerular hydrostatic pressure attenuates thickening and sclerosis of the GBM
ACEI on preload and afterload?
↓ Preload and afterload → ↓ cardiac remodeling after acute myocardial infarction or in chronic hypertensive disease
Increase in bradykinin concentration, which can lead to? 2
Dry cough (can be treated by discontinuing ACE inhibitor, consider switching to ARB)
Bradykinin-mediated angioedema due to increased vascular permeability and vasodilation
Why dry cough in bradykinin?
The mechanism is not fully understood. However, protussive and proinflammatory effects from local accumulation of bradykinin (and other mediators) in the lung are considered most likely.
Adverse of ACEI?
Hypotension
↓ GFR (with ↑ creatinine): can cause AKI in patients with preexisting renal hypoperfusion (e.g., renal artery stenosis, hypovolemia, heart failure)
Hyperkalemia!!!!
Proteinuria
Pemphigus vulgaris (unknown mechanism)
Teratogenicity: renal malformations
Leukopenia
Rash
Taste changes
Early DN effect on glomerular filtration pressure?
Elevated glomerular filtration pressure
+ATII further increases glomerular pressure by selective vasoconstriction of the efferent arteriole
Blockage of what decr. glomerular filtration pressure?
blockage of ATII, since it increases glomerular pressure by selective vasoconstriction of the efferent arteriole –> lowered glomerular pressure
ACEI use with caution in what condition? and why?
In bilateral renal artery stenosis. It leads to decr. renal blood flow –> decr. GFR THEREFORE –> ACTIVATION OF RAAS –> RELEASE OF ATII –> constr. of efferent –> maintain GFR.
ACEI - drop in systemic BP and dilation of efferent.
Drop in BP is no longer high enough to overcome the stenosis –> renal blood flow drops. Due to dilation of efferent –> reduction of intraglomerular filtration pressure -> decr GFR and filtration fraction.