Lecture 10 - ACE Inhibitors Flashcards
Physiological effects of RAAS and source?
regulate BP, intravasc. volume and fetal development; juxta-glomerular cells produce renin, RAA produced in myocardium, vasc. endothelium and adrenal gland
Pathophysiological effects?
increased activity in CCF and hypertension, CHF progression, hypertrophy, atherosclerosis, SNS action (NA), fibrosis (similar effects to aldosterone)
ACE inhibitors general benefits?q
decrease Angiotensin II, increase Angiotensin 1-9 and bradykinin
Prolonged ACE-inhibitor usage?
restoration of Angi-II (and thereore aldosterone) levels through decreased negative feedback on renin production + other enzymes restoring levels e.g. chymase
Sartan block?
Angio-II receptor blocker blocking type 1 receptors to reduce negative effets, but also does not block type II allowing positive effects e.g. vasodilation and tissue repair
Drug examples?
cilazapril - (ACE-inhib.), Candesartan (AII Antagonist)
ACEi PK?
prodrugs, variable half life, renally excreted (careful but no contraindication), bile excreted also
P.D.?
vasodilation (decreased BP, preload and afterload), decreased blood volume (natriuresis and mild diuresis), decreased SNS, decreased cardiac and vascular hypertrophy
ACEi indications?
hypertension (mono or combined with diuretic), congestive cardiac failure (combination therapy)
AIIA indications?
patients adverse to ACEi; hypertension, heart failure
SIde effects?
dry cough (bradykinin increase for ACEi), hyperkalaemia (decreased aldosterone), hypotension, angio-oedema
Contraindications - bilaterall renal artery stenosis?
stenosis decreasing perfusion @ glomerulus, increased AngioII produced to increase vasoconstriciton of efferent arteriole to maintain appropriate profusion pressure
Contraindications - pregnancy?
crosses placenta -> fetal renal defects, miscarriage
