ACE inhibitors Flashcards
physiological effects of RAAS
regulates:
- BP
- IV volume (Na+, K+)
- foetal development of kidneys
juxtaglomerular cells
- produce renin
locally produced - RAA
- myocardium, vascular endothelium, adrenal
pathophysiological effects of RAAS
- increases activity in CCF and hypertension
- involved in CHF progression
- adverse CVS effects e.g. hypertrophy, pro-inflammatory, atherosclerosis
- close relationship with SNS
role of angiotensin converting enzyme
breaksdown bradykinin therefore ACEi increase the level of bradykinin and prolong their action -> stimulation of NO from endothelium = vasodilation
ACE inhibitors
- inhibit angiotensin converting enzyme
- decrease angiotensin 2 activity
- change concentration of other vasoactive peptides
- increase bradykinin levels
ACE inhibitors use
hypertension
- synergistic with diuretic
CHF
- part of multiple tx e.g. ACEi, diuretic, beta-blocker, aldosterone antagonist
AIIA use
- in ACEi intolerant patients
- hypertension
- HF
side effects of these drugs
- dry cough (from bradykinin & substance P)
- hyperkalaemia (reduction in aldosterone)
- renal Fx deterioration
- contraindication in pregnancy
- angio-oedema
absolute contraindication
pregnancy
bilateral renal artery stenosis
conditions that provoke caution with use
- hyperkalemia
- renal impairment
- volume deplete/diuresed patients
example of an ACEi drug
cilazapril
example of an AIIA drug
candesartan
losartan
pharmacodynamic of ACEi/AIIA
vasodilation
- decrease arterial and venous pressure
- decrease ventricular preload and afterload
decrease BV
- natriuresis
- diuresis
decrease sympathetic activity
decrease cardiac and vascular hypertrophy
hyperkalemia risk groups
- CKD
- diabetes mellitus
- advanced age
- patients on NSAID or K+ sparing diuretics
important to monitor with blood tests
mechanism of AIIA
inhibit angiotensin 2 type 1 receptors
where do you find angiotensin type 1 receptors
- kidneys
- heart
- vascular SM
- brain
- adrenal glands
- placenta
