ACE inhibitors Flashcards
State the 4 common clinical indications for the use of ACE inhibitors and state why ACE inhibitors might be used.
1) HTN - first or second line treatment for HTN to reduce risk of stroke, MI or death from CV disease.
2) CHF - first line treatment for all grades to improve symptoms and prognosis.
3) IHD - to reduce risk of subsequent CV events such as stroke or MI.
4) Diabetic nephropathy and CKD with proteinuria - to reduce proteinuria and progression of nephropathy.
1) What is the primary mechanism of ACE inhibitors?
2) What is Angiotensin II and what does it do?
3) What does blocking the action of Angiotensin II do?
1) Inhibits angiotensin converting enzyme, preventing the formation of Angiotensin II from Angiotensin I.
2) A vasoconstrictor which stimulates aldosterone release.
3) Reduces peripheral vascular resistance (afterload), leading to decreased BP.
1) How do ACE inhibitors slow the progression of CKD?
2) What does a reduction in aldosterone level promote?
3) What effect of ACE inhibitors has a beneficial action for heart failure?
1) Dilation of efferent glomerular arteriole > reduction in intraglomerular pressure > slows progression of CKD.
2) Promotes Sodium and water excretion.
3) Sodium and water excretion reduces venous return (preload) to the heart which is beneficial for heart failure.
Give 3 adverse effects of ACE inhibitors and state why they happen.
1) Hypotension, particularly after the first dose.
2) Persistent dry cough, due to increased levels of Bradykinin which is usually inactivated by ACE.
3) Hyperkalaemia, because a lower aldosterone level promotes potassium retention.
1) What condition can be caused or worsened through use of ACE inhibitors?
2) Why is worsening of this condition particularly relevant in patients with renal artery stenosis?
1) Renal failure.
2) Because these patients rely on construction of the glomerular efferent arteriole to maintain glomerular filtration.
Give 2 rare and idiosyncratic side effects of ACE inhibitors.
Angioedema and Anaphylactoid reactions.
1) Name 4 conditions where use of ACE inhibitors is contraindicated.
2) In what condition should ACE inhibitors be used cautiously? What precautions should be taken?
1) Renal artery stenosis
Pregnant women
Women who are breastfeeding
Acute kidney injury.
2) Chronic kidney disease. Lower doses should be used, and the effect on kidney function closely monitored.
1) Name 2 classes of drug that ACE inhibitors should NOT be prescribed in conjunction with and state why.
2) In combination with what class of drugs can ACE inhibitors cause profound first dose hypotension?
1) Potassium elevating drugs (potassium supplements/ potassium sparing diuretics) due to risk of hyperkalaemia. NSAIDs because using both together increases risk of renal failure.
2) When used in combination with other diuretics.
1) Name the 3 P-drugs to be known for ACE inhibitors.
2) What is the common ACE inhibitor and dose prescribed for heart failure and nephropathy, and then for other indications.
3) Before prescribing ACE inhibitors for a patient, what should you check?
4) When else should you carry out these checks?
1) Enalapril, Ramipril, Lisinopril.
2) 1.25mg Ramipril for HF and nephropathy. 2.5mg Ramipril for other indications.
3) Electrolytes and renal function.
4) 1-2 weeks after starting treatment and after an increase in dose.
1) What do reduced tissue concentrations of Angiotensin II lead to?
2) Why is Angiotensin II production not completely inhibited?
3) Why is activity of these alternative pathways enhanced?
1) Arterial dilation and venous dilation (to a lesser extent).
2) There are alternative pathways that allow for Ang II generation through pro teases; Chymase and Chymotrypsin-like Angiotensin II generating enzyme (CAGE).
3) Activity enhanced due to the stimulation of renin release by the fall in BP after ACE inhibition.
1) Aside from inhibiting tissue ACE, what else do ACE inhibitors do?
2) How do ACE inhibitors prevent reflex tachycardia?
3) ACE inhibitors are better than beta blockers and and diuretics at doing what?
4) Why is this?
1) Competitive inhibition of plasma ACE reduces generation of circulating Angiotensin II and reduces aldosterone release. ACE inhibitors also increase bradykinin presence in the vascular walls, which may contribute to hypotension effects.
2) They reduce Angiotensin II potentiation of the sympathetic nervous system.
3) They are more effective at producing regression of LVH.
4) This is because Angiotensin II is implicated in developing arterial remodelling and LVH in hypertension, and ACE inhibitors reduce ACE.
