Most common medications used in the different branches of medicine including mental health, cardiology, respiratory and neurology. It discusses the MOA, Side effects and interactions.
Stage Criteria
Stage 1 hypertension Clinic BP >= 140/90 mmHg and subsequent ABPM
daytime average or HBPM average BP >= 135/85
mmHg
Stage 2 hypertension Clinic BP >= 160/100 mmHg and subsequent
ABPM daytime average or HBPM average BP >=
150/95 mmHg
Severe hypertension Clinic systolic BP >= 180 mmHg, or clinic diastolic
BP >= 120 mmHg
Stage 1- treat conservatively
ACE inhibitors:
Mode of action: binds to and inhibits ACE thereby preventing the conversion of angiotensin I to
angiotensin II. As plasma levels of angiotensin II fall, less activation of the G-protein coupled receptors
, angiotensin receptor I (AT1R) and angiotensin receptor II (AT2R) occurs. Angiotensin II, aldosterone, and
norepinephrine all increase blood pressure and urine production by the kidneys. If levels of these three
substances decrease in the body, this allows blood vessels to relax and dilate (widen), reducing both
blood and kidney pressure. ACE inhibitors also increase the production of bradykinin, another substance
that makes blood vessels dilate. ACE is also responsible for the breakdown of bradykinin. The resulting
buildup of bradykinin due to ACE inhibition is thought to mediate the characteristic dry cough as a side
effect of ACE inhibitor medications.
Decreases body production of substances that could raise your BP which allows your blood vessel to relax
and widen making it easier for your heart to pump blood around your body.
Indication: hypertension, HF, prophylaxis after MI, nephropathy
Side effects: angioedema, cough; diarrhoea; dizziness; drowsiness; dry mouth, hyperkalaemia
Interactions: patients receiving high-dose diuretic therapy (more than 80 mg of furosemide a day)
o significantly increases the risk of hypotension
Monitoring: urea and electrolytes should be checked before treatment is initiated and after increasing
the dose:
o a rise in the creatinine and potassium may be expected after starting ACE inhibitors
o acceptable changes are an increase in serum creatinine, up to 30% from baseline and an
increase in potassium up to 5.5 mmol/l.
o significant renal impairment may occur in patients who have undiagnosed bilateral renal
artery stenosis
Cautions and contraindications
pregnancy and breastfeeding - avoid
renovascular disease - may result in renal impairment
aortic stenosis - may result in hypotension
hereditary of idiopathic angioedema
specialist advice should be sought before starting ACE inhibitors in patients with a potassium >=
5.0 mmol/L
Ramipril- most commonly used ACE-I
Mode of action: ACE-I. is an inactive prodrug that is converted to ramiprilat in the liver, the main site of
activation, and kidneys. As it inhibits ACE enzyme, it prevents the conversion of angiotensin 1 into 2 thus
inhibits the RAAS system. This reduces the blood pressure.
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