Wk 5 HTN Flashcards
Understand that elevated blood pressure/hypertension is a cardiovascular risk factor
HTN is a risk factor for a series of CVD:
- stroke (↑BP causes vessel rupture or clot formation)
- heart failure (↑BP causes cardiac hypertrophy)
- myocardial infarction (cardiac hypertrophy)
- renal failure (↑BP causes arteries around the kidneys to narrow)
Discuss the non-pharmacological and pharmacological ways of treating hypertension
Non-pharmacological:
- lifestyle
- diet, healthy eating
- ↓ drinking, smoking
- physical activity
Pharmacological:
ACEI: ramipril, captopril, perindopril
- ↓angiotensin II, ↑bradykinin
- ↓[vasoconstriction, aldosterone release, Na+/H2O reabsorption]
- cough, hypotension, hyperkalemia, renal impairment
- CON: renal impairment, elderly, pregnancy
A2RA: irbesartan, candersartan
- same as ‘ACEI’
- cough, hypotension, hyperkalemia, renal impairment
- CON: renal impairment, elderly, pregnancy
Calcium channel blocker/CCB
- dihydropyridine: amlodipine, felodipine, nifedipine
- non-dihydropyridine: diltiazem, verapamil
[DHP CCB is more potent in vasodilation than non-DHP]
- MOA: primarily inhibit calcium entry into the vascular smooth muscle cells of blood vessels + cardiac muscle cells
- AEs: vasodilatory effects, including headache, flushing, dizziness, hypotension, peripheral oedema
Beta adrenoceptor antagonist/BB
- propranolol, atenolol, metoprolol
- MOA:
> block beta receptors in the heart (B1 receptor), lungs (B2 receptor), bladder (B3 receptor) etc
> ↓ HR, BP, cardiac contractility
- AEs: bradycardia, hypotension, bronchospasm, cold extremities
Diuretics
- MOA: ↓ Na+ & H2O reabsorption,
- Loop diuretics: frusemide
> potent, site: loop of henle
- thiazide diuretics: hydrochlorothiazide
> moderately potent, site: distal convoluted tubule
- potassium-sparing diuretics: spironolactone, amiloride
> weak, site: late distal convoluted tubule
- AEs:
> loop & thiazide: hypokalemia, hyponatraemia, hyperuricemia, hyperglycaemia
> potassium: hyperkalemia
What is Triple Whammy effect?
- ACEI/A2RA: cause vasodilation to efferent renal arteriole → ↓ glomerular filtration rate
- NSAIDs: (including COX 2 inhibitors): cause vasodilation to afferent renal arteriole [by reducing prostaglandin]
- Diuretics: cause hypovolemia