Hypertension Flashcards
Clinical hypertension definition - when to treat
BP above 160/100mmHg (diastolic >90 is important indicator of background resistance)
1˚ and 2˚
Primary is unknown cause, 2˚ due to something else e.g. phaeochromocytoma/Cushing’s etc
Diuretics MOA
Chlortalidone/indapamide (thiazide like diuretics), spironolactone, bendroflumethiazide (thiazide) initially has BP fall due to reduced volume but then peripheral resistance decreases, mechanism unknown
Thiazides especially effective in older patients
ACE inhibitors MOA
Captopril, ramipril, lisinopril, enalapril (prodrug, de-esterified in plasma) block conversion of angiotensin I to II in lungs so RAAS not activated and blood volume and TPR lowered (lack of angiotensin II), BP drops Also bradykinin (metabolised by ACE) is a vasodilator
K ATP channel activator MOA
Minoxidil blocks ATP from closing K channels, hyper-polarised cell so Ca channel close so vasodilation
Ca channel blockers (dihydropyridines) MOA
Nifedipine (short-acting), amlodipine (now used more as longer acting) block L-type Ca channels on vascular smooth muscle cells -> vasodilation
Hydralazine MOA
MOA unknown but may activate granulate cyclase (mimics NO), acts only on arteriolar smooth muscle
Sodium nitroprusside use
In an acute hypertensive crisis but just to bed bound patients, not ambulatory. Works as nitrovasodilator.
alpha-1 antagonist MOA and use
Prazosin and longer acting doxazosin block alpha-1 receptors -> vasodilation
Used with other antihypertensives in cases of resistant hypertension
alpha-2 agonist MOA
Clonidine acts on alpha 2 receptors in RVLM and NTS which results in inhibition of symp outflow to heart and vessels, and inc parasympathetic outflow to heart respectively
alpha-methyldopa MOA
Converted in adrenergic nerve endings to alpha-methylNA which stimulates alpha-2 in medulla
beta blockers possible MOA
Initially BP drop due to reduced CO and reduced renin secretion but peripheral resistance reset to lower level (?reset baroreceptors)
ARB MOA
Candesartan, losartan block AT1 receptors so RAS interfered with
thiazides SE
SE: hypokalaemia (unless K sparing), diabetes mellitus, gout, hypercalcaemia, hyponatraemia
ACE inhibitors SE
SE: Bradykinin cough, angioedema, neutropenia, hyperkalaemia
ARB SE
SE: angioedema, neutropenia, hyperkalaemia
beta blockers SE
SE: Cold hands, fatigue, provocation of asthma/heart failure/conductance block/diabetes
alpha-methyl dopa SE
SE: drowsiness, rarely haemolytic anaemia due to autoantibodies acting against RBCs
alpha-methyl dopa used in
pre-eclampsia
alpha-2 receptor agonist SE
Suddenly withdrawing causes rebound hypertension
alpha-1 antagonist SE
SE: postural hypotension, no tachycardia unlike non-selective alpha blockers
K ATP channel activator SE
SE: Causes hypertrichosis (baldness), severe fluid retention + oedema but this solved when given with beta-blocker and loop diuretic
Ca channel blockers SE
SE: Excess vasodilatation, hypotension, flushing, ankle oedema
1st line hypertension treatments
ACE inhibitors/ARBs
Ca channel blockers
Diuretics
beta blockers used
beta-1 selective (cardioselective) e.g. atenolol, metoprolol, bisoprolol used as cardioselective with fewest SEs
Hydralazine use
Used in combo with beta blocker to counter initial reflex tachycardia from BP drop
Hydralazine SE
SE: reflex tachycardia (can cause angina, headaches, fluid retention) and can induce lupus in slow acetylators
