Hypertension

Question 1

Clinical hypertension definition - when to treat

Answer 1

BP above 160/100mmHg (diastolic >90 is important indicator of background resistance)

Question 2

1˚ and 2˚

Answer 2

Primary is unknown cause, 2˚ due to something else e.g. phaeochromocytoma/Cushing’s etc

Question 3

Diuretics MOA

Answer 3

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

Question 4

ACE inhibitors MOA

Answer 4

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

Question 5

K ATP channel activator MOA

Answer 5

Minoxidil blocks ATP from closing K channels, hyper-polarised cell so Ca channel close so vasodilation

Question 6

Ca channel blockers (dihydropyridines) MOA

Answer 6

Nifedipine (short-acting), amlodipine (now used more as longer acting) block L-type Ca channels on vascular smooth muscle cells -> vasodilation

Question 7

Hydralazine MOA

Answer 7

MOA unknown but may activate granulate cyclase (mimics NO), acts only on arteriolar smooth muscle

Question 8

Sodium nitroprusside use

Answer 8

In an acute hypertensive crisis but just to bed bound patients, not ambulatory. Works as nitrovasodilator.

Question 9

alpha-1 antagonist MOA and use

Answer 9

Prazosin and longer acting doxazosin block alpha-1 receptors -> vasodilation
Used with other antihypertensives in cases of resistant hypertension

Question 10

alpha-2 agonist MOA

Answer 10

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

Question 11

alpha-methyldopa MOA

Answer 11

Converted in adrenergic nerve endings to alpha-methylNA which stimulates alpha-2 in medulla

Question 12

beta blockers possible MOA

Answer 12

Initially BP drop due to reduced CO and reduced renin secretion but peripheral resistance reset to lower level (?reset baroreceptors)

Question 13

ARB MOA

Answer 13

Candesartan, losartan block AT1 receptors so RAS interfered with

Question 14

thiazides SE

Answer 14

SE: hypokalaemia (unless K sparing), diabetes mellitus, gout, hypercalcaemia, hyponatraemia

Question 15

ACE inhibitors SE

Answer 15

SE: Bradykinin cough, angioedema, neutropenia, hyperkalaemia

Question 16

ARB SE

Answer 16

SE: angioedema, neutropenia, hyperkalaemia

Question 17

beta blockers SE

Answer 17

SE: Cold hands, fatigue, provocation of asthma/heart failure/conductance block/diabetes

Question 18

alpha-methyl dopa SE

Answer 18

SE: drowsiness, rarely haemolytic anaemia due to autoantibodies acting against RBCs

Question 19

alpha-methyl dopa used in

Answer 19

pre-eclampsia

Question 20

alpha-2 receptor agonist SE

Answer 20

Suddenly withdrawing causes rebound hypertension

Question 21

alpha-1 antagonist SE

Answer 21

SE: postural hypotension, no tachycardia unlike non-selective alpha blockers

Question 22

K ATP channel activator SE

Answer 22

SE: Causes hypertrichosis (baldness), severe fluid retention + oedema but this solved when given with beta-blocker and loop diuretic

Question 23

Ca channel blockers SE

Answer 23

SE: Excess vasodilatation, hypotension, flushing, ankle oedema

Question 24

1st line hypertension treatments

Answer 24

ACE inhibitors/ARBs
Ca channel blockers
Diuretics

Question 25

beta blockers used

Answer 25

beta-1 selective (cardioselective) e.g. atenolol, metoprolol, bisoprolol used as cardioselective with fewest SEs

Question 26

Hydralazine use

Answer 26

Used in combo with beta blocker to counter initial reflex tachycardia from BP drop

Question 27

Hydralazine SE

Answer 27

SE: reflex tachycardia (can cause angina, headaches, fluid retention) and can induce lupus in slow acetylators