hypertension

Question 1

Hypertesion

intro and causes

Answer 1

• systolic >140, diastolic >90
• pre hypertension systolic 120-139, diastolic 80-89
• MAP = CO/SVR
• Normally an acute increase in BP (by either increased HR or SVR) causes pressure natriuesis – increased renal artery pressure increses glomerular filtration and Na and H2O excretion
• Causes
  o Increased CO
• Increased blood volume through Na and H2O retention – impaired pressure natriuresis, curve shifted right when renal handling of Na and H2O changed from:
• Sympathetic activity
• Hormones – ANII, aldosterone, ADH
• Renal disease

o Increased SVR

• Thickening of walls so decreased radius
• Sympathetic activity
• Increased angiotensin II (also increase vascular hypertrophy)
• Endothelial dysfunction – less NO (also normally inhibits vascular hypertrophy), increased endothelin-1
• • From T2DM – insulin and glucose increase reactive oxygen specires and decrease NO bioavailabilty

Question 2

Essential (primary HTN) - 90%

Answer 2

o Hypothesis uncertain, related to genetics (?renal function and neurohumoral), older, african, low socioeconomic, obesity
o Increased blood volume and CO initiates increased SVR – impaired pressure natriuresis
o Increased SVR from vascular hypertrophy
o Diabetes – endothelial dysfunction
o Stress – sympathetic, adrenal secretion of catecholamines, activation of angiotensin II, aldosterone, vasopressin (incrased SVR an blood volume), vascular and cardiac hypertrophy from angiotensin II and catecholamines

Question 3

Causes of secondary hypertension

Answer 3

o Renal artery stenosis
• Atherosclerosis or fibromuscular lesion
• Less pressure in afferent, renin release, ANII vasoconstrcion (direct binding AT1, indirect augmenting sympathetic, increased Na and H2O, vascular and cardiac hypertrophy) and aldosterone
o Renal disease
• Diabetic nephropathy, glomerulonephritis, can’t excrete Na and H2O
• May also increase renin release
• Kidney is trying to increase perfusion to get a normal glomerular filtration rate
o Primary hyperaldosteronism
• Adrenal adenoma or hyperplasia, Na and H2O retention
• Acts on distal convoluted tubule and cortical collecting duct to increase Na+ resoption in exchange for K and H+
• Get hypokaleamia and decreased plasma renin (body tries to suppress)
o Pheochromocytoma
• Catecholamine secreting tumor in adrenal medulla, alpha and beta effects, can get arrhythmias from xs B1
• Dx – plasma or urine catecholamine (and their metabolite) levels.
o Aortic coarctation
• Narrow just distal to left subclavian artery, obstructs outflow, elevated pressure prox to it – head and neck
• Distal BP can be normal because of reduced systemic flow, but this can cause renin release and HTN anway
• Baroreceptors reset to higher pressure
• Congenital
o Pre eclampsia
• Decreased albumin due to renal damage and oedema
• Increased blood volume and tachycardia
• Increased responsiveness to vasoconstrictors and vasospasm
o Hyperthyroidism
• Systemic vasoconstriction, increased blood volume, increased cardiac activity
• Can also get if hypothyroid possibly due to reduced metabolism and release of vasodilators
o Cushings syndrome
• Xs glucocorticoid secretion, cortisol from adrenal cortex, can act like aldosterone

Question 4

treatment of hypertension

Answer 4

o Exercise (reduces arterial pressure and beneficial to endothelial function), diet, Na restriction

o Drugs:Target CO or SVR
• Diuretic, usually need another cos causes activation renin-angiotensinII-aldosterone which counteracts

• Angiotensin converting enzyme (ACE) inhibitor or angiotensin receptor blocker (ARB)

• Stops u holding on to Na H2O
• Also stops vasocontriction
• Alpha adrenoceptor antagonist
• BB – good if due to stress, also reduce renin release as this is Beta mediated
• Cardiac selective calcium channel blockers – verapamil
• Ca channel blockers – dihydropyridines, reduce SVR
• Hydralazine – direct acting arterial dilator