CT 6 Hypertension Flashcards
what metabolic products cause vasodilation
nitric oxide indicates damage to BVs
high carbon dioxide
what factors result in vasoconstriction in local blood vessels
low oxygen
acidity
potassium and bicarb
Sympathetic activation leads to what changes in BP
sympathetic fibres innervate all vessels except capillaries
activation leads to:
- vasoconstriction (increases resistance thus increasing BP (P = CO X R)
- increased HR (increases CO leading to increased BP)
- increased contractile strength (ionotropy) leads to increased SV –> increased CO and therefore increased BP)
also innervate the adrenal glands which release adrenaline and noradrenaline
what regulates sympathetic activity
baroreceptors in the aortic arch and internal carotid pick up stretch and for example in decreased BP there is decreased firing of these baroreceptors. this is conveyed to the vasomotor centre in the medulla which increases S activation thus increasing BP.
this is under negative feedback
effects of angiotensin II
potent vasoconstrictor
increased sympathetic activation which increases HR and BP
increased ADH secretion
increased NAcl reabsorption
increased aldosterone secretion
what stimulates release of ADH
low BP
high blood osmolarity (more concentrated, less water)
effects of natruitic peptides
vasodilation
diuresis
inhibition of aldosterone synthesis
inhibition of renin secretion
- lowers BP
essential hypertension
high salt intake
RAAS activation
SNS activation
macro and microvascular damage:
- chemical
- sheer stress
- endothelial dysfunction
epidemiology of hypertension
1 in 4 adults
2 in 3 adults > 60
M>F
causes of secondary hypertension
RA stenosis (reduced blood flow to kidneys – activation of RAAS)
obstructive sleep apnoea (diagnosis is via epworth score and treated with CPAP)
conn’s syndrome (bilateral hyperplasia of the adrenal glands – secrete too much aldosterone) measure renin: aldosterone ratio
phaeochromocytoma (excess release of catecholamines)
cushing’s syndrome:
coarctation of the aorta - narrowing of part of the aorta: mechanism is similar to RA stenosis.
there will be difference in BP between arms and legs
thyroid dysfunction (hypothyroid)
clues that it is secondary hypertension
<40 yr
resistant hypertension
sudden deterioration in BP control
any grade II hypertension
hypertensive crisis
hypertensive end organ disease HMOD
HMOD
- heart = LVH
- kidneys: CKD
- eyes = AV nipping, cotton wool spots and retinal haemorrhages
treatment of hypertension
1st line = ACEI OR ARB (IF <55 OR HAVE T2DM)
IF AFRICAN OR AFRO-CARRIBEAN WITHOUT T2DM OR >55 =
calcium channel blocker
titrate to top dose, add second agent
3rd line: thiazide or thiazide like diuretic
4th line: spirolnolactone or alpha blocker
examples of arbs
losartan
candesartan
valsartan
examples of mineralocorticoid receptor antagonists
spironolactone
eplerenone
examples of thiazides
bendroflumethiazide
indapamide
why are CCBs used in treating hypertension
reduce smooth muscle contraction causing vasodilation
amlodipine, felodipine and nifedipine
key diagnostic factors for HTN
presence of risk factors, BP over 140/90,
and retinopathy. Other diagnostic factors include headaches, dyspnoea, chest pain, and sensory or
motor deficits (suggests cerebrovascular disease)
