13. hypertension ii Flashcards
(31 cards)
what is hypokalaemia
low potassium levels in the blood
major unwanted effect of loop diuretics is what and why does it happen
potassium losss
lot more sodium is passed to distal parts of the nephron and is absorbed by orinciple cells of the collecting duct and this lowers the potential of the lumen of the nephron so k+ will move into the lumen. increased flushing due to increased volume of urine
potassium sparing diuretics
decrease sodium movement across the principle cells
spironolactone and amiloride
aldosterone
mineralcorticoid nuclear hormone receptor agonist
increases the transcriotion for the gene that codes for Na+/K+ ATPases
can also bind to a protein mediator and directly stimulate na channels non genomically in the luminal membrane
spironolactone
competitive antagonist of aldosterone
is a potassium sparing antagonist
amiloride
potassium sparing siuretic
blocks sodium channels in the luminal membrane
spironolactone uses
hyperaldosteronism in
liver cirrhosis - the fialaure to metanbolise aldosterone
conns syndrome - hypersecretion of aldosterone perhaps due to an aldosterone secreting tiumour in the adrenal medulla
draw the scheme for RAAS, what does it do to blood pressure
renin to angiotensin to aldosterone and vasoconstriction, aldosterone leads to salt and water retention and com ined with vasoconstricition will increase blood pressure
describe the generation of the angiotensin hormones
renin ( a protease) cleaves angiotensinogen into the inactive decamer angiotensin II.
ACE then cleves angiotensin I to angiotensin II which is an active octamer
where do angotesin II and III bind
to angiotensin II type 1 recptors which are g coupled protein receptors that increase aldosterone secretio and cause vasoconstriction
what is renin
renin is an enzyme secreted into the bloodstream by cells of the glomerular apparatus
how can the release of renin be stimulated
by adrenaline at Beta adrenceptors, prostacyclins and a decreased Na+ conc
out of renin and ACE whats an example of global control and whats an example of local control
renin is global and CE is local
ACE inhibitors
end in pril
unwanted effects: initial dose hypotension, cough as ACE inhibited so bradykinin not broken down so vasodilation
angiotensin II antagonists
compete with angiotensin II at angiotensin II type 1 receptors
hypotension but no cough
angiotensin receptors
g protein coupled receptors
angiotensin II type 1 recetpros are for aldosterone release and vascular effects
type 2 is for growth and development
adrenergic receptors
four types (beta 3 used to breakdown fats)
alpha 1 adrenergic receptor function `
vasoconstriction and contraction of smooth muscle
coupled with phospholipase c and stimulated by Gq
alpha 2
coupled to adenlyl cyclase and gi. causes transmitter relase and decrease in insulin release
beta 1
coupled to gs and adenylate cyclase
heart rateb and force
release of renin
beta two
coupled to gs and adenylate cyclase
bronchodilation and vasodilation
doxazoxin
antagonises alpha adrenergic receptors therefpre inhibiting vasoconsstrciton and contraction
phenoxybenzamine
INSURMOUNTABLE IRREVERSIBLE non competitive inhibitor to all four adrenergic receptors
propranolol
competive antagonist and is non selective to both beta adrenceptors
lipid soluble so can penetrate CNS
