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1

what is hypokalaemia

low potassium levels in the blood

2

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

3

potassium sparing diuretics

decrease sodium movement across the principle cells
spironolactone and amiloride

4

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

5

spironolactone

competitive antagonist of aldosterone
is a potassium sparing antagonist

6

amiloride

potassium sparing siuretic
blocks sodium channels in the luminal membrane

7

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

8

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

9

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

10

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

11

what is renin

renin is an enzyme secreted into the bloodstream by cells of the glomerular apparatus

12

how can the release of renin be stimulated

by adrenaline at Beta adrenceptors, prostacyclins and a decreased Na+ conc

13

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

14

ACE inhibitors

end in pril
unwanted effects: initial dose hypotension, cough as ACE inhibited so bradykinin not broken down so vasodilation

15

angiotensin II antagonists

compete with angiotensin II at angiotensin II type 1 receptors
hypotension but no cough

16

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

17

adrenergic receptors

four types (beta 3 used to breakdown fats)

18

alpha 1 adrenergic receptor function `

vasoconstriction and contraction of smooth muscle
coupled with phospholipase c and stimulated by Gq

19

alpha 2

coupled to adenlyl cyclase and gi. causes transmitter relase and decrease in insulin release

20

beta 1

coupled to gs and adenylate cyclase
heart rateb and force
release of renin

21

beta two

coupled to gs and adenylate cyclase
bronchodilation and vasodilation

22

doxazoxin

antagonises alpha adrenergic receptors therefpre inhibiting vasoconsstrciton and contraction

23

phenoxybenzamine

INSURMOUNTABLE IRREVERSIBLE non competitive inhibitor to all four adrenergic receptors

24

propranolol

competive antagonist and is non selective to both beta adrenceptors
lipid soluble so can penetrate CNS

25

atenolol and bisprolol

competitive antagonists
beta 1 selectivity
bisoprolol then atenolol then propranolol
water soluble- poor penetration of CNS

26

beta blockers in hypertension

reduces heart rate and stroke volume
reduce release of renin ( b1 anatagonist)
can reduce anxiety

27

unwanted effects of beta blocjers

big people hate vogue covers
brochoconstricition
precipitation of heart ailure or heart block
hypoglycaemia
vivid dreams
cold extremities

28

diabetic aptients experience what when becoming hypoglycaemic

major sympathetic activation

29

problem with propranolol and diabetes

non selective
decreased warning signs of hypoglycaemia problem for type 1
reduced insulin sensitivity problem for type 2

30

treatment for hypotension whats primary if black

calcium channel blocker