2.1 Nephron maintenance Flashcards
explain what acute tubular necrosis is, and why it happens
reduced BP and blood flow through glomerulus, vasa recta can’t support cells of nephron tubules, so fluid can leak, cells can fall in and block tubule
treatment for acute tubular necrosis
restore patient’s circulating volume
describe the myogenic response when blood pressure drops
(to cause an increase in GFR)
-EA constrict: pressure backs up in capillaries
-dilate AA: more blood can flow through capillary
describe the myogenic response when blood pressure increases
(to cause a decrease in GFR)
-constrict AA: blood backs up outside of glomerulus, so high BP isn’t transmitted
-dilate EA: stops pressure being retained in glomerulus
is EA or AA smaller at rest?
EA
which cells are responsible for tubuloglomerular feedback?
macula dense cells of DCT
explain the process of tubuloglomerular feedback when BP high
-macula dense cells detect high osmolality/high flow of Na+
-signal to juxtoglomerular cells
-ATP released covered to adenosine
-acts on A1 receptor of AA
-vasoconstrict AAs to decrease RPF and GFR
-so less Na+, Cl- so less H2O reabsorbed so BP can decrease
what happens if the ATPase can’t cope with the flow of NaCl into mesangial cells at macula densa?
cell water stays and cells swell
what is renin?
enzyme synthesised and stored in JGA, released when plasma Na+ low
overall aim of prostaglandin release
get rid of the systemic vasoconstriction
ang11 functions
-vasoconstricts EAs (backs up blood so more Na+ can be reabsorbed to increase BP)
-release ADH
-stimulate thirst
-zona glomerulosa to release aldosterone
action of aldosterone on DCT
increase Na+ reabsorption
what triggers prostaglandin release?
reduction in circulating volume
where are prostaglandin released from in kidneys?
-cortex (arterioles and glomeruli)
-medullary interstitial cells
-collecting duct epithelial cells
effects of prostaglandins
-remove systemic vasoconstriction by vasodilation, to increase blood flow through kidneys
-renin release
