Renal 2 Flashcards by Angelica J

what mainly happens in descending limb of henle

water reabsorption

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can water reabsorb in the ascending limb of henle

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what is the main transporter in the thick ascending limb

NKCC2

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what is special about K+ in ascending limb and what does it cause

K excreted into lumen which makes it ++++ so then Mg++ and Ca++ can be reabsorbed

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how does K+ enter the blood in the loop of henle

alongside Cl

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what do loop diuretics attack and where

NKCC2 in the thick ascending loop of henle

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what are theraputic uses for loop diuretics

hypercalcemia 
hyperkalemia
pulmonary edema
hypertension
heart failure
renal failure

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adversive effects of loop diuretics

hypokalemia
hypomagnesia
metabolic alkalosis

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how can loop diuretics cause metabolic alkalosis

increase in Na+ delivery to collecting duct causes increased urinary excretion of K and H

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what are main transporters in distal convoluted tubule

NCC and apical calcium channel

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what channel does PTH stimulate and where

apical Ca channel in the distal convoluted tubule

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how does Ca enter the blood in the distal convoluted tubule

Na/Ca antiport

Ca/H ATP antiport

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what do thiazides target and where in nephron

NCC transporter in distal tubule

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what is NCC transporter and where is it

Na Cl co transpor in the distal tubule

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what is the NKCC2 transporter and where is it

Na K 2Cl cotransporter in the loop of henle

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where is the TRPV5 transporter (ca apical)

distal tubule

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what does thiazides do to Na and Cl reabsorption

reduce

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what does thiazides do to Ca reabsorption

increase (increases Na Ca basolateral exchange cause Na is reduced)

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what are uses of thiazides

hypertension
edema
kidney stones
heart failure

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what are adverse effects of thiazides

hypokalemia
hyponatremia
Metabolic alkalosis

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where in the nephron is most important for K excretion

collecting tubule

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where is the ENaC pump

collecting tubule

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what does the ENaC pump exchange

just brings Na into principal cells in collecting tubules

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what receptor is in principal cells

aldosterone

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what does aldosterone do in principal cells

increase ENaC

what part of nephron has aldosterone receptors

principal cells of collecting tubules

what part of nephron has PTH receptors

distal convoluted tubule

what does Na+ exit from lumen do for the principal cells

drives negative lumen which increases K excretion and Cl-reabsorption into interstitium

what happens with volume depletion (aka what does this cause/or effect)

aldosterone secretion, which then increases K+ excretion

what 2 pumps are in A cells in collecting tubules

H-ATP sending H into lumen HCO3-/Cl- antiport sending HCO3- into blood

what 2 pumps are in B cells in collecting tubules

H-ATP sending H into blood HCO3-/Cl- antiport sending HCO3- into lumen

which cells of the collecting tubule react with acidemia and what do they do

A dominate to secrete excess H+

which cells of the collecting tubule react with acidemia and what do alkalemia do

dominates to secrete excess bicarbonate

what does aldosterone do to apical proton pump in type A cells

increases the # of them

what are the 2 potassium sparing diuretics

ENaC inhibitors and Aldosterone antagonists

how can antagonists of aldosterone cause metabolic acidosis

they reduce the amount of A cell type H+ pumps (less H+ pumped out into lumen)

what is the most efficacious diuretic agent

loop diuretics

what do loop diuretics do to na and cl reabsorption

reduce

what do loop diuretics do to ca and mg reabsorption

reduce

what types of diuretics cause vasocilation

loop diuretics and thiazides

what do thiazides do to na and cl reabsorption

reduce

what do thiazides do to ca reabsorption

increase

what receptor does aldosterone activate /potentialte

ENaC

what does increased Na into collecting tubules do to K

increases K excretion

what does volume depletion do to K and why

increases K excretion because it increases aldosterone secretion (which increases ENaC)

what does aldosterone do to H+ ATP pump

make more of them on apical side

how do ENaC inhibitors reduce K+ excretion

because less Na+ exit from lumen makes the lumen more positive so K doesnt enter

what are some theraputic uses for potassium sparing diuretics (both types)

hypertension hyperaldosteronism heart failure -really just whenever K+ loss is a concern

what are the 2 types of potassium sparing diuretics

ENaC inhibitors and aldosterone competitive antagonists

what are adverse effects of potassium sparing diuretics

hyperkalemia

where are aquaporin 2

apical membrane of collecting tubules

where are aquaporin 3 and 4

basolateral membrane of collecting tubules

where does ADH act on

V2 receptors on basolateral membrane

what is another name for ADH

vasopressin

what is another name for vasopressin

ADH

what does V2 activation cause

increased cAMP then increase AQP2 in apical membrane

what happens with increased AQP2 in apical membrane

promotes water reabsorption

what does V2 antagonist do to water and Na

reduces water reabsorption, increases plasma Na concentration (i think cause less water just makes na more concentrated)

when do you use V2 antagonists therapeutically

syndrome of innappropriate ADH secretion | hyponatremia

adverse effects of V2 antagonist

hypernatremia | hypotension

what do carbonic anhydrase inhibitors do to ph of body

decrease

what do loop agents do to ph of body

increase

what do thiazides do to ph of body

increase

what do K+ sparing agents do to ph of body

decrease

relationship between blood and urine pH

opposite (one high other low)

which diuretics increase NaCl in urine the most

loop agents and thiazides

which agents increase K+ in urine the most

loop agents and thiazides (but not a lot of them do it a lot)

which agents increase H3CO- in the urine the most

carbonic anhydrase inhibitors

which agents decrease K+ in blood the most

K sparing agents

what can be a bad side effect of heart failure

besides death, pulmonary edema

what is the best treatment for kidney stones and why

thiazide because it decreases Ca in urine

what are used for patients with mild renal insufficiency or heart failure

loop diuretics

what do diuretics do to ACE inhibitors

enhance

what are good drugs used to treat hypercalcemia

loop diuretics (reduce ca reabsorption) (less K+ making lumen ++++ so Ca Mg dont reabsorb)

why is ca and mg reabsoprtion inhibited by loop diuretics

reduce luminal positive potential (inhibit NKCC2) so less ca and mg reabsorption

Renal 2 Flashcards

(75 cards)