Renal 2 Flashcards
what mainly happens in descending limb of henle
water reabsorption
can water reabsorb in the ascending limb of henle
no
what is the main transporter in the thick ascending limb
NKCC2
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
how does K+ enter the blood in the loop of henle
alongside Cl
what do loop diuretics attack and where
NKCC2 in the thick ascending loop of henle
what are theraputic uses for loop diuretics
hypercalcemia hyperkalemia pulmonary edema hypertension heart failure renal failure
adversive effects of loop diuretics
hypokalemia
hypomagnesia
metabolic alkalosis
how can loop diuretics cause metabolic alkalosis
increase in Na+ delivery to collecting duct causes increased urinary excretion of K and H
what are main transporters in distal convoluted tubule
NCC and apical calcium channel
what channel does PTH stimulate and where
apical Ca channel in the distal convoluted tubule
how does Ca enter the blood in the distal convoluted tubule
Na/Ca antiport
Ca/H ATP antiport
what do thiazides target and where in nephron
NCC transporter in distal tubule
what is NCC transporter and where is it
Na Cl co transpor in the distal tubule
what is the NKCC2 transporter and where is it
Na K 2Cl cotransporter in the loop of henle
where is the TRPV5 transporter (ca apical)
distal tubule
what does thiazides do to Na and Cl reabsorption
reduce
what does thiazides do to Ca reabsorption
increase (increases Na Ca basolateral exchange cause Na is reduced)
what are uses of thiazides
hypertension
edema
kidney stones
heart failure
what are adverse effects of thiazides
hypokalemia
hyponatremia
Metabolic alkalosis
where in the nephron is most important for K excretion
collecting tubule
where is the ENaC pump
collecting tubule
what does the ENaC pump exchange
just brings Na into principal cells in collecting tubules
what receptor is in principal cells
aldosterone
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
