W2- renal mechanism for urine concentration Flashcards
in what regions of the kidney is water reabsorbed depending on the needs of the body
in the collecting duct
cortical specifically is only dependent on AQP and this is where the majority of the reabsorption occurs, where as medullary region has some independent mechanisms
Outline the mechanism of ADH dependent upregulation of AQP2
ADH acts on the Basolateral membrane by attaching to V2 receptors –> cAMK and PKA –> insertion of AQP2 into apical membrane
what things increase ADH
increased plasma osmolarity
decreased blood volume
via this the response to plasma osmolarity can be blunted when blood volume is high
what regions of the nephron are involved in the reabsorption of Ca
proximal –> paracellular
thick ascending limb –> paracellular
DCT –> TRP channel apical –> calmodulin –> exit via Na/c exchange
name two ways to increase Ca excretion
increase free Ca or increase GFP ( give saline)
how does the kidney contribute to calcium balance
reabsorption, forms VitD for the increased GI absorption of ca
what happens to PTH and phosphate when you have decreased Ca
both increases
what are the effects of increased PTH
determines calcium concentration increase calcitriol increase ca reabsorption in kidney and ca resorption in the bone decrease kidney reabsorption of phosphate
what are some of the effects of increased calcitriol
determines ca supply
decreased PTH
increased ca reabsorption in the gut
increased FGF
what are some of the effects of increased hyperphosphatemia
increased PTH
decrease phosphate
increase ca
increase FGF
what are some of the effects of increased FGF23
decreased phosphate and calcitriol but increased TRP in distal tubule
what are some of the effects of decreased calcitriol
decreased ca
increased serum phosphate which can also then increase FGF
increased PTH
describe the electrolyte balance of calcium, phosphate, potassium and magnesium in CKD
hypocalemia
hyperphophatemia
hypermagnesium
where is Mg reabsorbed and what things can create hypo magnesium and hyper
paracellular in other places but transcellular in DCT
hypo- alcohol and loop diuretics
hyper- declining kidney function cannot excrete
where is urea recycled
from the inter medullary collecting duct to the ascending limb of the loop of henle
what would occur if the flow in the vasa recta was disturbed
too fast of a flow will wash out the solutes and ruin the portico-medullary gradient
too slow and may not maintain the supply of o2 and nurtients
Describe the receptors available for Ca reabsorption along the nephron
proximal tubule paracellular apical: Na/H basolateral: Na/K TAL paracellular apical: NKCC basolateral: Na/K DCT apical: Na basolateral:Na/C
identify the impact of low Ca levels on muscle and Na channels
Low levels of calcium fool sodium channels into sensing more depolarization than actually exists, leading to spontaneous firing of motor neurons. In turn, this firing triggers inappropriate muscle contraction, called low-calcium tetany. If severe enough, it leads to
respiratory arrest because of spasms in the ventilatory muscles
describe why a PT with alkalosis would manifest tetany before an acidotic PT
An important modulator of the e!ect of calcium on nerve membranes is the plasma pH. Serum albumin has many anionic sites that reversibly bind both protons and calcium. These ions compete for occupancy of the binding sites. As pH rises, protons dissociate and calcium ions take their place, thereby lowering the concentration of free calcium ions. In turn, this reduces the di!use cationic layer associated with cell membranes. Thus, a patient with an acute alkalosis is more susceptible to tetany, whereas someone with acidosis will not manifest tetany at levels of total plasma calcium low enough to cause symptoms in normal people
when is the active absorption of ca in the duodenum important
when ca is limited
under normal circumstances the majority of calcium is passively diffused paracellularly in the intestines
Calcium enters duodenal cells passively through calcium-selective channels (members of the TRP family), binds reversibly to mobile cytosolic calcium-binding proteins (called calbindins), and is then actively transported out the basolateral side via a Ca-ATPase and to some extent by a Na-Ca antiporter
what occurs to calcium when na reabsorption decreased
it also decreases
in PCT its powered by water reabsorption and in the TAL it is driven by positive lumen potential, all which are indirectly driven by sodium
what stimulates and what inhibits the kidneys formation of calcitriol
PTH stimulates
FGF inhibits
what can you give to decrease hyperphosphatemia
calcium
where is the majority of magnesium reabsorbed
20% of the filtered load is reabsorbed in the proximal tubule and 70% in the thick ascending limb of the loop of Henle, in both cases by the paracellular route
what impact does ang II have on sodium reabsorption
increased Na reabsorption
also unregulated aldosterone which increases sodium and water reabsorption and k and H secretion
Summarize what would happen if the kidneys were unable to perform ADH functions
If the kidney is unable to respond to ADH, or the countercurrent mechanism / concentration multiplication system is disrupted, there is a large amt of water secretion – nephrogenic diabetes insipidus
If there is an issue with ADH secretion, there is also a large amt of water secretion – central diabetes insipidus
how is urea maintained in the interstitium
■ Regulation: thick ascending limb to collecting ducts are not permeable to urea which keeps it in the tubule and prevents exit into interstitium
● Some urea recycles in the inner medullary collecting ducts to drive urea to be secreted into the thin loops of henle
