W2- renal mechanism for urine concentration Flashcards

1
Q

in what regions of the kidney is water reabsorbed depending on the needs of the body

A

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

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2
Q

Outline the mechanism of ADH dependent upregulation of AQP2

A

ADH acts on the Basolateral membrane by attaching to V2 receptors –> cAMK and PKA –> insertion of AQP2 into apical membrane

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3
Q

what things increase ADH

A

increased plasma osmolarity
decreased blood volume

via this the response to plasma osmolarity can be blunted when blood volume is high

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4
Q

what regions of the nephron are involved in the reabsorption of Ca

A

proximal –> paracellular
thick ascending limb –> paracellular
DCT –> TRP channel apical –> calmodulin –> exit via Na/c exchange

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5
Q

name two ways to increase Ca excretion

A

increase free Ca or increase GFP ( give saline)

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6
Q

how does the kidney contribute to calcium balance

A

reabsorption, forms VitD for the increased GI absorption of ca

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7
Q

what happens to PTH and phosphate when you have decreased Ca

A

both increases

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8
Q

what are the effects of increased PTH

A
determines calcium concentration  
increase calcitriol
increase ca reabsorption in kidney and 
ca resorption in the bone 
decrease kidney reabsorption of phosphate
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9
Q

what are some of the effects of increased calcitriol

A

determines ca supply
decreased PTH
increased ca reabsorption in the gut
increased FGF

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10
Q

what are some of the effects of increased hyperphosphatemia

A

increased PTH
decrease phosphate
increase ca
increase FGF

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11
Q

what are some of the effects of increased FGF23

A

decreased phosphate and calcitriol but increased TRP in distal tubule

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12
Q

what are some of the effects of decreased calcitriol

A

decreased ca
increased serum phosphate which can also then increase FGF
increased PTH

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13
Q

describe the electrolyte balance of calcium, phosphate, potassium and magnesium in CKD

A

hypocalemia
hyperphophatemia
hypermagnesium

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14
Q

where is Mg reabsorbed and what things can create hypo magnesium and hyper

A

paracellular in other places but transcellular in DCT
hypo- alcohol and loop diuretics
hyper- declining kidney function cannot excrete

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15
Q

where is urea recycled

A

from the inter medullary collecting duct to the ascending limb of the loop of henle

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16
Q

what would occur if the flow in the vasa recta was disturbed

A

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

17
Q

Describe the receptors available for Ca reabsorption along the nephron

A
proximal tubule paracellular
apical: Na/H
basolateral: Na/K
TAL paracellular
apical: NKCC
basolateral: Na/K
DCT
apical: Na
basolateral:Na/C
18
Q

identify the impact of low Ca levels on muscle and Na channels

A

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

19
Q

describe why a PT with alkalosis would manifest tetany before an acidotic PT

A

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

20
Q

when is the active absorption of ca in the duodenum important

A

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

21
Q

what occurs to calcium when na reabsorption decreased

A

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

22
Q

what stimulates and what inhibits the kidneys formation of calcitriol

A

PTH stimulates

FGF inhibits

23
Q

what can you give to decrease hyperphosphatemia

A

calcium

24
Q

where is the majority of magnesium reabsorbed

A

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

25
Q

what impact does ang II have on sodium reabsorption

A

increased Na reabsorption

also unregulated aldosterone which increases sodium and water reabsorption and k and H secretion

26
Q

Summarize what would happen if the kidneys were unable to perform ADH functions

A

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

27
Q

how is urea maintained in the interstitium

A

■ 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