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renal > Urine concentration and dilution L07 > Flashcards

Urine concentration and dilution L07 Flashcards

1
Q

Is ADH released from the anterior or posterior pituitary gland?

A

posterior

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2
Q

Where is ADH synthesised?

A

hypothalamus

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3
Q

What is the action of ADH? How does it do this?

A

-increase retention of water by kidney
(-also causes constriction of blood vessels)

increases presence of AQP2 in distal tubule and collecting duct of nephron

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4
Q

what is vasopressin?

A

same as ADH!

*vaso-blood vessels, pressin-increase pressure

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5
Q

Describe the cellular pathway by which ADH stimulates the synthesis of AQP2 on the apical membrane of distal tubule cells.

A
  • ADH binds to vasopressin type 2 (V2) receptor on basolateral membrane
  • activates the Gstimulatory protein
  • activates Adenlyl Cyclase to synthesise secondary messenger cAMP from ATP
  • cAMP can either:
    1. activate transcription of AQP2 protein in nucleus of cell
    2. activate the PKA pathway
  • AQP2 produced by the cell is sent in vesicles to the apical membrane
  • PKA stimulates the insertion of these AQP2 channels onto the apical membrane
  • allows water to passively move from filtrate into cell and ultimately the medullary interstitium
  • 2 is the short term pathway - quick changes in H2O, no need for protein synthesis
  • 1 is the long term pathway - requires protein synthesis
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6
Q

State the osmolality (mOsm/kg) of different sections of the nephron when there is no ADH.

A 
PT - 285
start of descending limb - 285
tip of loop - around 600
end of thick ascending limb - 90
distal tubule - 90*
end of collecting duct - 60 (very dilute urine)

*note that no water movement as no ADH so osmolality remains low at 90 in distal tubule

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7
Q

State the flow rate* (ml/min) in different parts of the nephron when there is no ADH.

*state the total values calculated from the flow rates of all the nephrons in the kidney

A 
PT - 125
start of loop - 45
end of loop - 25
end of distal tubule - 25*
end of collecting duct - 17 (high urinary flow rate)

*no water movement so volume and therefore flow in tubule remain the same

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8
Q

State the osmolality (mOsm/kg) of different sections of the nephron when there is the maximum amount of ADH.

A 
PT - 285
start of descending limb - 285
tip of loop - around 1400
end of thick ascending limb - 90
end of distal tubule - 285
end of collecting duct - 1400 (very concentrated urine)
  • osmolality in distule tubule from 90 > 285 - due to water movement, it can equilibrate with the interstitial fluid
  • osmolality in collecting duct equilibrates with the very high osmolality deep in the renal medulla - 1400
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9
Q

State the flow rate* (ml/min) in different parts of the nephron when there is the maximum amount of ADH.

*state the total values calculated from the flow rates of all the nephrons in the kidney

A 
PT - 125
start of loop - 45
end of loop - 25
end of distal tubule - 3*
end of collecting duct - 0.1 (very low urinary flow rate)

*losing water (+ ions) due to presence of AQP2 so flow rate decreases across distal tubule and collecting duct

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10
Q

Why is urine more dilute in protein starvation?

A

-urea production is low
-urea has an effect in maintaining high osmolality in renal medulla to drive water movement
-therefore less urea = lower capacity to concentrate urine
>less able to cope with dehydration in protein malnutrition

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11
Q

Describe the cellular pathway by which ADH stimulates the synthesis of UT-A1 on the apical membrane of distal tubule cells.

A
  • ADH binds to vasopressin type 2 (V2) receptor on basolateral membrane
  • activates the Gstimulatory protein
  • activates Adenlyl Cyclase to synthesise secondary messenger cAMP from ATP
  • cAMP can either:
    1. activate transcription of UT-A1 protein in nucleus of cell
    2. activate the PKA pathway
  • UT-A1 produced by the cell is sent in vesicles to the apical membrane
  • PKA stimulates the insertion of these UT-A1 channels onto the apical membrane
  • allows urea to passively move from filtrate into cell and ultimately the medullary interstitium

*very similar to the pathway for water

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12
Q

If there is large water movement out of the distal tubule (in presence of ADH), how is it possible that medullary interstitial space maintains a very high osmolality?

A

urea is also transported out of tubule as well as water

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13
Q

How do cells of the renal medulla cope with the high extracellular osmolality?

A

the cells accumulate a range of organic osmolytes including sorbitol, inositol and betaine. These compounds keep intracellular osmolality high so the cells are not damaged.

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14
Q

What is diabetes insipidus?

A

-deficiency of ADH or loss in sensitivity of kidney to ADH
> patients produce large quantities of dilute urine (polyuria) and are constantly thirsty (due to dehydration and hypovalaemia)

*if fluid intake is inadequate, patients also become hyponatraemic

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15
Q

what is the difference between central and nephrogenic diabetes inspidus?

A 
central = loss of ADH secretion
nephrogenic = loss of sensitivity to ADH
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16
Q

What causes central diabetes inspidus and how is it treated?

A

causes:
-head injury, tumours, infection (basically problems with posterior pituitary/hypothalamus)

Treatement:

  • give desmopressin (vasopressin analogue) *has a longer half life- don’t need to administer as much
  • thiazide (diuretic) * bit weird as it is a diuretic but used to treat polyuria - probably due to other mechanisms
17
Q

Why are ADH analogues given to treat diabetes inspidus rather than ADH itself?

A
  • ADH is peptide > broken down in stomach > can’t take orally > must be injected
  • short half-life > would have to be given a lot/ in large doses
18
Q

What causes nephrogenic diabetes inspidus and how is it treated?

A

causes:

  • genetic mutation in either V2 receptor or AQP2 channel
  • toxicity in the kidney
  • hypercalcaemia (deposits?)

treatment:

  • NOT desmopressin - kidney is insensitive to it
  • thiazide diuretic
  • low sodium diet
19
Q

what does SIADH stand for?

A

syndromes in inappropriate ADH

20
Q

What is SIADH and how does it cause concentrated urine?

A
  • inappropriately high plasma levels of ADH
  • commonly caused by head injury although many causes
  • too much ADH > water retained when it shouldn’t be > body/plasma becomes diluted (hyponatraemia) > urine concentrated
21
Q

How is SIADH treated?

A
  • fluid restriction *hard for patients as ADH stimulates thirst
  • give urea - takes up circulating osmolaltiy > decrease in osmotic pressure *also urea acts as osmotic diuretic by staying in the filtrate and carrying water with it.
22
Q

what is the new therapy used to treat chronic hyponatraemia?

A

V2 receptor antagonists/ vaptans - e.g. tolvaptan

23
Q

what is the osmolality of urine in the presence of maximal ADH?

A

1400mOsm

24
Q

what is the osmolality of urine in the absence of ADH?

A

60-90mOsm

25
Q

What is the urine production rate in presence of maximal ADH?

A

300-400ml/day

26
Q

What is the urine production rate in absence of ADH?

A

25L/day

renal (16 decks)

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