6 Urine Concentration and dilution Flashcards

1
Q

Usually, how does osmolality change along the nephron?

A

not much over PCT
increases to base of loop of Henle
by end of loop, decreased
variable water reabsorption over remaining tubule

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2
Q

How does flow rate change over the nephron?

A

decreases along the whole lot tbh

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3
Q

How does ADH increase water reaborption?

A

binds to V2 receptor
increases synthesis of new AQP2 via PKA
causes insertion of AQP channels pre-formed in vesicles

also increases urea absorption by increasing UT-A1 by the same mechanisms

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4
Q

What happens to the nephron when there is no ADH?

A

we don’t have water reabsorption, so the urine is dilute, increasing flow rate and decreasing osmolality

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5
Q

What happens to the nephron when there is maximum ADH?

A

More water reabsorption, concentrated urine
higher osmolality
lower flow rate

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6
Q

What happens in selective protein starvation?

A

less nitrogen is excreted in the form of urine

it is therefore harder to concentrate urine

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7
Q

What happens to reabsorbed urea?

A

it accumulates in the medulla, forming an area of high osmolality

this is observed in the deeper areas of the loop of henle

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8
Q

Why might cells struggle to survive in the renal medulla? How do they survive?

A

because the osmolality is so high due to the amount of urine

they accumulate lots of organic osmolytes within them to hold the water there, preventing them from dehydrating

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9
Q

What osmolytes are within medullary cells?

A

sorbitol
inositol
betain
glycerophosphorylcholine

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10
Q

What are the 2 types of diabetes insipidus?

A

Central diabetes insipidus

nephrogenic diabetes insipidus

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11
Q

What is the pathogenesis behind central diabetes insipidus?

A

often due to head injnury (subarachnoid haemorrhage)

less ADH is released

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12
Q

How is central diabetes Insipidus treated?

A
ADH analogue (desmopressin)
paradoxical use of thiazide diuretics
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13
Q

what are the different causes of nephrogenic DI?

A

lithium toxicity (bipolar meds)
hypercalcaemia
genetic, mutations in V2 of AQP2 (very rare)

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14
Q

How is nephrogenic DI treated?

A

thiazide diuretic

low salt diet

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15
Q

Why would you not used desmopressin to treat Nephrogenic DI?

A

it is insensitive to it

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16
Q

What is SIADH?

A

syndromes in Inappropriate ADH (high ADH, concentrated urine)

17
Q

What might cause SIADH?

A

head injury

18
Q

What are the effects of SIADH?

A

become hyonatraemic, as water is retained, so it dilutes the sodium

19
Q

How might you treat SIADH

A
fluid restriction
give urea (although this sin't really done in the uk anymore as you would have to give so much)
Aquaretic drugs
20
Q

What do aquaretic drugs do?

A

cause water loss without salt loss
V2 receptor antagonists
Vaptans
act on the late portion of the distal tubule and the collecting duct