Osmoregulation Flashcards

1
Q

Where is ADH synthesised?

A

in the hypothalamus

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2
Q

Where is ADH released?

A

in the terminals of the hypothalamic neurones found within the posterior pituitary

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3
Q

How does ADH work?

A

acts in the distal tubule and collecting duct to increase the water permeability by increasing AQP2

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4
Q

How does ADH affect AQP2?

A

increases the number of AQP2 channels, increasing reabsorption

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5
Q

Before the number of AQP2 channels are increased, where are they stored?

A

in vesicles inside the epithelial cell (can be quickly inserted into the membrane (quicker mechanism as synthesis not requires))

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6
Q

Why does the osmolality stay the same along the proximal tubule?

A

even though salt is being reabsorbed so is water so they balance each other out

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7
Q

In terms of urine, what does low osmolality result in?

A

dilute urine

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8
Q

When is urea production low?

A

in the presence of selective protein starvation production is low so that the kidney has a lower capacity to concentrate urine

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9
Q

What is the urea transporter and what is it regulated by?

A

UT-A1
regulated by ADH
When ADH is high, urea absorption is increased, this increases the amount of urea in the extracellular space, increasing water reabsorption

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10
Q

What is the role of urea in the renal medulla?

A

role in maintaining osmolality

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11
Q

What is osmolality?

A

defined as the number of osmoles (Osm) of solute per kilogram of solvent

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12
Q

How are the cells of the medulla adapted to survive 1200mOsm? (high osmolality)

A

to prevent cell swelling, they have to have a high intercellular osmolality. They do this by accumulating a range of organic osmolytes inside the cells. These include: sorbitol, inoitol, glycerophosphorylcholine and betaine

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13
Q

Why does diabetes inspidus?

A
  • due to a loss of ADH secretion (central diabtetes inspidus) or a loss in the sensitivity of the kidney to ADH (usually due to a problem in the V2 receptors) (nephrogenic diabetes insipidus)
  • unable to produce concentrated urine
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14
Q

What does diabetes insipidus lead to?

A

polyuria
dehydration
hypovolaemia
can also cause people to drink too much

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15
Q

How is central diabetes insipidus treated?

A

uses desmopression (ADH analogue)

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16
Q

How is nephrogenic diabetes insipidus treated?

A

-low salt diet (prevents high sodium conc)

17
Q

How is nephrogenic diabetes insipidus caused?

A
  • toxicity
  • hypercalceamia
  • genetic due to mutations in either V2 or AQP2
18
Q

What is SIADH?

A

syndrome of inappropriate ADH (inappropriately high ADH)

19
Q

What is the urine like of someone with SIADH?

A

v conc

20
Q

How do you treat SIADH?

A
  • fluid restriction
  • give urea
  • V2 receptor antagonist
21
Q

What happens when there is inadequate water intake?

A
  • increase in osmolality in the plasma
  • osmolality is detected in the anteroventral third ventrical (AV3V) region
  • AV3V neurones project to the median preoptic area of the hypothalamus which increases thirst
22
Q

What is the max urine osmolality?

A

1400mOsm

23
Q

Can any animals drink sea water?

A

yes, in rats urine concs can reach 3000mOsm (so can some other animals)

24
Q

What are the dominant osmolytes in the circulation?

A

Na+ and Cl- (but aren’t dominat osmolytes ingested e.g carbs, fats and proteins)

25
Q

When can glucuse conc get so high that it contributes to osmolality?

A

diabetes mellitus