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*Urinary System > Regulation of Osmolality > Flashcards

Regulation of Osmolality Flashcards

1
Q

What are 2 other names for ADH?

A

Vasopressin

Arginine vasopressin (AVH)

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2
Q

Which nuclei of the hypothalamus is ADH synthesised in?

A

Supraoptic + paraventricular (SO + PVN)

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3
Q

Which type of pituitary hormone is ADH?

A

Posterior pituitary

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4
Q

What is the half life of ADH? What is the benefit of this?

A

~10 mins

Can be rapdly adjusted depending on the body’s needs for H2O conservation

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5
Q

What is the primary control of ADH secretion?

A

Plasma osmolarity

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6
Q

When the effective OP (osmotic pressure) of the plasma increases, what happens to ADH release?

A

Rate of discharge of ADH-secreting neurons in the SO and PVN is increased, leading to an increased release of ADH from the posterior pituitary

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7
Q

What are changes in neuronal discharge mediated by?

A

Osmoreceptors

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8
Q

Where are osmoreceptors found?

A

Anterior hypothalamus

Close to the SO and PVN

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9
Q

What do other receptors in the lateral hypothalamus mediate?

A

Thirst

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10
Q
A
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11
Q

Describe the mechanism of osmoreceptors in situations of both 1. increased and 2.decreased osmolarity

A
  1. Increased osmolarity = H2O leaves the cell, cell shrinks/stretch sensitive ion channel is activated = increased neuronal discharge = increased ADH secretion
  2. Decreased osmolarity = H2O enters the cell, cell swells = decreased neural discharge = decreased ADH secretion
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12
Q

What is normal plasma osmolality?

A

280-290mOsm/kg H2O

It is regulated very precisely

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13
Q

What do small changes in either direction of osmolality result in?

A

Rapid changes in ADH

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14
Q

For example, if the system has a very high ‘gain’ of 2.5% increase in osmolality, what increase in ADH would be stimulated?

A

10x increase in ADH

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15
Q

Why do we talk about effective OP rather than just OP?

A

An increase in osmolarity that does not cause an increase in tonicity is ineffective in causing an increase in [ADH]

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16
Q

[sidenote] Difference between osmolarity, osmolality and tonicity?

A

Tonicity is the term used to encompass solutes that are non-penetrating and therefore produce an osmotic drag

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17
Q

Solutes that can penetrate membranes move together with water and don’t produce any what?

A

‘osmotic drag’ or tonicity

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18
Q

The concentrating ability of the human kidney is relatively limited and the amount of urine produced depends on what 2 things?

A

[ADH]

Amount of solute to be excreted

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19
Q

Maximally concentrated urine is 1200-1400mOsm/l, so even if the amount was 2400mOsm, this would mean excretion of how much urine?

A

2L of urine

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20
Q

Ingestion of hypertonic solutions, such as seawater, increase the solute load to be excreted and therefore do what to urine flow?

A

Increase it, leading to dehydration because more H2O is required to excrete the solute load than was ingested with it

(shipwrecked sailors die if they drink seawater!!)

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21
Q

Is urea an effective osmole?

A

NO!

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22
Q

Where is the site of water regulation?

A

the collecting duct

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23
Q

The permeability of the collecting duct is under control of what?

A

ADH

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24
Q
A
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25
Q

Whether or not the dilute urine delivere to the distal tubule is conentrated and to what extent depends on the presence or absence of what?

A

ADH

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26
Q

Lovely wee diagram of the tubule system

A
27
Q

How does ADH increase permeability of collecting ducts to H2O?

A

By incorporating H2O channels into the luminal membrane (aquaporins)

28
Q

What are the 3 steps following the vasopressin binds to membrane receptor on the kidney tubule?

A
  • Receptor activates cAMP second messenger system
  • Cell inserts AQP2 water pores into apical membrane
  • Water is absorbed by osmosis into the blood
29
Q
A
30
Q

Describe the process of ADH and AQP2 again - diagram

A
31
Q

If ADH is present then H2O is able to leave the collecting duct, what does this mean for the cortical CD? Then what happens after?

A

It becomes equilibriated with that of the cortical interstitium i.e. 300mOsm/l

The CD then passes through the hypertonic medullary interstitial gradient

32
Q

What is the hypertonic medullary interstitial gradient created by?

A

Countercurrent multiplier of the loop of Henle

33
Q

If maximum ADH is present, what do the contents of the CD do with the medullary interstitium?

A

The contents equilibriate with that of the medullary interstitium via osmotic efflux of H2O and thus become highly oncentrated at the tip of the medulla

(effectively anti-diuretic effect)

34
Q

With maximal [ADH], what is the nature of the urine produced, to compensate for water deficit?

A

A small volume of highly concentrated urine, which contains relatively less H2O than of solute

35
Q

In maximal ADH, effectively pure H2O is added to the ECF, how is this then reabsorbed?

A

By the oncotic P of vasa recta, which will be even greater than usual in the presence of the H2O deficit

36
Q

What happens to collecting ducts in the absence of ADH? So how does the medullary interstitial gradient affect them?

A

They are impermeable to H2O, so that the medullary interstitial gradient is ineffective in inducing H2O movements out of the CD

37
Q

How does the nature of urine produced in absence of ADH compensate for H2O excess?

A

Large volume of dilute urine is excreted, compensatng for H2O excess

38
Q

Why then in the absence of CD can urine osmolarity even fall to 30-50 mOsm/l?

A

Further ions are absorbed in the CD and no water is lost

39
Q

What happens to urea in the CD in the presence of ADH?

A

Movement of H2O out of the CDs greatly concentrates the urea remaining in the ducts

40
Q

CD membranes are relatively permeable to urea, particularly towards the medullary tips, so what happens as urea approaches these tips?

A

There is an increasing tendency for it to move out down its concentration gradient; permeability of late medullary CD to urea is enhanced by ADH

41
Q

So in antidiuresis, what happens to urea in the CD and what does this act to reinforce?

A

In antidiuresis w high ADH levels, urea will be reabsorbed from CD into the interstitium, where it reinforces the interstitial gradient in the region of the thin ascending loops of Henle

42
Q

In max ADH, what then happens with urea? (one word)

A

Uraemia

43
Q

Why is it so important that urea should be reabsorbed?

A

If it remained in the tubule, it would exert an osmotic effect to hold H2O in the tubule and therefore reduce the potential for rehydration

(conservation of H2O is more important than the associated retention of urea)

44
Q

Any level of ADH between the extremes of [max] and absence is possible, so that…

A

the CD permeability can be precisely graded to meet the demands of the body for H2O regulation

45
Q

How does an increase v decrease in ECF volume affect ADH secretion?

A

Increased ECF vol = decreased [ADH]

Decreased ECF vol = increased [ADH]

46
Q

What is the relationship between the rate of ADH secretion and the rate of discharge of stretch receptor afferents in the low and high P areas of circulation?

A

Inverse relationship

47
Q

Where are the low P receptors and high P receptors?

A

Low P receptors = L and R atria and great veins

High P receptors = caroitic and aortic arch baroreceptors

48
Q

Moderate decreases in ECF volume primarly affect what?

A

The atrial receptors

49
Q

When ECF volume is within normal limits, what do low P atrial receptors do?

A

Exert tonic inhibitory discharge of ADH secreting neurones via the vagus nerve (the atrial receptors constantly send signals saying ‘we don’t need any ADH’)

50
Q

Decreased ECF volume = decreased atrial receptor discharge and therefore…

A

increased ADH release

51
Q

If volume changes enough to affect MBP - then what else gets involved?

A

Carotid (and aortic) receptors (high P) which will also contribute to changes in ADH secretion

52
Q

On volume expansion, what occurs?

A

The inverse of these changes

53
Q

What happens to ADH secretion when you go from lying down to standing up?

A

increase in ADH release

54
Q

Try to name stimuli which increase ADH release (7)

A

Pain

Stress

Emotion

Exercise (sweat - body loses fluid - pre-emptive ADH release)

Nicotine

Morphine

Traumatic surgery (innapropriate - need to be careful about monitoring H2O intake)

55
Q

Give a factor which decreases ADH release

A

Alcohol (diuretic)

56
Q

What type of cells are ADH secreting cells?

A

Neurones - receive multiple inputs which they integrate to dermine [ADH]

57
Q

Summary of receptor function

A
58
Q

What is diabetes insipidus?

A

ADH deficiency

59
Q

Why might the hypothalamic areas synthesising ADH become diseased/damaged? (central DI)

A

Due to tumours or in meningitis

Surgery (central DI)

60
Q

What is the pathology of peripheral DI?

A

CD may be insensitive to ADH

61
Q

How are DI patients characterised?

A

Passage of v large volumes of v dilure urine (generally >10l/day) = POLYURIA

Drink large volumes of water = POLYDIPSIA

62
Q

How can central DI be treated?

A

Giving ADH (AVP)

63
Q

How can peripheral DI be treated?

A

Importance of thirst mechanism for survival - cant give ADH

Usually secondary to hypercalcaemia/hypokalaemia so resolves when ion disorders corrected

May arise as a genetic defect in the V2 (ADH) receptor or in gene for aquaporins

64
Q

Changes in filtrate volume and osmolarity along the nephron graph

A

*Urinary System (26 decks)

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