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renal system > Regulation of Osmolality > Flashcards

Regulation of Osmolality Flashcards

1
Q

What is water regulation controlled by?

A

ADH (vasopressin)

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2
Q

What is ADH?

A

Polypeptide (9ass)

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3
Q

Where is ADH synthesised?

A

In the supraoptic (SO) and paraventricular (PVN) nuclei of the hypothalamus in the brain

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4
Q

What secretes ADH?

A

Posterior pituitary

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5
Q

What is the half life of ADH?

A
  • ~10 minutes

- can rapidly be adjusted depending on the body’s needs for H2O conservation.

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6
Q

How is ADH secretion controlled?

A
  • plasma osmolarity

- ECF volume

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7
Q

What is the primary control of ADH secretion?

A

Plasma osmolarity

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8
Q

How does increased osmolarity affect ADH secretion?

A
  • effective osmotic pressure of the plasma increases
  • rate of discharge of ADH-secreting neurones in the SO and PVN increases
  • release of ADH from the posterior pituitary increases
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9
Q

What are changes in neuronal discharge mediated by?

A

Osmoreceptors in the anterior hypothalamus, close to the SO and PVN

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10
Q

What mediates thirst?

A

Receptors in the lateral hypothalamus

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11
Q

Why does increased osmolarity increase ADH secretion?

A
  • increased H2O out of cell
  • cell shrinks (stretch sensitive ion channel activated)
  • increased neuronal discharge
  • increased ADH secretion
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12
Q

Why does decreased osmolarity decrease ADH secretion?

A
  • H2O enters cells
  • cells swell
  • decreased neuronal discharge
  • decreased ADH secretion
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13
Q

What does changes in the volume of the osmoreceptors lead to?

A

Changes in osmoreceptor discharge (stretch sensitive ion channels)

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14
Q

What is the normal plasma osmolarity?

A

280-290Osm/kg H2O

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15
Q

What does a small change in plasma osmolarity lead to?

A

Rapid changes in ADH

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16
Q

What increase in ADH does a 2.5% increase in osmolarity result in?

A

A 10x increase in ADH

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17
Q

Why is an increase in osmolarity that does not cause an increase in tonicity ineffective in causing a change in [ADH]?

A

Solutes that can penetrate membranes move together with water and don’t produce any osmotic drag or tonicity

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18
Q

Why does an increase in urea not cause an increase in [ADH]?

A

It is an ineffective osmole

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19
Q

What does the amount of urine produced depend on?

A

Depends not only on the [ADH] but also on the amount of solute to be excreted

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20
Q

How does ingestion of hypertonic solutions such as seawater effect excretion?

A
  • increases solute load to be excreted
  • increases urine flow
  • dehydration because more H2O is required to excrete the solute load than was ingested
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21
Q

How is the permeability of collecting ducts to H2O increased?

A

By incorporating H2O channels known as aquaporins into the luminal membrane

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22
Q

How does the presence of ADH affect the collecting duct?

A
  • H2O is able to leave the collecting duct
  • the cortical CD becomes equilibrated with that of the cortical interstitium ie 300 mOsm/l.
  • the CD then passes through the hypertonic medullary interstitial gradient, created by the countercurrent multiplier of the loop of Henle
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23
Q

What happens to the collecting duct if maximum ADH is present?

A
  • contents of the collecting duct equilibrates with that of the medullary interstitium
  • via osmotic efflux of H2O
  • thus becomes highly concentrated at the tip of the medulla.
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24
Q

What is produced when there is maximal [ADH]?

A
  • small volume of highly concentrated urine
  • contains less of the filtered H2O than solute
  • therefore compensating for water deficiency
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25
Q

In H2O deficit how is water reabsorbed?

A

H2O is reabsorbed by the oncotic pressure of vasa recta, which will be even greater then usual in the presence of the H2O deficit.

26
Q

What is produced in the absence of ADH?

A

Large volume of dilute urine is excreted compensating for H2O excess

27
Q

Why is a large volume of dilute urine produced in the absence of ADH?

A

In the absence of ADH collecting ducts are impermeable to H2O, so that the medullary interstitial gradient is ineffective in inducing H2O movements out of the CD

28
Q

How can urine osmolarity fall to 30-50mOsm/l

A

Further ions can be reabsorbed from the CD

29
Q

What plays an important part in the production of concentrate urine?

A

Urea

30
Q

What effect does ADH have on urea?

A

In the presence of ADH, movement of H2O out of the CDs greatly concentrates the urea remaining in the ducts. CD membranes are relatively permeable to urea, particularly towards medullary tips.

31
Q

What happens as urea approaches the medullary tips?

A

As urea approaches the medullary tips, there is an increasing tendency for it to move out down its concentration gradient. The permeability of the late medullary CD to urea is enhanced by ADH

32
Q

What happens to urea in an antidiuresis with high levels of ADH?

A

Urea will be reabsorbed from the CD into the interstitium, where it acts to reinforce the interstitial gradient in the region of the thin ascending loops of Henle.

33
Q

When does uraemia occur?

A

In an anti-diuresis with high levels of ADH, urea is retained in order to save water and reinforce medullary gradient in region of thin ascending limb of LoH. Uraemia occurs

34
Q

Why is it important that urea is 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.

35
Q

What is the conservation of water more important than?

A

The associated retention of urea

36
Q

How can the collecting duct permeability be precisely graded to meet the demands of the body fro H2O regulation?

A

Any level of ADH between the extremes of [max] and absence is possible

37
Q

How does an increase in ECF volume affect [ADH]?

A

Decreases

38
Q

How does a decrease in ECF volume affect the [ADH]?

A

Increases

39
Q

What is there an inverse relationship between the rate of ADH secretion and the rate of?

A

There is an inverse relationship between the rate of ADH secretion and the rate of discharge of stretch receptor afferents in the low and high pressure areas of the circulation.

40
Q

Where are low pressure receptors located?

A

In the left and right atria and the great veins

41
Q

Where are high pressure receptors?

A

Carotid and aortic arch baroreceptors

42
Q

Why are the low pressure receptors sometimes known as volume receptors?

A

They monitor the return of blood to the heart and the “fullness” of the circulation.

43
Q

What are the low pressure receptors sometimes known as?

A

Volume receptors

44
Q

What do moderate decreases in ECF volume primarily affect?

A

Atrial receptors

45
Q

How does a moderate decrease in ECF volume leads to an increase in ADH release?

A
  • Normally they exert tonic inhibitory discharge of ADH secreting neurones via the vagus nerve.
  • Decreased ECF volume leads to decreased atrial receptor discharge
46
Q

What receptors will also contribute to changes in ADH secretion if there is volume change enough to affect the MBP?

A

Carotid (and aortic) receptors

47
Q

What change in ADH occurs when someone stands up from lying down?

A

Increase in ADH release

48
Q

What type of cells are the ADH secreting cells?

A

Neurones

49
Q

What do the neurones which secrete ADH to the multiple inputs they receive?

A

They integrate them to determine [ADH]

50
Q

What stimuli can increase ADH?

A
  • Pain
  • Emotion
  • Stress
  • Exercise
  • Nicotine
  • Morphine
51
Q

What stimuli can decrease ADH?

A

-Alcohol

52
Q

What can happen to ADH secretion following traumatic surgery?

A

Inappropriate ADH secretion

53
Q

What is diabetes insipidus?

A

ADH deficiency

54
Q

What can cause central diabetes insipidus?

A

The hypothalamic areas synthesising ADH may become diseased due to tumours or in meningitis or in surgery leading to central DI

55
Q

What can cause peripheral diabetes insipidus?

A

A collecting duct which is insensitive to ADH

56
Q

What is diabetes insipidus characterised by?

A
  • Passage of very large volumes of very dilute urines generally >10l/day (Polyuria)
  • Drink very large volumes of H2O (Polydipsia)
57
Q

How can central DI be treated?

A

By giving ADH

58
Q

Why can ADH not be given in peripheral DI?

A

The importance of the thirst mechanism for survival means you can’t give ADH

59
Q

What is peripheral DI usually secondary to?

A

Hypercalcaemia or hypokalaemia so it usually resolves when ion disorders corrected

60
Q

What genetic defects may result in DI?

A

May arise as a genetic defect in the V2 (ADH) receptor or in gene for aquaporins (H2O channels)

renal system (26 decks)

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