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12. Year 2: Urinary System COPY > Regulation of Osmolarity > Flashcards

Regulation of Osmolarity Flashcards

1
Q

What is water regulation controlled by?

A

ADH (vasopressin)

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2
Q

ADH is also called vasopressin, but what else is it called?

A

Arginine vasopressin

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3
Q

What does AVP stand for?

A

Arginine vasopressin

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4
Q

Wha class of hormone is ADH?

A

Polypeptide

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5
Q

Where is vasopressin synthesised?

A

Supraoptic (SO) and paraventricular (PVN) nuclei of the hypothalamus

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6
Q

What does SO stand for?

A

Supraoptic

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7
Q

What does PNV stand for?

A

Paraventricular nuclei

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8
Q

Is vasopressin an anterior or posterior pituitary hormone?

A

Posterior pituitary

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9
Q

What are the 2 different ways ADH secretion is controlled?

A

1) Primary control is plasma osmolarity
2) ECF volume also affects ADH secretion

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10
Q

Explain how osmolarity controls ADH secretion?

A
  • When the effective OP of the plasma increases, the rate of discharge of ADH-secreting neurones in the SO and PVN is increased, increasing release of ADH from posterior pituitary
  • Changes in neuronal discharge is mediated by osmoreceptors in the anterior hypothalamus close to the SO and PVN
  • Other receptors in the lateral hypothalamus mediate thirst
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11
Q

How does an increase in osmolarity impact ADH secreting cells?

A

Increases ADH secretion

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12
Q

How does a decrease in osmolarity impact ADH secreting cells?

A

Decrease in ADH secretion

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13
Q

What ion channels control secretion of ADH?

A

Stretch-sensitive ion channels, changes of water volume due to osmolarity activate them

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14
Q

What is normal plasma osmolarity?

A

280-290MOsm/L

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15
Q

How is plasma osmolarity regulated tightly?

A

Small changes in plasma osmolarity causes radid changes in ADH

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16
Q

How does a 2.5% gain in plasma osmolarity impact ADH levels?

A

10x increase

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17
Q

Does an increase in osmolarity that does not cause an increase in tonicity impact secretion of ADH?

A

No

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18
Q

What is the difference between osmolarity and tonicity?

A
  • Osmolarity is the concentration of a solution expresses at the total number of solute particles per litre
  • Tonicity is a measure of the effective osmotic pressure gradient, the water potential of two solutions separated by a semipermeable cell membrane
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19
Q

What is osmolarity?

A
  • Osmolarity is the concentration of a solution expresses at the total number of solute particles per litre
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20
Q

What is tonicity?

A
  • Tonicity is a measure of the effective osmotic pressure gradient, the water potential of two solutions separated by a semipermeable cell membrane
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21
Q

What kinds of solutes do not produce any “osmotic” drag (impact tonicity)?

A

Solutes that can penetrate membranes, they move together with water

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22
Q

Is urea an effective osmole?

A

No, because it can penetrate membranes

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23
Q

Concentrating ability of the kidney is relatively limited, what does the amount of urine produced depend on?

A

[ADH] and the amount of solute excreted

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24
Q

How does ingesting hypertonic solutions, such as seawater, impact urine?

A

Increases the solute load to be excreted:

  • Therefore increase urine flow, causing dehydration because more water is required to excrete the solute load than was ingested with it
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25
Q

How does ADH impact the permeability of the collecting ducts to water?

A

Increases permeability by incorporating water channels into the limnal membrane (aquaporins)

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26
Q

How does ADH increase the permeability of the collecting ducts to water?

A

By incorporating water channels into the luminal membrane

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27
Q

What impact does ADH being present have on water in the collecting duct?

A
  • Water is able to leave the collecting duct
  • Meaning that the cortical CD becomes equilibrated with the cortical interstitium, ie 300mOsm/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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28
Q

How is the collecting duct impacted if maximum ADH is present?

A
  • The contents equilibrates with that of the medullary interstitium via osmotic efflux of water and thus becomes highly concentrated at the tip of the medulla
  • So produces small volume of highly concentrated urine, which contains relatively less of the filtered water than of solute therefore compensating for water deficit
    • Effectively adds pure water to the ECF
    • Which is reabsorbed by the oncotic P of vasa recta, which will be even greater than usual in the present of water deficit
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29
Q

How are the collecting ducts impacted by the absence of ADH?

A
  • Collecting ducts are impermeable to water
  • So medullary interstitial gradient is ineffective in inducing water movements out of the CD and therefore a large volume of dilute urine is excreted, compensating for water excess
  • Since further ions are reabsorbed from the CD, urine osmolarity can fall to 30-50 mOsm/L
30
Q

What does urea play an important role in?

A

Production of concentrated urine

31
Q

Are collecting duct membranes permeable to urea?

A

Yes, particularly towards medullar tips

So as urea approaches tips there is a tendency for it to move out down its concentration gradient

32
Q

How does ADH impact the collecting ducts permeability to urea?

A

Permeability of late medullary collecting duct to urea is enhanced

33
Q

Explain how urea has an important role in the production of concentrated urine?

A

In presence of ADH, movement of water out of CD greatly concentrates urea remaining in the ducts:

  • CD membranes are relatively permeable to urea, particular towards medullary tips
  • So as urea approaches tip, there is increasing tendency for it to move out down its concentration gradient
  • Permeability of late medullary CD to urea is enhanced by ADH
  • So in an antidiuresis with high levels of ADH urea will be reabsorbed from CD into interstitium where it acts to reinforce the interstitial gradient in the region of the thin ascending loops of Henle
34
Q

What is the medical term for raised level of urea in the blood?

A

Uraemia

35
Q

When can 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 (raised level in the blood of urea) occurs

36
Q

Why is it important that urea is reabsorbed?

A

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

37
Q

How does ECF volume impact ADH secretion?

A
  • Increase in ECF volume causes decrease in [ADH]
  • Decrease in ECF volume causes increase in [ADH]
38
Q

Is the relationship between the rate of ADH secretion and the rate of discharge of stretch receptors proportional or inverse?

A

Inverse

39
Q

What are the two classes of stretch receptors that impact ADH secretion?

A

Low pressure receptors

High pressure receptors

40
Q

Where are low pressure stretch receptors for ADH release found?

A

Left and right atrium

Great veins

41
Q

What are low pressure stretch receptors also called?

A
  • Sometimes called volume receptors because they monitor the return of blood to the heart and the “fullness” of circulation
42
Q

Where are high pressure stetch receptors found?

A

Carotic and aortic arch baroreceptors

43
Q

What receptors are primarily affected by moderate decreases in ECF volume?

A

Atrial receptors

44
Q

How does a moderate decrease in ECF volume impact atrial receptors?

A
  • Normally they exert tonic inhibitory discharge of ADH secreting neurons via the vagus nerve
  • Decrease ECF volume -> decreased atrial receptor discharge -> increased­ ADH release
45
Q

What happens if ECF goes from a moderate change to a small enough amount to impact mean blood pressure (MBP)?

A
  • Then carotid and aortic receptors will also contribute to changes in ADH secretion
  • Very important in haemorrhage, even when going from lying down to standing up there is an increase in ADH release
  • The inverse of these changes occur on volume expansion
46
Q

ADH secreting cells are neurons and receive multiple inputs that they integrate to determine [ADH], other than ECF volume what other stimuli impacts ADH secretion?

A
  • Increases ADH
    • Pain, emotion, stress, exercise, nicotine, morphine
    • Following traumatic surgery inappropriate ADH secretion occurs, so need to be careful about monitoring water intake
  • Decreases ADH
    • Alcohol, suppresses ADH release
47
Q

Other than ECF volume, what other stimuli increase ADH?

A
  • Pain, emotion, stress, exercise, nicotine, morphine
  • Following traumatic surgery inappropriate ADH secretion occurs, so need to be careful about monitoring water intake
48
Q

Other than ECF volume, what other stimuli decreases ADH secretion?

A
  • Alcohol, suppresses ADH release
49
Q

What is a decrease in blood pressure detected by?

A

Carotid and aortic baroreceptors

50
Q

What is low blood volume detected by?

A

Atrial stretch receptor

51
Q

What is a change in osmolarity detected by?

A

Hypothalamic osmoreceptors

52
Q

What is diabetes insipidus?

A

ADH deficiency

53
Q

What are some causes of diabetes insipidus?

A

Hypothalamic areas synthesising ADH may become diseases due to tumours or meningitis, or can be damaged during surgery causing central DI (diabetes insipidus)

54
Q

What are the different kinds of diabetes insipidus?

A

Central diabetes insipidus

Peripheral diabetes insipidus

55
Q

What does DI stand for?

A

Diabetes insipidus

56
Q

What are patients with DI characterised by?

A
  • Very large volumes of very dilute urine, generally >10L/day – polyuria
  • Drink large volumes of water – polydipsia
57
Q

What is the medical term for excess urination?

A

Polyuria

58
Q

What is the medical term for excess thirst?

A

Polydipsia

59
Q

What can central DI be treated by?

A

Giving ADH (AVP)

60
Q

Why can peripheral DI not be treated by giving ADH, but central DI can be?

A

Peripheral DI, due to importance of thirst mechanism for survival cannot give ADH, it is usually secondary to hypocalcaemia or hyperkalaemia so resolved when ion disorders are corrected:

  • May arise due to genetic defect in the V2 (ADH) receptor or in gene for aquaporins (H2O channel)
61
Q

What is peripheral DI usually secondary to?

A

Hypercalaemia or hypokalaemia

62
Q

What genetic deficit may peripheral DI arise due to?

A
  • May arise due to genetic defect in the V2 (ADH) receptor or in gene for aquaporins (H2O channel)
63
Q

What is the osmolarity of the fluid in the Bowman’s capulse?

A

300mOsM

64
Q

What is the osmolarity of the fluid at the end of the proximal tubule?

A

300mOsM

65
Q

What is the osmolarity of the fluid at the end of the loop of Henle?

A

100mOsM

66
Q

What is the osmolarity of the fluid at the end of the collecting duct?

A

50-1200mOsM

67
Q

What is the volume of the fluid in the Bowman’s capsule

A

180L/day

68
Q

What is the volume of the fluid at the end of the proximal tubule

A

54L/day

69
Q

What is the volume of the fluid at the end of the loop of henle

A

18L/day

70
Q

What is the volume of the fluid at the end of the collecting duct

A

1.5L/day (average)

12. Year 2: Urinary System COPY (30 decks)

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