Regulation of Osmolarity Flashcards

1
Q

What type of hormone is ADH?

A

Peptide hormone - neurohormone

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2
Q

Where is ADH synthesised?

A

Supraoptic and Paraventricular nuclei of the hypothalamus

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3
Q

Where is ADH secreted?

A

Posterior pituitary

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4
Q

What is the half life of ADH?

A

10 minutes

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5
Q

Why is the half life of ADH so short?

A

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

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6
Q

What is the primary control of ADH secretion?

A

Plasma osmolarity

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7
Q

How does increased osmotic pressure effect ADH secretion?

A

Increased supraoptic/paraventricular nuclei discharge causing increased ADH release

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8
Q

Where are neuronal discharge changes mediated?

A

Osmoreceptors in the anterior hypothalamus

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9
Q

Where is thirst mediated?

A

Lateral hypothalamus

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10
Q

How do osmoreceptors detect increased osmolarity?

A

↑ H2O outflow from cell
Cell shrinks → stretch sensitive ion channel activated
↑ neural discharge
↑ ADH secretion

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11
Q

How do osmoreceptors detect decreased osmolarity?

A

H2O enters cells
Cells swell
↓ Neural discharge
↓ ADH secretion

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12
Q

What is the effect on ADH when osmoreceptors detect a stretch?

A

Increased H2O levels, decreased ADH secretion

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13
Q

What is the normal plasma osmolarity?

A

280-290mOsm/kg

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14
Q

2.5% increase in osmolarity causes what increase in ADH?

A

10x increase

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15
Q

Why does urea concent not effect osmolarity?

A

Urea passes freely with water through membranes

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16
Q

What is the maximum concentration of urine?

A

1200-1400mOsm

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17
Q

Why does ingestion of hypertonic solutions cause dehydration?

A

The increased solute load increases urine flow as more H2O is needed to excrete than was ingested with it

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18
Q

Where is the main site of water regulation in the kidney?

A

Collecting duct

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19
Q

Via what mechanism does ADH cause increased water absorption?

A

ADH binds with basolateral membrane
Vesicles containing aquaporins exocytose onto brush border membranes membranes
Increased permeability to water

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20
Q

ADH levels affect aquaporins where?

A

On the brush border membrane of the collecting duct

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21
Q

What is the effect of ADH on aquaporin levels on the basolateral membrane of the collecting duct?

A

None - aquaporins here are constant

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22
Q

What is the collecting duct concentration if ADH is present?

A

Proportional to the cortical interstitium (300mOsm), then with the hypertonic medullary interstitial gradient

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23
Q

What is the collecting duct concentration if ADH levels are at maximum?

A

Contents equilibrates with medullary interstitium via osmotic efflux and become highly concentrated at the tip

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24
Q

How would urine present with maximal [ADH]?

A

Small volume, highly concentrated

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25
Q

How is H2O reabsorbed in the presense of Maximal [ADH]?

A

Via oncotic pressure of the vasa recta which will be high in the presence of a H2O deficit

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26
Q

How would urine present with absent ADH? What osmolarity?

A

Large volume
Very dilute
30-50mOsm

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27
Q

Why are urea concentrations high in the presence of ADH?

A

Water leaves the collecting duct and urea remains

28
Q

How does urea permeability vary in the collecting ducts?

A

More permeable to urea towards the medullary tips

29
Q

What is the role of urea reabsorbed into the interstitium from the collecting ducts?

A

Acts to reinforce the interstitial gdt in the region of the thin ascending loops of Henle

30
Q

What happens to urea during maximum anti-diuresis?

A

Urea is retained to save water and reinforce the medullary gradient in the thin ascending limb

31
Q

Why is the reabsorption of urea important in maximal ADH?

A

Too much urea in the collecting duct would have an osmotic effect and impede potential rehydration
Conservation of H2O more important than Urea excretion

32
Q

What is the effect of increased extracellular fluid volume on ADH?

A

Increased ECF volume = decreased ADH

33
Q

What is the effect of decreased extracellular fluid volume on ADH?

A

Decreased ECF volume = increased ADH

34
Q

Why does low blood volume cause increased ADH secretion?

A

Low blood volume = low stretch receptor afferent discharge = increased ADH secretion

35
Q

Where are the low pressure receptors located?

A

L and R atria

Great veins

36
Q

Where are the high pressure receptors located?

A

Carotid

Aortic arch baroreceptors

37
Q

Moderate decreases in ECF volume primary affect what?

A

Atrial - low pressure receptors

38
Q

How do atrial receptors effect ADH release?

A

Presence of reduced ECF volume
Decreased discharge (via vagus nerve)
Increased ADH release

39
Q

When do carotid/aortic baroreceptors engage to contribute to ADH secretion?

A

When volume changes are significant enough to affect MBP

40
Q

What type of cells secrete ADH?

A

Neurones

41
Q

What stimuli can increase ADH?

A

Pain, emotion, stress
Exercise
Nicotine, morphine
Surgery

42
Q

What stimuli can decrease ADH?

A

Alcohol

43
Q

What is the effect of Alcohol on ADH?

A

Suppresses ADH release

44
Q

Why is ADH an important factor post-surgery?

A

Surgery causes inappropriate ADH secretion - monitor H2O intake

45
Q

An osmolarity above what will trigger vasopressin secretion?

A

280mOsM

46
Q

Changes in blood pressure are detected where?

A

Carotid/aortic baroreceptors

47
Q

Changes in blood volume are detected where?

A

Atrial stretch receptors

48
Q

How do messages from the hypothalamic osmoreceptors reach the hypothalamus?

A

Interneurons to hypothalamus

49
Q

Changes in osmolarity are detected where?

A

Hypothalamic osmoreceptors

50
Q

ADH acts where?

A

Collecting duct epithelium

51
Q

What is central Diabetes insipidus?

A

ADH deficiency

52
Q

What factors can cause diabetes insipidus?

A

Meningitis
Tumours
Surgery

53
Q

What is peripheral diabetes insipidus?

A

Collecting ducts insensitive to ADH

54
Q

How are diabetes insipidus characterised?

A

Polyuria (>10L/day)

Polydipsia

55
Q

How is central diabetes insipidus treated?

A

Give patient ADH

56
Q

What is the typical cause of peripheral diabetes insipidus?

A

Hypercalcaemia

Hypokalemia

57
Q

What is the genetic cause of diabetes insipidus?

A

Gene for aquaporins

Gene for ADH receptors

58
Q

What is the normal fluid osmolarity in the bowmens capsule?

A

300mOsM

59
Q

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

A

300mOsM

60
Q

What is the normal fluid osmolarity at the end of the loop of henle?

A

100mOsM

61
Q

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

A

50-1200mOsM

62
Q

How much fluid passes the bowmans capsule a day?

A

180L

63
Q

How much fluid passes the ends of the proximal tubules a day?

A

54L

64
Q

How much fluid passes the ends of the loop of henle a day?

A

18L

65
Q

How much fluid passes the ends of the collecting ducts a day?

A

1.5L (average)