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Renal/Urology > Lecture 6 - Regulation of Osmolarity > Flashcards

Lecture 6 - Regulation of Osmolarity Flashcards

1
Q

Water regulation is controlled by what hormone?

A

ADH

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2
Q

What is ADH made from?

A

Polypeptide (made from 9 AAs)

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3
Q

Where is ADH produced?

A

Supraoptic and paraventricular nuclei of the hypothalamus

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4
Q

Where is ADH stored?

A

Posterior pituitary

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5
Q

What is the half life of ADH?

A

10 minutes This is good as it can be rapidly adjusted depending on body’s needs for water conservation

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6
Q

What primarily controls ADH secretion?

A

Plasma osmolarity (when osmotic pressure of plasma increases, rate of discharge from ADH secreting neurons in PVN and SO increase) Changes in neuronal discharge are mediated by osmoreceptors close to the PVN and SO in the anterior hypothalamus

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7
Q

Where are the receptors that mediate thirst?

A

Lateral hypothalamus

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8
Q

Describe what happens in the osmoreceptors when there is increased plasma osmolarity

A

Water leaves the cell Cell shrinks and stretches sensitive ion channels Increased neural discharge Increased ADH secretion

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9
Q

Describe what happens in the osmoreceptors when there is decreased plasma osmolarity

A

Water enters cell Cell swells Decreased neural discharge Decreased ADH secretion

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10
Q

What is normal plasma osmolality?

A

130-290mOsm/Kg

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11
Q

What do small changes in plasma osmolarity result in?

A

Rapid changes in ADH secretion System has a very high gain (e.g. 2.5% inc. in osmolality –> 10x inc. ADH)

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12
Q

An increase in osmolarity that does not cause an increase in what is ineffective at raising ADH concentration?

A

Tonicity

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13
Q

What is the difference between osmolarity and tonicity?

A

Osmolarity takes into account the penetrating and non-penetrating solutes Tonicity only takes account of the non-penetrating solutes Remember solutes that penetrate membranes move together with water and do not produce osmotic drag/tonicity

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14
Q

What two things does the amount of urine produced by the kidney depend on?

A

Amount of solute to be excreted ADH concentration

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15
Q

Explain why shipshreked sailors die if they drink seawater

A

Sea water is a hypotonic solution, and it increases the solute load to be excreted and so increases urine flow –> more dehydration as more water is req. to excrete the solute than that ingested with it

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16
Q

Describe the process whereby ADH increases collecting duct permeability to water

A

ADH binds to membrane receptor Receptor activates cAMP second messenger system Cell inserts AQP2 water pores into apical membrane Water reabsorbed by osmosis into the vasa recta (due to medullary gradient concentrated by the countercurrent multiplier of loop of henle)

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17
Q

What happens to water reabsorption at the collecting duct if the maximum amount of ADH is prsent?

A

Contents equilibrate with medullary interstitum via osmotic efflux of water and becomes highly concentrated at the tip of the medulla

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18
Q

What about the vasa recta favours water moving into them at the collecting duct?

A

Higher oncotic pressure due to H2O deficit

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19
Q

Maximal ADH concentration produces what kind of urine?

A

Concentrated, small volume

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20
Q

In the absence of ADH collecting ducts are _____ to water?

A

Impermeable Means medullary interstitial gradient ineffective in inducing H2O movements out CD

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21
Q

What kind of urine is produced in the absence of ADH?

A

Diluted, large colume

22
Q

What is the mimum osmolarity of urine?

A

30-50mOsmol/L (can fall this low as further ions are reabsorbed from the CD)

23
Q

Describe how the permeability of the CD to urea changes down its length

A

CD is relatively permeable to urea, esp at the medullary tips As urea reaches medullary tip there is an increasing tendency for it to move down its conc. gradient

24
Q

Is the permeability of the late medullary CD to urea enhanced or decreased by ADH?

A

Enhanced

25
Q

So what happens in antidiuresis (with high levels of ADH) to urea?

A

It is reabsorbed from the CD into the interstitium where it reinforces the interstitial gradient in the region of the thin ascending loop of henle NB uraemia occurs

26
Q

Why is it important that in antidiuresis urea is reabsorbed?

A

If it remained in the tubule it would exert an osmotic effect to hold water in the tubule + therefore reduce potential for rehydration CONSERVATION OF WATER MORE IMPORTANT THAT UREA RETENTION

27
Q

Why is the level of ADH precisely graded?

A

So CD permeability can meet demands of body for H2O regulation

28
Q

Apart from the osmoreceptors in the hypothalamus, how else is ADH concentration regulated?

A

ECF volume

29
Q

How does increased ECF volume affect ADH concentration?

A

Reduces it

30
Q

How does decreased ECF volume affect ADH concentration?

A

Increases it

31
Q

What are the two types of receptors that detect ECF volume?

A

Low pressure receptors (aka volume receptors) High pressure receptors

32
Q

What are the two low pressure receptors?

A

L and R atria Great veins

33
Q

What are the two high pressure receptors?

A

Carotid and aortic arch baroreceptors

34
Q

What do the low pressure receptors measure?

A

These are stretched if there is a big venous return so they indicate the fullness of the CV system

35
Q

What do the high pressure receptors measure?

A

There are baroreceptors and so measure the pressure in systole (when heart is pumping)

36
Q

Moderate decreases in ECF volume primarily affect what receptors?

A

Atrial receptors

37
Q

What do the atrial receptors normally do if ECF volume is adequate?

A

Exert tonic inhibitory discharge of ADH secreting neurones via the vagus

38
Q

If the atrial receptors notice a decreased ECF volume what happens?

A

There is reduced atrial receptor discharge and so increased ADH release

39
Q

If ECF volume changes enough to affect MBP then _______ receptors will also contribute to changes in ADH secretion.

A

Carotid and aortic

40
Q

With all the different inputs that could affect ADH secretion how is ADH concentration actually determined?

A

ADH secreting cells are neurons and they receive multiple inputs which they integrate to determine ADH

41
Q

What other stimuli can cause an increase in ADH concentration?

A

Pain Emotion Stress Exercise Nicotine Morphine Following traumatic surgery SIADH

42
Q

What other stimuli can cause a decrease in ADH concentration?

A

Alcohol

43
Q

How does alcohol lead to a decrease in ADH concentration?

A

It suppresses ADH release

44
Q

What are the two types of diabetes inspidius?

A

Central DI Peripheral DI

45
Q

What is the cause of central DI?

A

Hypothalamic areas producing ADH become damaged, e.g. due to tumours, surgery, meningitis

46
Q

What is the cause of peripheral DI?

A

Collecting duct becomes insensitive to ADH, e.g. metabolic abnormalities or genetic defect in ADH receptor or gene for AQPs

47
Q

What are the features of DI?

A

Polyuria (>10L/day) Polydipsia

48
Q

How is central DI treated?

A

Give ADH

49
Q

How is peripheral DI treated?

A

Can’t give ADH Usually secondary to hyperCa or hypoK so may resolve when there are treated

50
Q

SUMMARY SLIDE

A

Renal/Urology (29 decks)

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