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11. Urinary > 5. Plasma Osmolarity > Flashcards

5. Plasma Osmolarity Flashcards

1
Q

When does plasma osmolarity increase?

A

When water intake < excretion.

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2
Q

When does plasma osmolarity decrease?

A

When water intake > excretion.

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3
Q

What is body fluid osmolarity kept at?

A

275-295mOsm/kg.

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4
Q

How do disorders of water balance manifest?

A

Changes in body fluid osmolatiry.

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5
Q

How do disorders of Na+ balance manifest?

A

Changes in volume.

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6
Q

What are changes in plasma osmolarity detected by?

A

Hypothalamic osmoreceptors.

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7
Q

Where are hypothalamic osmoreceptors located?

A

Organum vasculoum of the laminae terminalis (OVLT).

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8
Q

Where is the OVLT?

A

Anterior and ventral to the third ventricle.

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9
Q

How is the OVLT exposed to the systemic circulation?

A

It has a fenestrated leaky epithelium.

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10
Q

How does the OVLT respond to increase in plasma osmolarity?

A

Concentrate urine and increase thirst respectively.

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11
Q

When do you begin to feel thirsty?

A

At 10% dehydration.

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12
Q

How does the posterior pituitary respond to increase in plasma osmolarity?

A

Releases ADH.

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13
Q

What is the structure of ADH?

A

It is a small peptide, 99 amino acids long.

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14
Q

What is the role of ADH?

A

It acts on the kidney to regulate the volume and osmolarity of the urine by increasing permeability of the kidneys to water and urea.

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15
Q

How does ADH affect the apical membrane of the nephron’s collecting duct?

A

It adds the water channel aquaporin-2 so water can be reabsorbed to decrease plasma osmolarity.

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16
Q

Which aquaporin channels are present on the apical and basolateral membranes?

A

Apical - aquaporin-2 in presence of ADH.

Basolateral - aquaporin-3, and aquaporin-4 always.

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17
Q

What is the implication of aquaporin-3 and 4 channels always being present on the basolateral membrane?

A

It is always permeable to water so water that enters across the apical membrane can always pass into the peritubular blood.

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18
Q

How does ADH affect the medullary part of the collecting duct?

A

It increases permeability to urea so it is reabsorbed and water folllows.

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19
Q

What happens when urea concentration rises?

A

It passively moves down its concentration gradient into the ascending limb. It then passes back into the collecting duct to be reabsorbed in the medullary portion - i.e. is recycled.

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20
Q

What is SIADH?

A

Syndrome of inappropriate anti-diuretic hormone secretion. It is secretion of ADH not inhibited by lowering of blood osmolarity.

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21
Q

What is the consequence of SIADH?

A

An excessive amount of water is retained so blood osmolarity drops and there is hyponatraemia.

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22
Q

What are symptoms of hyponatraemia?

A

Nausea and vomiting, headache, confusion, lethargy, fatigue, appetite loss, restlessness and irritability, muscle weakness, spasms, cramps, seizures, and decreased consciousness or coma.

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23
Q

How can hyponatraemia caused by SIADH be treated?

A

ADH receptor antagonists.

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24
Q

How does gradient of osmolarity change over the medullar?

A

It increases as you descend.

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25
Q

What sets up the osmotic gradient of the medulla?

A

Active transport of NaCl out of the thick ascending limb and the recycling of urea.

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26
Q

What is the crucial action of the thick ascending limb?

A

It removes solute without water, diluting the filtrate and increasing intersticium osmolarity.

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27
Q

What is the effect of loop diuretics on the medullary intersticium?

A

It blocks NaK2Cl transporters so the intersticium becomes isosmotic and large amount of dilute urine is produced.

28
Q

What does the loop of Henle act as in setting up the osmotic gradient?

A

A counter current multiplier.

29
Q

What is counter-current multiplication?

A

The tubule is filled with isotonic fluid initially. Then Na+ is pumped out of the ascending loop so the osmotic pressure outside the tubule is raised and lowered inside. More fluid enters from glomerulus and enters the descending limb, which is permeable to water, so it leaves via osmosis to raise osmotic pressure inside the descending tubule. More fluid enters and the concentrated fluid is pushed into ascending limb. The Na+ pump restores the 200mOsmol/L gradient across membrane so external osmolarity is 500mOsmol/L. More fluid enters and water leaves until the osmotic pressure in the descending tubule is 500mOsmol/L. It is then pushed into the ascending limb and Na+ pump makes the gradient so the interstitial osmolarity is 700mOsmol/L.

30
Q

What is the final gradients of the counter-current mechanism limited by?

A

The diffusional process.

31
Q

What maintains the counter current concentration gradient in the loop of Henle?

A

Vasa recta.

32
Q

What are the vasa recta?

A

Blood vessels that run alongside the loop of Henle but in opposite flow direction.

33
Q

Why do ions diffuse into the vasa recta and water out?

A

Isosmotic blood in the descending limb of the vasa recta enters the hyperosmotic milieu of the medulla, where there is a high concentration of ions. So ions move into vasa recta.

34
Q

In which direction does the osmolarity of blood in the vasa recta increase?

A

As it reaches the tip of the hairpin loop.

35
Q

What is the osmolarity of blood in the vasa recta as it reaches the tip of the hairpin loop?

A

It is isosmotic with the medullary intersticium.

36
Q

Why does solute move out of the blood ascending towards the cortex?

A

It has a higher solute content than surrounding intersticium so solute mvoes out.

37
Q

Where does water move between the loop of Henle and vasa recta?

A

Back in from the descending limb of the loop of Henle into the blood.

38
Q

Why is there little net dilution of the concentration of the interstitial fluid in the counter current system?

A

The U shape of the vasa recta allows it to act as a counter current exchanger.

39
Q

What is the role of the vasa recta?

A

Prevent the medullary hyperosmolarity from being dissipated.

40
Q

What is the range that free plasma [Ca2+] should be kept within?

A

1.0-1.3mmol/L.

41
Q

How does calcium exist in plasma?

A

As free ionised species, protein bound, and complexed.

42
Q

What controls the absorption of calcium?

A

Vitamin D.

43
Q

What happens to dietary calcium?

A

20-40% is absorbed and some excreted into the gut.

44
Q

When does calcium absorption increase?

A

In growing children, pregnancy, and lactation.

45
Q

When does calcium absorption decrease?

A

With advanced age.

46
Q

What reduces calcium absorption?

A

Complexing it, e.g. with oxalates.

47
Q

How much calcium do the kidneys filter a day?

A

250mmol.

48
Q

How much of filtered calcium is reabsorbed?

A

95-98%.

49
Q

What is urinary calcium excretion?

A

<10mmol/day.

50
Q

Where is calcium reabsorbed in the kidney?

A

65% in the proximal convoluted tubule, 20-25% in the loop of Henle, 10% in the distal convoluted tubule.

51
Q

How does vitamin D get into the body?

A

Absorbed in the gut or synthesised in the skin in the presence of sunlight.

52
Q

How is vitamin D kept for longer?

A

Converted to calciferol in the liver to extend the half life.

53
Q

What does parathyroid hormone regulate?

A

The conversion of calciferol in the kidney to the active form, calcitriol.

54
Q

What is the role of calcitriol?

A

It’s the active form of vitamin D and work by binding to calcium in the gut to increase its absorption.

55
Q

How does PTH affect calcium levels?

A

It increase its release from bone and reabsorption in the proximal convoluted tubule of the kidney. It also decreases the reabsorption of phosphate and bicarbonate.

56
Q

What causes hypercalcaemia?

A

Primary hyperparathyroidism, haematological malignancies, non-haematological malignancies.

57
Q

How does hypercalcaemia come about due to a malignancy?

A

Production of parathyroidhormone-related peptide (PTHrP).

58
Q

What is the function of PTHrP?

A

Increases plasma Ca2+ concentration.

59
Q

What are the gastrointestinal symptoms of hypercalcaemia?

A

Anorexia, nausea/vomiting, constipation, acute pancreatitis (rare).

60
Q

What are the cardiovascular symptoms of hypercalcaemia?

A

Hypertension, shortened QT interval on ECG, enhanced sensitivity to digoxin, renal, polyuria and polydipsia, occasional nephrocalcinosis.

61
Q

What are the central nervous system symptoms of hypercalcaemia?

A

Cognitive difficulties and apathy, depression, drowsiness, and coma.

62
Q

How is hypercalcaemia managed generally?

A

Hydration and loop diuretics to increase Ca2+ excretion.

63
Q

How is hypercalcaemia managed specifically?

A

Bisphosphonates inhibit the breakdown of bone, calcitonin opposes the action of PTH.

64
Q

What is the risk of developing renal stones in men and women over a lifetime?

A

Men 20%, women 5-10%.

65
Q

What proportion of renal tract stone are made of calcium?

A

70-80%.

66
Q

What factors are involved in stone formation?

A

Low urine volume, hypercalcuria, and low urine pH (<5.47).

67
Q

What is the conservative management of renal stones?

A

Increasing fluid intake, restricting dietary oxalate and sodium, consider restricting calcium and animal protein intake.

11. Urinary (12 decks)

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