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Physiology of thirst and fluid balance and its disorders Flashcards

1
Q

What is the difference between osmolality and osmolarity?

A

Osmolality - measures solute concentration in osmoles of solute per KG of solution.
Osmolarity - measures solute concentration in osmoles of solute per LITRES of solution.

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2
Q

Which receptors detect changes in plasma osmolality and extracellular tonicity?

A

Osmoreceptors

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3
Q

Where are osmoreceptors found?

A

In the anterior wall of the third ventricle

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4
Q

How small a change in tonicity can osmoreceptors detect?

A

1-2% change

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5
Q

What is tonicity?

A

Measure of osmotic pressure gradient.

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6
Q

An increase in extracellular fluid will stimulate what receptors?

A

Osmoreceptors

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7
Q

When activated, osmoreceptors cause what?

A

Thirst - causes an increase in water intake
Vasopressin release - causes renal water reabsorption
These increase the circulating volume and decrease extra cellular fluid osmolality.

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8
Q

What is the normal range of plasma osmolality?

A

285 - 295 mosmol/kg.

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9
Q

Is there increased thirst with high or low plasma osmolality?

A

High.
No thirst with low plasma osmolality.

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10
Q
A
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11
Q

Which lobe of the pituitary gland secretes ADH?

A

posterior

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12
Q

Which neuroendocrine cells are located in the hypothalamus?

A

Magnocellular neurons

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13
Q

What do magnocellular neurons synthesise and where?

A

Synthesise a precursor of ADH.
Located in the hypothalamic paraventricular and supraoptic nuclei.

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14
Q

Where is synthesised ADH located?

A

Packaged in secretory granules/vesicles in the cell body of magnocellular neurons.

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15
Q

Where does the axon of the magnocellular neurons travel to?

A

The axons travel along the pituitary stalk and extend into the posterior pituitary.

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16
Q

How is ADH released into circulation?

A

Osmoreceptors activate the paraventricular and supraoptic neurons –> Ca2+ entry increases –> ADH released.

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17
Q

What is ADH also known as?

A

Vasopressin or Arginine vasopressin (AVP)

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18
Q

What is the role of ADH?

A

Prevents excessive urine synthesis (anti-diuretic)
Causes vasoconstriction (Vasopressin)
Overall causes water retention –> water replenishes the plasma and decreases plasma osmolality.

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19
Q

Where does ADH act in the kidney?

A

Distal tubule
Collecting tubule
Collecting duct epithelia

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20
Q

What is the mechanism of ADH?

A

ADH binds to V2 receptors on basolateral membrane of tubular cells.
Activates Gas pathway –> AC –> cAMP –> PKA –> Protein phosphorylation.
Aquaporin 2 is released/activated by phosphorylation.
Aquaporin 2 fuses with the apical membrane via exocytosis.
Water channels formed (aquaporins 3+4) –> allows diffusion of water across cell.
Water enters blood circulation.

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21
Q

What happens if there is a 2% increase or decrease in normal osmolality?

A

Decrease - Inhibition of thirst
Increase - Thirst and ADH release

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22
Q

What happens if there is a 20% increase or decrease in normal osmolality?

A

Seizures and death.

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23
Q

What is polyuria?

A

Passing excessive urine
>3L/day or >30ml/kg/24hours

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24
Q

What is polydipsia?

A

Excessive thirst and water consumption - there is decrease in plasma osmolality.

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25
Q

What are the main causes of polyuria and polydipsia?

A

Diabetes mellitus
Central (cranial) diabetes insipidus
Nephrogenic diabetes insipidus
Dipsogenic diabetes insipidus (Primary polydipsia)

26
Q

Why can central diabetes insipidus cause cause polyuria and polydipsia?

A

There is a lack of ADH secretion.

27
Q

Why can nephrogenic diabetes insipidus cause polyuria and polydipsia?

A

There is a lack of renal tubule response to ADH

28
Q

What is dipsogenic diabetes insipidus?

A

Also called psychogenic polydipsia - causes by excessive drinking without a psychological stimulus to do so.

29
Q

How does primary polydipsia affect ADH?

A

Fluid intake is increased so much that plasma osmolality is lowered to below the threshold for ADH secretion.

30
Q

Which condition is associated with primary polydipsia?

A

Schizophrenia

31
Q

What are the clinical features of primary polydipsia?

A

Usually mild
Impaired cognitive function, seizures
Permanent neurological deficits
Death - rare

32
Q

What is diabetes insipidus characterised by?

A

Hypotonic polyuria - >3L urine/day with reduced urine osmolality <295 mosmol/kg.

33
Q

What are the causes of central diabetes insipidus?

A

Idiopathic - autoimmune damage to neurons that secrete ADH
Head trauma, neurosurgery
Pituitary tumours
Genetic (<5%) - mutation of ADH gene. DIDMOAD (Wolfram’s syndrome)

34
Q

What are some rare causes of central diabetes insipidus?

A

Histiocytosis
Sarcoidosis
CNS infections
Vascular causes (Sheehan’s syndrome - excessive blood loss in childbirth damages pituitary gland).

35
Q

What are the causes of nephrogenic diabetes insipidus?

A

Genetic;
- X-linked mutation in V2 encoding gene
- AD mutation in aquaporin 2 encoding gene
Persistent high Ca2+
Severe low K+
Drugs - Lithium, demeclocycline, antifungals, antineoplastic agents (chemo).

36
Q

What is gestational diabetes insipidus caused by?

A

Increased placental vasopressinase activity that degrades vasopressin and resolves after delivery.

37
Q

What test is done to diagnose diabetes insipidus?

A

Water deprivation test

38
Q

How is a water deprivation test done?

A

Period of dehydration - measure plasma and urine osmolality and weight
Infect synthetic vasopressin (Desmopressin) - measure plasma and urine osmolality.

39
Q

From the water deprivation test, what does it mean if there is normal plasma osmolality and high urine osmolality?

A

Normal response - no diabetes insipidus

40
Q

From the water deprivation test, what does it mean if there is poor urine concentration after dehydration, and a rise in urine osmolality are desmopressin?

A

Central diabetes insipidus

41
Q

From the water deprivation test, what does it mean if there if poor urine concentration after dehydration and no rise in urine osmolality after desmopressin?

A

Nephrogenic diabetes insipidus

42
Q

How is central diabetes insipidus treated?

A

Desmopressin
Be careful of hyponatraemia.

43
Q

How is nephrogenic diabetes insipidus treated?

A

Correct cause (metabolic/drug)
Thiazide diuretics/NSAIDS

44
Q

How is primary polydipsia treated?

A

Explanation
Psychological therapy

45
Q

What happens to the tonicity in true hyponatraemia?

A

Decreased tonicity

46
Q

What are the four types of hyponatraemia?

A

Acute <48hrs
Chronic >48hrs
True
Pseudo

47
Q

What are the symptoms of severe hyponatraemia?

A

Vomiting
Cardio-resp arrest
Seizures
Coma

48
Q

What are the symptoms of moderately severe hyponatraemia?

A

Nausea
Confusion
Headaches

49
Q

How is hyponatraemia classified based on volume?

A

Hypovolaemia
Euvolaemia
Hypervolaemia

50
Q

What are the causes of hypovolaemic hyponatraemia?

A

Gi loss
Burns
Renal
Pancreatitis
Blood loss

51
Q

What are the causes of euvolaemic hyponatraemia?

A

Thiazide diuretics (or hypovolaemia)
Hypothyroidism
Adrenal insufficiency (or hypovolaemia)
SIADH

52
Q

What are the causes of hypervolaemic hyponatraemia?

A

HF
Cirrhosis
Nephrotic syndrome

53
Q

What is SIADH?

A

Syndrome of inappropriate anti-diuretic hormone secretion.
Inappropriate anti-diuresis.
Urine is not maximally dilute, despite reduction in serum osmolality.

54
Q

What is the criteria to diagnose SIADH?

A

Serum osmolality <275 mOsm/KG
High urine osmolality >100
Urine Na+ 30mmol/L
No other causes found.

55
Q

What type of cancer can cause SIADH?

A

Bronchogenic (lung)

56
Q

What lung conditions can cause SIADH?

A

Pneumonias
TB

57
Q

Which neurological disorders can cause SIADH?

A

Encephalitis/Meningitis
Trauma
Stroke
ETOH withdrawal

58
Q

Which drugs can cause SIADH?

A

Carbamazepine - anti-epileptic
Anti-depressants
PPIs
Opiates
NSAIDS
Anti-psychotics - Haloperidol
Amitriptyline
Ecstasy

59
Q

What is the risk of treating hyponatraemia too quickly?

A

Can cause osmotic demyelination and oligodendrocyte degeneration (central pontine myelinosis).
Alcoholics and malnourished particularly at risk.

60
Q

How quickly can hyponatraemia be treated?

A

No more than 0.5mmol/L = no more than 8mmol/day.

61
Q

How is SIADH treated?

A

Treat underlying cause.
1L Fluid restriction
Aim -ve balance of 500mls
Demeclocycline - induces mild nephrogenic DI
Vasopressin antagonists - induce a water diuresis but expensive and variable response.

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