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203: Theme 1: The Endocrine System > Physiology of thirst and fluid balance and its disorders > Flashcards

Physiology of thirst and fluid balance and its disorders Flashcards

1
Q

Importance of physiology of water balance

A

Regulation of water balance ensures plasma osmolality remains stable

Narrow range of plasma osmolality
- 285-295 mosmol/kg

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2
Q

3 key determinants of physiology of water homeostasis

A

Antidiuretic hormone

  • osmotically stimulated secretion
  • acts on renal tubule to allow changes in water excretion

Kidney
- wide variation in urine output

Thirst

  • osmoregualted
  • stimulates fluid intake
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3
Q

Osmorecepetors

A

Groups of specialised cells which detect changes in plasma osmolality

Located in the anterior wall of the 3rd ventricle

Alter their volume by a transmembrane flux of water in response to changes in plasma osmolality

Initiates neuronal impulses that are transmitted to the hypothalamus to synthesise ADH and to the cerebral cortex to register thirst

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4
Q

ADH

A

Nonapeptide- 9 amino acid peptide

Vasporessin synthesised in neurones in supraoptic and paraventricular nuclei of the hypothalamus

Secretory granules migrate down axons to posterior pituitary form where AVP is released

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5
Q

ADH action in the kidney

A

ADH action mediated via V3 receptors

ADH sensitive water channel normally stored in cytoplasmic vesciles, moves to and fuses with the luminal membrane

Increases water permeability of renal collecting tubules, promoting water reabsorption

When ADH cleared, water channels removed from the luminal surface and returned to cytoplasm

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6
Q

Osmoregulation: AVP and the kidney

A

Low plasma osmolality

  • AVP undetectable
  • dilute urine
  • high urine output

High plasma osmolality

  • High AVP secretion
  • concentrated urine
  • low urine output
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7
Q

Osmoregulation: thirst

A

Low plasma osmolality
- no thirst

High osmolality

  • increased thirst sensation
  • drinking immediately transiently suppresses AVP secretion and thirst
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8
Q

Three main causes of polyuria and polydipsia

A

Cranial (central) diabetes insipidus
- lack of osmoregulated AVP secretion

Nephrogenic diabetes insipidus
- lack of response of the renal to AVP

Primary polydipsia
- psychogenic polydipsia, social/ cultural

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9
Q

Cranial diabetes insipidus causes

A

Idiopathic (27%)

Genetic (5%)

  • familial mutation of AVP gene
  • DIDMOAD

Secondary (commonest cause)

  • post- surgical (pituitary/ other brain operations)
  • traumatic (head injury, including closed injury)
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10
Q

Cranial diabetes insipidus

A

Decreased osmoregulated AVP secretion

Excess solute free renal water excretion
- polyuria

Provided thirst sensation remain intact and there is ready access to fluids, thirst is stimulated to maintain a stable, normal plasma osmolality

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11
Q

Hypothalamic syndrome

A

Disordered thirst and DI

Disordered appetite

Disordered temperature regulation

Disordered sleep rhythm

Hypopituitarism

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12
Q

Nephrogenic diabetes insipidus

A

Renal tubules resistant to AVP
- polyuria

Thirst stimulated
- polydipsia

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13
Q

Nephrogenic diabetes insipidus causes

A

Idiopathic

Genetic (rare) Xr or Ar
- mutations of V2 receptor gene/ aquaporin gene

Metabolic
- high (calcium) or low (potassium)

Drugs
- lithium

Chronic kidney disease

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14
Q

Primary polydipsia (psychogenic)

A

Increased fluid intake

Lower plasma osmolality

Suppressed AVP secretion

Low urine osmolality, high urine output

Also lose renal interstitial solute, reducing renal concentrating ability

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15
Q

Investigating polyuria and polydipsia

A

Medical history

Exclude diabetes mellitus

Document 24 hour fluid balance
- urine output and fluid intake, day and night

Exclude hypercalcaemia/ hypokalaemia

Water deprivation test

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16
Q

Water deprivation test

A

Period of dehydration

Measure plasma and urine osmolalties and weigh

Injection of synthetic vasopressin
- desmopressin

Measure plasma and urine osmolalities

17
Q

Water deprivation test results

A

Normal response to dehydration
- normal plasma osmolality, high urine osmolality

Cranial diabetes insipidus

  • poor urine concentration after dehydration
  • rise in urine osmolality after desmopressin

Nephrogenic diabetes insipidus

  • poor urine concentration after dehydration
  • nor rise in urine osmolality after desmopressin
18
Q

Treatment for cranial diabetes insipidus

A

DDAVP (desmopressin)

Over treatment can cause hyponatreamia

19
Q

Treatment for nephrogenic diabetes insipidus

A

Correction of cause (metabolic. drug cause)

Thiazide diuretics/ NSAIDs

20
Q

Treatment for primary polydipsia

A

Explanation, persuasion

Psychological therapy

21
Q

Definitions of hyponatreamia

A

[Sodium] <135 mmol/L

Severe [Na] <125 mmol/L

22
Q

Symptoms of hyponatraemia

A

May be asymptomatic

Depends on rate of fall as well as absolute value

Non specific
- headache, nausea, mood change, cramps, lethargy

Severe/ sudden
- confusion, drowsiness, seizures, coma

23
Q

Classification of hyponatraemia

A

Exclude drug causes
- thiazide diuretics

Exclude high concentrations of
- glucose, plasma lipids or proteins

Classify by extracellular fluid volume status

  • hypovalaemia
  • normovolaemia
  • hypervolaemia
24
Q

Hypovolaemia

A

Renal loss

Non renal loss (D&V, burns, sweating)

25
Q

Normovolaemia

A

Hypoadrenalism, hypothyroidism

Syndrome of inappropriate ADH secretion

26
Q

Hypervolaemia

A

Renal failure

Cardiac failure

Cirrhosis

Excess IV dextrose

27
Q

Diagnosis of SIADH

A

Clinically euvolaemic patient

Low plasma sodium and low plasma osmolality

Inappropriately high urine sodium concentration and high urine osmolality

28
Q

Causes of SIADH

A

Neoplasias

Neurological disorders

Lung disease

Drugs

Endocrine

29
Q

SIADH treatment

A

Identify and treat the underlying cause

Fluid restriction (<1000ml daily)

  • induce negative fluid balance 500ml
  • aim ‘low normal’ sodium

Democlocycline

Vasporessin (V2 receptor) antagonists

30
Q

Democlocycline

A

Drug that induces mild nephrogenic DI

31
Q

Vasporessin (V2 receptor) antagonists

A

Vaptans- induce water diuresis

Expensive, variable responses, some attenuation

Lack of clinically significant outcome data

32
Q

Hyponatraemia treatment

A

Correct severe hyponatraemia slowly

Rapid correction risks oligodendrocyte degeneration and CNS myelinolysis

  • severe neurological sequelae, may be permanent
  • alcoholics and malnourished particularly at risk

203: Theme 1: The Endocrine System (22 decks)

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