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203 - Theme 1 - The Endocrine System > L10 - Physiology of thirst and fluid balance and its disorders > Flashcards

L10 - Physiology of thirst and fluid balance and its disorders Flashcards

1
Q

What is the physiology?

A

Regulation of thirst and fluid balance

Water homeostasis

Featured hormone:
-ADH aka arginine vasopressin (AVP)

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2
Q

What is the pathophysiology?

A

Polyuria and polydipsia
-Diabetes Insipidus (DI)

Hyponatraemia
-Syndrome of inappropriate ADH secretion (SIADH)

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3
Q

Physiology of water homeostasis: Importance

A

Regulation of water balance ensures plasma osmolality (and extracellular fluid osmolality) remains stable

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

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4
Q

Physiology of water homeostasis: 3 key determinants

A

ADH

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

Kidney
-wide variation in urine output (0.5-20L/day)

Thirst

  • osmoregulated
  • stimulates fluid intake
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5
Q

What are osmoreceptors?

A

Osmoreceptors are groups of specialised cells which detect changes in plasma osmolality (esp sodium)

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6
Q

Where are osmoreceptors located?

A

Located in the anterior wall of 3rd ventricle

-Fenestrations in the blood-brain barrier allow circulating solutes (osmoles) to influence brain osmoreceptors

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7
Q

How do osmoreceptors work?

A

Osmoreceptor cells alter their volume by a transmembrane flux of water in response to changes in plasma osmolality

This initiates neuronal impulses that are transmitted to the hypothalamus to synthesise ADH, and to the cerebral cortex to register thirst

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8
Q

Anti-diuretic hormone (ADH)

A

ADH = ‘against diuresis’ - water conserving

Human form of ADH is arginine vasopressin AVP

Like oxytocin

  • Nonapeptide - 9 amino acid peptide
  • Vasopressin synthesised in neurons in supraoptic and paraventricular nuclei of the hypothalamus
  • Secretory granules migrate down axons to posterior pituitary from where AVP is released
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9
Q

ADH action in the kidney

A

ADH action mediated via V2 receptors

ADH-sensitive water channel (aquaporin) normally stored in cytoplasmic vesicles, moves to & 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 (endocytosis) and returned to cytoplasm

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10
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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11
Q

Osmoregulation: Thirst

A

Low plasma osmolality
-No thirst

High osmolality

  • Increased thirst sensation
  • Drinking immediately transiently suppresses AVP secretion and thirst
  • avoids overshoot
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12
Q

Relationship between plasma AVP and plasma osmolality/urine osmolality

A

positive, when one increases so does the other

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13
Q

What do polyuria and polydipsia exclude?

A

diabetes mellitus

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14
Q

3 main causes of polyuria and polydipsia

A

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

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

Primary polydipsia
-psychogenic polydipsia, social/cultural

all may be ‘partial’

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15
Q

Causes of cranial diabetes insipidus

A

Idiopathic (27%)

Genetic (<5%)

  • familial (AD) mutation of AVP gene
  • DIDMOAD (wolfram) (Ar, incomplete penetrance)

Secondary (comments causes)

  • post-surgical (pituitary/other brain operations)
  • traumatic (head injury, including closed injury)
  • rarer causes (tumours, histiocytosis, sarcoidosis, encephalitis, meningitis, vascular insults, autoimmune)
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16
Q

What is cranial diabetes insipidus?

A

Decreased osmoregulated AVP secretion

Excess solute-free renal water excretion
-polyuria

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

17
Q

Hypothalamus syndrome

A

Disordered thirst and DI

Disordered appetite (hyperphagia)

Disordered temperature regulation

Disordered sleep rhythm

Hypopituitarism

18
Q

Nephrogenic diabetes insipidus

A

Renal tubules resistant to AVP
-polyuria

Thirst stimulated
-polydipsia

19
Q

Causes of nephrogenic diabetes insipidus

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

20
Q

Primary polydipsia (psychogenic)

A

Increases fluid intake
-polydipsia

Lower plasma osmolality

Suppressed AVP secretion

Low urine osmolality, high urine output
-polyuria

Also lose renal interstitial solute, reducing renal concentrating ability

21
Q

Investigating polyuria and polydipsia

A

Medical history

Exclude diabetes mellitus

Documents 24hr fluid balance
-urine output and fluid intake, day and night

Exclude hypercalcaemia/hypokalaemia

Water deprivation test

22
Q

Water deprivation test

A

Period of dehydration

Measure plasma and urine osmolalities & weight

Injection of synthetic vasopressin
-desmopressin (DDAVP)

Measure plasma and urine osmolalities

23
Q

Water deprivation test: normal response to dehydration

A

normal plasma osmolality, high urine osmolality

24
Q

Water deprivation test: cranial diabetes insipidus

A

poor urine concentration after dehydration

rise in urine osmolality after desmopressin

25
Q

Water deprivation test: nephrogenic diabetes insipidus

A

poor urine concentration after dehydration

no rise in urine osmolality after desmopressin

26
Q

Treatment: cranial diabetes insipidus

A

DDAVP (desmopressin)

Over-treatment can cause hyponatraemia

27
Q

Treatment: nephrogenic diabetes insipidus

A

Correction of cause (metabolic/drug cause)

Thiazide diuretics/NSAIDs

28
Q

Treatment: primary polydipsia

A

Explanation, persuasion

Psychological therapy

29
Q

Definitions of hyponatraemia

A

Na < 135mmol/L

Severe Na <125 mol/L

30
Q

Classification of hyponatraemia

A

Exclude ‘drug’ causes
-thiazide diuretics, others

Exclude high concentrations of
-glucose, plasma lipids or proteins

Classify by extracellular fluid volume status

  • hypovolaemia => renal loss, non-renal loss (D&V, burns, sweating)
  • normovolaemia (euvolaemia) => hypoadrenalism, hypothyroidism, SIADH
  • hypervolaemia
  • renal failure, cardiac failure, cirrhosis, excess IV dextrose
31
Q

Diagnosis of SIADH

A

Clinically euvolaemic patient

Low plasma sodium and low plasma osmolality

Inappropriately high urine sodium concentration and high urine osmolality

assess renal, adrenal and thyroid function

32
Q

Causes of SIADH

A

neoplasias

neurological disorders (CNS)

lung disease

drugs

endocrine (hypothyroid/hypoadrenalism)

33
Q

Hyponatraemia treatment

A

Correct severe hyponatraemia slowly

Rapid correction risks oligodendrocyte degeneration and CNS myelinolysis (osmotic demyelination)

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

203 - Theme 1 - The Endocrine System (11 decks)

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