Physiology of thirst and fluid balance and its disorders Flashcards
Importance of physiology of water balance
Regulation of water balance ensures plasma osmolality remains stable
Narrow range of plasma osmolality
- 285-295 mosmol/kg
3 key determinants of physiology of water homeostasis
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
Osmorecepetors
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
ADH
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
ADH action in the kidney
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
Osmoregulation: AVP and the kidney
Low plasma osmolality
- AVP undetectable
- dilute urine
- high urine output
High plasma osmolality
- High AVP secretion
- concentrated urine
- low urine output
Osmoregulation: thirst
Low plasma osmolality
- no thirst
High osmolality
- increased thirst sensation
- drinking immediately transiently suppresses AVP secretion and thirst
Three main causes of polyuria and polydipsia
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
Cranial diabetes insipidus causes
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)
Cranial diabetes insipidus
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
Hypothalamic syndrome
Disordered thirst and DI
Disordered appetite
Disordered temperature regulation
Disordered sleep rhythm
Hypopituitarism
Nephrogenic diabetes insipidus
Renal tubules resistant to AVP
- polyuria
Thirst stimulated
- polydipsia
Nephrogenic diabetes insipidus causes
Idiopathic
Genetic (rare) Xr or Ar
- mutations of V2 receptor gene/ aquaporin gene
Metabolic
- high (calcium) or low (potassium)
Drugs
- lithium
Chronic kidney disease
Primary polydipsia (psychogenic)
Increased fluid intake
Lower plasma osmolality
Suppressed AVP secretion
Low urine osmolality, high urine output
Also lose renal interstitial solute, reducing renal concentrating ability
Investigating polyuria and polydipsia
Medical history
Exclude diabetes mellitus
Document 24 hour fluid balance
- urine output and fluid intake, day and night
Exclude hypercalcaemia/ hypokalaemia
Water deprivation test
Water deprivation test
Period of dehydration
Measure plasma and urine osmolalties and weigh
Injection of synthetic vasopressin
- desmopressin
Measure plasma and urine osmolalities
Water deprivation test results
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
Treatment for cranial diabetes insipidus
DDAVP (desmopressin)
Over treatment can cause hyponatreamia
Treatment for nephrogenic diabetes insipidus
Correction of cause (metabolic. drug cause)
Thiazide diuretics/ NSAIDs
Treatment for primary polydipsia
Explanation, persuasion
Psychological therapy
Definitions of hyponatreamia
[Sodium] <135 mmol/L
Severe [Na] <125 mmol/L
Symptoms of hyponatraemia
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
Classification of hyponatraemia
Exclude drug causes
- thiazide diuretics
Exclude high concentrations of
- glucose, plasma lipids or proteins
Classify by extracellular fluid volume status
- hypovalaemia
- normovolaemia
- hypervolaemia
Hypovolaemia
Renal loss
Non renal loss (D&V, burns, sweating)