Thirst and fluid balance Flashcards
Osmoreceptors
- Function
- Location
- Mechanism
Receptors that detect changes in plasma osmolarity
- Especially in changes to Na+
Located in the anterior wall of the third ventricle.
- Contains leaky blood vessels close to the hypothalamus.
Mechanism:
When changes in osmolarity occurs—> Alters the volume of the cell
- Changes water influx into cell.
Triggers the secretion of ADH [hypothalamus] and directs thirst [cortex]
ADH
- Synthesis and secretion
- Action
Peptide hormone made in hypothalamus nuclei
- Supraoptic
- Paraventricular
Secreted into the posterior pituitary gland via secretory granules.
Action
- Binds to V2 receptors on the basolateral membrane of tubule cells in collecting duct.
- Triggers the insertion of aquaporins [AQP2 in lumen, 3+4 in basal membrane]
Physiology in low plasma osmolarity
- ADH
- Urine
- Thirst
ADH negligible.
Urine dilute, large volume.
No thirst
Physiology in high plasma osmolarity
- ADH
- Urine
- Thirst
ADH secreted, high levels.
Urine concentrated, low volume.
Thirst triggered.
- Drinking suppresses ADH secretion to prevent overshooting.
Plasma osmolarity ranges
285-295 mosmol/kg
This is maintained under normal physiology using
- Kidneys
- ADH secretion
- Thirst
Diabetes insipidus
- Definition
- Causes
Diabetes= urine Insipidus= insipid [lacking flavour, watery]
Characterised by polydipsia and polyuria.
Causes
- Cranial/ Central: brain
- Nephrogenic: Kidney
- Secondary
Cranial/ central diabetes insipidus.
- Description
- Causes
- Treatment
Polyuria and Polydipsia caused by inadequate synthesis/ secretion of ADH.
Causes:
- Idiopathic [27%]
- Genetic [<5%]
- Secondary [most common]
Treatment
- Administering artificial AVP [desmopressin]
Genetic causes of cranial diabetes insipidus
Mutations to do with AVP:
- Familial mutation of the AVP gene-
- Wolfram syndrome [DIDMOAD]—> Autosomal recessive, incomplete penetrance.
Secondary causes of cranial DI
Most common cause of cranial DI.
- Post-surgical brain surgeries, esp. pituitary
- Brain trauma
- Tumours
- Infections [TB, encephalitis, meningitis]
- Autoimmune
- Sarcoidosis
- Histiocytosis
Nephrogenic diabetes insipidus
- Description
- Causes [6]
- Treatment
Polydipsia and polyuria caused by the kidneys inability to respond to AVP.
Causes:
- Idiopathic
- Genetic
- Metabolic [hypercalcaemia, hypokalaemia]
- Drugs: lithium
- CKD.
Treatment
- Treat underlying causes
- Thiazide diuretics
- NSAIDs
Hypothalamic syndrome
Damage to the hypothalamus
- Affects the HPA axis.
Consequences
- Disrupted thirst, DI
- Hyperphagia
- Abnormal temperature regulation
- Hypopituitarism
- Sleep rhythm disruptions.
Primary polydipsia
- Consequences
- Treatment
Excessive intake of water despite plasma osmolarity being normal.
- Causes high urine output and low plasma osmolarity.
- Can be caused by psychotic disorders [delusions, hallucinations]
Consequences
- Suppresses AVP secretion
- Low plasma osmolality
- Low urine plasma osmolality
- High urine output
- Loss of renal interstitial solute
Treatment
- Psychological therapy
- Explaining the reason
Investigations into polyuria and polydipsia.
Medical history
- Familial?
- Water intake?
- Exclude diabetes mellitus
24 hour fluid balance documented
- Urine out put
- Water intake
- Weight day and night
Exclude hypercalcemia and hypokalemia
Water deprivation test
Water deprivation test
Diagnostic test to dehydration.
- After a period of dehydration
- Plasma and urine osmolarity measured
- Weight measured - Desmopressin is administered
- Plasma and urine osmolality measured again
Water deprivation test results
- Normal person
After period of dehydration
- Plasma osmolality increases
- Urine osmolality increases
