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ADH Disorders (Thirst Axis (ADH binds to V2R receptor and aquaporin…
ADH Disorders
Thirst Axis
ADH binds to V2R receptor and aquaporin channels are inserted into the apical membrane of the collecting duct
The water permeability of the collecting duct is increased. More water is absorbed resulting in a concentrated urine
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Osmoreceptors in hypothalamus detect large falls in BP or blood volume and this stimulates the release of ADH
The relationship between osmolality and ADH is linear - the more concentrated the blood, the more ADH is released
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Diabetes Insipidus
Aetiology
Nephrogenic DI: Drugs e.g. lithium, hypokalaemia, hypercalcaemia, renal tubular acidosis, mutation of ADH receptor
Cranial DI: head trauma, pituitary tumour, congenital defects in ADH gene, idiopathic
Symptoms
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Hypernatraemia: high sodium due to water loss in excess of Na+ loss. Symptoms = lethargy, weakness, confusion, irritability
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Investigations
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Water deprivation test
Serum and urine osmolality, urine volume and body weight are measured hourly for 8 hours during fasting with no fluids
In DI, serum osmolality rises without a concentrated urine
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Give IM desmopressin to differentiate between cranial and nephrogenic DI. Desmopressin will concentrate urine in cranial DI
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Treatment
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Nephrogenic
Oral bendroflumethiazide - a thiazide diuretic. Causes water and sodium loss which then lowers the GFR and encourages kidneys to take up more water and sodium in the proximal tubule
Ibuprofen - an NSAID. Will lower urine volume by inhibiting prostaglandin synthase. Prostaglandins inhibit ADH.
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Osmolality = Concentration of solution per kg. The higher the osmolality, the more concentrated the solution.