Diabetes Insipidus (Cranial + Nephrogenic) Flashcards
Epidemiology
Uncommon
Females = Males
Risk Factors
Family history
Aetiology - CRANIAL DI
Idiopathic
ADH gene mutation
Pituitary adenomas
Aetiology - NEPHROGENIC DI
Renal tubular acidosis
ADH-R mutation
Polyuria
Drugs:
- Lithium chloride
- Glibenclamide
Hypokalaemia
Hypercalcaemia
Pathophysiology
Reduced ADH secretion or impaired response to ADH
= Increased H2O loss in urine - dilute high volumes
Nephrogenic = poor kidney response to vasopressin, lithium
Cranial/Neurogenic = hypothalamus/ pituitary injury.
Signs
Polyuria
Polydipsia
HypERnatremia
Inappropriately hypotonic urine
Dry mucosa
Sunken eyes
Changes to skin turgity
Symptoms
Extreme dehydration
Lethargy
Confusion
Coma
Diagnosis
FIRST LINE: Bloods = hypernatremia
Serum glucose - exclude DM
Low urine osmolality, high serum osmolality
GOLD STANDARD: 8 hour water deprivation test
- normally serum osm stays normal, urine osm increases
- DI = serum osm RISES while urine osm unchanged
THEN desmopressin test
- desmopressin determines cranial or nephrogenic = cranial will respond, nephrogenic won’t.
- cranial urine osm before <300 after >800
- nephrogenic urine osm before <300 after <300
Treatment
Cranial: DEMOPRESSIN
Nephrogenic: BENDOFLUMETHIADIZE + treat underlying cause (+ maybe NSAIDS)
- Increase H20 loss at DCT therefore encourages Na+ reabsorption (and H20 retention) which will concentrate urine and increase retention volume