Diabetes Insipidus (Cranial + Nephrogenic)

Question 1

Epidemiology

Answer 1

Uncommon
Females = Males

Question 2

Risk Factors

Answer 2

Family history

Question 3

Aetiology - CRANIAL DI

Answer 3

Idiopathic
ADH gene mutation
Pituitary adenomas

Question 4

Aetiology - NEPHROGENIC DI

Answer 4

Renal tubular acidosis
ADH-R mutation
Polyuria
Drugs:
- Lithium chloride
- Glibenclamide
Hypokalaemia
Hypercalcaemia

Question 5

Pathophysiology

Answer 5

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.

Question 6

Signs

Answer 6

Polyuria
Polydipsia
HypERnatremia
Inappropriately hypotonic urine
Dry mucosa
Sunken eyes
Changes to skin turgity

Question 7

Symptoms

Answer 7

Extreme dehydration
Lethargy
Confusion
Coma

Question 8

Diagnosis

Answer 8

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

Question 9

Treatment

Answer 9

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