Diabetes Insipidus (Cranial + Nephrogenic) Flashcards

1
Q

Epidemiology

A

Uncommon
Females = Males

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2
Q

Risk Factors

A

Family history

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3
Q

Aetiology - CRANIAL DI

A

Idiopathic
ADH gene mutation
Pituitary adenomas

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4
Q

Aetiology - NEPHROGENIC DI

A

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

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5
Q

Pathophysiology

A

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.

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6
Q

Signs

A

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

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7
Q

Symptoms

A

Extreme dehydration
Lethargy
Confusion
Coma

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8
Q

Diagnosis

A

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

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9
Q

Treatment

A

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

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