Sodium abnormalities: hypernatraemia and diabetes insipidus Flashcards
What are the 2 main causes of diabetes insipidus? What do they both lead to?
- ADH deficiency (Cranial DI) in posterior pituitary - so signal to kidneys to reabsorb water and concentrate urine is weak/absent.
- ADH end- organ resistance (Nephrogenic DI) - kidneys do not respond to ADH and fail to reabsorb water and concentrate urine.
Both lead to passing of large volumes of dilute urine with unquenchable thirst.
What is the difference between cranial and nephrogenic DI in terms of what causes them?
Causes of Cranial DI
- pituitary disease
- meningitis
- vascular lesions
Causes of Nephrogenic DI
- electrolyte disturbance eg. hypokalaemia, hypercalcaemia
- renal disease eg. pyelonephritis, hydronephrosis
- drugs affecting the kidney eg lithium
What are the key features of DI?
- High urine volume (pale urine)
- Low urine osmolality
- High serum osmolality
- Extreme thirst
What can severe hypernatraemia lead to?
Dehydration and death
How is DI confirmed biochemically?
How is DI excluded biochemically?
urine volume > 3L per 24 hours and
- SERUM osmolality > 295 mosmol/Kg (high)
- URINE osmolality < 300 mosmol /Kg. (low)
DI is excluded if urine osmolality > 600 mosmol/Kg or double the serum osmolality.
What is the name of the test used to diagnose DI?
How is it done?
Water Depriviation Test - useful in partial DI as diagnosis less clear cut. If DI clinically obvious, no need to perform WDT.
1. The patient is fluid restricted
2. In diabetes insipidus, the urine remains abnormally dilute despite water
deprivation
3. When desmopressin/DDAVP (a ADH/vasopressin analogue) is administered:
• Cranial DI - urine will become CONCENTRATED (good)
• Nephrogenic DI - urine will continue to be dilute
4. DI excluded if if patients concentrate urine osmolality > 600 mosmol/Kg and serum osmolality remains < 300 mosmol/Kg.
What is the management of a patient with confirmed cranial DI?
Investigate for pituitary disease
Administer DDAVP (synthetic ADH) /desmopressin - intranasal, oral, sublingual, paraenteral
> overtreatment: dilutiutional hyponatraemia - headaches, reduced cognitive ability
>undertreatment: excessive thirst, polyuria
What is the management of a patient with confirmed nephrogenic DI?
Treat underlying cause.
Drugs - carbamazepine, chlorpropramide (sulfonylurea)
if symptoms persist - patients drink according to thirst and keep up with water loss.
Specific measures:
- low salt, low protein diet
- diuretics
- NSAIDs
What are the 3 main causes of hyperantraemia?
Pure water loss
- extrarenal (reduced water intake, hypothyroidism)
- renal`(DI, CKD)
Hypotonic loss
- extrarenal (GI eg vomiting, diarrhoea), escessive sweating
- renal (osmotic diuresis eg glucose, urea,])
Salt gain
- iatrogenic eg hypertonic saline
- salt ingestion
What is a rare form of DI where patients have impaired thirst mechanism?
Hypodipsic DI.
Hypothalamus affected - eg hypothalamic infiltrative disorders - require specialist care as risk of severe hypernatraemia and dehydration.
What are the differential diagnoses for polyuria? (make sure patient clarifies whether they pee often or in large amounts - confirm by 24h urine collection)
- diabetes mellitus
- diabetes insipidus
- diuretics including caffeine and alcohol
- heart failure
- hypercalcemia
- hyperthyroidism
- primary polydipisa