SIADH and Diabetes Insipidus Flashcards
ADH is produced in the ______ and secreted by the ______.
It stimulates ______ reabsorption from the CDs in the kidneys.
hypothalamus, posterior pituitary, water
What is SIAD?
A condition where there is inappropriately large amounts of ADH
Compare primary vs secondary SIADH
Primary: posterior pituitary secreting too much ADH
Secondary: ADH coming from elsewhere ie. small cell lung cancer
Pathophysiology of SIADH?
↑ ADH = ↑ H20 reabsorption in CD
Dilutes Na in the blood but not enough to cause fluid overload → Euvolaemic Hyponatraemia
Less water excreted by kidneys, so urine becomes more concentrated → High urine Na and osmolality
Symptoms of SIADH?
Symptoms are non-specific
- Headache
- Fatigue
- Muscle aches and cramps
- Confusion
- Severe hyponatraemia can cause seizures and reduced consciousness
List 4 causes of SIADH
- Medications (most common)
- Surgery
- Infection (esp atypical pneumonia and lung abscesses)
- Head injury
- Malignancy (small cell lung cancer)
- Meningitis
List 4 drugs known of cause SIADH
- Thiazide diuretics
- Carbamazepine
- Vincristine
- Cyclophosphamide
- Antipsychotics and SSRIs
- NSAIDSs
How is an initial diagnosis of SIADH made?
No test to directly measure ADH activity so diagnosis is based on:
- Clinical examination → will show euvolaemia
- U+Es → will show hyponatraemia
- Urine sodium and osmolality will be high
List 4 differentials for hyponatraemia
- Adrenal insufficiency
- Diuretic use
- Diarrhoea, vomiting, burns, fistula or excessive sweating
- Excessive water intake
- CKD or AKI
If you suspect pneumonia, lung abscess or lung cancer, what investigation will you perform?
Chest xray
If you suspect malignancy, what investigation will you perform?
CT TAP and MRI brain
Management of SIADH?
- Correct Na slowly
- Fluid restriction (to 500mls-1litre)
- ADH receptor blockers ie. Tolvaptan
- Demeclocycline (tetracycline antibiotic) rarely used anymore
Why is it important to correct Na slowly in SIADH?
To prevent central pontine myelinolysis (osmotic demyelination syndrome)
What is CMP
A complication of long term severe hyponatraemia (< 120 mmols/l) being treated too quickly (> 10 mmol/l increase over 24 hours)
Pathophysiology of CMP?
- ↓ blood Na causes H20 to cross BBB by osmosis
- brain adapts by ↓ its solutes to prevent oedema (takes a few days)
- In hyponatraemia, brain cells have a ↓ osmolality
- when fluid is restored to fast, blood Na levels ↑ rapidly, so H20 moves out of brain cells into blood
- this causes destruction of myelin (2 phases of symptoms)
What is the first phase of symptoms in CPM?
Why?
Due to electrolyte imbalance
Presents as encephalopathic and confused
What is the second phase of symptoms in CPM?
Why?
Due to demyelination of neurones in pons a few days after rapid correction (risk of death)
Present as:
- spastic quadriparesis
- pseudobulbar palsy
- cognitive and behavioural changes
What is Diabetes insipidus?
A condition characterised by either a decreased secretion of ADH from pituitary or an insensitivity to ADH
What are the 2 types of Diabetes insidious and how do they differ?
Cranial - hypothalamus does not produce ADH for pituitary to secret
Nephrogenic - collecting ducts of the kidneys do not respond to ADH
What is Primary polydipsia?
Patient has a normally functioning ADH system, but they are drinking excessive quantities of water leading to excessive urine production
They don’t have diabetes insipidus
List 4 causes of cranial DI
- Idiopathic
- Head injury
- Pituitary or brain surgery
- Brain tumour
- Brain infections (meningitis, encephalitis, TB)
List 4 causes of Nephrogenic DI
- Congenital
- Lithium
- Intrinsic kidney disease
- Hypokalaemia and hypercalcaemia
What gene mutation is associated with congenital nephrogenic DI?
AVPR2 gene on the X chromosome that codes for the ADH receptor
List 4 clinical features of DI
- Polyuria
- Polydipsia
- Dehydration
- Postural hypotension
- Hypernatraemia
List 3 Investigations for DI
- Low urine osmolality (< 700)
- High serum osmolality (>295)
- Water deprivation test
What is the gold standard investigation to diagnose DI?
The water deprivation test
Also known as the desmopressin stimulation test
Explain the Water Deprivation Test
- patient should avoid taking in any fluids for 8 hours - “fluid deprivation”
- urine osmolality is measured and synthetic ADH is administered
- 8 hours later urine osmolality is measured again
Water deprivation test findings indicative of cranial vs nephrogenic DI
Cranial:
- Before deprivation urine osmolality is LOW
- After ADH urine osmolality is HIGH
Nephrogenic DI:
- Before deprivation urine osmolality is LOW
- After ADH urine osmolality is LOW
What findings on the water deprivation differentiate indicate primary polydipsia?
HIGH before deprivation and after ADH
In PP, 8 hours of water deprivation will cause urine osmolality to be HIGH even before ADH is given
Management of DI?
- Treat underlying cause (If possible)
- Cranial DI: Desmopressin
- Nephrogenic DI: thiazides and NSAIDs, low salt/protein diet, high dose desmopressin
