Lecture 10: Case Based Learning Sessions: Diabetes Insipidus, Cushings and Prolactinoma Flashcards

1
Q

signs and symptoms of diabetes insipidus

A
  • large volumes of dilute urine (> 3 litres in 24hrs and a urine osmolality of < 300 mOsm/kg
  • nocturia
  • excessive thirst

in children, additional symptoms:
- failure to thrive
- enuresis

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2
Q

diabetes insipidus investigations and diagnosis

A

baseline investigations:
- U&Es (sodium may be raised)
- blood glucose (to rule out DM)
- urine dip
- paired serum and urine osmolality measurements

DI is present when the serum osmolality is raised (> 295 mOsm/kg) with inappropriately dilute urine (urine osmolality < 300 mOsm/kg).

If diagnosis remains uncertain, a water deprivation test is performed.

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3
Q

expected findings of water deprivation test in diabetes insipidus

A
  • in central DI, urine osmolality increased with ADH administration.
  • in nephrogenic DI, urine osmolality remains low/unchanged despite ADH administration.
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4
Q

what is the management of cranial diabetes insipidus?

A
  • desmopressin, a medication which mimics the action of endogenous ADH.
  • sodium levels should be monitored routinely due to risk of hyponatraemia.
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5
Q

what is the management of nephrogenic diabetes insipidus?

A
  • correct any underlying metabolic abnormalities and discontinuing offending drugs.
  • high-dose desmopressin has been used with variable results.
  • other potential treatments include using a thiazide diuretic and a NSAID to reduce urine volume.
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6
Q

what is the aetiology of ACTH-dependent Cushing’s disease?

A
  • caused by excessive production of ACTH, most often due to a pituitary tumour (Cushing’s disease) or ectopic ACTH-producing tumours (e.g. lung carcinoids, thymic carcinoids, and others).
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7
Q

what is the aetiology of ACTH-independent Cushing’s syndrome?

A
  • this arises from primary adrenal diseases, such as adrenal adenomas or adrenal carcinomas, which produce excess crotisol independently of ACTH stimulation.
  • exogenous steroids can also cause ACTH independent Cushing’s.
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8
Q

Cushing’s syndrome investigations

A

Biochemical evidence of cortisol excess:
- 24hr urinary free cortisol test
- low-dose dexamethasone suppression test: not suppressed by low dose > Cushing’s syndrome, not suppressed by low dose but is suppressed with high dose > Cushing’s disease, not suppressed by either low or high dose > ectopic ACTH (not under axis control, likely ACTH producing tumour)

Localisation of the source:
- plasma ACTH levels
- high-dose dexamethasone suppression test for suspected Cushing’s disease
- inferior petrosal sinus sampling
- MRI of the pituitary and/or CT of chest and abdomen for tumour localisation

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