D&E - Pituitary Disorders Flashcards
What are the causes of prolactinaemia?
- pregnancy
- medications (e.g. anti-emetics, antipsychotics)
- hypothyroidism
- PCOS
- prolactinoma
What are micro-prolactinomas?
The commonest pituitary tumour, presenting with menstrual disturbances, hypogonadism and galctorrhoea.
Infertility may be a feature.
Micro-prolactinomas are <1cm.
What are macro-prolactinomas?
Large pituitary adenomas (>1cm), causing extremes in serum prolactin levels.
How are prolactinomas treated?
Dopamine receptor agonists suppress prolactin secretion from the pituitary gland.
Even large macro-prolactinomas are medically treated.
Describe the growth hormone axis.
- Hypothalamus produces GHRH
- GHRH stimulates release of GH from anterior pituitary gland
- GH stimulates the release of IGF-1 from the liver
What are the actions of growth hormone?
- stimulates muscle growth
- increases bone density and strength
- stimulates cell regeneration and reproduction
- stimulates growth of internal organs
What is acromegaly?
A condition that is as a result of excess growth hormone.
What are the causes of excess growth hormone?
- pituitary adenoma
- paraneoplastic ectopic GHRH or GH secretion
Presentation of acromegaly.
- frontal bossing
- coarse, sweaty skin
- large nose
- macroglossia
- large hands and feet
- large protruding jaw
Which other medical conditions may have acromegaly as an underlying cause?
- hypertrophic heart
- hypertension
- T2DM
- carpal tunnel syndrome (esp. bilaterally)
- arthritis
- colorectal cancer
How does a space occupying pituitary tumour present?
- headaches
- visual field defect (bitemporal hemianopia)
Investigations for acromegaly.
IGF-1 on blood sample (cannot test GH as fluctuates too much).
Growth hormone suppression test - consume 75g glucose drink with growth hormone tested at baseline and 2 hours following the drink. Glucose should suppress the growth hormone level in healthy individuals.
MRI of the pituitary to diagnose a pituitary adenoma.
What is the treatment of acromegaly?
Trans-sphenoidsal surgery to remove a pituitary adenoma if this is the cause.
Medical options include:
- pegvisomant
- somatostatin analogues
- dopamine agonists
What are non-functioning pituitary adenomas?
Biochemically inactive tumours of the pituitary gland, which can be removed surgically if there is a visual field defect or there is a threat to vision.
What is the pathophysiology of syndrome of inappropriate ADH (SIADH)?
Excessive ADH results in increased water reabsorption in the collecting ducts, causing a euvolaemic hyponatraemia.
Presentation of SIADH?
- headache
- fatigue
- muscle aches / cramps
- confusion
What are the causes of SIADH?
- post-operative
- SSRIs
- small cell lung cancer
What are the clinical features of SIADH?
- euvolaemia
- hyponatraemia
- low serum osmolality
- high urine sodium
- high urine osmolality
NOTE SIADH can only be diagnosed after the exclusion of hypothyroidism, total salt depletion and ACTH deficiency.
How should SIADH be managed?
- admission if severe or symptomatic hyponatraemia
- treat the underlying cause
- fluid restriction
- vasopressin receptor antagonists to block ADH receptors
What is the major complication of treating SIADH quickly?
Osmotic demyelination syndrome.
As blood sodium concentration falls, water moves via osmosis across the BBB into the brain, causing the brain to swell.
The brain adapts to this by reducing the solutes in the brain cells, so that it does not become oedematous. If hyponatraemia has been present, the brain cells therefore have low osmolality.
When sodium levels rise rapidly during treatment, demyelination of the pons causes cognitive and behavioural changes, and carries a significant risk of death.
What is:
a) cranial diabetes insipidus?
b) nephrogenic diabetes insipidus?
The kidneys are unable to reabsorb water and concentrate urine due to:
a) lack of ADH
b) lack of response to ADH
What are the causes of nephrogenic diabetes insipidus?
- medications (lithium)
- genetic mutations in ADH receptor gene
- hypercalcaemia
- hypokalaemia
- PCKD
What are the causes of cranial diabetes insipidus?
- brain tumours
- brain injury
- brain infections
- genetic mutations in the ADH gene
Presentation of diabetes insipidus.
- polyuria
- polydipsia
- dehydration
- postural hypotension
How is diabetes insipidus investigated?
- low urine osmolality
- high serum osmolality
- ≥3L/24hr on catheter
How is diabetes insipidus diagnosed?
Water deprivation test.
Describe how the water deprivation test is performed and interpreted.
Patient avoids fluids for 8 hours before the test, and urine osmolality is measured. If osmolality is low, synthetic ADH is given. Urine osmolality is measured again in 2-4 hours.
In primary polydipsia, water deprivation will cause urine osmolality to be high when first measured, ruling out diabetes insipidus.
If urine osmolality is low, desmopressin is given. If urine osmolality rises, this is cranial diabetes inspidus. If it doesn’t, this is nephrogenic diabetes insipidus.
How is cranial diabetes insipidus managed?
Desmopressin (synthetic ADH) to replace absent ADH.
How is nephrogenic diabetes insipidus managed?
- access to plenty of water
- high dose desmopressin
- thiazide like diuretics
- NSAIDs
