3.5 - Pituitary tumours Flashcards

1
Q

What hormones do anterior pituitary cells release?

A
  • somatotrophs - growth hormone (somatotrophin)
  • lactotrophs - prolactin
  • thyrotrophs - thyroid stimulating hormone (thyrotrophin)
  • gonadotrophs - luteinising hormone, follicle stimulating hormone
  • corticotrophs - adrenocorticotrophic hormone (corticotrophin)
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2
Q

What would a functioning tumour of somatotrophs cause?

A

Acromegaly

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3
Q

What would a functioning tumour of lactotrophs cause?

A

Prolactinoma

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4
Q

What would a functioning tumour of thyrotrophs cause?

A

TSHoma

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5
Q

What would a functioning tumour of gonadotrophs cause?

A

Gonadotrophinoma

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6
Q

What would a functioning tumour of corticotrophs cause?

A

Cushing’s disease (corticotroph adenoma)

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7
Q

What are the different ways to classify a pituitary tumour? (3)

A
  • radiological (MRI)
  • function
  • benign or malignant
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8
Q

How is a pituitary tumour classified radiologically?

A
  • size - microadenoma is <1cm, macroadenoma is >1cm
  • sellar or suprasellar (grows out of sella turcica)
  • compressing optic chiasm or not (suprasellar grows up)
  • invading cavernous sinus or not (suprasellar grows sideways)
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9
Q

How is a pituitary tumour classified by function?

A
  • functioning tumour - excess secretion of a specific pituitary hormone e.g. prolactinoma
  • no excess secretion of pituitary hormone (non functioning adenoma)
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10
Q

How is a pituitary tumour classified as benign or malignant?

A
  • pituitary carcinoma (cancer) very rare (<0.5% of pituitary tumours)
  • mitotic index measured using Ki67 index - benign is <3%
  • pituitary adenomas can have benign histology but display malignant behaviour
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11
Q

What does hyperprolactinaemia caused by a prolactinoma do to the HPG axis?

A
  • PRL binds to PRL receptors on kisspeptin neurons in hypothalamus
  • inhibits kisspeptin release
  • decreases downstream GnRH –> LH/FSH –> T/Oes
  • oligo-amenorrhoea / low libido / infertility / osteoporosis
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12
Q

What do prolactinomas do to serum prolactin?

A
  • commonest functioning pituitary adenoma
  • usually serum PRL > 5000 mU/L
  • serum PRL proportional to tumour size
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13
Q

How do prolactinomas present? (5)

A
  • menstrual disturbance
  • erectile dysfunction
  • reduced libido
  • galactorrhoea (leaking of milk outside of lactation)
  • subfertility

NB remember effects of prolactin on inhibiting HPG axis for symptoms!!

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14
Q

What are other types of causes of an elevated prolactin aside from a prolactinoma? (3)

A
  • physiological
  • pathological
  • iatrogenic
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15
Q

What are examples of physiological causes of an elevated prolactin? (3)

A
  • pregnancy/breastfeeding
  • stress - exercise, seizure, venepuncture
  • nipple/chest wall stimulation
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16
Q

What are examples of pathological causes of an elevated prolactin? (3)

A
  • primary hypothyroidism
  • PCOS
  • chronic renal failure
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17
Q

What are examples of iatrogenic causes of an elevated prolactin? (5)

A
  • antipsychotics
  • selective serotonin reuptake inhibitors (SSRIs)
  • anti-emetics
  • high dose oestrogen
  • opiates
18
Q

What do you do once you have confirmed a true pathological elevation of serum prolactin?

A

Organise a pituitary MRI

19
Q

How do we treat prolactinomas?

A
  • first-line treatment is medical not surgical
  • dopamine receptor agonists mainstay of treatment e.g. cabergoline (bromocriptine)
  • safe in pregnancy
  • aim to normalise serum PRL and shrink prolactinoma
  • microprolactinomas need smaller doses than macroprolactinomas
20
Q

How do dopamine receptor agonists work?

A
  1. the agonist mimics dopamine and binds to D2 receptors on anterior pituitary lactotrophs
  2. works like dopamine and prevents lactotrophs making PRL
21
Q

What does a pituitary tumour secreting excess growth hormone cause in children and adults?

A
  • children - gigantism
  • adults - acromegaly
22
Q

What is the mean diagnosis time for acromegaly?

A

10y - often insidious presentation

23
Q

What are the symptoms of acromegaly? (8)

A
  • sweatiness
  • headache
  • coarsening of facial features - macroglossia, prominent nose
  • large jaw - prognathism
  • increased hand and feet size
  • snoring and obstructive sleep apnoea
  • hypertension
  • impaired glucose tolerance/diabetes mellitus
24
Q

What are the mechanisms of growth hormone action?

A
  • direct via growth hormone receptor from APG to tissues
  • indirect via insulin-like growth factor (somatomedin) to tissues - APG –> liver –> tissues
25
Q

How do we diagnose acromegaly?

A
  • GH is pulsatile - so random measurement unhelpful
  • elevated serum IGF-1
  • failed suppression (paradoxical rise) of GH following oral glucose load - oral glucose tolerance test
  • prolactin can be raised - co-secretion of GH and PRL
26
Q

What do we do once we confirm growth hormone excess?

A

Pituitary MRI to visualise pituitary tumour

27
Q

What can untreated acromegaly cause?

A

Increased cardiovascular risk in untreated acromegaly

28
Q

What is the treatment of acromegaly?

A
  • first-line treatment is surgical - trans-sphenoidal pituitary surgery
  • aim to normalise serum GH and IGF-1
  • could use radiotherapy (slow)
29
Q

What can we use to shrink an acromegaly tumour prior to surgery?

Or after surgery to improve outcome?

A
  • somatostatin analogues e.g. octreotide - ‘endocrine cyanide’
  • dopamine agonists e.g. cabergoline (GH secreting pituitary tumours frequently express D2 receptors)
30
Q

What is Cushing’s syndrome?

A

Occurs due to an excess of cortisol or other glucocorticoid

31
Q

What are the two types of causes of Cushing’s syndrome?

A
  • ACTH dependent
  • ACTH independent
32
Q

What are the ACTH dependent causes of Cushing’s syndrome? (2)

A
  • Cushing’s disease (pituitary corticotroph adenoma)
  • ectopic ACTH (e.g. lung cancer)
33
Q

What are the ACTH independent causes of Cushing’s syndrome? (2)

A
  • taking steroids by mouth (common)
  • adrenal adenoma/carcinoma
34
Q

What are some symptoms of Cushing’s syndrome? (12)

A
  • red cheeks
  • moon face
  • fat pads (buffalo hump)
  • thin skin
  • easy bruising
  • impaired glucose tolerance and high BP
  • osteoporosis
  • mental changes
  • proximal myopathy
  • purple striae
  • pendulous abdomen
  • poor wound healing
35
Q

What is the difference between Cushing’s syndrome and Cushing’s disease?

A
  • syndrome - excess cortisol
  • disease - pituitary corticotroph adenoma secreting ACTH
36
Q

What is the normal rhythm of cortisol release?

A

Diurnal - highest early morning, decreases throughout day (lowest at night) then increases to early morning

37
Q

How do we investigate Cushing’s disease?

A
  • elevation of 24h urine free cortisol - increased cortisol secretion
  • elevation of late night cortisol - salivary or blood test - loss of diurnal rhythm
  • failure to suppress cortisol after oral dexamethasone (exogenous glucocorticoid) - increased cortisol secretion (should decrease as increased plasma cortisol reduces ACTH, suppressing cortisol levels)
38
Q

Once we have confirmed hypercortisolism, how do we further investigate?

A

Measure ACTH and if high (ACTH dependent), do a pituitary MRI

39
Q

What are non-functioning pituitary adenomas?

A

Do not secrete any specific hormones (but the tumour still causes symptoms)

40
Q

What do non-functioning pituitary adenomas often present with?

A

Visual disturbance - bitemporal hemianopia

41
Q

What hormonal issues can non-functioning pituitary adenomas cause?

A
  • can present with hypopituitarism
  • serum prolactin can be raised as dopamine cannot travel to pituitary stalk from hypothalamus
42
Q

How do we treat large non-functioning pituitary adenomas?

A

Trans-sphenoidal surgery needed for larger tumours, particularly if visual disturbance