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Z YEAR 2 BRS NEURO > Pituitary Tumours > Flashcards

Pituitary Tumours Flashcards

1
Q

What do somatotrophs produce?

A

growth hormone (somatotrophin)

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2
Q

What do lactotrophs produce?

A

prolactin

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3
Q

What to thyrotrophs produce?

A

TSH

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4
Q

What do gonadotrophs produce?

A

LH + FSH

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5
Q

What do corticotrophs produce?

A

ACTH

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6
Q

What is a functioning pituitary tumour involving somatotrophs

A

acromegaly

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7
Q

What is a functioning pituitary tumour involving lactotrophs?

A

Prolactinoma

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8
Q

What is a functioning pituitary tumour involving thyrotrophs?

A

TSHoma

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9
Q

What is a functioning pituitary tumour involving gonadotrophs

A

gonadotrophinoma

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10
Q

What is a functioning pituitary tumour involving corticotrophs?

A

Cushing’s disease (corticoadenoma)

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11
Q

How do you classify pituitary tumour radiologically?

A 
1. Size
 Microadenoma <1cm (10mm)
 Macroadenoma >1cm (10mm)
2. Sellar or suprasellar
3. Compressing optic chiasm or not
4. Invading cavernous sinus or not (internal carotid artery risk)
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12
Q

How do you classify a pituitary tumour depending on function?

A
  1. Excess secretion of a specific pituitary hormone
    eg prolactinoma
  2. No excess secretion of pituitary hormone (Non Functioning Adenoma)
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13
Q

How do you classify a pituitary tumour depending on benign or malignant?

A
  1. Pituitary carcinoma very rare (<0.5% of pituitary tumours)
  2. Mitotic index measured using Ki67 index – benign is <3%
  3. Pituitary adenomas can have benign histology but display malignant behaviour
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14
Q

Describe the process of hyperprolactinaemia inhibiting Kisspeptin Neurons

A
  1. Prolactin binds to prolactin receptors on kisspeptin neurons in hypothalamus
  2. Inhibits kisspeptin release
  3. Decreases in downstream GnRH/LH/FSH/T/Oest
  4. Oligo-amenorrhoea/Low libido/Infertility/Osteoporosis
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15
Q

How do you measure prolactinomas?

A
  • Usually serum [prolactin] >5000 mU/L

* Serum [prolactin] proportional to tumour size

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16
Q

How common are prolactinomas?

A

Commonest functioning pituitary adenoma

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17
Q

What is the presentation of a prolactinoma?

A
  1. Menstrual disturbance
  2. Erectile dysfunction
  3. Reduced libido
  4. Galactorrhoea (more common in women)
  5. Subfertility
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18
Q

What are the other physiological reasons for elevated prolactin?

A
  1. Pregnancy/breastfeeding
  2. Stress: exercise, seizure, venepuncture
  3. Nipple/chest wall stimulation
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19
Q

What are the other pathological reasons for elevated prolactin?

A
  1. Primary hypothyroidism (TRH goes up, but this can also increase prolactin if high enough)
  2. Polycystic ovarian syndrome
  3. Chronic renal failure
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20
Q

What are the other latrogenic reasons for elevated prolactin?

A
  1. Antipsychotics
  2. Selective serotonin re-uptake inhibitors
  3. Anti-emetics
  4. High dose oestrogen
  5. Opiates
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21
Q

How do you confirm true elevation in serum prolactin?

A
  • Confirm true elevation in serum prolactin (lots of false positives)
  • No diurnal variation, not affected by food
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22
Q

What should you think if there is a mild elevation in serum prolactin but no clinical features consistent with this?

A
  1. Macroprolactin

2. Stress of venepuncture

23
Q

What is the majority of circulating prolactin like?

A

monomeric & biologically active

24
Q

What is macroprolactin?

A
  • ‘sticky prolactin’ (so higher reading)
  • a polymeric form of prolactin
  • an antigen–antibody complex of monomeric prolactin and IgG (normally <5% of circulating prolactin)
25
Q

How is macroprolactin recorded?

A

-Recorded on assay as elevation of prolactin – needs alternative method to confirm
•Limited bioavailability and bioactivity
•Can reassure patient

26
Q

How do you check a stress of venipuncture?

A
  • Exclude by a cannulated prolactin series

- Sequential serum [prolactin] measurement 20 mins apart with an indwelling cannula to minimise venepuncture stress

27
Q

When do you do a pituitary MRI?

A

Only once you have confirmed a true pathological elevation of serum prolactin

28
Q

What is the treatment of prolactinoma?

A
  • Dopamine receptor agonists mainstay of treatment
    e. g. Cabergoline (bromocriptine)
  • Safe in pregnancy
29
Q

What is the aim of dopamine receptor antagonists?

A

to normalise serum prolactin + shrink prolactinoma

30
Q

When do you need to change the dose of dopamine receptor antagonists?

A

Microprolactinomas will need smaller doses than macroprolactinomas

31
Q

What is the difference between gigantism and acromegaly?

A

Gigantism-children

Acromegaly-adults

32
Q

When does acromegaly present?

A

Often insidious presentation – mean time to diagnosis from onset of symptoms = 10y

33
Q

What are the symptoms of acromegaly?

A
  • Sweatiness
  • Headache
  • Large jaw - prognathism
  • Increased hand and feet size
  • Snoring & obstructive sleep apnoea
  • Hypertension
  • Impaired glucose tolerance/diabetes mellitus
34
Q

What facial features coarsen in acromegaly?

A
  • Macroglossia

* Prominent nose

35
Q

Why can you not take a random measurement of GH?

A

Its pulsatile

36
Q

How do you diagnose acromegaly?

A
  1. Elevated serum IGF-1
  2. Failed suppression (‘paradoxical rise’) of GH. (rises in acromegaly not down as in normal) following oral glucose load – oral glucose tolerance test
  3. Prolactin can be raised – co-secretion of GH + prolactin
  4. Once confirm GH excess, pituitary MRI to visualise pituitary tumour
37
Q

What is the first line of treatment for acromegaly?

A

surgical – trans-sphenoidal pituitary surgery

38
Q

What is the aim in the surgery for acromegaly?

A

normalise serum GH and IGF-1

39
Q

What is at an increased risk in untreated acromegaly?

A

Increased cardiovascular risk

40
Q

What can you use before medical treatment?

A

•Can use medical treatment prior to surgery to shrink tumour or if surgical resection incomplete

  1. Somatostatin analogues eg octreotide – ‘endocrine cyanide’
  2. Dopamine agonists eg cabergoline (GH secreting pituitary tumours frequently express D2 receptors)
  3. Radiotherapy (slow)
41
Q

What are the symptoms of Cushing’s syndrome?

A
  1. Red cheeks
  2. Fat pads (buffalo hump)
  3. Easy bruising
  4. Thin skin
  5. Moon Face
  6. Purple Striae
  7. Pendulous abdomen
  8. Poor would healing
  9. Proximal myopathy (thin arms and legs)
  10. Impaired glucose tolerance and High BP
  11. Osteoporosis
  12. Mental changes (depression)
42
Q

Why does Cushing’s syndrome occur?

A

excess of cortisol or other glucocorticoid

43
Q

What are the causes of Cushing’s syndrome?

A
  1. Taking steroids by mouth (common)
  2. Pituitary dependent Cushing’s disease (pituitary adenoma)
  3. Ectopic ACTH (lung cancer)
  4. adrenal adenoma or carcinoma
44
Q

What are ACTH dependent causes of Cushing’s?

A
  • Cushing’s disease (corticotroph adenoma)

* Ectopic ACTH (lung cancer)

45
Q

What are ACTH independent causes of Cushing’s?

A
  • Taking steroids by mouth (common)

* Adrenal adenoma or carcinoma

46
Q

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

A
  • Cushing’s syndrome = excess cortisol

* Cushing’s disease is due to a corticotroph adenoma secreting ACTH

47
Q

How do you investigate Cushing’s disease?

A
  1. Elevation of 24h urine free cortisol- increased cortisol secretion (lost normal diurnal rhythm)
  2. Elevation of late night cortisol – salivary or blood test – loss of diurnal rhythm
  3. Failure to suppress cortisol after oral dexamethasone (exogenous glucocorticoid works like big dose of cortisol) – increased cortisol secretion, in healthy person should switch off cortisol prod as negative feedback to pituitary and shut down ACTH
48
Q

What happens once you confirm hypercortilolism?

A
  • measure ACTH

- If ACTH high, pituitary MRI ACTH dependent

49
Q

What happens in a non-functioning pituitary adenomas?

A

•Don’t secrete any specific hormone

-Often present with visual disturbance (bitemporal hemianopia

50
Q

What can happen with hormones in a non- functioning pituitary adenomas? How do you treat?

A
  1. Can present with hypopituitarism (can stop anterior pituitary working properly as big)
  2. Serum prolactin can be raised (dopamine can’t travel down pituitary stalk from hypothalamus)
  3. Trans-sphenoidal surgery needed for larger tumours, particularly if visual disturbance
51
Q

What is the majority of circulating prolactin?

A

monomeric and biologically active

52
Q

How do dopamine receptor agonists reduce prolactin and shrink prolactinomas?

A
  1. Dopamine reduces prolactin secretion
  2. Lactotroph in anterior pituitary expresses D2 receptors
  3. Dopamine comes from hypothalamic dopaminergic neurons binds to D2. receptor and stops prolactin from being released from lactotrophs
  4. D2 receptor agonist binds to D2 receptor and stops prolactin secretion and causes cell and tumour to shrink
53
Q

What does growth hormone do?

A
  1. Direct effect on body tissues (growth and development)
  2. Travels to liver and tells to make Insulin-like growth factor (somatomedin (IGF-1 and IGF-2)) and this also goes body and tissues and growth and development and increasing glucose?

Z YEAR 2 BRS NEURO (21 decks)

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