1b Pituitary Tumours Flashcards

1
Q

What is a functioning tumour of the somatotrophs called?

A

Acromegaly

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2
Q

What is a functioning tumour of the lactotrophs called?

A

prolactinoma

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3
Q

What is a functioning tumour of the Corticotrophs called?

A

Cushings Disease

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4
Q

What is the name for a radiologically small and large pituitary tumour?

A

Microadenoma (<1cm) and macroadenoma (>1cm)

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5
Q

What things are we looking for in an MRI?

A

Seller or suprasellar
Compressing optic chiasm or not
Invading carvenous sinus or not

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6
Q

What are the two functional classifications for tumours?

A

excess hormone secretion or not (non-functioning adenoma)

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7
Q

Are pituitary tumours generally malignant?

A

No (<0.5%)

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8
Q

How do you tell the difference between malignant or benign tumour?

A

Mitotic index measured using Ki67 index - benign is <3%

Pituitary adenomas can have benign histology but display malignant behaviour

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9
Q

Describe how hyperprolactinaemia leads to the associated symptoms?

A

Prolactin binds to prolactin
receptors on kisspeptin
neurons in hypothalamus

Inhibits kisspeptin release.

Decreases in downstream
GnRH/LH/FSH/T/Oest
Oligo-amenorrhoea/Low
libido/Infertility/Osteoporosis

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10
Q

What is serum prolactin proportional to in prolactinomas?

A

The size of the tumour

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11
Q

What is the hormonal presentation of prolactinomas?

A

low GnRH, low FSH and low LH
Usually serum concentration of prolactin >5000mU/L

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12
Q

What are the clinical symptoms of prolactinoma?

A

Menstrual disturbance
Erectile dysfunction
Reduced libido
Galactorrhoea
Subfertility

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13
Q

What are other causes of elevated prolactin?

A

Physiological
Pregnancy, stress, nipple stimulation

Pathological
Hypothyroidism, pcos or renal failure

Iatrogenic
Antipsychotics, oestrogen, opiates

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14
Q

Why is prolactin levels higher in pregnancy?

A

Lactotrophs undergo hypertrophy

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15
Q

Why does primary hypothyroidism cause elevated prolactin?

A

thyroid gland not working, therefore not producing thyroxine, so TSH rises which stimulates prolactin release

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16
Q

How should a prolactinoma be investigated?

A

MRI - look for pituitary tumour

17
Q

What is the first line treatment of prolactinoma?

A

Cabergoline - dopamine receptor agonist

18
Q

How do dopamine receptor agonists reduce prolactin and shrink prolactinomas?

A

Dopamine is the off switch for prolactin, therefore dopamine binds to the D2 receptors on the lactotrophs and reduces prolactin production - can also used dopamine agonists like Cabergoline

19
Q

Where does the dopamine come from?

A

The dopaminergic neurones

20
Q

What is the difference between acromegaly and giganticism?

A

acromegaly is in adults, gigantism in children

21
Q

What is the problem with insidious prsentation of acromegaly?

A

long time between symptoms appearing and mean time to diagnosis

22
Q

What are some clinical symptoms of acromegaly?

A

Sweatiness
* Headache
* Coarsening of facial features
* Macroglossia
* Prominent nose
* Large jaw - prognathism
* Increased hand and feet size
* Snoring & obstructive sleep
apnoea
* Hypertension
* Impaired glucose
tolerance/diabetes mellitus

23
Q

What are the two mechanisms of growth hormone action?

A

direct and indirect

Direct = growth hormones acting on tissues
Indirect = GH act on liver, which makes IGF-1 which then acts on other body tissues

24
Q

How do you diagnose acromegaly?

A

GH pulsatile so random measurement is unhelpful

Failed suppression (‘paradoxical
rise’) of GH following oral
glucose load – oral glucose
tolerance test

Elevated IGF-1

25
Q

Why is it important that acromegaly must be treated?

A

Increased cardiovascular risk in untreated
acromegaly

26
Q

What is the first line treatment of acromegaly?

A

First-line treatment is surgical – trans-sphenoidal
pituitary surgery

27
Q

what is the medical treatment to do before surgery for treating acromegaly?

A

Somatostatin analogues eg octreotide –
‘endocrine cyanide’

Dopamine agonists eg cabergoline (GH
secreting pituitary tumours frequently express
D2 receptors)

Radiotherapy

28
Q

What are the clinical features of Cushings?

A
  • Red Striae
  • Buffalo humps - fat pads
  • Lemon on sticks - centripedal obesity
  • Moon face
  • Proximal Myopathy - cannot get up from squat
  • Easily bruising
29
Q

What us Cushings Syndrome?

A

Too much cortisol

30
Q

What is cushings Disease?

A

pituitary dependant adenoma

31
Q

What are ACTH dependant causes of hypercortisolism?

A

ACTH dependent
* Cushing’s disease (corticotroph
adenoma)
* Ectopic ACTH (lung cancer)

32
Q

What are ACTH indepedant causes of hypercortisolism?

A

ACTH dependent
* Taking steroids by mouth
(common)
* Adrenal adenoma or carcinoma

33
Q

What would you see in an investigation of Cushings?

A
  1. Elevation of 24h free urine cortisol
  2. Elevation of late night cortisol
  3. Failure to suppress cortisol after oral dexamethasone so increased cortisol secretion
34
Q

What do you do when hypercortisolism is confirmed?

A

Measure ACTH - if high then pituitary MRI, CTH dependant

35
Q

What are the main effects of non-functioning pituitary adenomas

A

visual disturbances - bitemporal hemianopia

36
Q

What are the hormonal affects of non-functioning pituitary adenomas?

A

Can present with hypopituitarism
* Serum prolactin can be raised
(dopamine can’t travel down
pituitary stalk from hypothalamus)