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BRS YEAR 2 > Endo - Pituitary Tumours > Flashcards

Endo - Pituitary Tumours Flashcards

1
Q

What is functioning tumour of somatotrophs called?

A

Acromegaly

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2
Q

What is functioning tumour of lactotrophs called?

A

Prolactinoma

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3
Q

What is functioning tumour of gonadotrophs called?

A

Gonadotrophinoma

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4
Q

What is functioning tumour of thyrotrophs called?

A

TSHoma

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5
Q

What is functioning tumour of corticotrophs called?

A

Corticotroph adenoma

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6
Q

What are the 3 criteria for classifying pituitary tumours?

A

Function
Size
Benign vs malignant

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7
Q

What is a functioning tumour?

A

Secretes excess hormone

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8
Q

What is a non functioning pituitary adenoma?

A

Doesn’t secrete excess

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9
Q

What is a micro adenoma?

A

<1cm

Sellar

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10
Q

What is a macro adenoma?

A

> 1cm

Suprasellar

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11
Q

What other 2 questions do we need to ask when assessing tumour size?

A

Is it compressing on the optic chiasm?

Is it invading the cavernous sinus?

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12
Q

What is the risk when a tumour has invaded the cavernous sinuses?

A

There are to many cranial nerves and the internal carotid therefore removing a tumour in the cavernous sinus is too risky

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13
Q

How do we determine whether a tumour is malignant or benign?

A

Determined by mitotic index by ki67 index - if it is less than 3% then it’s benign

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14
Q

When may a benign tumour have malignant behaviour?

A

For example, if it causing a visual disturbance

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15
Q

Describe the secretion pattern of GnRH

A

Pulsatile

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16
Q

How does hyperprolactinemia cause hypogonadism?

A

Prolactin binds to prolactin receptors on kisspeptin neurones which inhibits the release of GnRh therefore we inhibit the release of FSH and Lh in turn causing T or Oestrogen to fall

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17
Q

What is the commonest functioning pituitary adenoma?

A

Prolactinoma

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18
Q

What is the normal range of prolactin?

A

<300 M mU/L

<600 F mU/L

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19
Q

What is the prolactin level in a prolactinoma?

A

> 5000 mU/L

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20
Q

What increases serum prolactin?

A

Increase in tumour size

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21
Q

What is the presentation in a prolactinoma?

A 
Menstrual disturbance 
Erectile dysfunction 
Low libido 
Galactorrhoea 
Subfertility
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22
Q

What are the 3 classes of causes for hyperprolactinemia?

A

Physiological
Pathological
Iatrogenic

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23
Q

What are physiological causes of increased PRL?

A

Prengancy/breast feeding
Stress: exercise, seizure, venepuncture
Nipple/chest wall stimulation

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24
Q

What are the pathological causes of increased PRL?

A

Primary hypothyroidism
PCOS
Chronic renal failure (PRL not excreted properly)

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25
Q

What are the iatrogenic causes of increased PRL?

A 
Anti-psychotic 
SSRI
Anti-emetics
High dose oestrogen 
Opiates
26
Q

When should we consider other differentials aside from prolactinoma when looking at an increased PRL?

A

When we have confirmed it is a true elevation not a false positive
If there are not 2 clinical features of prolactinoma and we’ve checked the drug chart

27
Q

What do we consider after ruling out PRL?

A

Macroprolactin

Stress to venepuncture

28
Q

What is macroprolactin?

A

Most prolactin is monomeric however in some people PRL will clump together and stick to IgG therefore during a blood test this will show up as high PRL - benign blood test error

29
Q

What is the stress response to venepuncture?

A

Prolactin secreted in response to stress therefore we take patient to a relaxing unit and place needle in their arm for a long period, measuring PRL every 20 minutes waiting for PRL to fall

30
Q

What should we do if we have rules out macroprolactin and stress for venepuncture?

A

Order a pituitary MRI

31
Q

What is the first line treatment for prolactinoma?

A

DA receptor agonist such as cabergoline to normalise serum prolactin

32
Q

Is cabergoline safe fro pregnant women?

A

Yes

33
Q

When do we increase the dose of cabergoline?

A

When there is a bigger tumour

34
Q

How does cabergoline work?

A

Binds to D2 receptors on lactotrophs therefore stimulates the inhibitory effect they have on PRL secretion, and there is less PRL secretion

35
Q

What do we call a functioning Gh tumour in children?

A

Gigantism

36
Q

What do we call a functioning GH tumour in adults?

A

Acromegaly

37
Q

What is the onset of acromegaly and how does this affect its presentation as a tumour?

A

Insidious onset (10 years) therefore often reveals as a big tumour

38
Q

What are the symptoms of acromegaly?

A 
Sweatiness
Headache
Coarsening of facial features
Spade like hands due to increased soft tissue size
Large jaw (prognathism)
Increase in foot and hand size
Snoring/OSA
Hypertension 
Impaired glucose tolerance/ diabetes mellitus
39
Q

How does acromegaly cause headaches?

A

Due to IGF-1/GH behaviour, not because of tumour size

40
Q

Why do we not measure GH to diagnose acromegaly?

A

GH is too pulsatile

41
Q

How do we diagnose acromegaly?

A

Increased IGF-1 serum level with failed suppression test after 75g glucose load, instead a paradoxical rise is seen

42
Q

What may we also see in acromegaly patients in terms of other hormones?

A

Increase in prolactin

43
Q

What should we do after confirming excess GH?

A

Pituitary MRI

44
Q

What is the first line treatment for acromegaly?

A

Surgery: trans-sphenoidal pituitary surgery due to increased CVD risk

45
Q

What should we do prior to acromegaly surgery?

A

Somatostatin analogue e.g. ocreotide injection

46
Q

What is a side effect of octreotide injection?

A

Endocrine cyanide therefore can disturb gut enzymes to cause diarrhoea

47
Q

Why do GH tumours co-secrete PRL?

A

Some GH tumours have D2 receptors

48
Q

When else may drugs be used for a GH tumour?

A

If surgical resection is incomplete

49
Q

What is the con of using radiotherapy for Gh tumour?

A

Slow

50
Q

What happens in Cushings syndrome?

A

Too much cortisol

51
Q

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

A

Cushing’s syndrome is when there is too much cortisol from any cause
Cushing’s disease is when there is a tumour causing increased ACTH therefore increased cortisol

52
Q

What are the causes of Cushing’s syndrome?

A

Too much steroids

Adrenal adenoma

53
Q

What are the causes of Cushing’s disease?

A

Corticotroph adenoma

Ectopic ACTH e.g. from lung cancer

54
Q

How do we show Cushing’s on a test?

A

We want to demonstrate that we have either lost diurnal cortisol rhythm or we can show that we have produced too much cortisol over a 24 hours period

55
Q

Where can we test for cortisol?

A

Can be tested for in the saliva or the blood

56
Q

What can we use to try and suppress cortisol?

A

We can give oral dexamethasone which is an exogenous glucocorticoid

57
Q

What should we do once hypercortisolism is confirmed?

A

Measure ACTH - if that is high then we order a pituitary MRI

58
Q

What do non functioning pituitary adenomas secrete?

A

They do not secrete any specific hormone

59
Q

What do non functioning pituitary adenomas cause?

A

Often cause a visual disturbance such as bitemporal hemianopia

60
Q

What may non functioning pituitary adenomas cause?

A

As they get larger they may disrupt the stalk and thus cause hypopituitarism

61
Q

What is an exception to adenomas causing hypopituitarism?

A

Inhibitory dopamine won’t be able to travel down the stalk therefore we may get hyperprolactinemia

BRS YEAR 2 (37 decks)

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