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BRS 1b > 3.5 Pituitary Tumours > Flashcards

3.5 Pituitary Tumours Flashcards

1
Q

A tumour is a proliferation of a cell type, what would be caused by a tumour arising from somatotrophs.

A

Acromegaly - too much GH

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2
Q

What is a tumour made up from lactotrophs called?

A

prolactinoma

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3
Q

What is a tumour made up from thyrotrophs called?

A

TSHoma

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4
Q

What is a tumour made up from gonadotrophs called?

A

Gonadotrophinoma

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5
Q

What is a tumour made up from corticotrophes called?

A

cotricotroph adenoma

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6
Q

What is an adenoma?

A

Benign tumour of the pituitary gland

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7
Q

What disease does a corticotroph adenoma cause?

A

Cushing’s disease

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8
Q

How do we measure the size of a pituitary tumour?

A

MRI

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9
Q

What are the 4 ways we can radiologically classify a pituitary tumour?

A

size
sellar or suprasellar
compressing optic chiasm or not
invading cavernous sinus or not

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10
Q

What are the two size classifications of a pituitary tumour and the parameters?

A

microadenoma <1cm

macroadenoma >1cm

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11
Q

How do we classify pituitary tumours according to function?

A

Functioning: causes excess secretion of a specific pituitary hormone (e.g. prolactinoma - will go by this name)
Non-functioning: no excess secretion

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12
Q

Why can pituitary adenomas have benign histology but display malignant behaviour?

A

lack of space, lots of other structures easily affected.

*benign according to classification but can cause many symptoms as affecting other structures so seems malignant

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13
Q

Are pituitary tumours typically benign or malignant?

A

benign

pituitary carcinoma very rare <0/5%

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14
Q

What are the three factors to consider when classifying pituitary tumours?

A

Radiological
Function
Benign/malignant

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15
Q

How does (too much) prolactin inhibit GnRH?

A
  1. prolactin binds to prolactin receptors on kisspeptin neurones in hypothalamus
  2. inhibits kisspeptin release
  3. decreases in downstream GnRH (and therefore LH/FSH)
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16
Q

What is the pattern of GnRH release?

A

pulsatile

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17
Q

What are the symptoms will you see if excess PRL inhibits GnRH?

A
  • low libido
  • erectile dysfunction
  • loss of periods
  • reduced pubic hair
  • infertility
  • osteoporosis
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18
Q

What does excess PRL inhibiting GnRH an example of?

A

secondary hypogonadism

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19
Q

What is the commonest functioning pituitary adenoma?

A

prolactinoma

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20
Q

What is serum prolactin in a patient with prolactinoma

A

> 5000mU/L

usually men ~300, women <600

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21
Q

In a patient with prolactinoma, what does the level of serum prolactin indicate?

A

serum prolactin proportional to tumour size

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22
Q

How does prolactinoma usually present? (5)

A 
menstrual disturbance
erectile dysfunction
reduced libido
galactorrhoea (usually in women) - production of milk outside of normal
subfertility
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23
Q

What are other physiological causes of an elevated prolactin, that isn’t prolactinoma? (3)

A

pregnancy/breastfeeding
stress: exercise, seizure, venepuncture
nipple/chest wall stimulation

24
Q

What are other pathological causes of elevated prolactin, that isn’t prolactinoma? (3)

A

primary hypothyroidism
PCOS
chronic renal failure - kidneys don’t excrete prolactin properly

25
Q

What are other iatrogenic (drug) causes of an elevated prolactin, that isn’t prolactinoma? (5)

A 
antipsychotics
selective serotonin re-uptake inhibitors
anti-emetics
high dose oestrogen
opiates
---> mental health drugs affect dopaminergic system
26
Q

What does physiological cause mean?

A

Something that happens naturally in the body

27
Q

What is the release pattern of prolactin ?

A

none, (not diurnal, or pulsatile, or affected by food)

28
Q

What are the two causes of high prolactin, without symptoms, not caused by prolactinoma?

A
  1. Macroprolactin

2. stress of venopuncture

29
Q

What has to be done before diagnosing macroprolactin or stress venepuncture?

A

confirm elevation in serum prolactin, check if no clinical features consistent with this, review medication list

30
Q

What is macroprolactin?

A

majority of circulating porlactin is monomeric & biologically active
macroprolactin is ‘sticky’ prolactin:
- a ploymeric form of prolactin
- an antigen-antibody complex of monomeric prolactin and IgG (normally <5% of circ. prolactin)
-limited bioavaliability and bioactivity
–> can reassure patient

31
Q

How to confirm stress of venepuncture?

A

exclude by a cannulated prolactin series

- sequential serum measurement 20 mins apart with an indwelling cannula to minimise stress

32
Q

If elevation of prolactin is true, what next test should be done?

A

Pituitary MRI –> look for prolactinoma

33
Q

What is the first line treatment for prolactinoma?

A

Cabergoline - Dopamine receptor agonist (medical not surgical)

Aims to normalise serum prolactin& shrink prolactinoma

Safe in pregnancy

34
Q

How do we adjust the dose of dopamine receptor agonists for prolactinoma treatment?

A

based on size of tumour;

microprolactinoma will need smaller doses than macroprolactinoma

35
Q

Why do dopamine receptor agonists reduce prolactin levels?

A

When dopamine binds to the D2 receptors on an anterior pituitary lactotroph, it inhibits the production of prolactin.
Dopamine receptor agonists acts like dopamine and binds to D2 receptor
Prevents lactotrophs from making prolactin

36
Q

Whats the difference between gigantism and acromegaly?

A

gigantism is excess GH before growth plates close so affect height.

excess GH after growth plates close = acromegaly (and no excess height)

37
Q

Why does acromegaly present with such big pituitary tumours?

A

often insidious presentation - mean time from onset of symptoms to diagnosis =10 years

38
Q

What are the symptoms of acromegaly?

A 
sweatiness
headache
hypertension
impaired glucose tolerence/ diabetes mellitus
coarsening of facial features:
- macroglossia
- prominent nose
- large jaw
- inc. hand and foot size
39
Q

What are two ways in which GH affects growth?

A

GH direct from anterior pituitary to bone/muscle

GH to the liver, causing the liver to secrete Insulin - like Growth factor (IGF-1)

40
Q

Why is it unhelpful to do a random measurement of GH when trying to diagnose acromegaly?

A

GH is pulsatile

41
Q

How do we diagnose acromegaly?

A

elevated serum IGF-1 –> HIGH
failed supression of ‘paradoxical rise’ in GH following oral glucose load (oral glucose tolerance test)
normal after glucose –> GH falls after glucose load
acromegalic after glucose –> GH rises after glucose load

42
Q

Why is it important that acromegaly is treated?

A

Increased cardiovascular risk in untreated acromegaly

43
Q

What is the first line treatment for acromegaly?

A

surgical –> trans sphenoidal pituitary surgery

44
Q

What is the aim for treatement of acromegaly?

A

aim to normalise serum GH and IGF-1

45
Q

What can drugs be used for treatment of acromegaly

A

medical treatment can be used prior to surgery to shrink tumour or if surgical resection incomplete

46
Q

What are the options for medical treatment of acromegaly?

A 
somatostatin analogues (octreotide) - endocrine cyanide (can cause many problems with gut)
Dopamine agaonists (cabergoline) - GH secreteing pituitary tumours frequently express D2 receptors
47
Q

What hormone is cushings syndrome caused by?

A

excess cortisol

48
Q

What are the physical features of cushing syndrome?

A 
red cheeks
moon face
fat pads (buffalo humps)
thin skin
easy bruising
purple striae (stretch marks)
poor wound healing
pendulous abdomen
proximal myopathy (muscle weakness causing thin arms and legs)
49
Q

What are the non-physical features of cushing syndrome?

A 
mental changes - depression
osteoporosis
imparied glucose tolerance (diabetes)
hypertension
cardiac hypertrophy
females: amenorhea, hirsutism
males: erectile dysfunction
50
Q

What are some causes of excess cortisol leading to Cushing’s? (4)

A 
ACTH dependent: pituitary dependent Cushing's disease (pituitary adenoma)
ectopic ACTH (lung cancer)

ACTH independent:
adrenal adenoma or carcinoma
taking steroids by mouth (over prescription)

51
Q

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

A

Cushing’s disease caused by corticotroph adenoma

Cushing’s syndrome is the symptoms caused by excess cortisol

52
Q

How is Cushing’s disease investigated?

A
  1. Elevation of 24h urine free cortisol - increase cortisol secretion
  2. Elevation of late night cortisol (salivary or blood test) - loss of diurnal rhythm
  3. Failure to supress cortisol after oral dexamethasone (exogenous glucocorticoid) - increased cortisol secretion
53
Q

What should be done after confirming hypercortisolism to explore the cause of the Cushing’s symptoms?

A

Measure ACTH,
if low –> look at ACTH independent
if high –> pituitary MRI (cause is ACTH dependent)

54
Q

How do non-functioning pituiatry adenomas typically present?

A

visual disturbances (e.g. bitemporal hemianopia)

*don’t secrete any hormones so no hormone symptoms

55
Q

When can a non-functioning pituitary adenoma cause hormone related symptoms?

A

Don’t present with symtoms causes by excess hormones

Can present with hypopituitarism and raised serum prolactin, as pituitary is squished and dopamine can’t travel down pituitary stalk from hypothalamus

56
Q

What is the treatment for non-functioning pituitary adenoma?

A

Trans-sphenoidal surgery, esp for large tumours causing visual disturbances

BRS 1b (25 decks)

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