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AE > 1 - Pituitary Gland > Flashcards

1 - Pituitary Gland Flashcards

1
Q

How does the hypothalamus communicate with the anterior pituitary gland?

A

Neurohormones

Through a specialised portal vascular system.

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2
Q

Do direct neural connections exist between the hypothalamus and the anterior pituitary gland?

A

No.

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3
Q

How does the hypothalamus communicate with the posterior pituitary gland?

A

Through axons that originate within hypothalamic neuronal cell bodies.

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4
Q

What are the two inhibitory neurohormones produced by the hypothalamus?

A

Dopamine

Somatostatin

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5
Q

What anterior pituitary hormones does dopamine inhibit?

A

FSH
LH
Prolactin
TSH

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6
Q

What anterior pituitary hormones does somatostatin inhibit?

A

Growth Hormone

TSH

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7
Q

What hormone does POMC (pro-opiomelanocortin) give rise to?

A

ACTH

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8
Q

POMC and MSH (melanocyte-stimulating hormone) result in what change? And occur in what disease?

A

Hyperpigmentation

Addison’s disease
Nelson syndrome

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9
Q

Where does vasopressin (ADH) act and how does it work?

A

Distal tubule

Increases permeability to water

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10
Q

At high concentrations, what can ADH cause?

A

Vasoconstriction

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11
Q

What are the two main stimuli of ADH secretion?

Sensed by which receptors?

A

Increased osmotic pressure + volume depletion.

Osmoreceptors (within hypothalamus) and baroreceptors.

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12
Q

What 4 locations are baroreceptors located?

A

Carotid sinus
Aortic arch
Left atrium
Pulmonary veins

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13
Q

A lack of ADH results in what condition?

A

Central diabetes insipidus

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14
Q

What pathology occurs in nephrogenic diabetes insipidus?

A

Inability of kidney to respond to ADH.

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15
Q

What are the two target areas of oxytocin?

A

1) Uterine smooth muscle

2) Myoepithelial cells within the breast

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16
Q

What stimulates oxytocin release?

A

1) Suckling

2) Increases gradually throughout pregnancy

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17
Q

What 6 hormones are produced by the anterior pituitary gland?

A 
ACTH
GH
TSH
LH
FSH
Prolactin
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18
Q

What 2 hormones are produced by the posterior pituitary gland?

A

Oxytocin

ADH (vasopressin)

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19
Q

What are the two possible effects arising from pituitary tumours?

A

1) Mass effect (headache, visual loss)

2) Hormonal effects (hormone overproduction)

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20
Q

What is a clonal tumour?

A

A tumour made up of all the same cells.

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21
Q

What pathology arises as as a result of a clonal tumour of somatotrophs?

A

Acromegaly (GH excess)

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22
Q

What features are present in acromegaly?

A

Tall stature
Enlarged hands, feed
Metabolic effects: HTN + diabetes
Sweating (gland proliferation)

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23
Q

What is a clonal tumour of lactotrophs called?

A

Prolactinoma

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24
Q

What symptoms occurs as a result of a prolactinoma?

A

Lactation

Amenorrhoea

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25
Q

What pathology arises as as a result of a clonal tumour of corticotrophs?

A

Cushing’s disease

ACTH-secreting pituitary tumour from POMC

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26
Q

What are the characteristic features of Cushing’s disease?

A 
Moon face (fat deposition)
Striae
Recession of hair
Hirsutism
Bruising
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27
Q

Which two clonal tumours are termed ‘non-functioning’ adenomas?

And why?

A

Gonadotroph adenomas

Thyrotroph adenomas

Both very rare

28
Q

What are craniopharyngiomas?

A

Rare, benign tumours

Form as solid tissue, cysts or calcified nodules.

29
Q

Name 3 destructive lesions which result in hypopituitarism

A

Rathke’s cleft cyst
Meningiomas
Gliomas

30
Q

Hypopituitarism lesions results in which 3 hormones insufficiencies?

A

Hypoadrenalism
Hypothyroidism
Hypogonadism

31
Q

Polyclonal tumours arise from what pathology?

A

Hormone dysregulation resulting in hyperplasia

e. g. high-dose estrogen = PRLoma
(e. g. Transgenic GH-RH excess = GHoma)

32
Q

What are the 4 candidates for protein mutation in polyclonal tumours?

A

Receptors
G-protein subunits
Kinases
Nuclear proteins

(cell signalling capital)

33
Q

What two receptors result in a prolactinoma if mutated?

A

Dopamine D2 receptor
(K/o studies get them because Dopamine is an important inhibitor of prolactin secretion)

FGF4-Receptor
(splice variant may be associated, but not causative)

34
Q

What are the 5 diseases involving adenomas?

A

1) McCune-Albright Syndrome
2) Multiple Endocrine Neoplasia (MEN) 1
3) Familial isolated pituitary adenoma
4) X-linked acromegaly
5) Carney complex

35
Q

What is the underlying pathophysiology of McCune-Albright Syndrome?

A

G-protein activating mutation in the protein GSP, resulting in excess GH.

36
Q

How does a GSP mutation result in excess GH?

A

GalphaS mutation (GSP)

1) Inhibition of GTP-ase activity
2) Constitutive activation of adenylate cyclase
3) LOTS OF cAMP
4) Protein kinase A activation
5) CREB phosphorylation
6) Excess gene expression

37
Q

In what % of GHomas is a GSP mutation found?

A

40%

38
Q

What inheritance trait is the GSP mutation?

A

Dominant

39
Q

As a result of its effect, what type of gene is GSP?

A

Oncogene

40
Q

MEN-1 is what kind of gene?

A

Tumour suppressor gene

41
Q

For MEN-1 to manifest, however, given its TSG trait, what has to occur?

A

Two-hit hypothesis

42
Q

What is the difference in protein expression between the 1st and 2nd hit?

A

1st = reduced protein expression

2nd = NO Protein expressed (phenotype)

43
Q

MEN-1 results in tumours forming in which 3 glandular organs?

A

Pituitary
Parathyroid
Pancreas

44
Q

What NUCLEAR protein does MEN-1 gene code for?

A

Menin

45
Q

What inheritance pattern does MEN-1 have?

A

Autosomal dominant trait (occurs even in heterozygous)

**High-penetrance

46
Q

On what chromosome is MEN-1 mutation found?

A

Chromosome 11

11q33

47
Q

Describe what happens in the process of ubiquination?

A

Protein targeting for degradation.

48
Q

What kind of protein is USP8?

A

A de-ubiquitinase

49
Q

A mutation in USP8 results in what condition?

A

Cushing’s disease

50
Q

How does Cushing’s disease arise from a USP8 mutation?

A

Increases de-ubiquitination of EGFR.

Rescues EGFR from lysosomal degradation.

Increase in EGFR signalling.

Increase in ERK

Increased ATH production.

51
Q

Explain the combined model of pathogenesis in regards to pituitary adenomas.

A

Hormonal / environmental induced proliferation occurring.

More divisions = more likely for mutation.

Incidental mutation (e.g. GSP / USP8) results in monoclonal tumour forming.

52
Q

What are the 3 main modalities to treat pituitary tumours?

A

1) Surgery
2) Radiotherapy
3) Drug therapy

53
Q

What type of surgery is used to remove pituitary tumours?

A

Transsphenoidal adonectomy

54
Q

Name two important structures that need to be avoided in Transsphenoidal surgery

A

Optic nerve

Internal carotid artery

55
Q

Possible complications from pituitary surgery?

A

Visual field defects
Various endocrine complications
CSF leak

56
Q

Radiotherapy is often an adjuvant. What consequence will occur after therapy?

A

Hypopituitarism

57
Q

What 3 consequences occur from a prolactinoma?

A

Anovulation
Amenorrhoea
Galactorrhoea

58
Q

Name 3 drugs that can cause prolactinaemia

A

Dopamine antagonists (metoclopramide)

SSRI (e.g. fluoxetine)

Tricyclic anti-depressants

59
Q

What pharmaceutical therapy can be used to treat prolactinomas / hyperprolactinaemia?

A

Dopamine agonists (e.g. bromocriptine)

60
Q

Name a few side effects of bromocriptine

A

12% get them

Nausea
Postural hypotension
Abdo pain

61
Q

Name one novel dopamine agonist

And why is it better?

A

Quinagolide (similar to bromocriptine)

Less common SE

62
Q

What pharmaceutical therapy can be used to treat acromegaly?

A

Somatostain receptor agonists

OR

GH antagonists

63
Q

Name a GH antagonist

A

Pegvisomant

64
Q

What is the mechanism of action of Pegvisomant?

A

Binds to one half of the GH-receptor, inhibiting the binding of GH and subsequent dimerisation.

Reduces levels of IGF-1 and GH production.

65
Q

Pegvisomant is a modified GH molecule. It is also pegylated for two reasons - what are they?

A

Decrease immunogenicity

Increase half-life

AE (7 decks)

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