Endo 2: Hypersecretion of adenohypophysial hormones Flashcards

1
Q

Overall causes of hyperpituitarism. What is it associated with

A

Pituitary tumour or ectopic (i.e. cancer producing pituitary hormones).

It’s associated with visual field defect due to compression of overlying optic chiasm or other cranial nerve defects (due to compression of the nerves in the wall of the choroid plexus).

And endorcrine-related signs and symptoms

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2
Q

Specific effect of a large pituitary gland on vision and how this is assessed

A

Compresses optic chiasm by growth of SUPRASELLAR tumour. The fibres that cross over at the optic chiasm are those from the nasal retina. The light rays that hit the nasal retina are those from the periphery. So you get bitemporal heminopia (because vision lost on the temporal side). Assess with perimetry

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3
Q

What is the result of excess of each of the pituitary hormones?

A
ACTH: cushing's
TSH: thyrotoxicosis 
FSH/LH: precocious puberty in kids
Prolactin: hyperprolactinaemia
Somatotrophin: Gigantism/acromegaly
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4
Q

Physiological and pathological cause of hyperprolactinaemia. What other hormone is affected by this

A

Phys: pregnancy and breastfeeding
Path: prolactin secreting adenoma (prolactinoma). It’s the most common function pituitary tumour. GnRH is suppressed

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5
Q

Presentation of hyperprolactinaemia in M and F

A

F: galactorreah even when not pregnant, secondary amenorreah/oligomenorrhoea, infertility, loss of libido
M: galactorreah (less common since appropriate steroid background usually inadequate), loss of libido, erectile dysfunction, infertility

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6
Q

Regulation of prolactin secretion?

A

Under constant inhibition from dopaminergic neurons in the hypothalamus- level increases when dopamingergic neurons suppressed

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7
Q

Treatment for hyperprolactinaemia

A

MEDICAL TREATMENT FIRST LINE. Give D2-receptor agonists (to stimulate dopaminergic neurons to release dopamine which inhibits prolactin release AND it reduces tumour size). e.g cabergoline and bromocriptine oral administration

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8
Q

Side effects of dopamine receptor agonists

A

cabergoline: depression, nausea and vomiting, postural hypotension, dyskinesia, pathological gambing

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9
Q

2 effects of excess GH

A

childhood: gigantistm
adulthood: acromegaly

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10
Q

What usually causes excess GH

A

benign growth hormone secreting pituitary adenoma

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11
Q

How do symptoms progress of too much GH?

A

Gradually- insidious on onset

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12
Q

What causes the increase in morbidity and mortality in acromegaly

A

Cardiovascular disease (60%) as sugar is increased by GH so diabetes and there is also HTN, respiratory complications (25%), cancer (15%)

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13
Q

What grows in acromegaly

A

periosteal bone, cartilage, fibrous tissue, connective tissue, orgnans (cardiomegaly, splenomegaly, hepatomegaly etc.)

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14
Q

Clinical features of acromegaly

A

MAIN: excessive sweating and headache.
Also: Enlargement of superorbital ridges, nose hands and feet (SPADE SHAPED HANDS), thickening of lips and coarseness of features, macroglossia, mandible grows causing protrusion of lower jaw (prognathism), carpal tunnel syndrome (compresses median nerve), barrel chest and hyphosis

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15
Q

Metabolic effects of acromegaly

A

Increases blood glucose levels, decreased muscle glucose uptake, leading to insulin resistance and T2DM

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16
Q

Complications of acromegaly

A

Obstructive sleep apnea
Hypertension
Cardiomyopathy
Cancer

17
Q

Why does acromegaly cause obstructive sleep apnea

A

due to soft tissue changes in the neck casues collapse during sleep

18
Q

Why does acromegaly cause hypertension

A

direct effect of GH and IGF-1 on vascular tree and GH mediated renal sodium reabsorption

19
Q

Why does acromegaly cause cardiomypathy

A

hypertension, DM, toxic effects of GH on myocardium`

20
Q

Why does acromegaly cause cancer. Which regular test is required.

A

increased cell growth e.g. colonic polyps, regular colonoscopy needed

21
Q

Which hormone often cosecreted with GH

A

Prolactin (may relect tumour secreting prolactin and GH) - so may get secondary hypergonadism due to hyperprolactinaemia

22
Q

How to diagnose acromegaly

A

Not GH as pulsatile

  1. IGF-1 blood test (increased serum IGF implies it)
  2. Oral glucose tolerance test (see tutorial questions for how this works)
23
Q

Treatment for acromegaly

A
  1. Surgical removal of pituitary tumour (transphenoidal)
  2. Somatostatin agalogues e.g. octreotide (increase release of hypothalamic SS which inhibits GH secretion) and perhaps dopamine agonists e.g. cabergoline (as prolactin often cosecreted)
  3. Radiotherapy
24
Q

Outline the regulation of GH secretion

A

GHRH releasing neurons from hypothalamus main stimulation
Inhibition from SS.

GH causes release of SOMATOMEDINS e.g. mostly IGF1 and a bit of IGF2 from liver

25
Q

Outline how somatostatin analogues work and what it would be used for

A

For treatment of acromegaly (increased GH): ‘endocrine cyanide’- reduces GH secretion and tumour size. Injected or monthly depot

USE: pre-treatment before surgery to make resection easier, post operatively if not cured or whilst waiting for radio to take effect.

26
Q

Side effects of somatostatin

A

Nausea, diarroea, gall stones (also suppresses CCK release etc)