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Year 2 - LCRS - Endocrinology > Hypersecretion of Anterior Pituitary Hormones > Flashcards

Hypersecretion of Anterior Pituitary Hormones Flashcards

07.10.2019

1
Q

Hyperpituitarism

A

Symptoms associated with excess production of adenohypophysial hormones

  • Usually due to isolated pituitary tumours but can also be ectopic (i.e. from non-endocrine tissue) in origin
  • can be associated with visual field and other (e.g. cranial nerve) defects as well as endocrine-related signs and symptoms
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2
Q

Bitemporal hemianopia

A
  • loss of vision from the outer temporal vision fields

- can be caused by compression of the optic chasm by a suprasellar tumour

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3
Q

How do you asses bitemporal hemianopia?

A

Visual field test?

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4
Q

Excess ACTH leads to..

A

Cushing’s syndrome

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5
Q

Excess TSH leads to..

A

Thyrotoxicosis

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6
Q

Excess LH and FSH lead to..

A

precocious puberty in children

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7
Q

Excess Prolactin leads to…

A

Hyperprolactinaemia

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8
Q

Excess GH leads to..

A

Acromegaly, Gigantism

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9
Q

What are the 2 forms of hyperprolactinaemia?

A
  • Physiological (in pregnancy and breastfeeding)
  • Pathological (prolactinoma, often microadenomas < 10mm diameter)

High prolactin suppresses GnRH pulsatility!!!

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10
Q

How does hyperprolactinaemia due to pituitary adenoma show in women?

A
  • galactorrhoea (milk production)
  • secondary amenorrhoea (or oligomenorrhoea)
  • loss of libido
  • infertility
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11
Q

How does hyperprolactinaemia due to pituitary adenoma show in men?

A
  • galactorrhoea uncommon (since appropriate steroid background usually inadequate)
  • loss of libido
  • erectile dysfunction
  • infertility

-> presents with symptoms of testosterone deficiency

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12
Q

What receptors do lactotrophes express?

A

D2 receptors

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13
Q

Where does the dopamine that acts on lactotrophes come from?

A

HYPOTHALMIC DOPAMINERGIC NEURONES

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14
Q

How is the release of prolactin regulated?

A

Dopamine suppresses the release of prolactin.

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15
Q

How do you treat hyperprolactinaemia?

A
  • 1st line treatment: D2 agonists (decrease PRL secretion, reduce tutor size)
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16
Q

What are examples of D2 agonists?

A

BROMOCRIPTINE
CABERGOLINE

-> oral administration

17
Q

What are side effects of D2 agonists?

A
  • Nausea and vomiting
  • Postural hypotension
  • Dyskinesias
  • Depression
  • Impulse control disorder e.g. Pathological gambling
  • hyper sexuality

-> good to have a close relative to monitor them

18
Q

What does excess GH result in in children and in adults?

A

Children: gigantism
Adults: acromegaly

-> usually due to a benign GH secreting pituitary adenoma

19
Q

Tallest man recorded in world history

A

Robert Wadlow

died at age 22

20
Q

Acromegaly

A
  • insidious in onset
  • signs and symptoms progress very gradually, can be undiagnosed for years.
  • untreated, excess GH is associated with increased morbidity and mortality

-> soft tissue growth

21
Q

What grows in acromegaly?

A
  • periosteal bone
  • cartilage
  • fibrous tissue
  • connective tissue
  • internal organs (cardiomegaly, splenomegaly, hepatomegaly, etc.)
22
Q

What additional screening do acromegaly patients have and why?

A

Bowel cancer screening as bowel cancer is common in patients with acromegaly.

23
Q

What are the causes of death in acromegaly?

A
  • Cardiovascular disease 60%
  • Respiratory complications 25%
  • Cancer 15%
24
Q

Clinical features of acromegaly (8)

A
  • excessive sweating (hyperhidrosis)
  • headache
  • enlargement of supraorbital ridges, nose, hands and feet, - thickening of lips and general coarseness of features
  • enlarged tongue (macroglossia)
  • mandible grows causing protrusion of lower jaw (prognathism)
  • carpal tunnel syndrome (median nerve compression)
  • barrel chest, kyphosis

-> old photos are useful with diagnosis

25
Q

What are the metabolic effects of acromegaly?

A
  1. excess GH production ->
  2. increased endogenous glucose production, decreased muscle glucose uptake ->
  3. increased Insulin production = increased insulin resistance ->
  4. impaired glucose tolerance ->
  5. Diabetes Mellitus
26
Q

What does GH do to muscle glucose uptake?

A

it suppresses it.

27
Q

What are some complications of acromegaly?

A
  • obstructive sleep apnoea
  • Hypertension
  • Cardiomyopathy
  • increased risk of cancer (e.g. colonic polyps -> regular screening with colonoscopy)
28
Q

Obstructive sleep apnoea in acromegaly

A

Bone and soft-tissue changes surrounding the upper airway lead to narrowing and subsequent collapse during sleep

29
Q

Hypertension in acromegaly

A
  • Direct effects of GH &/or IGF-1 on vascular tree

- GH mediated renal sodium reabsorption

30
Q

Cardiomyopathy in acromegaly

A
  • Hypertension
  • DM
  • direct toxic effects of excess GH on myocardium
31
Q

What hormone is often co-secreted in acromegaly?

A
  • Prolactin is often high in acromegaly – may reflect tumour secreting GH AND prolactin
  • Hyperprolactinaemia will cause secondary hypogonadism (see clinical features of hyperprolactinaemia)
32
Q

How do you diagnose acromegaly?

A
  • Elevated serum IGF-1
  • Failed suppression (‘paradoxical rise’) of GH following oral glucose load – oral glucose tolerance test
  • measuring GH is unhelpful as it is pulsatile!!
33
Q

Treatment of Acromegaly

A
  • trans-sphenoidal surgery (first line)
  • Medical (somatostatin analogues (e.g. octreotides), dopamine agonists (e.g. cabergoline))
  • radiotherapy
34
Q

Why are dopamine agonists sometimes used to treat acromegaly?

A

GH secreting pituitary tumours often express D2 receptors.

35
Q

What are side effects of somatostatin analogues?

A

GI side effects common eg nausea, diarrhoea, gallstones can occur

36
Q

How/when are somatostatin analogues given to treat acromegaly?

A
  • Injection: short acting or monthly depot
  • Pre-treatment before surgery may make resection easier
  • Use post-operatively if not cured or whilst waiting for radiotherapy to take effect (slow)
37
Q

What do somatostatin analogues do in acromegaly?

A

reduces GH secretion and tumour size

Year 2 - LCRS - Endocrinology (18 decks)

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