Hypersecretion of APG hormones Flashcards

1
Q

Hyperpituitarism?

A

Symptoms associated with excess production of adenohypophysial hromones

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2
Q

What are some causes or hyperpituitarism?

A

Isolated pituitary tumours
BUT
could be ectopic (from non-endocrine tissue) in origin

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3
Q

What is hyperpituitarism often associated with?

A

Visual field & CN defects e.g. bitemporal hemianopia

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4
Q

Excess ACTH (corticotrophin) can result in……

A

Cushing’s Disease

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5
Q

Excess TSH (thyrotrophin) can result in……

A

Thyrotoxicosis

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6
Q

Excess gonadotrophins (LH/FSH) can result in……

A

Precocious puberty in children

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7
Q

Excess prolactin can result in……

A

Hyperprolactinaemia

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8
Q

Excess GH can result in……

A

Gigantism (in children)

Acromegaly (in adults)

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9
Q

Physiological causes of hyperprolactinaemia?

A

Pregnancy

Breastfeeding

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10
Q

Pathological causes of hyperprolactinaemia?

A

Prolactinoma (often microadnenomas) - most common functioning pituitary tumour

High prolactin suppresses GnRH pulsatility

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11
Q

Signs/symptoms of hyperprolactinaemia in women?

A

x Galactorrhoea (milk production)
x 2o amenorrhoea (or oligomenorrhoea)
x loss of libido
x infertility

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12
Q

Signs/symptoms of hyperprolactinaemia in men?

A

x galactorrhoae UNCOMMON (as do not have appropriate steroid for it)
x loss of libido
x erectile dysfunction
x infertility

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13
Q

What is different about prolactin to the other APG hormones?

A

Has an INHIBITORY regulation

via. Dopamine

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14
Q

How is prolactin inhibited?

A

Dopamine from hypothalmic dopaminergic neurones

BINDS to

D2 receptors on the lactotrophs to switch OFF prolactin secretion

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15
Q

What is the 1st line treatment for hyperprolactinaemia?

A

D2 receptor agonists (oral!)

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16
Q

Examples of the 1st line treatment for hyperprolactinaemia?

A

Bromocriptine

Cabergoline

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17
Q

How does the 1st line treatment for hyperprolactinaemia work?

A
  1. Decreases prolactin secretion

2. Reduces tumour size

18
Q

Side-effects of the 1st line treatment for hyperprolactinaemia work?

A

x Impulse control disorder - dopamine receptors found elsewhere as well
x Nausea & vomiting
x Postural hypotension
x Dyskinesias (impairment of voluntary movement)
x Depression (exhaustion of dopamine stores)
x pathological gambling

19
Q

Why does excress GH (somatotrophs) present differently in children & adults?

A

In adults, the growth plates have fused so cannot grow in height
BUT
in children this has not happened yet

20
Q

Why does excess GH usually result in the 2 conditions?

A

Usually due to benign GH secreting pituitary adenoma

21
Q

Why is acromegaly associated w. increased morbidity and mortality?

A

Insidious onset (gradual but harmful on onset) - signs/symptoms progress gradually so can remain undiagnosed hence untreated results in increased…..

22
Q

What complications are normally seen in those w. acromegaly when they die?

A

CVS disease - 60%
Respiratory complications - 25%
Cancer - 15% e.g. bowel cancer

23
Q

Whats grows in acromegaly?

A
x Periosteal bone 
x Cartilage
x Fibrous tissue
x Connective tissue
x Internal organs (cardiomegaly, splenomegaly, hepatomegaly etc)
24
Q

Clinical features of acromegaly?

A

x Hyperhidorsis (excess sweating)
x Headache
x Face enlargement (e.g. supraorbital ridges)
x Macroglossia (enlarged tongue) - which can cause sleep apnoea
x Prognathism (mandible grows, protruding the lower jaw)
x Carpal tunnel syndrome (median nerve compression)
x Barrel chest
x Kyphosis (spinal disorder)

25
Q

How can patients help with the diagnosis of acromegaly?

A

Bring old photos

26
Q

What are the metabolic effects of acromegaly?

A

Diabetes mellitus development

27
Q

How does acromegaly cause the seen metabolic effects?

A
  1. Excess GH
  2. Increased endogenous glucose production
  3. Decreased muscle glucose uptake
  4. Increase insulin production = increased insulin resistance
  5. Impaired glucose tolerance
  6. diabetes mellitus
28
Q

4 complications of acromegaly?

A
  1. Obstructive sleep apnoea
  2. Hypertension
  3. Cardiomyopathy
  4. Increased risk of cancer
29
Q

OSA in acromegaly?

A

Increased soft tissue growth in throat = narrowing and subsequent collapse during sleep

30
Q

Hypertension in acromegaly?

A

Direct effects of GH & IGF-1 on vascular tree

GH mediated renal sodium reabsorption

31
Q

Cardiomyopathy on acromegaly?

A

Hypertension, DM, direct toxic effects of excess GH on myocardium

32
Q

Increased risk of cancer on acromegaly?

A

Colonic polyps SO need regular screening with colonoscopy

33
Q

Relationship betw. prolactin & GH in acromegaly?

A

Prolactin is often high in acromegaly - reflects tumour secreting both GH & prolactin

34
Q

How can the relationship betw. prolactin & GH in acromegaly imapct another hormone?

A

Hyperprolactinaemia will cause 2o hypogonadism

35
Q

How can you diagnose acromegaly (GH is pulsatile so random measurement unhelpful) ?

A

Give an oral glucose load (OGTT)!

The GH should DROP in a healthy person as the insulin rises
BUT
in acromegaly, there is a paradoxial rise of GH

36
Q

Another method to diagnose acromegaly (GH is pulsatile so random measurement unhelpful) ?

A

Elevated levels of serum IGF-1 so measure that!

37
Q

1st line of treatment for acromegaly?

A

Surgery - trans-sphenoidal

up the nose through a fassure as PG lies behind

38
Q

Medical treatment of acromegaly?

A

Somatostain analogues (e.g. octreotide)

Dopamine agonists - GH secreting P. tumours often express D2 receptors (cabergoline)

39
Q

Another treatment method for acromegaly?

A

Radiotherapy

40
Q

Why are somatostain analogues negative?

A

‘endocrine cyanide’

Can switch off digestive peptides in gut leading to GI side-effects e.g nausea, diarrhoea, gallstones etc.