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Year 2 - endocrinology > Hyposecretion of anterior pituitary hormones > Flashcards

Hyposecretion of anterior pituitary hormones Flashcards

1
Q

Give examples of anterior pituitary hormones

A 
FSH/LH
Prolactin
GH
TSH
ACTH
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2
Q

What do levels of endocrine diseases mean?

A

If a defect lies in the adenohypophysis then it is a secondary endocrine disease - the level of the defect determines the category
E.g. endocrine gland is primary
Hypothalamus is tertiary

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3
Q

What is hypopituitarism and panhypopituitarism?

A

Decreased production of all adenohypophysial hormones

Congenital or acquired

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4
Q

What are the signs of panhypopituitarism?

A

Short stature and more

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5
Q

What investigations are conducted to diagnose panhypopituitarism

A

Hypoplastic adenohypophysis on MRI - underdeveloped

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6
Q

What are the types of acquired panhypopituitarism?

A
  • tumours (hypothalamic(craniopharyngioma) or pituitary(adenoma, metasteses, cysts))
  • radiation - hypothalamic/pituitary damage
  • infection - meningitis
  • traumatic brain injury - explosion
  • infiltrative disease - neurosarcoidosis
  • pituitary apoplexy - unconsciousness from haemorrhage
  • peripartum infarction
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7
Q

During radiation which hormones is most and least likely to be affected?

A

GH - most vulnerable

TSH - resistant

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8
Q

What is Sheehan’s syndrome?

A

Infarcts pituitary upon giving birth

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9
Q

What does panhypopituitarism present with? (Specify which hormone causes each effect)

A

FSH/LH - secondary hypogonadism(gonad not problem the pituitary is), reduced libido, secondary amenorrhoea, erectile dysfunction
ACTH - secondary hypoadrenalism, fatigue
TSH - secondary hypothyroidism, fatigue, weight gain

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10
Q

What causes congenital panhypopituitarism and what does it result in?

A

RARE
due to mutations of transciption factor genes needed for normal pituitary development
Leads to deficiency of GH and at least another pituitary hormone

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11
Q

Which parts of the world is Sheehan’s syndrome common in?

A

less developed countries

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12
Q

How is Sheehan’s disease presented? (easily noticed and not well noticed)

A

Hard to notice – lethargy, anorexia, weight gain (TSH, ACTH, GH deficiency)

Easy to notice – failure of lactation (prolactin deficiency), failure to resume menstrual cycles post-delivery

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13
Q

What is pituitary apoplexy?

A

Dramatic presentation in patients with pre-existing pituitary adenomas (known or not known)

  • Haemorrhage or a bleed
  • Can be precipitated by anti-coagulants
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14
Q

What are the symptoms of pituitary apoplexy?

A
  • severe sudden onset headache
  • bitemporal hemianopia (pressing on the optic chiasm)
  • diplopia (double vision)
  • ptosis (drooping upper eyelid)
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15
Q

What are the ways in which hypopituitarism can be diagnosed?

A

Biochemical diagnosis

Radiological diagnosis- MRI can show if the sella turcica is empty for example

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16
Q

How are different hormones tested for through a biochemical diagnosis?

A
  • Stimulated pituitary function tests

ACTH GH = ‘stress hormones’ – stress is defined as hypoglycaemia (<2.2mM glucose)

  • An insulin-induced hypoglycaemia stimulates GH and ACTH (cortisol measured) release
  • TRH (in injection) then stimulates TSH release and GnRH stimulates FSH and LH release
17
Q

Why is it not useful to measure basal plasma concentrations of different hormones?

A
  • cortisol is in small volumes and varies throughout the day
  • T4/thyroxine has a long half-life (6 days) and so may take a while for it to fall
  • FSH/LH is cyclical.
  • GH/ACTH is pulsatile
18
Q

What are the therapies for ACTH, TSH, FSH/LH and GH deficiency and how is effectiveness checked?

A

ACTH - hydrocortisone (cortisol)
TSH - thyroxine (T4)
LH/FSH (female) - E2 and progestagen (symtpoms improve)
LH/FSH - testosterone (symptoms improve and testosterone)
GH - GH (IGF1, growth in children)

19
Q

What is the definition of short stature?

A

Children = <2 SDs from the mean.

Adults = less clear definition.

20
Q

What are the causes of short stature?

A

Genetic – e.g. Downs, Turner’s, Prader-Willi syndromes

Emotional deprivation

Systemic disease

Malnutrition - Malabsorption – e.g. coeliac disease.

Endocrine disorders – e.g. Cushing’s, hypothyroidism, GH deficiency

Skeletal dysplasia – e.g. Achondroplasia, osteogenesis imperfecta

21
Q

Summarise the main parts of the growth axis

A

Hypothalamus makes GHRH and SS
This causes GH release or inhibition
this acts on target tissues
It can also act on the liver to produce IGF1 and IGF2 which act on target tissues

PROBLEMS WITH THE HYPOTHALAMUS, LACK OF GH, GH RECEPTOR DEFECTS

22
Q

Describe some of the different types of short stature

A

Dwarfism – achondroplasia
Mutation in Fibroblast Growth Factor Receptor 3 (FGF3). Abnormalities in growth plate chondrocytes that impairs linear growth resulting in an average sized trunk and short arms/legs.

Pituitary dwarfism – childhood GH deficiency

Prader Willi syndrome – GH deficiency secondary to hypothalamic dysfunction

Laron dwarfism – high local incidence, mutation in GH receptor treated with IGF-1 in childhood

23
Q

How can short stature be diagnosed?

A
  • A predicted height is calculated using parents heights and then the child’s length (later height) mapped against its weight is followed.
  • If they fall below the lowest line, they often need referring to a paediatrician.
24
Q

What are the causes of acquired GH deficiency in adults?

A

trauma, pituitary tumour/surgery and cranial radiotherapy

25
Q

How can acquired GH deficiency in adults be diagnosed?

A

Provocative Challenge (stimulation) test

  • Cannot measure GH as it is pulsatile

Provocation tests include:

  • GHRH + Arginine (IV)
  • Insulin (IV)
  • glucagon (IM)
  • exercise (10mins)

Plasma GH is then measured at specific time points after. In response to hypoglycaemia GH deficient people have a low GH response (normally hypoglycaemia induced GH release)

26
Q

What is the NICE cutoff for hormone replacement therapy for GH?

A

3mcg/L

27
Q

GH replacement therapy -prep, administration, absorption and distribution, metabolism and duration of action

A
  • Preparation – human recombinant GH
  • Administration – daily, subcutaneous injection, monitor clinical responses and adjust dose to IGF-1
  • Absorption & distribution – maximal concentration in plasma in 2-6 hours.
  • Metabolism – hepatic/renal with a short half-life of 20 minutes.
  • Duration of action – lasts well beyond clearance, peak IGF1 levels at approx. 20 hours.
28
Q

What are the symptoms of GH deficiency?

A
  • Reduced lean mass
  • Increased adiposity - Increased waist: hip ratio
  • Reduced muscle strength/bulk
  • Reduced exercise performance
  • Decreased plasma HDL-cholesterol
  • Raised LDL-cholesterol
  • Impaired psychological well-being

Benefits of HRT are opposite

29
Q

Risk of GHRT

A

Increased susceptibility to cancer – no currently supported data.

Expensive.

30
Q

What causes Sheehan’s syndrome?

A

The anterior pituitary often enlarges in pregnancy
(lactotroph hyperplasia) and then the hypotension from loss of blood from giving
birth can mean the
pituitary becomes under perfused and then infarcts

31
Q

What is Simmond’s disease?

A

Disease characterized by panhypopituitarism that causes progressive emaciation, atrophy of the gonads, thyroid, and adrenal cortex, and loss of body hair

32
Q

Why is glucose found in the urine of patients with acromegaly?

A

chronically high GH inhibits insulin (also insulin resistance) and so glucose remains high so the kidneys begin to expel glucose

33
Q

Why do patients with acromegaly have polydipsia?

A

glucose osmotic diuretic affected

Year 2 - endocrinology (18 decks)

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