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ENDO- OBG > Hyposecretion of Anterior Pituitary Hormones > Flashcards

Hyposecretion of Anterior Pituitary Hormones Flashcards

1
Q

What is the difference between primary, secondary and tertiary endocrine gland disease?

A

Primary – problem with the endocrine gland/hormone released

Secondary – problem with the pituitary gland/hormone released

Tertiary – problem with the hypothalamus

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2
Q

What is the term given to decreased secretion of all anterior pituitary hormones?

A

Panhypopituitarism

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3
Q

Broadly speaking, what can panhypopituitarism be caused by?

A

Congenital defects (rare)

Gene mutations (more rare)

acquired- injury etc…

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4
Q

In what order does loss of secretion occur?

A

Usually develops in adults with progressive loss of pituitary secretion

Gonadotrophins

GH

Thyrotrophin

Corticotrophin

Prolactin

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5
Q

What are three main types of panhypopituitarism?

A

Simmond’s Disease

Sheehan’s Syndrome

Pituitary Apoplexy

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6
Q

Describe the onset of Simmond’s disease and state some of its causes and symptoms.

A 
Insidious (slow) onset  
Can be caused by: 
 Infiltrative diseases  
 Craniopharyngioma 
 Cranial injury 
 Pituitary adenomas  
 Following surgery 
Symptoms: (mainly due to loss of adrenal, gonadal and thyroid function) 
 Impotence  
 Loss of libido 
 Hypotension 
 Tirednesss 
 Secondary amenorrhoea or oligomenorrhoea 
 Loss of body hair  
 Waxy skin
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7
Q

State the cause of Sheehan’s syndrome and describe its onset.

A

This is specific to WOMEN

It is caused by vasoconstrictor spasm of hypophysial arteries as a result of post-partum haemorrhage

This spasm causes pituitary infarction

This develops very RAPIDLY

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8
Q

What is pituitary apoplexy? Describe its onset.

A

This is similar to Sheehan’s syndrome but isn’t specific to women

It is caused by intra-pituitary infarction or haemorrhage

This also has a RAPID presentation

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9
Q

Why is a single measurement of most hypothalamic hormones not useful?

A

Most hypothalamic hormones tend to be released in pulses

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10
Q

What type of test do you do to test if someone is producing a hormone?

A

Stimulation/provocation test

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11
Q

How are the releasing hormones administered in these tests? (Stimulation/provocation test )

A

Intravenous

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12
Q

What is the name given to the secondary endocrine gland failure that results from a lack of corticotrophin release from the pituitary?

A

secondary Hypoadrenocorticalism

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13
Q

What are the effects of a lack of somatotrophin in children and in adults?

A

Children – stunted growth (pituitary dwarfism)

Adults – loss of GH effects are uncertain

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14
Q

State some other causes of short stature.

A

Genetic

Malnutrition

Emotional deprivation

Endocrine disorders

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15
Q

State some genetic and acquired causes of GH deficiency in children.

A

Genetic:
 Deficiency of hypothalamic GHRH
 Mutations of GH gene
 Developmental abnormalities (e.g. aplasia or hypoplasia of the pituitary gland)

Acquired:
 Tumours of the hypothalamus and pituitary
 Other intracranial tumours nearby (e.g. optic nerve glioma)
 Irradiation
 Head injury
 Infection or inflammation
 Severe psychosocial deprivation

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16
Q

What are most endocrine-related causes of short statue due to (with reference to the HP axis)?

A

Decreased production of GHRH

17
Q

As well as being its own hormone, GH stimulates the production of other hormones. State one important hormone that is stimulated by GH, its side of production and its effects.

A

IGF I = insulin-like growth factor I

It is produced in the LIVER

It mediates growth effects

18
Q

What type of dwarfism is caused by a GH receptor defect?

A

Laron Dwarfism

19
Q

Describe the IGF I levels in people with this type of dwarfism. (Laron)

A

LOW IGF I

Because functioning GH receptors are necessary for GH to stimulate the production of IGF I

20
Q

Why are the Pygmies in Africa naturally short?

A

Their IGF I doesn’t function properly

21
Q

Using GnRH as an example. State and describe two examples of tertiary hypopituitarism.

A

Kallmann’s Syndrome
 Hypogonadism + Anosmia
 Genetic defect where the neurones in the embryo that will go on to produce GnRH are unable to migrate to the hypothalamus
 So they have a hypothalamus that lacks GnRH neurones
 The defect also affects the migration of neurones involved in olfaction (which causes anosmia)

Prader-Willi Syndrome
 Hypogonadism is one of the aspects of this disorder and the problem is at the level of the hypothalamus

22
Q

What is the gold standard method of testing the ability of the pituitary to release growth hormone?

A

Insulin-induced hypoglycaemia

Hypoglycaemia is a potent stimulus for growth hormone release

23
Q

State three other triggers for an increase in GH release.

A

Arginine

Glucagon (seems odd as this increases blood glucose but it turns out that in people who have GH deficiency, glucagon is good at stimulating growth hormone release)

Exercise

24
Q

Describe how the insulin-induced hypoglycaemia test is used to test GH secretion.

A

In a normal subject, the insulin-induced hypoglycaemia will give a massive rise in GH secretion

If you have a partial deficiency of GH then your response will be reduced

25
Q

For each of the following anterior pituitary hormone deficiencies, state the replacement used and the parameter that is monitored during treatment:

a. ACTH
b. TSH
c. Women - LH/FSH
d. Men - LH/FSH
e. GH

A

a. ACTH
Give hydrocortisone
Monitor serum cortisol

b. TSH
Give thyroxine
Monitor serum T4

c. Women – LH/FSH 
Give ethinyloestradiol (E2) and medroxyprogesterone (progestagen)
Monitor libido and oestrogen deficiency

d. Men – LH/FSH
Give testosterone undecanoate
Monitor libido and serum testosterone

e.GH
Give GH
Monitor IGF I

26
Q

State some of the effects of growth hormone therapy in children.

A

Increased linear growth

Decease in body fat

Younger children respond better

Obese children respond better

27
Q

What is a problem with growth hormone therapy in children?

A

Tolerance may develop so you need to think about when to start GH therapy

28
Q

How is the human recombinant GH used in GH therapy administered and how frequently must it be given?

A

Subcutaneous or Intramuscular

It is given daily or 4/5 times a week

29
Q

Describe the absorption, metabolism and duration of action of the drug (human recombinant GH).

A

It has a maximal plasma concentration after 4-6 hours
Metabolism – renal and hepatic with a short half-life (20 mins)

Duration of action – it works on protein synthesis so it’s duration of action is going to be quite long.
IGF I levels peak after around 20 hours

30
Q

State some adverse effects of GH therapy.

A

Lipoatrophy at the site of administration

Intracranial hypertension

Headaches (due to intracranial hypertension)

GH is also a cell stimulation hormone so there is an increased risk of tumours

31
Q

State some signs and symptoms of GH deficiency in adults.

A

Decreased muscle mass

Increased adiposity

Increased waist: hip ratio

Decrease HDL and increased LDL

Reduced muscle strength and bulk

Impaired psychological wellbeing and quality of life

32
Q

How can you diagnose GH deficiency in adults?

A

Lack of response to GH stimulation test (e.g. insulin-induced hypoglycaemia)

Low plasma IGF I

Low plasma IGF-BP3

33
Q

What are the potential benefits of GH therapy in adults?

A

Improved body composition

Improved muscle strength and exercise capacity

Normalisation of HDL-LDL

Increased bone mineral content

Improved psychological and mental wellbeing and quality of life

34
Q

What are the potential risks of GH therapy in adults?

A

Increased risk of cardiovascular accidents

Increased growth of soft tissue e.g. cardiomegaly

Increased susceptibility to cancer

ENDO- OBG (17 decks)

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