Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Endocrinology year 2 > Hyposecretion of anterior pituitary hormones > Flashcards

Hyposecretion of anterior pituitary hormones Flashcards

1
Q

How is the posterior pituitary gland different

A 
Differs embryologically (neurohypophysis- formation from diencephalon- that is all neural tissue)
Different hormones secreted (oxytocin and vasopressin)

A.P is glandular- adenohypophysis,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

List the hormones released by the anterior pituitary gland

A

FSH/LH- controls gonads
PROLACTIN- involved in post-partum lactation
GH
TSH- tells thyroid gland to make T4 and T3
ACTH- tells adrenal gland to make cortisol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is important to remember about aldosterone

A

Released is under the control of renin and not ACTH

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Summarise the hypothalamo-pituitary- thyroid axis

A

Hypothalamus- A.P- TSH– Thyroid gland- T4+T3

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How do autoimmune diseases effect the endocrine glands

A

The endocrine system is very scuppered by autoimmune diseases

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Compare primary and secondary disorders

A

Primary- problem with the gland itself

Secondary- problem not with the gland but problem from signal from the anterior pituitary (i.e no TSH)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Define panhypopituitarism

A

DECREASED PRODUCTION OF ALL ANTERIOR PITUITARY HORMONES (PANHYPOPITUITARISM)

PAN= ALL OR COVERING

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Summarise hypopituitarism

A

DECREASED PRODUCTION OF ALL ANTERIOR PITUITARY HORMONES (PANHYPOPITUITARISM)

OR: OF SPECIFIC HORMONES

CONGENITAL (rare) OR ACQUIRED
Uncommon to be born with an abnormal anterior pituitary gland

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Summarise panhypopituitarism

A

Rare
Usually due to mutations of transcription factor genes needed for normal anterior pituitary development
eg PROP1 mutation
Deficient in GH and at least 1 more anterior pituitary hormone
Short stature - what you present with
Hypoplastic anterior pituitary gland on MRI- small, underdeveloped gland

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Describe PROP1

A

PROP1 has both DNA-binding and transcriptional activation ability. Its expression leads to ontogenesis of pituitary gonadotropes, as well as somatotropes, lactotropes, and caudomedial thyrotropes

Homeobox protein prophet of PIT-1 is a protein that in humans is encoded by the PROP1 gene.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How can tumours cause acquired panhypopituitarism

A

Large non-functioning pituitary tumours can produce anterior pituitary hypofunction by compressing the pituitary cells against the bone of the sella turcica.

hypothalamic - craniopharyngiomas (tumour of the pituitary gland embryonic tissue)
pituitary – adenomas, metastases, cysts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

How can radiation lead to acquired panhypopituitarism

A

hypothalamic/pituitary damage
GH most vulnerable, TSH relatively resistant

Late effects from cancer treatment- radiotherapy for nasophargyneal carcinomas or head and neck cancers- may damage hypothalamus and pituitary gland.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe the other causes of acquired panhypopituitarism

A

Infection eg meningitis
Traumatic brain injury
Infiltrative disease – often involves pituitary stalk
eg neurosarcoidosis- Neurosarcoidosis (sometimes shortened to neurosarcoid) refers to sarcoidosis, a condition of unknown cause featuring granulomas in various tissues, involving the central nervous system
Inflammatory (hypophysitis)
Pituitary apoplexy
haemorrhage (or less commonly infarction)- sad, unhappy and damaged pituitary gland
Peri-partum infarction (Sheehan’s syndrome)- infarcted pituitary upon giving birth).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What was panhypopituitarism originally called

A

Simmond’s disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Summarise the presentation of panhypopituitarism

A 
FSH/LH	Secondary hypogonadism
			Reduced libido
			Secondary amenorrhoea
			Erectile dysfunction
ACTH	Secondary hypoadrenalism (cortisol 			deficiency)- no ACTH
			Fatigue
TSH		Secondary hypothyroidism
			Fatigue
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is a feature of the neurohypophysis

A

neural tissue and so is the same colour as the brain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Summarise sheehan’s syndrome

A

Specifically describes post-partum hypopituitarism secondary to hypotension (post partum haemorrhage - PPH)
Less common in developed countries
Anterior pituitary enlarges in pregnancy (lactotroph hyperplasia)
PPH leads to pituitary infarction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Describe how Sheehan’s syndrome exposes a design flaw in the anterior pituitary gland

A

During pregnancy, the anterior pituitary gland enlarges- due to hyperplasia of the lactotrophs preparing to make prolactin to breast feed the baby- therefore blood supply to the tissue increases
However in PPH- blood pressure decreases and vasoconstriction occurs- less blood flow to a metabolically active tissue- so the gland dies off

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Describe sheehan’s syndrome presentation

A

Lethargy, anorexia, weight loss – TSH/ACTH/(GH) deficiency
Failure of lactation – PRL deficiency
Failure to resume menses post-delivery- lost LH and FSH
Posterior pituitary usually not affected

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Describe the epidemiology of a pituitary adenoma

A

10% of the population will have a pituitary adenoma without being aware of it- an intra-pituitary haemorrhage (pituitary apoplexy) can then be the first presentation of a pituitary adenoma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Summarise pituitary apoplexy

A

Intra-pituitary haemorrhage or (less commonly) infarction
Often dramatic presentation in patients with pre-existing pituitary tumours (adenomas)
May be first presentation of a pituitary adenoma
Can be precipitated by anti-coagulants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How can pituitary apoplexy be precipitated by anti-coagulants

A

May be aware of existing pituitary adenoma
May present with chest pain and breathlessness- given sub-cutaneous heparins to stabilise unstable plaque- but this precipitates to haemorrhage- pituitary apoplexy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Describe the ease of seeing the symptoms of sheehan’s syndrome

A

Hard to notice – lethargy, anorexia, weight loss (TSH, ACTH, GH deficiency). Easy to notice – failure of lactation (prolactin deficiency, but still, many women can’t lactate naturally), failure to resume menstrual cycles post-delivery.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

What should you see between the optic chiasm and the pituitary gland

A

Black space- CSF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Describe the effects of a pituitary tumour or pituitary apoplexy on the optic chiasm and relate this to the symptoms observed and the anatomy.

A

SEVERE sudden onset headache (growing tumour maty have more insidious onset)
Visual field defect – compressed optic chiasm, bitemporal hemianopia (lose outer fields of vision)
Cavernous sinus involvement may lead to diplopia- double vision (IV, VI), ptosis- drooping eyelid (III)

see diagram!!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Why is a single measurement of most hypothalamic hormones not useful- essentially why is the interpretation of anterior pituitary hormones limited

A

Most hypothalamic hormones tend to be released in pulses

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Summarise the biochemical diagnosis of hypopituitarism

A
  1. Basal plasma concentrations of pituitary or target endocrine gland hormones
    - interpretation may be limited
    - undetectable cortisol – what time of day?
    - T4 – circulating t1/2 6 days- may take a while for it to fall
    - FSH/LH – cyclical
    - GH/ACTH - pulsatile
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What do we use as a surrogate to measure ACTH

A

Cortisol- timing important- measure at 9:00 am. Will be low in the evening anyway- so futile measuring cortisol in the evening- as it won’t be an exclusive measure of pathology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

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

A

Stimulation/provocation test

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

How are the releasing hormones administered in these tests

A

Intravenous

33
Q

Summarise the stimulated pituitary function tests

A
  • ACTH & GH = ‘stress’ hormones
    • Hypoglycaemia (<2.2mM) = ‘stress’
    • Insulin-induced hypoglycaemia stimulates:
      GH release
      ACTH release (cortisol measured)
    • TRH stimulates TSH release
    • GnRH stimulates FSH & LH release
34
Q

Why do the stimulated pituitary function tests work

A

The brain essentially hates hypoglycaemia- so we have counter-regulatory hormones (ACTH, GH and glucagon) that are released to bring glucose levels back to normal

35
Q

Describe the inadequacy of the use of CT scans to look at the pituitary gland

A

May be able to see blood in pituitary fossa- but nothing more- MRI best

36
Q

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

A

Hypoadrenocorticalism

37
Q

Summarise the radiological diagnosis of hypopituitarism

A

Pituitary MRI
May reveal specific pituitary pathology
eg haemorrhage (apoplexy), adenoma

Empty sella – thin rim of pituitary tissue- due to hypopituitarism- not much of the pituitary gland left

38
Q

How can we easily identify the pituitary gland on an MRI in some patients

A

The posterior bright spot (although not every one may have this)

39
Q

What is the issue with treatment of pituitary diseases

A

Treatments often given in tablet form, leading to a steady-state release of the hormone. Whereas, naturally, pituitary gland releases the hormone in pulses and in specific circumstances- so it is difficult to mimic the pituitary gland- why the patient’s quality of life never fully returns

40
Q

Describe hormone replacement for the deficiencies in different hormones

A

GH- replace with GH- Check IGF1 and growth chart in children
Men LH/FSH- replace with testosterone- check symptom improvement and testosterone
Women LH/FSH- replace with HRT (E2 plus progestagen)- check symptom improvement and withdrawal bleeds
TSH- replace with thyroxine- check serum fT4
ACTH- replace with hydrocortisone- check serum cortisol

41
Q

Why don’t we replace ACTH directly and when is the biggest dose of hydrocortisone given

A

ACTH is very pulsatile- so we replace cortisol instead

Biggest dose given in the morning- to mimic the diurnal variation of cortisol

42
Q

Why don’t we measure TSH in secondary hypothyroidism (I,e hypopituitarism)

A

Because TSH won’t be low

Measure T4 as most T3 is converted to T4

43
Q

Why don’t we give oestrogen unopposed

A

To reduce the risk of endometrial cancer- take of oestrogen for a few days- to allow the endometrial lining to be shred and menstruated

44
Q

Consequence of no LH

A

Can’t make testosterone

Need different regimen to improve sperm count

45
Q

Summarise growth hormone (somatotrophin deficiency)

A

in children results in short stature (=2 SDs < mean height for children of that age and sex)

in adults, effects (and definition) less clear

46
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

47
Q

State some other causes of short stature

A 
Genetic 
Malnutrition 
Emotional deprivation 
Endocrine disorders 
Systemic disease
Malabsorption
Skeletal dysplasias
48
Q

Describe the genetic causes of short stature

A

Down’s syndrome, Turner’s syndrome, Prader Willi syndrome

49
Q

Describe emotional deprivation as a cause of short stature

A

Activates the stress axis- which can shut down Growth Hormone

50
Q

Describe malnutrition and malabsorption as a cause of short stature

A 
Need calories growth
In malabsorption (i.e coeliac disease)- can't absorb the calories needed for growth
51
Q

Describe endocrine disorders and skeletal dysplasias as a cause of short stature

A

Endocrine Disorders:
Cushing’s syndrome, Hypothyroidism, GH deficiency, poorly controlled T1DM
Skeletal dysplasias:
Achondroplasia, osteogenesis imperfecta

52
Q

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

A

Decreased production of GHRH

53
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

IGF2 is also produced

54
Q

Describe laron dwarfism

A

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

NOTHING WRONG WITH GH PRODUCTION

55
Q

Why are the Pygmies in Africa naturally short

A

Their IGF I doesn’t function properly

56
Q

Summarise the different causes of short stature

A

§ Dwarfism – achondroplasia.
o Mutation in Fibroblast Growth Factor Receptor 3 (FGF3).
o 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

57
Q

Describe PWS

A

Food-seeking behaviour- very distressing
Learning difficulties
GH deficiency 2o to hypothalamic dysfunction- no signa (GHRH) from hypothalamus to tell Anterior Pituitary to release growth hormone
Thus giving growth hormone will help them grow and also lose weight.

58
Q

Summarise Laron dwarfism

A

High incidence in a specific village in Ecuador – descendants of Spanish Sephardic Jews fleeing Spain during Inquisition

Mutation in GH receptor

IGF-1 treatment in childhood can increase height

59
Q

Describe mid parental height

A

MID PARENTAL HEIGHT
A predicted adult height –
based on father’s & mother’s height

60
Q

When is short stature an issue

A

When you fall of the growth curves

9th centile at aged 5y, started to fall down the curves – a drop of more than 2 centiles is flagged, by aged 11y, below the 0.4th centile – diagnosis of coeliac disease made, gluten free diet – starts to grow as predicted

61
Q

Summarise the diagnosis of short stature

A

§ A predicted height is calculated 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.

62
Q

Describe the causes of GH deficiency in adults

A

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

Ultimately, injury to pituitary gland or hypothalamus

63
Q

Summarise the diagnosis of GH deficiency

A

Random GH little use – pulsatile
PROVOCATIVE CHALLENGE
(i.e. STIMULATION) TEST

64
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

65
Q

State three other triggers for an increase in GH release.

A

Arginine- may stimulate GH release by inhibiting somatostatin release
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

66
Q

Summarise the GH provocation tests

A

GHRH + ARGININE (i.v.) (in combination more effective than each alone) (give as marmite for children- easier)
INSULIN (i.v.) – via hypoglycaemia
GLUCAGON (i.m.)
EXERCISE (e.g. 10 min step climbing; when appropriate)- doesn’t really work in adults

Measure plasma GH at specific time-points (before and after)

67
Q

Describe how the insulin provocation test can be used to diagnose acquired GH deficiency in adults

A

§ In response to hypoglycaemia, GH deficient people have a very low GH response obviously.
§ The NICE cut-off for HRT is less than 3mcg/L.

68
Q

How can glucagon stimulate GH release

A

Powerful stimulus to make GH and ACTH

Induced vomiting in patients- which probably drives up GH and ACTH.

69
Q

Summarise GH therapy

A

§ Preparation – human recombinant GH.
§ Administration – daily, subcutaneous injection, monitor clinical responses (energy levels etc) 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.

70
Q

Describe the absorption, metabolism and duration of action of the drug.

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

71
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

72
Q

Describe the signs and symptoms of GH deficiency in adults

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’ and reduced quality of life

73
Q

Describe the benefits of GH treatment in adults

A

Improved body composition – decreased waist circumference, less visceral fat

Improved muscle strength and exercise capacity

More favourable lipid profile - higher HDL-cholesterol, lower LDL-cholesterol

Increased bone mineral density

Improved psychological well being and quality of life

74
Q

Describe the POTENTIAL RISKS OF GH THERAPY IN ADULTS

A

Increased susceptibility to cancer
– no data to support this currently

Expensive – NICE estimated cost of lifelong GH treatment in adult = £42K

Increased risk of cardiovascular accidents
Increased growth of soft tissue e.g. cardiomegaly

75
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

76
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-BP

77
Q

Describe the onset of Simmond’s disease

A

Slow, insidious osnet

78
Q

What are three main types of panhypopituitarism?

A

Simmond’s Disease
Sheehan’s Syndrome
Pituitary Apoplexy

79
Q

Why is GH deficiency less clear in adults

A

No effect on growth- growth plates have fused

Endocrinology year 2 (13 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions