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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,

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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

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3
Q

What is important to remember about aldosterone

A

Released is under the control of renin and not ACTH

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4
Q

Summarise the hypothalamo-pituitary- thyroid axis

A

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

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5
Q

How do autoimmune diseases effect the endocrine glands

A

The endocrine system is very scuppered by autoimmune diseases

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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)

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7
Q

Define panhypopituitarism

A

DECREASED PRODUCTION OF ALL ANTERIOR PITUITARY HORMONES (PANHYPOPITUITARISM)

PAN= ALL OR COVERING

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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

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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

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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.

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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

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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.

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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).

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14
Q

What was panhypopituitarism originally called

A

Simmond’s disease

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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
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16
Q

What is a feature of the neurohypophysis

A

neural tissue and so is the same colour as the brain

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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

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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

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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

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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

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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

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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

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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

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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

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25
Describe the ease of seeing the symptoms of sheehan's syndrome
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.
26
What should you see between the optic chiasm and the pituitary gland
Black space- CSF
27
Describe the effects of a pituitary tumour or pituitary apoplexy on the optic chiasm and relate this to the symptoms observed and the anatomy.
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!!
28
Why is a single measurement of most hypothalamic hormones not useful- essentially why is the interpretation of anterior pituitary hormones limited
Most hypothalamic hormones tend to be released in pulses
29
Summarise the biochemical diagnosis of hypopituitarism
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
30
What do we use as a surrogate to measure ACTH
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
31
What type of test do you do to test if someone is producing a hormone?
Stimulation/provocation test
32
How are the releasing hormones administered in these tests
Intravenous
33
Summarise the stimulated pituitary function tests
- 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
Why do the stimulated pituitary function tests work
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
Describe the inadequacy of the use of CT scans to look at the pituitary gland
May be able to see blood in pituitary fossa- but nothing more- MRI best
36
What is the name given to the secondary endocrine gland failure that results from a lack of corticotrophin release from the pituitary?
Hypoadrenocorticalism
37
Summarise the radiological diagnosis of hypopituitarism
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
How can we easily identify the pituitary gland on an MRI in some patients
The posterior bright spot (although not every one may have this)
39
What is the issue with treatment of pituitary diseases
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
Describe hormone replacement for the deficiencies in different hormones
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
Why don't we replace ACTH directly and when is the biggest dose of hydrocortisone given
ACTH is very pulsatile- so we replace cortisol instead | Biggest dose given in the morning- to mimic the diurnal variation of cortisol
42
Why don't we measure TSH in secondary hypothyroidism (I,e hypopituitarism)
Because TSH won't be low | Measure T4 as most T3 is converted to T4
43
Why don't we give oestrogen unopposed
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
Consequence of no LH
Can't make testosterone | Need different regimen to improve sperm count
45
Summarise growth hormone (somatotrophin deficiency)
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
What are the effects of a lack of somatotrophin in children and in adults?
Children – stunted growth (pituitary dwarfism) | Adults – loss of GH effects are uncertain
47
State some other causes of short stature
``` Genetic Malnutrition Emotional deprivation Endocrine disorders Systemic disease Malabsorption Skeletal dysplasias ```
48
Describe the genetic causes of short stature
Down’s syndrome, Turner’s syndrome, Prader Willi syndrome
49
Describe emotional deprivation as a cause of short stature
Activates the stress axis- which can shut down Growth Hormone
50
Describe malnutrition and malabsorption as a cause of short stature
``` Need calories growth In malabsorption (i.e coeliac disease)- can't absorb the calories needed for growth ```
51
Describe endocrine disorders and skeletal dysplasias as a cause of short stature
Endocrine Disorders: Cushing’s syndrome, Hypothyroidism, GH deficiency, poorly controlled T1DM Skeletal dysplasias: Achondroplasia, osteogenesis imperfecta
52
What are most endocrine-related causes of short statue due to (with reference to the HP axis)?
Decreased production of GHRH
53
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
IGF I = insulin-like growth factor I It is produced in the LIVER It mediates growth effects IGF2 is also produced
54
Describe laron dwarfism
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
Why are the Pygmies in Africa naturally short
Their IGF I doesn’t function properly
56
Summarise the different causes of short stature
§ 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
Describe PWS
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
Summarise Laron dwarfism
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
Describe mid parental height
MID PARENTAL HEIGHT A predicted adult height – based on father’s & mother’s height
60
When is short stature an issue
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
Summarise the diagnosis of short stature
§ 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
Describe the causes of GH deficiency in adults
· 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
Summarise the diagnosis of GH deficiency
Random GH little use – pulsatile PROVOCATIVE CHALLENGE (i.e. STIMULATION) TEST
64
What is the gold standard method of testing the ability of the pituitary to release growth hormone?
Insulin-induced hypoglycaemia | Hypoglycaemia is a potent stimulus for growth hormone release
65
State three other triggers for an increase in GH release.
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
Summarise the GH provocation tests
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
Describe how the insulin provocation test can be used to diagnose acquired GH deficiency in adults
§ 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
How can glucagon stimulate GH release
Powerful stimulus to make GH and ACTH | Induced vomiting in patients- which probably drives up GH and ACTH.
69
Summarise GH therapy
§ 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
Describe the absorption, metabolism and duration of action of the drug.
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
How is the human recombinant GH used in GH therapy administered and how frequently must it be given?
Subcutaneous or Intramuscular | It is given daily or 4/5 times a week
72
Describe the signs and symptoms of GH deficiency in adults
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
Describe the benefits of GH treatment in adults
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
Describe the POTENTIAL RISKS OF GH THERAPY IN ADULTS
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
State some adverse effects of GH therapy.
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
How can you diagnose GH deficiency in adults?
Lack of response to GH stimulation test (e.g. insulin-induced hypoglycaemia) Low plasma IGF I Low plasma IGF-BP
77
Describe the onset of Simmond's disease
Slow, insidious osnet
78
What are three main types of panhypopituitarism?
Simmond’s Disease Sheehan’s Syndrome Pituitary Apoplexy
79
Why is GH deficiency less clear in adults
No effect on growth- growth plates have fused

Endocrinology year 2 (13 decks)

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