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Endocrinology > Hyposecretion of anterior pituitary hormones > Flashcards

Hyposecretion of anterior pituitary hormones Flashcards

1
Q

Panhypopituitarism

Simmond’s disease

A

Decreased production of all anterior pituitary hormones

-congenital (rare) or acquired (common)

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2
Q

Hypopituitarism

A

Decreased production of a specific anterior pituitary hormone

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3
Q

Congenital panhypopituitarism

A
  • rare
  • typically caused by mutations of transcription factor genes needed for normal anterior pituitary development (eg: PROP1)
  • Patients are deficient in GH and at least 1 more anterior pituitary hormone
  • patients present with short stature from GH deficiency
  • pituitary MRI shows hypoplastic (not developed properly) anterior pituitary gland
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4
Q

Acquired panhypopituitarism

A

-Common
Can result from:
Tumours (most common=squash anterior pituitary gland to prevent hormone release)
-hypothalamic (craniopharyngiomas=benign brain tumours)
-pituitary (adenomas, metastases, cysts)
Radiation (more common cause now increased cancer survival rate=late effects of cancer treatment impacting adult life)
-hypothalamic/pituitary damage (GH most vulnerable, TSH relatively resistant)
Infection
-eg: meningitis
Traumatic brain injury
Infiltrative disease
-often involves pituitary stalk from which pituitary gland hangs from (eg: neurosarcoidosis)
Inflammatory (autoimmune destruction)
-hypophysitis= inflammation of the pituitary gland
Pituitary apoplexy
-damage from haemorrhage (or less commonly infarction)
Peri-partum infarction
-Sheehan’s syndrome

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5
Q

Panhypopituitarism presentation

A

SYMPTOMS RESULT FROM HORMONE DEFICIENCIES

  • FSH/LH deficiency gives secondary hypogonadism->missing signals to gonads (ovaries and testes) to synthesise oestrogen and testosterone (reduced libido, secondary amenorrhoea, erectile dysfunction)
  • ACTH deficiency gives secondary hypoadrenalism-> reduced ACTH signal so reduced cortisol released from adrenal cortex=cortisol important for staying well in terms of energy, getting out of bed etc(fatigue)
  • TSH deficiency gives secondary hypothyroidism (fatigue, weight gain)
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6
Q

Sheehan’s syndrome/

A
  • Post-partum hypopituitarism secondary to hypotension/severe blood loss (post partum haemorrhage=heavy bleeding after birth)
  • less common in developed countries as good obstetric care
  • anterior pituitary gland enlarges in pregnancy because lactotrophs get big to prepare for large prolactin production needed for breastfeeding (lactotroph hyperplasia)
  • pituitary stalk has blood supply to pituitary gland (particularly anterior pituitary gland)
  • Haemorrhage
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7
Q

Sheehan’s syndrome presentation

A
  • TSH/ACTH/GH deficiency: lethargy, anorexia, weight loss
  • Prolactin deficiency: failure of lactation
  • FSH/LH deficiency: failure to resume menses post-delivery

POSTERIOR PITUITARY GLAND USUALLY UNAFFECTED

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8
Q

Pituitary apoplexy

A
  • due to intra-pituitary haemorrhage or infarction (less common cause)
  • dramatic presentation in patients with pre-existing pituitary tumours (patients typically have this pre-existing adenoma)
  • haemorrhage into pituitary gland may be first presentation of pituitary adenoma
  • can be precipitated by anti-coagulants
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9
Q

Pituitary apoplexy presentation

A
  • HALLMARK PRESENTATION: severe sudden onset headache (bleed into anterior pituitary gland stretches dura to give headache)
  • Bitemporal hemianopia-> loss of outer fields of vision (resulting from compressed optic chiasm due to enlarged pituitary gland=loss of normal space between pituitary gland and optic chiasm)

Cavernous sinus surrounding pituitary gland contains many cranial nerves-> enlarged pituitary can squash these cranial nerves

  • Diplopia (CN IV, CN VI) due to cavernous sinus involvement= double vision
  • Ptosis (CN III) due to cavernous sinus involvement= upper eyelid drooping
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10
Q

Hypopituitarism diagnosis (biochemical)

A

1) Measure basal plasma concentration of pituitary/target endocrine gland hormones (blood sample)
-interpretation limited are hormone profiles are up and down->do not know if measurement of low anterior pituitary hormone is because it is a genuine deficiency or if you have caught the bottom of the peak in the pulsatile profile (different measurements at different times)
HORMONE PROFILES:
-GH/ACTH=pulsatile (cortisol measured as surrogate in ACTH instance)
-cortisol=high right at start of day and decreases as day goes by until low when sleeping (may be undetectable depending on the time of day)
-FSH/LH=cyclical
-T4=circulating half life of 6 days

2) Stimulated (‘dynamic’) pituitary function tests
- performed when patient is well to determine if pituitary gland is functional
- ACTH and GH are both stress hormones (increasing in times of stress, particularly in intercurrent illness)
- Induce this stress by administering insulin to cause hypoglycaemia (insulin-induced hypoglycaemia where glucose <2.2 mmol/L)
- Insulin co-administered alongside TRH and GnRH (TRH should stimulate TSH release and GnRH should stimulate FSH/LH release)
- Hypoglycaemia stimulates GH and ACTH release to increase blood glucose levels

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11
Q

Hypopituitarism diagnosis (radiological)

A
  • Pituitary MRI (looks at pituitary gland in detail=CT not effective for this)
  • May reveal specific pituitary pathology (eg: haemorrhage (apoplexy), adenoma, empty sella etc)
  • Pituitary MRI may show white crescent shaped area=posterior bright spot representing posterior pituitary gland (not found in every individual)
  • Pituitary gland sits in sella turcica (sphenoid bone depression)=if pituitary MRI shows empty sella with a thin rim of pituitary tissue, hypopituitarism is likely
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12
Q

Causes of short stature

A

-Genetic: Down’s syndrome, Turner’s syndrome, Prader-Willi syndrome
-Emotional deprivation: chronic stress (shuts down hormone axis)
-Systemic disease: Cystic fibrosis, Rheumatoid arthritis
-Malnutrition
-Malabsorption: Coeliac disease (need to absorb calories and nutrients to grow properly)
Endocrine disorders: Cushing’s syndrome, Hypothyroidism, GH deficiency, poorly controlled T1DM
Skeletal dysplasia: (not related to endocrine dysfunction) Achondroplasia (form of short-limbed dwarfism with FGF3 mutation resulting in short limbs with average trunk size), osteogenesis imperfecta

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13
Q

Growth hormone (somatotrophin) deficiency in children

A

Results in short stature

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14
Q

Growth hormone (somatotrophin) deficiency in adults

A

Less clear effects compared to children (adult growth already complete)

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15
Q

Growth hormone therapy

A

Preparation: human recombinant GH (SOMATOTROPIN)
Administration: daily subcutaneous injection, monitor clinical response and adjust dose to IGF-1 (produced by liver in response to GH)

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16
Q

Benefits of growth hormone therapy in adults

A
  • Improved body composition (decreased waist circumference, less visceral fat which is beneficial for the cardiovascular system)
  • Improved muscle strength and exercise capacity
  • More favourable lipid profile (higher HDL-cholesterol and lower LDL-cholesterol)
  • Increased bone mineral density
  • Improved psychological well being and quality of life
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17
Q

Risks of growth hormone therapy in adults

A
  • Increased cancer suscepitibility (no supporting data currently)
  • Expensive (lifelong GH treatment in adults ~ £42k=estimated by NICE)
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18
Q

Signs and symptoms of GH deficiency in adults

A

VAGUE PRESENTATION

  • Reduced lean mass, increased adiposity, increased waist:hip ratio
  • Reduced muscle strength and bulk (reduced exercise performance)
  • Bad lipid profile=decreased plasma HDL-cholesterol and raised LDL-cholesterol
  • Impaired psychological well being and reduced quality of life
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19
Q

Hormone replacement therapy in hypopituitarism (ACTH deficiency)

A
  • Hydrocortisone replacement

- Check: serum cortisol

20
Q

Hormone replacement therapy in hypopituitarism (TSH deficiency)

A
  • Thyroxine replacement

- Check: serum free T4

21
Q

Hormone replacement therapy in hypopituitarism (LH/FSH deficiency in women)

A
  • HRT (estradiol plus progestagen replacement)

- Check: symptom improvement, withdrawal bleeds

22
Q

Hormone replacement therapy in hypopituitarism (LH/FSH deficiency in men)

A
  • Testosterone replacement

- Check: symptom improvement, serum testosterone

23
Q

Hormone replacement therapy in hypopituitarism (GH deficiency)

A
  • GH replacement

- Check: IGF-1, growth chart (children)

24
Q

Adenohypophysis

A

Anterior pituitary gland composed of glandular tissue

25
Q

The 5 anterior pituitary hormones

A
  • FSH/LH
  • Prolactin
  • GH
  • TSH
  • ACTH
26
Q

The growth axis

A
  • Hypothalamus synthesises GHRH which promotes GH release from the anterior pituitary gland
  • Somatostatin is also produced from the hypothalamus and stops GH release from the anterior pituitary gland
  • Both GHRH and Somatostatin regulate GH secretion from the anterior pituitary gland
  • GH signals liver to synthesise somatomedins (mainly IGF-1, IGF-2 is important in fetal growth)
27
Q

Causes of short stature in children

A
  • Problem with hypothalamus (GHRH production)=Prader Willi Syndrome
  • Not enough GH produced (problem with anterior pituitary gland)=Pituitary dwarfism
  • Problem with GH receptor=Laron dwarfism
28
Q

Achondroplasia

A
  • form of short-limbed dwarfism
  • mutation in FGF3 (Fibroblast Growth Factor Receptor 3)
  • abnormality in growth plate chondrocytes (impaired linear growth)
  • patient present with average sized trunk but short arms/legs
  • no problem with endocrine system
29
Q

Pituitary dwarfism

A

Problem with GH production from somatotrophs in the anterior pituitary gland (childhood GH deficiency)

30
Q

Laron dwarfism

A
  • mutation in GH receptor means it does not work properly
  • enough GH production from somatotrophs in anterior pituitary gland but problem with GH receptor means signal not sent to liver to synthesise IGF-1 (low IGF-1 levels)
  • growth happens through combination of GH and IGF-1
  • Treatment: IGF-1 infections in childhood can increase height
31
Q

Mid parental height

A

Predicated adult height based on father’s and mother’s height (genetic programming accountable for this)

32
Q

Monitoring height in children

A

USE GROWTH CHART

-a drop of more than 2 centiles is flagged on the curve

33
Q

Causes of acquired GH deficiency (short stature) in adults

A
  • typically caused by injury to hypothalamus or anterior pituitary gland that makes you not able to grow anymore
  • Eg: trauma, pituitary tumour, pituitary surgery, cranial radiotherapy etc
34
Q

GH deficiency diagnosis

A
  • Use GH provocation tests (eg: GH stimulation test)

- Can’t measure random GH as pulsatile (up and down all day)

35
Q

GH provocation tests

A
  • Give combination of GHRH and the amino acid Arginine (intravenously administered in adults, children given marmite)-> combination more effective than alone
  • GHRH and arginine= potent stimulus of GH release by inhibiting somatostatin release (if GH levels do not increase-> problem synthesising GH)
  • Give insulin intravenously=stimulates hypoglycaemia which should stimulate GH and ACTH release if no problem
  • Give glucagon (intramuscular)->administation causes vomiting and stress of vomiting believed to drive ACTH and GH release
  • Exercise->effective GH stimulation in children but not adults (eg: 10 min step climbing)

IN ALL TESTS, MEASURE PLASMA GH LEVELS BEFORE AND AFTER PROVOCATION (observe if GH synthesis and secretion has increased or if the patient is GH deficient)

36
Q

Chain of command

A
  • Starting point of hypothalamus which synthesises releasing/inhibiting hormones (hypothalamic signals)
  • Anterior pituitary gland synthesises specific anterior pituitary hormone in response to releasing/inhibiting hormone
  • Anterior pituitary hormone tells endocrine gland (eg: thyroid, gonads, adrenal cortex) to synthesise and release primary hormone
37
Q

Primary endocrine gland disease

A

-problem/disorder with endocrine gland itself

38
Q

Secondary endocrine gland disease

A
  • problem/disorder with signal from anterior pituitary gland to the endocrine gland
  • not problem with endocrine gland but endocrine gland does not work as not receiving signals from anterior pituitary gland (anterior pituitary hormone AND primary hormone at low levels)
39
Q

Vulnerability of endocrine system

A
  • Very vulnerable to autoimmune destruction (eg: T1DM)

- In autoimmune disease, the body attacks itself rather than attacking the foreign antigens

40
Q

Effectiveness of hormone replacement therapy

A
  • Hormones typically pulsatile=depending on time
  • replacement is steady so can’t exactly mimic this biology
  • can’t completely return to quality of life before dysfunctional pituitary gland
41
Q

ACTH deficiency

A

Replacement:
-Hydrocortisone tablet (given several times a day with largest dose in morning to mimic diurnal cortisol variation)=replaces cortisol
Check:
-measure serum cortisol released from adrenal cortex (surrogate as ACTH measurement difficult)

42
Q

TSH deficiency

A

Replacement:
-Thyroxine
Check:
-serum free T4 (majority of T3 converted to T4 by enzymes in body)

43
Q

LH/FSH deficiency in females

A 
Replacement:
-HRT (E2 plus oestrogen)
Check:
-symptom improvement
-withdrawal bleeds (need withdrawal bleed each month because of intact uterus-> unopposed oestrogen gives increased endometrial cancer risk)
44
Q

LH/FSH deficiency in males

A 
Replacement:
-Testosterone (gel/patch/injection)
-different regiment for inducing sperm production (LH and FSH injections to harvest sperm in short time period)
Check:
-symptom improvement
-serum testosterone
45
Q

GH deficiency

A

Replacement:
-daily GH injections
Check:
-measure IGF-1 levels in adults to guide GH replacement (GH from anterior pituitary gland signals liver to synthesise IGF-1)
-measure growth on growth chart for children

46
Q

Short stature

A

<2 standard deviations below mean height for children of that age and sex

47
Q

Growth hormone secretion in response to hypoglycaemia

A

INSULIN TOLERANCE TEST

  • Intravenous insulin given into cannula in arm at 0 mins
  • normal response= anterior pituitary gland makes lots of GH in response to hypoglycaemic stimulus
  • GH deficiency= GH not synthesised and secreted in response to hypoglycaemic stimulus
  • NICE sets cut-off at 3mcg/L (GH deficiency below cut off warrants treatment-> important because GH therapy is expensive)

Endocrinology (18 decks)

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