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MRCOG Part one > Endocrinology: Hypothalamus and Pituitary Gland > Flashcards

Endocrinology: Hypothalamus and Pituitary Gland Flashcards

1
Q

Describe the location of the pituitary gland

A

Protrudes from base of hypothalamus, sits in the sella turcica, close proximity to the optic chiasm.

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2
Q

What happens to the pituitary gland in pregnancy.

A

Becomes larger

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3
Q

Which hormones are secreted by the hypothalamus?

A 
Thyrotrophin releasing hormone TRH
Corticotrophin releasing hormone CRH
Somatostatin 
Growth Hormone releasing hormone GHRH
Dopamine
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4
Q

What is the embrological origins of the anterior and posterior lobes of the pituitary gland

A

Anterior lobe: Ectodermal cells of the oropharynx in the primitive gut
Posterior lobe: Neural crest cells

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5
Q

What is 3 elements that regulate the anterior pituitary gland

A

Hypothalamic input
Feedback from hormones
Paracrine and autocrine secretions of the pituitary gland

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6
Q

What hormones do the anterior pituitary gland produce?

A 
Growth Hormone GH
Thyroid stimulating hormone (TSH)
ACTH
FSH
LH
Prolactin
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7
Q

What inhibits GH secretion

A

IGF I - negative feedback

Somatostatic from hypothalamus

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8
Q

What increases GH secretion

What increases sensitivity of GH

A

GHRH

Estadiol

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9
Q

How many pulses of GH secretion a day during adulthood

A

5

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10
Q

GH is produced by what cell, what % of the total cells of the anterior pituitary gland

A

Somatotophs

40-50%

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11
Q

Prolactin is produced by which cells? What % of total cells

A

Lactotrophs

10-15%

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12
Q

What are the effects of prolactin

A

Important in lactation, other roles not clear.
Prolactin levels of non-lactating female same as men
Prolactin receptors on many tissues

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13
Q

Want is the overall effect of hypothalamus hormones on prolactin production?

A

Most inhibitory (different to all other ant pituitary hormones) - somatostatin and dopamine

Prolactin also has negative feedback

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14
Q

What stimulation prolactin

A 
Suckling
TRH
Pregnancy
Ostrogen 
Dopamine D2 receptor antagonist 
Sleep & stress
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15
Q

What cells make gonadatophins? What % of cells

A

Gonadotroph

10-15%

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16
Q

Where does LH bind in the testes/ovaries

A

Testes: Leydig cells
Ovaries: Theca/granulosa cells

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17
Q

Where does FSH bind in the testes/ovaries

A

Testes: Granulosa cells
Ovaries: Theca/granulosa cells

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18
Q

What hormones are produced from the posterior pituitary gland?

A

Arginine vasopressin

Oxytocinin

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19
Q

What is the effect of vasopressin in the kidney?

A

Binds to DCT & collecting ducts, adds aquaporins.

Increased H20 reabsorption and therefore decreased osmolality

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20
Q

What stimulated the release of vasopression

A 
Increased osmolality 
Decreased BP
N+V
Stress 
Exercise
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21
Q

What drinks release of vasopressin

A

Caffeine

ETOH

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22
Q

Where is oxytocin produce

A

Posterior pituitary
Hypothalaus
Peripheral tissue (uterus, plancenta, corpus lute, testies, heart)

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23
Q

What are the effects of oxytocin

A

Lactation

Uterine contraction

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24
Q

What hormonal change are seen at onset of puberty?

A

Increased GnRH production and therefore increased LH and FSH production.

During puberty nocturnal rhythm with rise in LH overnight. This is lost in adulthood.

These stimulate the gonads to release sex steroids and induce physical changes.

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25
Q

What are the easiest signs of puberty in males and females?

A

Males: Tesitcular growth
Females: Breast development

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26
Q

When does mensus start?

A

When ostrogen has stimulated the growth of the uterus enough so that the withdrawal of the hormones cause first mensus

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27
Q

What hormones stimulate hair growth?

A

Gonadal steroids & adrenal steroids

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28
Q

What is considered precocious puberty in males & females?

A

Males < 9 yrs

Females < 8 years

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29
Q

In central precious puberty what is the cause in 90% of girls

A

Idiopathic

Can be associated with CNS abnormalities - tumours, brain injury, congenital brain abnormality

30
Q

What is the deifinition of delayed puberty in males and females

A

Males: Testicular volume increased of less than 4ml by the age of 14years
Females: No breast development by the age of 13-15 years.

31
Q

What is the most common cause of delayed puberty

A

Idiopathic (constitutional) delay (90%) more common in boys

32
Q

What are causes of physiological amenorrhoea

A

Pregnancy

Lactation

33
Q

What is the definition or primary amenorrhoea

A

No menses before the age of 16

34
Q

What is the definition of secondary amenorrhoea

A

No menstruation for at least 3 months in a female previously menstruating/woman of reproductive age

35
Q

If a patient has a uterus but no breast what could be the causes of primary ammenhorea

A 
Hypothalamic hypogonadism - e.g. Kallman syndrome (anosmia) GnRH deficiency 
Hypertrophic hypogonadism (ovarian failure)- seen in Turner Syndrome 45X

before the onset of puberty
If breasts present → after puberty

36
Q

If uterus is absent

A

Androgen insensitivity

Congential abscence of uterus

37
Q

In disease of the hypothalamic-pituitary axis, what is meant by the terms
Primary
Secondary
Tertiary

A

Primary - the end organ (thyroid/ovary/adrenal)
Secondary - the pituitary hormone secretion
Tertiary - Hypothalamus

38
Q

95% cases of acromegaly are cause by what?

A

GH producing pituitary tumour - if > 1cm in diameter macroadenomas

Pituitary tumours usually produce 1 hormone.

39
Q

What are the symptoms of acromegaly

A
  • Arthritis
  • Carpel tunnel
  • Excessive sweating
  • Angina
  • Polydipsia
  • Renal colic
  • Menstrual irregularity
  • Impotence
40
Q

What are the signs of acromegaly

A
  • Enlarged hands and feet
  • Jaw protrusion
  • Osteoarthritis
  • Greesy skin
  • HTN/Cardiomyopathy
  • OSA
  • Neuropathy
  • Renal stones
  • Hypogonadism
41
Q

Treatments for acromegaly + SE

A

Medical/surgical/radiotherapy
Surgey if < 10mm
15-20% radiotherapy have panhypopituitarism with a lag of a few years

42
Q

What are the effects of pregnancy on GH?

A

Induced state of high GH IGF-1 excess

Placenta produced variety GH and GH releasing hormone stimulates liver hepatic IGF-1

43
Q

When does acromegaly present

A

3rd/4th decade of life insidious

Symptoms before diagnosis is 5-10 years

44
Q

How do you diagnose acromegaly

A

OGTT and test serum GH > 12 hours. Should be <2

Acromegaly failure to suppress GH after glucose load, may even increase

45
Q

Causes of hyperprolactinaemia

A

Drugs: Neurloptic agents, dopamine receptor antagonists used as antiemetics metoclopramide → 90%
Primary hypothyroidism
Macroprolactinaemia
Stalk syndrome (interference with dopamine to lactrtrophs)
Pituitary tumour
Renal failure

46
Q

By the end of pregnancy what % of lactotrophs make up the anterior pituitary gland

A

10-20 → 50%

47
Q

In pregnancy where is PRL produced

A

Maternal decidua → no inhibition by dopamine or dopaminergic agnoist drugs

48
Q

What is the presentation of prolactinoma in women/men

A

Women - smaller tumours galactorrhea or ammenorhoea - inhibitory effect of PRL on pituitary gland and ovaries

Men - tend to be bigger and diagnosed later more subtle features of hypogonadism

49
Q

What % of microadenomas <10mm progress to macro adenomas

A

5%

50
Q

Management of prolactinoma

A

Mircoadenoma + no fertility desired → serial PRL and imaging
Microadenoma + fertility desired or macro adenoma → dopamine agonist drugs (cabergoline or bromocriptine)

Features mass effect → surgery

51
Q

Affect of pregnant on prolactinoma

A

Risk enlargement microadenoma 1.3%

Risk of macroadeoma thats untreated 23.2%, treated 2.3%

52
Q

Are bromocriptine and cabergoline safe in pregnancy

A

Yes

53
Q

What are the features of craniopharygioma?

A

Slow growing
Extra axial
Epithelial-squamous
Calcified
Arise from remnant of craniophargeal duct/Rathke duct
Benign histology but malignant behaviour → invade surrounding tissue and reoccur despite total resection

54
Q

How do craniopharygiomas cause symptoms in 3 categories?

A
  • Increased intracranial pressure
  • Disrupt the function of pituitary gland resulting in hypopituitarism and diabetes incipidus
  • Compress optic chiasm resulting in visual field defect
55
Q

Appearance of craniopharygiomas on MRI

A

Cystic/lobulated
Filled with oily green fluids seen on MRI

usually picked up < 20

56
Q

Tx of craniopharygiomas

A

Surgery + radiotherapy

Medical Tx - replacing deficient hormone

57
Q

What is the presenting features of diabetes insipidus

A

Poluria

Polyuria

58
Q

2 main categories of diabetes insipidus

A

Central DI → decreased secretion of vasopressin/ADH from hypothalalmus or posterior pituitary gland, increased excretion of water in urine, increased osmalility of blood, thirsty

Nephrogenic diabetes - kidney unresponsive to ADH - hereditary, lithium, chronic renal insufficiency.

59
Q

Treatment of diabetes insidious, what electrolyte must be mointored

A

Desmopressin - Na risk of hyponatraemia

60
Q

What conditions is described by lymphocytes infiltrating the pituitary gland, causing it to enlarge.

Rare condition most often seen in 3rd trimester or postpartum?

A

Lymphocytic Hypophysitis

61
Q

How does Lymphocytic hypophysitis present?

A

Headache, nausea, vomiting, fatigue, hypopituitarism, diabetes incipidous, bitemporal hemianopia

62
Q

What is the Tx for Lymphocytic Hypophysitis

A

High dose steroids + pituitary hormone replacement → 72% need this lifelong

63
Q

What is the cause of sheehan syndrome?

A

During pregnancy 50% growth in the pituitary gland.

Hypotension/severe haemorrhage leads to postpartum pituitary necrosis.

64
Q

Which part of the pituitary gland is most vulnerable to sheenhan syndrome

A

Anterior pituitary gland

65
Q

If 90-95% of the anterior pituitary gland is destroyed how does sheenhans present

A 
PP failure to lactate 
Secondary ammenhorroea 
Loss axially/pubic hair
Genital and breast atrophy 
Secondary hypothyroidism 
Adrenocoritcol insufficiency 
T1DM → Less insulin requirement
66
Q

What is the description of premature ovarian function

A

Sex steroid deficiency, elevated gonadotrophin & amennorhea below the age of 40

67
Q

% of people of POF with
I) Primary amennhorea
2) Secondary amennhorea

A

1) 10-30%

2) 5-20%

68
Q

After Dx of POF how long can intermittent ovarian function occur?

A

15 years

69
Q

What are the long term health risks of POF

A

Osteoporosis
Cardiovascular disease
Stroke
Cancer

70
Q

Causes of POF

A

Mostly unexplained
X chromsome abnormality (Turner 45,X) triple x syndrome, fragile X syndrome
Autoimmune - +ve antiovarian antibodies
Iatrogenic (pelvic surgery, raiodtherapy, chemo)
Environmental (viral)

71
Q

Investigations to consider for POF

A

2 x FSH measurements a few weeks apart - >40IU/L
Consider autoimmune screen - thyroid and adrenal autoantibodies
If Fhx consider genetic screening

72
Q

3 main components to managing POF

A

1) Medical Tx - replacing hormones
2) fertility preservation - oocyte donation
3) Psychological support
4) Long term health → bone support, monitor for other autoimmune conditions

MRCOG Part one (28 decks)

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