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1
Q

complications of pituitary tumours

A
  1. press on local structures eg optic chiasm
  2. hypopituitism
  3. hyperpituitism (acromegaly, cushings, prolactinoma)
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2
Q

anterior pituitary hormones

A

FLAT PeG

GnRH > FSH* + LH* > act on gonads for germ cell development and hormone secretion

CTH > ACTH* > acts on adrenal gland to produce corticosteroids

TRH > TSH* > acts on thyroid to release T3, T4

DA > prolactin* > acts on mammary glands for milk production and breast development

endorphins

GHRH > GH* > stimulates IGF-1 production, growth

(ones with * are the ones released from anterior pituitary)

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3
Q

functions of cortisol

A

-increases insulin resistance
-suppresses immune response
-upregulates alpha 1 in arterioles to increase BP
-increases osteoclast activity (so osteoporotic)
-increased protein and carb breakdown

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4
Q

insulin action

A

biphasic release
insulin increases peripheral glucose uptake (glucose> glycogen)

1.glucose binds to GLUT2 receptors on pancreatic beta cells, stimulating insulin release

2.insulin binds to peripheral insulin receptors which activates intracellular tyrosine kinases and cascade resulting in increased GLUT4 channel expression on CSM (so increased peripheral uptake)

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5
Q

posterior pituitary hormones

A

oxytocin (paraventricular nucleus)- milk ejection and labour induction

vasopressin (ADH) (supraorbital nucleus)- recruited when decrease in BV, stress, major RAAS player
-increases APO II expression
-vasoconstricts BV
-increases aldosterone

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6
Q

which region of the adrenal gland releases which hormone

A

go find rex, make good sex

zona glomerulosa- mineralocorticoids (aldosterone)
zona fasciculata- glucocorticoids (cortisol)
zona reticularis- sex hormones (androgens)

salt, sugar, sex, deeper you go the sweeter in gets (moving inwards, controls production of salt etc)

adrenal medulla- adrenaline and noradrenaline

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7
Q

when is cortisol released

A

released with chronic stress and increasing blood sugar

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8
Q

Cushing’s disease/syndrome definition

A

hypercortisolaemia
clinical manifestation of prolonged elevated cortisol
Cushing’s syndrome- abnormal high cortisol of any cause
Cushing’s disease- high cortisol due to high ACTH from pituitary adenoma

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9
Q

Cushing’s epidemiology (G)

A

obesity, diabetes, older women

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10
Q

Cushing’s aetiology (G)

A

ACTH dependent- excessive ACTH from the pituitary gland (pituitary adenoma), or ectopic ACTH producing tumour eg small cell lung cancer, or excess ACTH administration

non ACTH dependent- excess glucocorticoid administration (iatrogenic) eg steroids eg prednisolone or adrenal adenomas

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11
Q

Cushing’s risk factors (G)

A

pituitary adenoma
adrenal adenoma
corticoid steroids
hypertension
uncontrolled diabetes

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12
Q

Cushing’s presentation

A

big in the middle, thin limbs, signs of stress

-central obesity
-round moon face
-buffalo hump (fat on back of neck)
-abdominal straie
-osteoporosis
-hypertension
-hyperglycaemia
-depression
-easy bruising and poor skin healing
-cardiac hypertrophy
-irregular periods
-erectile dysfunction
-hirsutism

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13
Q

Cushing’s pathophysiology (G)

A

negative feedback:
low blood cortisol > increased CRH from hypothalamus> ACTH from pituitary > increased cortisol from adrenal gland > negative feedback slows ACTH production when cortisol levels are sufficient

released with circadian rhythm- peaks in the mornings, least at night. With Cushing’s this rhythm is lost so unregulated CRH, ACTH, cortisol levels

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14
Q

Cushing’s investigations (G)

A

1: random plasma cortisol (midnight), if positive ACTH plasma
urinary free cortisol (24 hours)

gold:
dexamethasone overnigth test
dexamethasone is a glucocorticoid so should trigger negative feedback loop
give 1mg at 11pm and measure control, measure again at 8AM
with Cushings’s: not suppressed, >50nanomol/L
without Cushing’s: suppressed (negative feedback)

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15
Q

Cushing’s management (G)

A

stop taking steroids
-Cushing’s disease: transspheinoidal resection to remove pituitary adenoma
-if adrenal- adrenalectomy
-ectopic ACTH- remove neoplasm

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16
Q

Cushing’s complications (G)

A

osteoporosis, type 2 diabetes,

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17
Q

Cushing’s prognosis

A

untreated- 50% mortality in 5 years
treated is good prognosis

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18
Q

Acromegaly definition (G)

A

excess secretion of growth hormone from a pituitary tumour or hyperplasia results in bone and soft tissue overgrowth

acromegaly in adults

gigantism in children (before epiphyseal plates fuse)

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19
Q

acromegaly epidemiology (G)

A

2-13/100000

effects men and women equally

median age of diagnosis: 50s

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20
Q

acromegaly aetiology (G)

A

Unregulated GH secretion due to anterior pituitary adenoma
rarely ectopic GH from non-endocrine tumour eg lung

21
Q

acromegaly risk factors (G)

A

MEN-1
(multiple endocrine neoplasia)

22
Q

Acromegaly pathophysiology (G)

A

GHRH (released from hypothalamus) > excessive GH (anterior pituitary) > excessive production of IGF-1 (insulin growth factor 1)

IGF-1 stimulates growth of bone and muscle, increased protein synthesis, lipolysis

23
Q

acromegaly presentation (G)

A

-box jaw
-coarse facial features

-spade like hands and feet
-increase in shoe size

-interdental separation
-macroglossia

-snoring
-deep voice
-obstructive sleep apnoea
-sweating

-arthritis
-back pain
-arthralgia
-carpal tunnel

tumour related symptoms:
-visual disturbances (bitemporal hemianopia)
-headaches

24
Q

Acromegaly investigations (G)

A

1st:
serum IGF-1 (raised)
random serum GH (raised, not diagnostic as fluctuates with circadian rhythm)

gold:
oral glucose tolerance test
(failure of glucose to suppress GH)

other:
MRI pituitary

25
acromegaly management (G)
1st: transsphenoidal removal of pituitary tumour medication: 2nd: somatostatin analogue to block GH release eg octreotide 3rd: dopamine agonist to block GH release eg carbergoline 4th: growth hormone receptor antagonist: pegvisomant radiotherapy
26
acromegaly monitoring and prognosis (G)
-lifelong monitoring of IGF-1 and GH -prognosis good with surgery
27
acromegaly DD (G)
pseudo-acromegaly
28
Acromegaly complications (G)
T2DM, sleep apnoea
29
prolactinoma definition (G)
benign lactotroph adenoma releases excess prolactin, resulting in hyperprolactinaemia
30
prolactinoma epidemiology (G)
more women than men, child bearing years, 20-40, presents earlier in women than men
31
prolactinoma aetiology (G)
prolactin is released from the anterior pituitary and is inhibited by dopamine from the hypothalamus excess prolactin: pituitary adenoma, other non-functioning tumour compressing the infundibulum lack of dopamine: reduced dopamine levels, drug induced: dopamine antagonist or antipsychotics
32
Prolactinoma risk factors (G)
women 20-50, pregnant, oestrogen therapy men 30-60
33
prolactinoma presentation
infertility loss of libido tumour: visual disturbances, headaches women: amenorrhea/ oligomenorrhea galactorhhea men: gynecomastia hypogonadiam osteoporosis erectile dysfunction
34
prolactinoma pathophysiology (G)
increased prolactin inhibits GnRH decreased GnRH > decreased LH + FSH > decreased oestrogen/ progesterone in women, less testosterone in men prolactin stimulates mammary glands > galactorrhoea can be micro <10mm or macro
35
prolactinoma investigations (G)
1st/gold: basal serum prolactin (elevated) other: pituitary MRI, CT head
36
prolactinoma management
dopamine agonist: 1.carbergoline, 2.bromocriptine transsphenoidal removal of tumour hormone replacement therapy radiotherapy
37
prolactinoma complications (G)
infertility sight loss raised ICP
38
prolactinoma DD (G)
drug induced hyperproclactinaemia primary hypothyroidism renal insufficiency pregnancy PCOS
39
Adrenal insufficiency/ Addison's disease definition (G)
Insufficient production of steroids (mainly cortisol (glucocorticoid), aldosterone (mineralocorticoid) from the adrenal gland. Steroids are essential to life so can be fatal primary- Addison's disease. Due to autoimmune destruction of the adrenal gland secondary- pathology of the pituitary gland results in inadequate ACTH stimulating the adrenal gland tertiary- pathology of the hypothalamus results in inadequate CRH release CRH> ACTH> cortisol and aldosterone
40
Adrenal insufficiency/ Addison's disease epidemiology (G)
more women than men mostly autoimmune 30-50
41
Adrenal insufficiency/ Addison's disease aetiology (G)
1. -developed world: autoimmune destruction of adrenal antibodies (21-alpha-hydroxylase) results in destruction of adrenal gland -developing world: TB -adrenal metastases eg liver, lung, breast -adrenal haemorrhage (AKA waterhouse-Friderichsen syndrome commonly caused by meningococcol menigitis) -antiphospholipid syndrome 2. pituitary insufficiency due to long term steroid (iatrogenic) use or pituitary adenoma 3. hypothalamus insufficiency due to long term steroid use or radiotherapy
42
Adrenal insufficiency/ Addison's disease risk factors (G)
female adrenal haemorrhage adrenocortical antibodies other autoimmune conditions
43
Adrenal insufficiency/ Addison's disease pathophysiology
1. autoimmune destruction of adrenal antibodies (21-alpha-hydroxylase), destruction of adrenal gland so less cortisol/aldosterone production. This results in excess ACTH as lack of negative feedback. Rising ACTH acts on melanocytes to produce melanin resulting in hyperpigmentation 2. Pituitary/ hypothalamus insufficiency causes HPA axis suppression, causing decreased ACTH so no hyperpigmentation
44
Adrenal insufficiency/ Addison's disease presentation (G)
remember 4Ts- tanned, tired, tearful, thin -hyperpigmentation (tanned, bronzed, in palmar creases especially) -vitiligo -weight loss/ anorexia -tearful/ depressed -loss of axillary/ pubic hair in women -tired -N+V -weakness -abdominal cramps -postural hypotension -hypoglycaemia -headaches
45
Adrenal insufficiency/ Addison's disease investigations
1: serum electrolytes (Na+ low, K+ high, due to low aldosterone, high glucose) morning serum cortisol (low) plasma ACTH (1-high, 2-low) gold: ACTH stimulation Short Synacthen test (to test adrenal reserve) -measure basal cortisol at 9am (highest here, if low, major problem) -administer synacthen -measure cortisol 30 and 60 mins after failure for ACTH to stimulate rise in cortisol (less than double baseline) shows primary adrenal insufficiency <500nmol/l. If over 580 can rule out addisons other: renin: aldosterone (renin high in addisons, aldosterone low) FBC (anaemia)
46
Adrenal insufficiency/ Addison's disease DD (G)
1/2/3 adrenal insufficiency, adrenal suppression due to glucocorticoid drugs, hyperthyroidism
47
Adrenal insufficiency/ Addison's disease management (G)
1: hydrocortisone (glucocorticoid to replace cortisol) fludrocortisone (mineralocorticoid to replace aldosterone) -will correct Na K+ and postural hypotension double steroid use in illness/ trauma/ infection/ stress as cortisol needed in stress respone patients given steroid card and emergency ID to alert emergency services as dependent on steroids for life secondary: long term steroids weaned off, treat cause
48
Adrenal insufficiency/ Addison's disease red flags (G)
trauma infection dehydration ending steroid treatment
49
Adrenal insufficiency/ Addison's disease complications (G)
Addisonian/ adrenal crisis: -severe adrenal insufficiency (esp cortisol), -presents with shock, reduced consciousness, hypotension, hypoglycaemia, hyponatraemia, hypokalaemia, -management: immediate IV hydrocortisone, IV fluid resus, correct hypoglycaemia with dextrose - shock, coma, death if not treated

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