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RB Y2 Endocrine - 3 Pituitary > Cushing's Syndrome > Flashcards

Cushing's Syndrome Flashcards

1
Q

what 3 types of steroids does the adrenal cortex produce

A

glucocorticoids

mineralocorticoids

androgens

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2
Q

glucocorticoids

A

eg cortisol

affect carbohydrate, lipid and protein metabolism

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3
Q

mineralocorticoids

A

control Na and K balance eg aldosterone

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4
Q

androgens

A

sex hormones that have a weak effect until peripheral conversion to testosterone and dihydrotestosterone

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5
Q

cushing syndrome

A

the clinical state produced by chronic glucocorticoid excess and loss of the normal feedback mechanisms of the HPA axis and loss of circadian rhythm in cortical secretion

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6
Q

describe cortisol secretion

A
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7
Q

what is the chief cause of cushings syndrome

A

oral steroids

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8
Q

cushing’s disease

A

pituitary adenoma causing increased ACTH

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9
Q

signs due to protein loss

A

myopathy and wasting - proximal

osteoperosis leading to fractures

thin skin, striae and bruising

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10
Q

other signs

A

altered carbohydrate/lipid metabolism, DM, central obesity, intrascapular and supraclavicular fat pads

buffalo hump

altered psyche, depression

moon face

plethoric - florid/red face

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11
Q

how does Cushing’s lead to DM

A

Glucocorticoid excess induces a stimulation of liver gluconeogenesis, and inhibition of insulin sensitivity

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12
Q

how does Cushings cause osteoporosis

A

increased cortisol causes a decrease in calcium

compensatory increase in PTH

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13
Q

what does excess mineralocorticoid cause

A

fluid and sodium retention:

hypertension and oedema

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14
Q

what does excess androgen cause

A

virilism

hirsutism

acne

oligo/amenorrhoea

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15
Q

what are the two ACTH dependent causes

A

cause increased ACTH

Cushing’s disease and ectopic ACTH production

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16
Q

cushing’s disease

A

ACTH secreting pituitary adenoma

more common in females

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17
Q

what are the majority of ACTH secreting pituitary adenomas

A

microadenomas

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18
Q

ectopic ACTH production

A

especially SCLC and carcinoid tumours

seen in the thymus, lung and pancreas

19
Q

what are the ACTH independent causes

A

decreased ACTH due to negative feedback

adrenal adenoma or cancer

adrenal nodular hyperplasia - bilateral macronodular hyperplasia

20
Q

pseudo Cushing’s

A

alcohol and depression and steroid medication can mimic Cushing’s and cause positive screening tests

21
Q

what can alcohol cause

A

cushingoid appearance

22
Q

what does confirmation of Cushing’s rest on

A

demonstrating inappropriate cortisol secretion, not suppressed by exogenous glucocorticoids (eg Dexamethasone)

23
Q

outpatient screening test

A

overnight dexamethasone suppression test

  • 1mg dexamethasone PO at midnight, serum cortisol performed at 8am

normal test/positive suppression: plasma cortisol <100nmol/L

24
Q

what is the problem with overnight dexamethasone suppression test

A

there are some false positives

25
Q

name 2 other screening tests

A

24 hour urinary free cortisol (a total of <250 is normal and a cortisol/creatinine ratio of <25 is normal)

Circadian rhythm (cortisol taken at 0900 then 2400)

  • peaks in the morning and should be virtually 0 at midnight
26
Q

what is the formal diagnostic test

A

48h low dose dexamethasone suppression test

  • normal/positive suppression results in plasma cortisol <50nmol/L on second sample

2 day 2 mg dose

27
Q

what is used to evaluate the pituitary gland

A

MRI scan

28
Q

what is used to lateralize the tumour prior to surgery

A

inferior petrosal sinus sampling

29
Q

DD: what does a low ACTH suggest

A

non-ACTH dependent disease

likely to be adrenal in origin: adrenal adenoma/carcinoma or adrenal nodular hyperplasia

30
Q

DD: what does a high ACTH suggest

A

need to distinguish beween Cushing’s disease and ectopic ACTH

31
Q

DD: what is a classical ectopic ACTH syndrome presentation

A

short history

pigmentation and weight loss

unprovoked hypokalaemia

plasma ACTH levels > 300

32
Q

DD: what does a rise in cortisol and ACTH on a CRH test indicate

A

a pituitary source (rather than ectopic)

33
Q

DD: what is used to distinguish between pituitary and other sources

A

a high dose Dexamethasone test (4x the dose of the low test)

  • failure of significant plasma cortisol suppression indicates an ectopic source of ACTH or an adrenal tumour
34
Q

DD: what should be done if an adrenal tumour is suspected

A

CT the adrenal glands

35
Q

management of Cushing’s disease

A

selective removal of pituitary adenoma (trans-sphenoidally)

bilateral adrenalectomy if the source is unlocatable/recurrence post-op

radiotherapy if recurs

36
Q

trans sphenoidal approach

A

via the nasal cavities and sphenoid sinus

37
Q

management of adrenal adenoma/carcinoma

A

adrenalectomy cures adenomas but rarely cures cancer

radiotherapy if cancer

38
Q

management of ectopic ACTH

A

remove source

or bilateral adrenalectomy

39
Q

metyrapone

A

inhibits cortisol production (and aldosterone to a lesser extent), this resuts in increased ACTH production and increased cortisol precursors

side effects are common

40
Q

when is Metyrapone used

A

if other treatments fail, or when waiting for radiotherapy to work

41
Q

Ketoconazole

A

classic anti-fungal drug

hepatotoxic

42
Q

pasireotide

A

a new somatostatin analogue (blocks receptors 2 and 5)

43
Q

what are the implications of prolonged steroid therapy

A

chronic suppression of pituitary ACTH production (negative feedback) and atrophy of the adrenal cortex.

The implications of this are:

  • One is unable to respond to stress (e.g. illness/surgery)
  • Extra doses of steroid are required when one is ill or having a surgical procedure
  • Steroids must not be stopped suddenly, there must be a gradual withdrawal over 4-6 weeks.

RB Y2 Endocrine - 3 Pituitary (7 decks)

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