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(endo) hyperadrenalism Flashcards

1
Q

how do you test for adrenal hypofunction?

A

assess cortisol levels when they should be high

i.e. 9am cortisol

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2
Q

how do you test for adrenal hyperfunction?

A

assess cortisol levels when they should be low

i.e. midnight cortisol

(NB - different for night-shift workers)

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3
Q

what are the clinical features of Cushing’s syndrome?

A

centripetal obesity

moon face

buffalo hump

proximal myopathy

red striae

thin skin

easy bruising

hypertension and hypokalaemia

osteoporosis

diabetes

depression

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4
Q

how does excess cortisol lead to hypertension?

A

cortisol, when in excess, acts on the mineralocorticoid receptor to have aldosterone-like effects

(i.e. increased sodium, and therefore water reabsorption = hypertension)

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5
Q

list four causes of Cushing’s syndrome

A

taking too many steroids

pituitary-dependent Cushing’s disease

ectopic ACTH from lung cancer

adrenal adenoma secreting cortisol

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6
Q

list the investigations carried out to determine the PRESENCE of Cushing’s syndrome

A

1) 24 hour urine collection for urinary free cortisol
2) blood diurnal cortisol levels
3) low dose dexamethasone suppression test

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7
Q

what tests results are expected in a patient with Cushing’s syndrome?

A

1) 24h urine collection = consistently elevated levels of cortisol
2) blood diurnal cortisol levels = consistently elevated levels of cortisol
3) low dose dexamethasone = failure to suppress elevated cortisol levels

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8
Q

explain how a low dose dexamethasone suppression test works

A

dexamethasone = artificial glucocorticoid

when it is given, the pituitary gland detects it and via negative feedback, inhibits ACTH secretion, suppressing cortisol biosynthesis

if, despite dexamethasone administration, cortisol levels remain elevated, Cushing’s syndrome is present (can be ANY of the four main causes)

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9
Q

how does cortisol compare to dexamethosone?

A

dexamethasone is formed when fluorine is added to cortisol, making it a lot more potent & long-acting

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10
Q

how is a low dose dexamethasone suppression test given?

A

0.5mg every 6 hours for 48 hours

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11
Q

what is the expected cortisol level following a low dose dexamethasone suppression test?

A

cortisol levels following a LDDST should fall to ZERO (!!)

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12
Q

how is a pituitary adenoma treated?

A

hypophysectomy = removal of the pituitary gland

most commonly via the transphenoidal route

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13
Q

why can patients with Cushing’s present with pitting oedema?

A

Cushing’s
= high cortisol
= increased sodium and therefore water retention
= increased blood pressure in the vessels
= increased risk of fluid leakage into surrounding tissue
= oedema

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14
Q

what measures are taken before pituitary surgery to treat Cushing’s disease?

A

prior to the hypophysectomy, usually drugs are given to control excess cortisol levels

1) enzyme inhibitors
2) receptor blocking drugs

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15
Q

which two drug types are normally given to control excess cortisol levels in Cushing’s?

A

1) enzyme inhibitors

2) receptor blocking drugs

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16
Q

which two disease are associated with hypersecretion of hormones in the adrenal cortex?

A

1) Conn’s syndrome = excess aldosterone

2) Cushing’s syndrome = excess cortisol

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17
Q

which two enzyme inhibitors are used to treat Cushing’s disease?

A

1) metyrapone = inhibition of 11B-hydroxylase

2) ketoconazole = inhibition of 17a-hydroxylase

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18
Q

explain the mechanism of action of metyrapone

A

inhibition of 11B-hydroxylase

= inhibits biosynthesis of cortisol + corticosterone (and therefore aldosterone)

= reduced cortisol levels in Cushing’s

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19
Q

how does metyrapone affect the adrenal gland?

A

in the zona glomerulosa = arrests steroid synthesis in the 11-deoxycorticosterone stage

in the zona fasciculata = arrests steroid synthesis in the 11-deoxycortisol stage

= so no aldosterone or cortisol is produced

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20
Q

what are the main uses of metyrapone?

A

1) control Cushing’s syndrome prior to surgery

2) control Cushing’s symptoms after radiotherapy (which is usually slow to take effect)

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21
Q

explain why metyrapone is used to control Cushing’s syndrome prior to surgery

A

1) adjust dose according to cortisol levels (aim for mean serum cortisol 150-300 nmol/L)
2) improves patient’s symptoms and promotes better post-op recovery (better wound healing, less infection)

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22
Q

when using metyrapone, what is the desired cortisol level?

A

aim for a cortisol level of 150-300 nmol/L

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23
Q

what are the metabolic consequences of metyrapone?

A

metyrapone reduces cortisol levels so

1) less protein catabolism
2) less fat lipolysis
3) less hepatic gluconeogenesis

= lower blood glucose levels

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24
Q

explain why patients with Cushing’s syndrome have thin skin

A

in Cushing’s
= excess cortisol
= increased protein catabolism of tissues, collagen and decreased muscle mass
= thin skin + easy bruising

25
Q

explain why patients with Cushing’s syndrome have osteoporosis

A 
excess cortisol causes
1) reduced intestinal calcium absorption
2) more urinary calcium excretion
3) increased compensatory PTH secretion
4) increased bone resorption + decreased bone formation 
= osteoporosis
26
Q

which two adrenal disorders can cause a tan in patients?

explain how in each case

A

1) Addison’s disease = excess aMSH due to increased POMC cleavage to meet increased ACTH demand
2) Cushing’s = if cause is a pituitary adenoma that secretes ACTH excessively (requires more POMC cleavage)

27
Q

what are the main unwanted effects of metyrapone?

A

1) accumulation of 11-deoxycorticosterone = hypertension
2) accumulation of 11-deoxycortisol = increased ACTH levels (tan?)
3) accumulation of 17-OH progesterone = hirsutism

28
Q

how can metyrapone use lead to hypertension?

A

inhibition of 11-hydroxylase

= 11-deoxycorticosterone accumulates and has aldosterone-like (mineralocorticoid) effects

= leading to salt retention, water reabsorption and therefore hypertension

29
Q

how can metyrapone use lead to hirsutism?

A

inhibition of 11-hydroxylase

= 17-OH progesterone accumulates
= increased adrenal androgen production (i.e. testosterone)
= hirsutism

30
Q

explain the mechanism of action of ketoconazole

A

(inhibits steroidogenesis by inhibiting mainly 17-hydroxylase

= inhibiting cortisol production

31
Q

when is ketoconazole normally used?

A

to control Cushing’s syndrome prior to surgery

32
Q

what are the side effects of ketoconazole?

A

hepatotoxicity

= liver damage is possible (can be fatal)

33
Q

how is the hepatotoxicity associated with ketoconazole use managed?

A

monitor liver function weekly, both clinically and biochemically

34
Q

how is Cushing’s treated surgically?

A

pituitary adenoma = transphenoidal hypophysectomy

adrenal adenoma = unilateral/bilateral adrenalectomy

35
Q

how is Cushing’s treated medically?

A

1) metyrapone

2) ketoconazole

36
Q

what is Conn’s syndrome?

A

a syndrome of excess aldosterone

caused mainly by benign adenoma of the zona glomerulosa

37
Q

what causes Conn’s syndrome?

A

benign adrenal cortical tumour of the zona glomerulosa

38
Q

what are the main implications of Conn’s syndrome?

A

hypernatraemia = hypertension

hypokalaemia

39
Q

what is Conn’s syndrome alternatively known as?

A

primary hyperaldosteronism

40
Q

differentiate between primary and secondary aldosteronism

A

primary = problem w the adrenal glands themselves (e.g. adenoma of the zona glomerulosa)

secondary = problem elsewhere in the body that causes excess aldosterone release from the adrenal glands

41
Q

how can primary aldosteronism be confirmed?

A

if primary = then problem in the adrenal glands so RAS (renin-angiotensin system) should be suppressed

42
Q

how is Conn’s syndrome managed medically?

A

1) spironolactone

2) epleronone

43
Q

explain the mechanism of action of spironolactone

A

converted into several active metabolites e.g. canrenone

active metabolites will act as competitive antagonists at the mineralocorticoid receptor

= block Na+ reabsorption and K+ excretion in the collecting duct
(i.e. potassium-sparing diuretic)

44
Q

what are the pharmacokinetics of spironolactone?

A

orally active

highly protein bound and metabolised in the liver

45
Q

what are the side effects of spironolactone?

A

1) menstrual irregularities = acts on the progesterone receptor
2) gynaecomastia = acts to block the androgen receptor

46
Q

why does spironolactone cause menstrual irregularities in women?

A

spironolactone is non-specific and so binds to the progesterone receptor
= causing menstrual irregularities (very common)

47
Q

why does spironolactone cause gynaecomastia in men?

A

spironolactone is non-specific and so binds to and blocks the androgen receptor & therefore androgen production
= gynaecomastia

(spironolactone also is similar to and so can act on the oestrogen receptor)

48
Q

explain the mechanism of action of epleronone

A

like spironolactone, it is also a MR antagonist

BUT is more specific than spironolactone

49
Q

how does eplerenone compare to spironolactone?

A

epleronone is more specific than spironolactone so does not bind to the progesterone/androgen receptors
= so better tolerated

50
Q

what is a phaeochromocytoma?

A

a tumour of the adrenal medulla that secrete catecholamines in excess

(adrenaline & noradrenaline)

51
Q

what are the clinical features of a phaeochromocytoma?

A

when it is a primary tumour = episodic, severe hypertension

usually after abdominal palpation

52
Q

why is episodic hypertension usually seen in patient with phaeochromocytomas upon abdominal palpation?

A

abdominal palpation
= degranulation of the tumour
= sudden release of adrenaline
= sudden, sharp increase in blood pressure

53
Q

why are phaeochromocytomas a medical emergency?

A

the sudden release of loads of adrenaline causes severe, episodic hypertension

= can cause MI/stroke/ventricular fibrillation
= can lead to death

54
Q

how are phaeochromacytomas managed?

A

1) alpha blockade
2) IV fluids
3) beta blockade
4) surgery

55
Q

why can patients with phaeochromacytomas never be operated on immediately?

A

need to be prepped before surgery as anaesthetic administration can precipitate a hypertensive crisis

(tachycardia, pulmonary oedema, vasoconstriction)

56
Q

why is alpha blockade administered first in patients with phaeochromacytomas?

A

to block the effects of adrenaline in case there is accidental degranulation of the phaeo prior to surgery

(NB - alpha adrenoreceptor blocking drug)

57
Q

why are IV fluids given after alpha blockade administration in patients with phaeochromacytomas?

A

after alpha blockade = sudden fall in blood pressure (as adrenaline can no longer be detected by the adrenergic receptors)

this fall needs to be dealt with quickly to prevent a hypotensive crisis so = IV fluid administration

58
Q

why is beta blockade administered in patients with phaeochromacytomas?

A

to prevent tachycardia

brs (phase 1b) (71 decks)

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