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Endo: Sem 2 > Disorders of Adrenal Cortex > Flashcards

Disorders of Adrenal Cortex Flashcards

1
Q

what are the two parts of the adrenal gland?

A

cortex and medulla

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2
Q

what are the three layers of the adrenal cortex?

A

zona glomerulosa - aldosterone
zone fasiculata - cortisol
zona reticularis - testosterone

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3
Q

what does the medulla release?

A

adrenaline and noradrenaline

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4
Q

what do glucocorticoids respond to?

A

stress

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5
Q

how do glucocorticoids increase plasma glucose levels?

A
  • increase gluconeogenesis
  • decrease GLUT 4 expression so less glucose utilisation
  • increase glycogenesis
  • increase glycogen storage
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6
Q

what is the effect of cortisol on lipolysis?

A

increases so provides energy

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7
Q

effect of cortisol on protein catabolism?

A

increases in muscle which releases amino acids that can be made available to the liver for use in gluconeogenesis

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8
Q

other effects of cortisol?

A
  • Na+/H20 retention to maintain BP
  • anti-inflammatory effect
  • increased gastric acid production to prevent infection
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9
Q

what is cushings syndrome?

A

clinical features of chronic exposure to excessive cortisol levels

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10
Q

incidence of cushings syndrome

A

2 in 1 million, higher in females. onset of 20-40 years of age

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11
Q

signs and symptoms of cushings syndrome?

A

changes in body shape, central obesity, moon face, buffalo hump, thin skin, diabetes and osteoporosis.
changes in sex hormones, excessive hair growth, irregular periods, problems conceiving. salt and water retention so high BP and fluid retention

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12
Q

how is cushings disease tested?

A
  • screening via urinary test for free cortisol

- test urine at midnight when cortisol should be lowest but also doa 24 hour test

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13
Q

how many stages in confirming Cushing’s disease?

A

three (screening, confirmation, differentiation of the cause)

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14
Q

how is the cushings diagnosis confirmed?

A

overnight dexamethasone suppression test

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15
Q

how is the cushings cause differentiated?

A

find out if exogenous or if its from ectopic source

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16
Q

what does it mean if cortisol is on circadian rhythm pattern?

A

24-25 hour cycle so is lowest at night.

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17
Q

what is the normal axis in the negative feedback loop?

A

cortisol decreases both CRH release from the hypothalamus and ACTH from the anterior pituitary

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18
Q

what is dexamethasone?

A

drug version of cortisol

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19
Q

how does the dexamethasone test work?

A

given to normal and healthy person as dexamethasone should inhibit release of CRH and ACTH. ACTH should fall as should cortisol

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20
Q

what is the overnight low dose dexamethasone suppression test?

A
  • cortisol measured at 8am
  • 1mg of dexamethasone given at 11pm, person sleeps and then cortisol measured next morning at 8am
  • if cortisol suppressed to less than 50nmol/L = normal
  • if cortisol is still detectable = cushings
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21
Q

what are the three causes of cortisol levels being high after the low dost dexamethasone test?

A

1 - patient has Cushings, would be pituitary adenoma releasing high levels of ACTH resulting in high cortisol
2 - patient has adrenal tumour secreting cortisol, could be a benign tumour or a malignant one
3 - patient has an ectopic source of ACTH production meaning tumour is somewhere outside the normal glandular tissue secreting ACTH

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22
Q

what is the high dose dexamethasone test?

A
  • 2 mg of dexamethasone every 6 hours for 48 hours

- if cortisol suppresses to less than 50% of the baseline patient has Cushings disease

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23
Q

why does this result determine if patient has cushings?

A

shows that -ve feedback loop is in tact and working at greater baseline level so with high dose it should turn down ACTH production but if cortisol still high, patient must have ectopic ACTH production or adrenal tumour

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24
Q

how do we distinguish between ectopic ACTH production and adrenal tumour?

A
  • adrenal tumour secretes high levels of cortisol completely unregulated by ACTH
  • high levels of cortisol = decreased CRH and ACTH release into blood
  • so in adrenal tumour, ACTH will be low
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25
Q

adrenal tumour

A

ACTH low

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26
Q

ectopic tumour

A

ACTH high

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27
Q

what are some laboratory features of someone with cushings?

A
  • hypokalaemia (low K+)
  • metabolic alkalosis
  • hyperglycemia (caused by effects of cortisol on increasing gluconeogenesis)
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28
Q

why does someone with cushings have hypokalaemia and metabolic alkalosis

A

at high levels, cortisol can bind to mineralcorticoid receptor in the kidneys. usually enzyme 11-beta hydroxysteroid dehydrogenase converts cortisol to inactive cortisone so cant do this. at high level, enzyme gets overwhelmed and cortisol will bind and the effects of aldosterone will increase

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29
Q

what will aldosterone cause?

A

increases transcription so there is increased Na+ absorption from the tubule into tubular cells so actively pumps out into the blood via Na+/K+/ATPase pump

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30
Q

how will aldosterone affect?

A

lots of ATPase pump activity due to aldoestrone so lots of K+ removal from blood and H+ removal leading to alkalosis.

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31
Q

what is ACTH derived from?

A

POMC

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32
Q

What is a CRH test

A

test for Cushings. Small dose of CRH given and blood is assayed for ACTH and cortisol at intervals over 2 hours

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33
Q

what would exaggerated response in CRH test mean?

A

suggests pituitary cushings disease

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34
Q

what would flat response in CRH test mean?

A

ectopic ACTH production as ectopic source is producing high ACTH at a set level that isn’t being up-regulated by CRH or down regulated by anything. So its levels wont increase by giving CRH

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35
Q

how do we localise pituitary tumours?

A

via MRI and IPSS

36
Q

how do we localise adrenal tumours?

A

CT or MRI

37
Q

how do we localise ectopic tumours?

A

octreotide scan or ACTH sampling (test blood ACTH in diff parts of the body)

38
Q

how is cushings disease treated?

A
  • high cortisol is counteracted via cortisol production blockers (metyrapone or ketaconazole)
  • radiotherapy
39
Q

how is cushings treated if source of high cortisol is adrenal?

A

tumour is removed and patients and they will need steroid replacement tablets at the time and following surgery, this is because adrenal tumour suppresses the function of the normal gland.

40
Q

what is addisons?

A

primary adrenal failure where there is chronic low blood cortisol and aldosterone

41
Q

what are clinical features of addisons?

A

tiredness, weakness, anorexia, weight loss, hyperkalemia, acidosis, salt craving

42
Q

causes of addisons

A

autoimmune, TB, steroid withdrawal, infection, drugs, enzyme defect

43
Q

what are the two tests for low cortisol?

A

synacthen test or stress test

44
Q

what is synacthen?

A

synthetic ACTH

45
Q

what is the short synacthen test?

A

250mcg of synacthen given and monitor how much ACTH produced over the next hour. Diagnoses primary adrenal failure as cortisol wont rise

46
Q

what is the long synacthen test?

A

1mg intramuscular injection given to test for pituitary disease. First hour, ACTH levels would be low as if theres a disease, adrenals would be shrunk so wouldnt work well. But over 24 hours, we get some adrenal growth.

47
Q

what is the insulin tolerance test?

A

induce stress by making person hypoglycemic using same parameters (low dose then high dose) and see response in levels of cortisol and ACTH

48
Q

treatment for hypo-cortisol

A
  • hydrocortisone (mimics diurnal rhythm)

- fludocortisone (replaces aldosterone)

49
Q

what is CAH

A

congenital adrenal hyperplasia, deficiency in enzymes needed to make specific hormones

50
Q

what is 21- hydroxylase deficiency?

A

most common form of CAH, autosomal recessive disorder that is HLA linked

51
Q

what is 21HD?

A

needed for cortisol production

52
Q

what happens with lack of 21HD?

A

build up of 17-OHP so more sex steroids made. Aldosterone synthesis will impair

53
Q

what will excess sex steroids result in?

A

hirsutism, virillisation, infertility, premature adrenarche (early maturity)

54
Q

no aldosterone?

A

= salt losing crisis = hyperkalaemia and hypotension

55
Q

what is 11-Beta Hydroxylase Deficiency?

A

autosomal recessive. Inability to produce cortisol and aldosterone so there is shuttling to sex steroids and DOC is synthesised instead of aldosterone

56
Q

what happens with no aldosterone but high DOC?

A

= agonist at mineralocorticoid receptor = hypertension and hypokalaemia

57
Q

how is 11 BHD investigated?

A

synacthen test = no cortisol rise

increased 170HP progesterone levels

58
Q

how is 11 BHD treated?

A

fludrocortisone used to replace absent mineralocorticoid activity

59
Q

where is aldosterone produced?

A

zona glomerulosa of the adrenal cortex and acts on kidney via mineralocorticoid receptor

60
Q

what else does mineralcorticoid receptor bind with?

A

cortisol with equal affinity

61
Q

how does blood flow into glomeruli of kidneys?

A

via afferent arterioles

62
Q

what activated RAAS system?

A
  • low blood pressure
  • low Na+ just before DCT
  • High Sympathetic activity
63
Q

what happens with RAAS system is activated?

A

renin is released and ACE

64
Q

what does renin do?

A

enzyme that converts angiotensinogen to angiotensin I

65
Q

what is ACE?

A

angiotensin converting enzyme

66
Q

what does ACE do?

A

coverts angiotensin I to angiotensin II

67
Q

how does angiotensin II effect vasoconstriction?

A

acts on adrenal cortex to cause release of aldosterone

68
Q

what will aldosterone do to affect water retention?

A

increases Na+ and hence water retention and increased loss of K+

69
Q

why cant the kidney negatively feedback?

A

there are no aldosterone receptors in kidney, instead gets turned off by reducing stimulating factors (e.g. low BP)

70
Q

what is the syndrome for primary excess of aldosterone?

A

Conn’s Syndrome, Bilateral adrenal hyperplasia, aldosterone producing adrenal carcinoma

71
Q

what is the syndrome for secondary excess with hypertension?

A

renal artery stenosis, renin secreting tumour

72
Q

what is the syndrome for secondary excess with normal BP?

A

cirrhosis, nephrotic syndrome

73
Q

what does it mean by primary excess?

A

due to aldosterone secreting tumour

74
Q

what does it mean by secondary excess?

A

overactivity of RAAS system

75
Q

hyperaldosteronism

A

Conn’s syndrome, renal artery stenosis, renin secreting tumour, cirrhosis, nephrotic syndrome

76
Q

treatment of Conn’s?

A
  • spironolactone (aldosterone antagonist)
  • potassium supplementation for the hypokalemia
  • treatment of primary tumour
77
Q

what is phaeochromocytoma?

A

tumour of the enterochromaffin cells of the adrenal medulla producing adrenaline

78
Q

what is the rule of 10 for phaechromocytoma?

A

10% bilateral
10% malignant
10% extra adrenal
10% inherited

79
Q

symptoms of phaeochromocytoma?

A
  • sweating
  • anxiety
  • fever
  • angor aminii
  • constipation
  • abdominal pain
80
Q

chemical signs of high adrenaline

A
  • eosinophilia
  • hyperglycaemia
  • hyperclacemia
  • raised urinary catecholamines
81
Q

management of phaechromocytoma

A

alpha blockage, non-competitive alpha antagonist. then beta blockage with non-selective beta blocker (propranolol). Surgery

82
Q

Pheochromacytoma related syndromes?

A
  • MEN2A
  • MEN2B
  • Von Hipple Lindau Disease
83
Q

what is polyglandular endocrinopathy?

A

adrenal disorder, two distinct types

84
Q

two organs of adrenal gland?

A

adrenal cortex and adrenal medulla

85
Q

adrenal over-activity

A
  • cushings syndrome
  • conns syndrome
  • adrenal hyperplasia
  • phaeochromocytoma
86
Q

adrenal under-activity

A
  • addisons disease
  • congenital adrenal hyperplasia (CAH)
  • secondary adrenal failure

Endo: Sem 2 (11 decks)

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