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Endocrine > Adrenal gland > Flashcards

Adrenal gland Flashcards

1
Q

What is produced in the zona glomerulosa?

A

mineralocorticoids

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2
Q

What is produced in the zona fasciculata?

A

glucocorticoids (a little bit of androgen as well)

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3
Q

What is produced in the zona reticularis

A

androgens

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4
Q

What is the order of the zones from the capsule to the medulla in the adrenal gland?

A

glomerulosa; fasciculata; reticularis

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5
Q

What regulates aldosterone?

A

renin-angiotensin system and plasma potassium

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6
Q

What is CRH?

A

corticotropin release hormone produced by the hypothalamus in response to illness; stress and time of day which stimulate ACTH release from the anterior pituitary

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7
Q

How does angiotensin II cause BP increase?

A

direct- vasoconstriction; indirect- aldosterone

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8
Q

What are the 6 classes of steroid receptors?

A

glucocorticoid; mineralocorticoid; progestin; oestrogen; androgen; vitamin D

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9
Q

What are the major actions of glucocorticoid on the CNS?

A

mood lability; euphoria/psychosis; decreased libido

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10
Q

What are the effects of cortisol on bone/connective tissue?

A

accelerates osteoporosis; decreases serum calcium; decreases collagen formation; decreases wound healing

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11
Q

What are the immunological effects that cortisol has?

A

decreased capillary dilatation/permeability; decreased macrophage actvitiy; inflammatory cytokine production

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12
Q

What are the metabolic effects of cortisol?

A

increases blood sugar; increased lipolysis; central redistribution; increased proteolysis

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13
Q

What are the circulatory/renal effects of cortisol?

A

increased cardiac output; increased BP; increased renal blood flow and GFR

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14
Q

Where is the mineralocorticoid receptor found?

A

kidneys; salivary glands; gut; sweat glands

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15
Q

What are the effects of aldosterone?

A

sodiumpotassium balance; BP regulation; rgulation of ECF

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16
Q

What are the causes of primary adrenal insufficiency?

A

Addison’s disease; congenital adrenal hperplasia; adrenal TB/malignancy

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17
Q

What are the causes of secondary adrenal insufficiency?

A

iatrogenic; pituitary/hypothalamic disorders

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18
Q

What happens in Addison’s disease?

A

AI destruction of adrenal cortex

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19
Q

What are the symptoms of Addison’s disease?

A

anorexia; wt loss; fatigue; dizziness and low BP; abdo pain; vomiting; diarrhoea; skin pigmentation

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20
Q

How is Addison’s diagnosed?

A

U&E- hyponatraemia; hyperkalaemia; short synacthen test; ACTH lvels; renin/aldosterone levels; autoantibodies

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21
Q

What is the treatment for adrenal insufficiency?

A

hydrocortisone as cortisol replacement; fludrocortisone and aldosterone replacement

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22
Q

What is the commonest cause of secondary adrenal insufficiency?

A

exogenous steroid use

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23
Q

What is the difference between secondary and primary adrenal insufficiency in terms of clinical features?

A

secondary- pale skin (no increased ACTH) and aldosterone production is intact

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24
Q

What are clinical features of cortisol excess?

A

easy bruising; facial plethora; striae; proximal myopathy

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25
Q

What are the causes of Cushing’s ?

A

pituitary adenoma; ectopic ACTH or CRH; adrenal adenoma/carcinoma; nodular hyperplasia

26
Q

What are the tests to diagnose Cushing’s?

A

overnight dexamethasone suppression test; 24hr urinary free cortisol; late night salivary cortisol; low dose dexamethasone suppression test

27
Q

What is the commonest cause of cortisol excess?

A

prolonged high dose steroid therapy- chronic suppression of pituitary ACTH production and adrenal atrophy

28
Q

What is important about long term steroid therapy?

A

cannot be stopped suddenly; need extra doses of steroid when ill/surgery

29
Q

What is primary aldosternoism?

A

autonomous production of aldosterone independent of its regulators

30
Q

What are the regulators of aldosterone ?

A

angiotesin II and potassium

31
Q

What are the cardiovascular actions of aldosterone?

A

increased cardiac collagen; increased sympathetic outflow; cytokeine and ROS synthesis; sodium retention; altered endothelial function- increased pressor reponse—-increased BP; LVH; atheroma

32
Q

What are the clinical features of primary aldosteronism?

A

significant HT; hypokalaemia; alklaosis

33
Q

What is Conn’s syndrome?

A

adrenal adenoma causing primary aldosteronism

34
Q

What is the commonest cause of primary aldosteronism?

A

bilaterla adrenal hyperplasia

35
Q

What happens when potassium channels in aldosterone producing cells are mutated?

A

the potassium channel loses ion selectivity and sodium ions are able to enter through the channel, resulting in pathological depolarisation and continuous aldo. synthesis. leading to aldo. producing adenomas and hereditry HT

36
Q

What are the two steps in diagnosing primary aldosteronism?

A

1- confirm aldosterone excess

2- confirm subtype

37
Q

When should a secondary cause for HT be investiagted?

A

if young; if resistant HT

38
Q

How is aldosterone excess confirmed?

A

measure plasm aldosterone and renin ratio (ARR); then if raised to a saline suppression test

39
Q

What is a normal saline suppression test?

A

if plasma aldosterone is suppressed by more than 50% in response to 2 litres of saline

40
Q

What is used to confirm an adrenal adenoma?

A

adrenal CT

41
Q

What is the management of an adrenal adenoma?

A

unilateral laparoscopic adrenalectomy

42
Q

Waht is the Tx fro bilateral adrenal hyperplasia?

A

MR antagonists- spironolactone

43
Q

What is congeintal adrenal hyperplasia?

A

rare conditions associated with enzyme defects in the steroid pathway

44
Q

What is the inheritance of congenital adrenal hyperplasia?

A

autosomal recessive

45
Q

What is the most common enzyme affected in congenital adrenal hyperplasia?

A

21-alpha hydorxylase deficiency

46
Q

What is the classical symptoms of 21-alpha hydorxylase deficiency?

A

salt-wasting and simple virilising

47
Q

How is the diagnosis of CAH made?

A

basal or stimulated 17-OH progesterone

48
Q

What is the classical presentation of CAH in males?

A

adrenal insuffiency (2-3 weeks); poor weight gain; biochemical pattern- same as Addison’s

49
Q

What is the classica presentation in females?

A

genital ambiguity

50
Q

What are the non-classical features of CAH?

A

hisute; acne; oligomenorrhoea; precocious puberty; infertility or sub-fertility

51
Q

What are the priniciples of treatemtn of CAH for peads?

A

steroid (and maybe mineralocorticoid ) replacement; surgical correction; achieive max growth portential

52
Q

What is the main principles of tx in CAH fro adults?

A

control androgen excess; restore fertility; avoid steroid over-replacement

53
Q

What are the symptoms of phaeochromoctyoma?

A

labile HT; postural hypotension; paroxysmal sweating; headache; pallor; tachy;

54
Q

What is a phaeo called if it is extra adrenal- within the sympathetic chain?

A

paraganglioma

55
Q

Why is there a brown colour of tumour?

A

chromaffin cells reduce chrome salts to metal chromium

56
Q

What is the classical triad of symptoms in a phaeo?

A

HT (50%- paroxysmal); headache; sweating

57
Q

What pther symptoms may be seen with a phaeo?

A

palpitations; SOB; constipation; anxiet/fear; wt loss; flushing; pallor; postural hypotension; tachy

58
Q

What are the biochemical abnormalities seen with a phaeo?

A

hyperglycaemia; low potassium; high haemotocrit; mild hypercalcaemia; lactic acidosis

59
Q

How is a phaeo diagnosed?

A

confirm catecholamine excess- 2x24 hour catecholamines; plasma- at time of symptoms; identify source of catecholamine excess- MRI or MIBG or PET

60
Q

What are the treatments for a phaeo?

A

full alpha and beta blockade; surgery; chemo (if maligannt)

61
Q

What clinical syndromes are phaeo’s associated with?

A

MEN2; von-hippel-lindau syndrome; neurofibromatosis; tuberose sclerosis; succinate dehydrogenase mutations

62
Q

How is adrenaline synthesised?

A

dopamine—norepinephrine—adrenaline

Endocrine (27 decks)

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