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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
What are the causes of Cushing's ?
pituitary adenoma; ectopic ACTH or CRH; adrenal adenoma/carcinoma; nodular hyperplasia
26
What are the tests to diagnose Cushing's?
overnight dexamethasone suppression test; 24hr urinary free cortisol; late night salivary cortisol; low dose dexamethasone suppression test
27
What is the commonest cause of cortisol excess?
prolonged high dose steroid therapy- chronic suppression of pituitary ACTH production and adrenal atrophy
28
What is important about long term steroid therapy?
cannot be stopped suddenly; need extra doses of steroid when ill/surgery
29
What is primary aldosternoism?
autonomous production of aldosterone independent of its regulators
30
What are the regulators of aldosterone ?
angiotesin II and potassium
31
What are the cardiovascular actions of aldosterone?
increased cardiac collagen; increased sympathetic outflow; cytokeine and ROS synthesis; sodium retention; altered endothelial function- increased pressor reponse----increased BP; LVH; atheroma
32
What are the clinical features of primary aldosteronism?
significant HT; hypokalaemia; alklaosis
33
What is Conn's syndrome?
adrenal adenoma causing primary aldosteronism
34
What is the commonest cause of primary aldosteronism?
bilaterla adrenal hyperplasia
35
What happens when potassium channels in aldosterone producing cells are mutated?
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
What are the two steps in diagnosing primary aldosteronism?
1- confirm aldosterone excess | 2- confirm subtype
37
When should a secondary cause for HT be investiagted?
if young; if resistant HT
38
How is aldosterone excess confirmed?
measure plasm aldosterone and renin ratio (ARR); then if raised to a saline suppression test
39
What is a normal saline suppression test?
if plasma aldosterone is suppressed by more than 50% in response to 2 litres of saline
40
What is used to confirm an adrenal adenoma?
adrenal CT
41
What is the management of an adrenal adenoma?
unilateral laparoscopic adrenalectomy
42
Waht is the Tx fro bilateral adrenal hyperplasia?
MR antagonists- spironolactone
43
What is congeintal adrenal hyperplasia?
rare conditions associated with enzyme defects in the steroid pathway
44
What is the inheritance of congenital adrenal hyperplasia?
autosomal recessive
45
What is the most common enzyme affected in congenital adrenal hyperplasia?
21-alpha hydorxylase deficiency
46
What is the classical symptoms of 21-alpha hydorxylase deficiency?
salt-wasting and simple virilising
47
How is the diagnosis of CAH made?
basal or stimulated 17-OH progesterone
48
What is the classical presentation of CAH in males?
adrenal insuffiency (2-3 weeks); poor weight gain; biochemical pattern- same as Addison's
49
What is the classica presentation in females?
genital ambiguity
50
What are the non-classical features of CAH?
hisute; acne; oligomenorrhoea; precocious puberty; infertility or sub-fertility
51
What are the priniciples of treatemtn of CAH for peads?
steroid (and maybe mineralocorticoid ) replacement; surgical correction; achieive max growth portential
52
What is the main principles of tx in CAH fro adults?
control androgen excess; restore fertility; avoid steroid over-replacement
53
What are the symptoms of phaeochromoctyoma?
labile HT; postural hypotension; paroxysmal sweating; headache; pallor; tachy;
54
What is a phaeo called if it is extra adrenal- within the sympathetic chain?
paraganglioma
55
Why is there a brown colour of tumour?
chromaffin cells reduce chrome salts to metal chromium
56
What is the classical triad of symptoms in a phaeo?
HT (50%- paroxysmal); headache; sweating
57
What pther symptoms may be seen with a phaeo?
palpitations; SOB; constipation; anxiet/fear; wt loss; flushing; pallor; postural hypotension; tachy
58
What are the biochemical abnormalities seen with a phaeo?
hyperglycaemia; low potassium; high haemotocrit; mild hypercalcaemia; lactic acidosis
59
How is a phaeo diagnosed?
confirm catecholamine excess- 2x24 hour catecholamines; plasma- at time of symptoms; identify source of catecholamine excess- MRI or MIBG or PET
60
What are the treatments for a phaeo?
full alpha and beta blockade; surgery; chemo (if maligannt)
61
What clinical syndromes are phaeo's associated with?
MEN2; von-hippel-lindau syndrome; neurofibromatosis; tuberose sclerosis; succinate dehydrogenase mutations
62
How is adrenaline synthesised?
dopamine---norepinephrine---adrenaline

Endocrine (27 decks)

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