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endocrine > adrenal physiology > Flashcards

adrenal physiology Flashcards

1
Q

causes of primary insufficiency

A

addison’s disease
congenital adrenal hyperplasia (CAH)
adrenal TB/malignancy

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2
Q

secondary (and tertiary) insufficiency

A

due to lack of ACTH stimulation
iatrogenic (excess exogenous steroid)
pituitary/hypothalamic disorders

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3
Q

clinical features of addison’s disease

A

anorexia, weight loss
fatigue/lethargy
dizziness and low BP
abdominal pain, vomiting, diarrhoea
skin pigmentation

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4
Q

commonest cause of PAI ?

A

addison’s

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5
Q

cause of addison’s

A

autoimmune destruction of adrenal cortex (90% destrtoyed before symptomatic, autoantibodies positive in 70%)

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6
Q

what other autoimmune diseases associated w/ addison’s ?

A

T1DM, autoimmune thyroid disease, pernicious anaemia

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7
Q

diagnosis of adrenal insufficiency

A

“suspicious biochemistry” (decrease Na, increase K) (hypoglycaemia)

“short synacthen test” (measueing plasma cortisol before and 30 mins after IV/IM ACTH injection)

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8
Q

what are ACTH levels in addison’s ?

A

should be high (causes skin pigmentation)

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9
Q

renin/ aldosterone levels in addisons ?

A

inc renin dec aldosterone

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10
Q

management of adrenal insufficiency

A

hydrocortisone as cortisol replacement
(iv first if unewell, usually 15-30mg daily in divided doses, try to mimic diurnal rhythm)

fludrocortisone as aldosterone replacement
(careful monitoring of BP and K)

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11
Q

adrenal crisis management

A

fluids - normal saline
100mg iv - steroids hydrocortisone 50mg IM every 6hrs or 24hr infusion
treat underlying cause

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12
Q

secondary adrenal insufficiency (lack or CRH/ACTH) causes

A

pituitary/hypothalamic disease, tumours
(surgery/radiotherapy to manage)

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13
Q

more of a tertiary adrenal isufficiency

A

exogenous steroid use

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14
Q

secondary adrenal insufficiency (lack or CRH/ACTH) clinical features

A

pale skin (no increase ACTH)
aldosterone production intact (regulated by RAS)

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15
Q

SAI treatment

A

trear w/ hydrocortisone replacement (fludrocortisone unnecessary)

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16
Q

cushing’s syndrome

A

excess cortisol secretion
high mortality

17
Q

clinical features of cortisol excess

A

easy bruising
facial plethora
striae
proximal myopathy

18
Q

endogenous cause of cushings

A

ectopic
ACTH independent (too much cortisol) adenoma, adrenal carcinoma

19
Q

diagnosing cushing’s

A

establishing cortisol excess
overnight dexamethasone suppression test
24hr urinary free cortisol
late night salivary cortisol
low dose dexamethasone suppression test
repeat to confirm

20
Q

diagnostic test for cushings syndrome

A

low dose dexanthesone suppresion ACTH and cortisol measured base line and 24hrs (2mg per day)

21
Q

what is the commonest cause of cortisol excess

A

iatrogenic cushing’s syndrome

22
Q

iatrogenic cushing syndrome happens due to…

A

prolonged high dose steroid therpay (asthma, RA, IBD, transplants)
chronic suppression of pituitary ACTH production and adrenal atrophy

23
Q

adrenal suppression

A

atrophy of adrenal cortex

24
Q

implications of adrenal suppression

A

unable to response to stress(illness, surgery)
need extra doses of steroid when ill/surgical procedure
cannot stop suddenly
gradually withdrawal of steroid therapy (if >4-6 weeks)

25
Q

what are the endocrine causes of hypertension ?

A

too much aldosterone
too much GH
too much adrenaline and noradrenaline

26
Q

hypertension and hypokalaemia raises the possibility of…?

A

primary aldosteronism

27
Q

primary aldosteronism reflects…

A

autonomous production of aldosterone independent of its regulators (angiotensin II/potassium)

28
Q

what appearance would sample have ?

A

fleshy appearance

29
Q

what is commonest secondary cause of hypertension

A

primary aldosteronism (up to 10% of cases, 20% resistant hypertension)

30
Q

clinical features of primary alodsteronism

A

significant hypertension
hypokalaemia (in around 30%)
alkalosis

31
Q

subtypes of primary aldosteronism

A

adrenal adenoma
(conn’s syndrome)
bilateral adrenal hyperplasia (commonest cause)
rare causes (genetic mutations, unilateral hyperplasia)

32
Q

diagnosing primary aldosteronism

A
  1. confirm aldosterone excess
    measure plasma aldosterone and renin and express as ratio (ARR-aldosterone to renin ratio)
  2. confirm subtype
    adrenal CT to demonstrate adenoma
    sometimes adrenal vein sampling to confirm adenoma is true source of aldosterone excess
33
Q

management of PA

A

surgical (only if clear)
- unilateral laparoscopic adrenalectomy
ONLY IF ADRENAL ADENOMA (and excess confrimed in adrenal vein sampling)
- cure of hypokalaemia
- cures hypertension in 30-70% cases

medical
- in bilateral adrenal hyperplasia
- use MR antagonists (spironolactone)

endocrine (15 decks)

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