Adrenal insufficiency and Addison's Flashcards

1
Q

description

A

destruction of the adrenal cortex
reduction in adrenal hormones - ie glucocorticoids (cortisol) and mineralocorticoids (aldosterone)

primary insufficiency (addison's disease):
inability of adrenal glands to produce enough steroid hormones. most common cause is autoimmune disease

secondary insufficiency:
inadequate pituitary or hypothalamic stimulation of the adrenal glands
can be caused by exogenous effects leading to the suppression of the hypothalamic-pituitary axis. most common = exogenous steroid use

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2
Q

epidemiology

A

primary:
relatively rare
1 in 10,000
women more than men

secondary:
relatively common
150-280/1,000,000
women more than men
peak age 50-60yo
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3
Q

aetiology

A

85% of primary have an autoimmune basis in the west
TB is a common cause worldwide

autoimmune adrenal destruction is isolated in 40% of cases
part of autoimmune polyendocrinopathy syndrome in 60%
progressive immune mediated destruction of the adrenal glands
antibodies against steroid 21-hydroxylase found in 85%

administration of exogenous steroids is the most common cause of secondary

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4
Q

AIDS patients

A

can have CMV necrotising adrenalitis
adrenal tests are common in HIV patients
may be due to drug interactions

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5
Q

critically ill patients

A
at risk of adrenal dysfunction - known as critical illness-related corticosteroid insufficiency (CIRCI)
conditions where this may occur include:
sepsis
severe pneumonia
ARDS
trauma
HIV infection
after treatment with etomidate

unclear pathophysiology
reduction in production and effect of glucocorticoids
consider in critically ill and unresponsive to treatments for hypotension (particularly if septic)

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6
Q

presentation

A

acute:
may be a crisis precipitated by infection, surgery or trauma
features include: hypotension, hypovolaemic shock, acute abdo pain, low grade fever and vomiting
sudden onset of insufficiency, such as Waterhouse-Friderichsen syndrome (infarction secondary to septicaemia - eg meningococcal) presents with collapse and shock

chronic:
Sx develop insidiously and may be mild

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7
Q

non-specific Sx

A
fatigue and weakness (common)
anorexia
n&v
weight loss
abdo pain
diarrhoea
constipation
salt/salty food cravings (primary)
muscle cramps and joint pain
syncope and dizziness (hypotension)
confusion
personality change
irritability
loss of pubic/axillary hair in women
delayed onset of puberty
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8
Q

signs

A

hyperpigmentation - buccal mucosa, lips, palmar creases, new scars, areas subject to pressure eg elbows
hypotension
postura; hypotension

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9
Q

consider addison’s if:

A

hypothyroidism with worsening Sx after thyroxine is started
unexplained recurrent hypo’s in T1DM
presence of other autoimmune disease
low Na, high K (due to reduced aldosterone)

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