B5.034 Prework 2 Endogenous Steroids and Adrenal Insufficiency Flashcards

1
Q

what is adrenal insufficiency (AI)

A

hypofunction of the adrenal cortex (production of cortisol)

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2
Q

why does AI arise?

A

destruction of the adrenal gland itself (primary AI, Addisons disease (AD))
lack of ACTH (secondary AI)

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3
Q

most common cause of AD

A

autoimmune destruction of the adrenal gland (80%)

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4
Q

infectious causes of AI

A

viral, mycobacterial, fungal

AIDs the most common

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5
Q

hemorrhagic causes of AI

A

anticoagulants/ coagulopathy, sepsis, thrombosis

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6
Q

metastatic cancers causing AI

A

brast, lung, GI, renal

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7
Q

infiltrative causes of AI

A

amyloidosis, sarcoidosis, hemochromatosis, demyelination

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8
Q

what causes secondary AI

A

adrenal gland atrophy from ACTH deficiency
most often results from:
-pituitary corticotroph atrophy owing to previous exogenous glucocorticoid use (prednisone)
-panhypopituitarism
-isolated ACTH deficiency

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9
Q

diagnosis of AI

A

demonstrate diminished responsiveness of the hypothalamic-pituitary-adrenal axis to stimulation

  • morning cortisol value less than 4 mg
  • cosyntropic (ACTH) stimulation test usually required and is the gold standard
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10
Q

describe the cosyntropin stimulation test

A

rise in cortisol level to 18, or a change in 9 in 30-60 min after 250 mg of cosyntropin (ACTH) administration is normal response

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11
Q

what causes hyperpigmentation in primary AI

A

excess ACTH can interact with melanocytes

usually occurs in areas exposed to light and pressure

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12
Q

acute therapy for AI

A

IV fluid

high dose IV glucocorticoids

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13
Q

chronic therapy for AI

A

physiologic oral glucocorticoid replacement
mineralocorticoid replacement (for primary)
patient education
-medic alert bracelet
-dosage increases for stress and surgery
-parenteral admin is oral not an option

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14
Q

agents used for oral glucocorticoid replacement

A

prednisone

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15
Q

agent for IV glucocorticoids

A

hydrocortisone

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16
Q

mineralocorticoid activity

A

maintains BP

17
Q

general rule of AI during sickness

A

double current steroid for 3 days

if major surgery or critical illness change to IV steroids

18
Q

physiologic effects of cortisol

A

affects vascular and bronchial smooth muscles with the relationship to catecholamines
in absence of cortisol there is vasodilation and hypotension

19
Q

physiologic effect of glucocorticoids

A

stimulate gluconeogenesis and glycogen synthesis in the fasting state
increase serum glucose by inhibiting uptake of glucose in the muscle
stimulates hormone sensitive lipase and lipolysis (minor effect)

20
Q

action of short acting steroids

A

hydrocortisone
may mimic diurnal rhythm best, 100% bioavailability
short half life, generally recommended once in the morning and once in the early afternoon

21
Q

action of long acting steroids

A

dexamethasone and prednisone provide longer duration of action
better for noncompliance
greater inter individual variability

22
Q

what is fludrocortisone

A

potent steroid which is mainly a mineralocorticoid
dose 0.1 mg per day
given to individuals with primary AI that have little or no mineralocorticoid steroids

23
Q

function of fludrocortisone

A

helps sodium retention at the level of the kidney

has a side effect of hypokalemia due to excessive mineralocorticoid activity

24
Q

steroid side effects

A
immunosuppression
hypertension
weight gain
osteoporosis
insomnia
mood swings
peptic ulcers
redistribution of fat