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Endocrine > Adrenal Pathophysiology > Flashcards

Adrenal Pathophysiology Flashcards

1
Q

Cushing’s syndrome

A

having excess cortisol secretion regardless of cause or source

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2
Q

The most common cause of Cushing’s

A

iatrogenic from exogenous glucocorticoid use

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3
Q

3 Pathologic derangements of Cushing’s

A

loss of diurnal variation of cortisol secretion, autonomy from central ACTH control (loss of feedback inhibition), excess cortisol secretion

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4
Q

T/F Iatrogenic Cushing’s is ACTH independent

A

T

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5
Q

Most common Cushing’s ACTH dependent

A

pituitary adenoma secreting ACTH followed by ectopic ACTH syndrome (tumor outside pituitary)

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6
Q

Most common ectopic ACTH syndromes

A

lung cancers

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7
Q

Most common ACTH independent Cushing’s other than iatrogenic

A

Adrenal adenoma, adrenal carcinoma

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8
Q

Target of cortisol action

A

glucocorticoid nuclear receptor

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9
Q

Where is the glucocorticoid receptor?

A

almost all cells

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10
Q

How long will effects of disease last after a cure for Cushings?

A

long time –> nuclear transcription affected

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11
Q

3 metabolic derangements due to excess glucocorticoids

A

hyperglycemia, muscle loss, lipogenesis and insulin resistance

carbohydrate metabolism stimulates gluconeogenesis –> hyperglycemia, fat metabolism increases lipogenesis –> insulin resistance, protein catbolism from increased gluconeogenesis —> muscle loss

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12
Q

Effects of fat metabolism: fat deposition pattern

A

dewlap, buffalo hump, supraclavicular fat pads, moon facies –> central lipogenesis + muscle loss

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13
Q

Effects of cortisol excess

A

impaired immunity, increased clotting factors, cataract formation, proximal myopathy, osteoporosis, fat redistribution, htn, PE, thin skin, bruising, striae, acne, hirsutism, mood lability

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14
Q

ACTH dependent Cushing’s is characterized by _________

A

bilateral adrenal hyperplasia

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15
Q

Excess of cortisol on mineralocorticoid and androgens

A

htn, hypokalemia, increased testosterone in females, abnormal menses

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16
Q

Severe hypokalemia is associated more with _____ ACTH production

A

ectopic

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17
Q

T/f negative feedback is still somewhat intact in ACTH dependent Cushings

A

T –> pituitary adenoma cells do not listen to the feedback but the feedback is still there

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18
Q

T/F frank/marked virilization of a woman is sign of Cushing’s

A

F –> more worried about malignant adrenal tumor

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19
Q

ACTH independent Cushing’s has high/low ACTH

A

low ACTH because negative feedback from elevated cortisol is still intact

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20
Q

How do we measure loss of diurnal variation of cortisol secretion?

A

measure late night salivary cortisol

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21
Q

How do we test autonomy form ACTH control?

A

1mg dexamethasone suppression test

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22
Q

How do we measure cortisol excess?

A

24h urinary free cortisol

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23
Q

What does the DST indicate?

A

inappropriate cortisol secretion but does not tell you the source –> normally should be low b/c DST should negative feedback on cortisol production

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24
Q

Cushing’s is more likely if urinary cortisol is > ___X upper limit of normal

A

3

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25
Q

You suspect Cushing’s in apt. Urine cortisol is elevated and cortisol is elevated after DST. ACT is normal. What is hte source of Cushing’s?

A

pituitary adenoma

26
Q

Plasma ACTH should be low if Cushing’s is from ___ source

A

adrenal

27
Q

Plasma ACTH should be normal/elevated if Cushing’s is from ___

A

pituitary or ectopic source

28
Q

ACTH is suppressed if source is ___

A

exogenous glucocorticoids

29
Q

Tx of adrenal adenoma

A

remove adrenal/cortex

30
Q

Tx of pituitary adenoma

A

trans sphenoidal hypophysectomy

31
Q

T/F symptoms of hypercortisolism can take a year to resolve

A

T –> might need to steroid taper as well

32
Q

Addison’s

A

primary adrenal failure –> cortisol deficiency

33
Q

Typically ___% of cortex is destroyed prior to presentation of Addison’s

A

90

34
Q

Clinical marker of Addison’s/Cortisol deficiency

A

elevated ACTH

35
Q

T/F in Addision’s all adrenal hormones can be lost

A

T

36
Q

What laboratory findings would you expect with Addison’s

A

hyponatremia (low aldosterone) and hyperkalemia (no K+ exchange), and hypertension (no cortisol and no mineralocorticoids)

37
Q

Clinical findings in Addison’s

A

hyperpigmentation, weight loss, muscle/joint pain, fatigue, nausea, hypoglycemia

38
Q

Addison’s etiology

A

autoimmune destruction (60% of cases), infectious (TB, fungus, HIV), bilateral hemorrhage/infarct, metastatic cancer, drugs

39
Q

Waterhouse-Friderichsen syndrome

A

meningococcemia caused hypotension and bleeding into adrenals

40
Q

Drugs that can cause addison’s

A

aminoglutethimide, ketoconazole, etomidate, rifampin, phenytoin

41
Q

Most common autoimmune Ab in Addison’s

A

21 hydroxylase Ab

42
Q

Dx of Addison’s

A

early morning cortisol and ACTH (low cortisol, high ACTH), cosyntropin simulation testing, hypotension

43
Q

T/F if hypotensive with strong clinical suspicion of Addisons, should start treating immediately while assaying

A

T –> give dexamethasone becuase wont interfere with cortisol assay

44
Q

Addisonian Crisis

A

acute deficiency in cortisol and mineralocorticoids –> hypotension, shock, fatigue, fever, abdominal pain, hypoglycemia

45
Q

Etiology of addisonian/adrenal crisis

A

primary adrenal failure, acute illness, acute withdrawal of glucocorticoids, pituitary apoplexy

46
Q

Tx for adrenal crisis

A

saline IV, dexamethasone, monitor electrolytes and bp

47
Q

Primary hyperaldosteronism

A

mineralocorticoid excess –> hypertension, hypokalemia, mild hypernatremia, metabolic alkalosis, muscle weakness can occur

48
Q

Pituitary apoplexy

A

large pituitary adenomas infarct –>acute headache and loss of normal pituitary function due to hemorrhage

49
Q

Primary hyperaldosteronism and potassium

A

potassium may fall to severely low levels –> may be normal but usually severe K wasting

50
Q

Screening for primary hyperaldosteronism

A

persons under 30 with htn and no obesity/family hx // unexplained hypokalemia and hypertension //resistant htn

51
Q

Diff Dx of Primary hyperaldosteronism

A

benign adrenal adenoma or bilateral adrenal hyperplasia

52
Q

Dx of Primary hyperaldosteronism

A

early morning aldosterone:renin ratio (>20 usggestive), inappropriate aldosterone secretion after salt loading, CT/MRI

53
Q

Tx of Primary hyperaldosteronism

A

surgical resection for unilateral, mineralocorticoid antagonist if bilateral

54
Q

T/F adrenal adenomas often cause androgen excess

A

F –> efficient at secreting cortisol

55
Q

Androgen excess in men

A

reduced gnrh

56
Q

Androgen excess in women

A

hirsutism, baldness, menstrual irregularity

57
Q

T/F cushing’s can cause elevated testosterone and dhea-s

A

T

58
Q

Pheocromocytoma

A

tumor that secretes catecholamiens in adrenal medulla (chromaffin cells) –> tachycardia, HTN, headache, sweating

59
Q

T/F pheocromocytomas are associated with familial syndromes

A

T –> 15%

60
Q

T/F pheocromocytomas are associated with familial syndromes

A

T –> 15%

Endocrine (26 decks)

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