Pathology of the Adrenal I Flashcards

1
Q

glucocorticoid production

A

zona fasciculata

cortisol

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2
Q

mineralocorticoid production

A

zona glomerulosa

aldosterone

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3
Q

sex steroid production

A

zona reticularis

estrogens and androgens

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4
Q

chromaffin cells

A

in adrenal medulla

secrete catecholamines

epinephrine

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5
Q

cushings syndrome

A

hypercortisol

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6
Q

central obesity, moon facies, abdominal striae

A

cushings

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7
Q

elevated glucocorticoid levels

A

cushing

exogenous and endogenous

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8
Q

exogenous cushings

A

iatrogenic

admin of exogenous glucocorticoids

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9
Q

endogenous cushings

A

ACTH dependent

ACTH independent

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10
Q

ACTH dependent cushings

A

pituitary adenoma - producing ACTH

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11
Q

ectopic ACTH

A

small cell lung cancer

but rare

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12
Q

ACTH independent cushings

A

adrenal adenoma or carcinoma

elevated cortisol and low ACTH

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13
Q

majority of endogenous hypercortisolism

A

ACTH secreting pituitary adenoma

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14
Q

cushing disease

A

ACTH producing pituitary adenoma

more in women - young adults

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15
Q

most common cause of ACTH-indepenent cushing syndome

A

primary adrenal neopalsms

adenomas and carcinomas

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16
Q

crooke hyaline change

A

pituitary adenoma
-producing ACTH

cushings disease

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17
Q

adrenal cortex color

A

yellow

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18
Q

HTN and weight gain

A

seen early with cushings syndrome

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19
Q

buffalo hump

A

cushings

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20
Q

hypercortisol and muscle

A

atrophy of type 2 myofibers

decreased muscle mass and proximal limb weakness

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21
Q

striae in cushings

A

glucocorticoids induce gluconeogenesis - hyperglycemia, glucosuria, polydipsia - secondary diabetes

loss of collagen and bone resorption

skin thin fragile and easily bruised - striae occurs

22
Q

lady stops menstruating

overweight, HTN, striae, increased cortisol

A

cushings

23
Q

decreased libido

A

in cushings

24
Q

lab diagnosis of cushings

A

24 hour urine free cortisol increased

loss of normal diurnal (high morning/low afternoon) pattern of cortisol release

25
Q

dexamethasone suppression test

A

dexamethasone - suppresses ACTH secretion

in pituitary adenoma - low dose will not work, but high dose will

in ectopic ACTH or adrenal tumor low and high dose will not work

ectopic - high ACTH
adrenal tumor - low ACTH

26
Q

ectopic ACTH vs. adrenal tumor

A

ectopic - high ACTH

adrenal tumor - low ACTH

27
Q

primary hyperaldosteronism

A

excess aldosterone secretion

may be primary or secondary

decreased renin activity

28
Q

common symptom in primary hyperaldosteronism

A

BP elevation

due to too much Na

29
Q

conns syndrome

A

primary hyperaldosteronism

adrenal aldosteronoma

solitary aldosterone secreting adenoma

-surgery

30
Q

bilateral adrenal hyperplasia

A

primary adrenal hyperaldosteronism

tx - spironolactone

31
Q

CYP11B2

A

chromosome 8

altered in glucocorticoid remediable hyperaldosteronism

32
Q

most common primary hyperaldosteronism

A

idiopathic - bilateral enlargement

tx - medical - spironolactone

33
Q

secondary hyperaldosteronism

A

with increased plasma renin

1 - renal artery stenosis
2 - arterial hypovolemia and edema
3 - pregnancy

34
Q

renal artery stenosis

A

decreased renal perfusion

  • increased renin
  • secondary hyperaldosteronism
35
Q

spironolactone bodies

A

in aldosterone producing adenoma

36
Q

hyperaldosteronism clinical

A

hypertension

long term - left ventricular hypertrophy and reduced diastolic volume

strokes and MI

37
Q

diagnosis of primary hyperaldosteronism

A

elevated ratio of plasma aldosterone to plasma renin

confirmatory aldosterone suppression test must be performed**

38
Q

virilization

A

development of sex differences in male and female

39
Q

adrenal causes of androgen excess

A

adrenocortical neoplasms

congenital adrenal hyperplasia

40
Q

two compounds from adrenal cortex that can be converted to testosterone

A

dehydroepiandrosterone

androstenedione

41
Q

21 hydroxylase deficiency

A

too much testosterone formation

female gets hairy

42
Q

congenital adrenal hyperplasia

A

auto recessive

deficiency or total lack of enzymes involved in biosynthesis of cortical steroids

43
Q

mutation in CYP21A2

A

21 hydroxylase deficiency

main cause of congenital adrenal hyperplasia**

3 adrenogenitalism syndromes:
1 - salt wasting - classic
2 - virilizing
3 - nonclassic

44
Q

salt wasting syndrome

A

congenital adrenal hyperplasia
-total lack of 21 hydroxylase

no synthesis of mineralocorticoids

also deficient cortisol

excess androgens - virilization occurs

male - unrecognized

a birth - see a salt wasting crisis**

45
Q

higher K/Na ratio

A

severe tetany

46
Q

simple virilizing adrenogenital syndrome

A

genital ambiguity

1/3 pt with 21-hydroxylase deficiency

enough mineralocorticoids to prevent salt wasting crisis

increased testosterone - progressive virilization

47
Q

salt wasting crisis at birth**

A

21 hydroxylase deficiency

  • congeintal adrenal hyperplasia
  • salt wasting syndrome

produce no mineralocorticoids

48
Q

late onset adrenal virilism

A

nonclassic congenital adrenal hyperplasia

partial 21 hydroxylase deficiency

49
Q

hirsutism, acne, menstrual irregularity

A

nonclassic - adrenal virilism

partial deficiency of 21 hydroxylase

50
Q

all cases of congenital adrenal hyperplasia

A

adrenals are bilaterally hyperplastic

51
Q

congeintal adrenal hyerplasia in males

A

21 hydroxylase deficiency
-excessive androgens

enlarged external genitalia and other evidence of precocious puberty

older males - oligospermia

52
Q

ambiguous genitalia

A

suspect congneital adrenal hyperplasia