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Endo II > adrenals > Flashcards

adrenals Flashcards

1
Q

causes cushings syndrome

A
  • most common cause is exogenous glucocorticoids
  • ACTH secreting pituitary adenoma
  • corticotroph cell hyperplasia
  • secretion of ectopic ACTH
  • primary adrenal neoplasms
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2
Q

ACTH secreting pituitary adenoms

A

most common endongenous cause
cushings DISEASE
young adults
usually microadenoma

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3
Q

corticotroph cell hyperplasia

A

primary or secondary d/t excessive ACTH from hypothalmic CRH producing tumor

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4
Q

secretion of ectopic ACTH

A

SCC of lung

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5
Q

primary adrenal neoplasms

A

adenomas and carcinomas most common cause of ACTH independent endogenous cushings

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6
Q

secondary hyperadrenocoritcal function morphology

A

pituitary shows Crooke hyaline change

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7
Q

adrenal Cx atrophy

A

b/l if exogenous cushings

u/l if ACTH independent hypersecretion is u/l

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8
Q

diffuse hyperplasia of adrenals

A

ACTH dependent cushings

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9
Q

adrenal adenomas morphology

A

YELLOW WITH CAPSULE

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10
Q

adrenal carcinomas

A

NOT capsulated

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11
Q

symptoms of cushings

A 
HTN and weight gain
truncal obestiy, moon facies, buffalo hump
hyperglycemia, glucosuria, polydipsia
decreased mm and weakness
skin is thin, striae
osteoporosis
at risk for infections, poor wound healing
mental disturbances
hirsuitism and menstrual abnormalities
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12
Q

Dx of cushings

A

Dexamethasone suppression test

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13
Q

primary hyperaldosteronism

A

HTN most common manifestation

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14
Q

causes of primary hyperaldosteronism

A

b/l hyperaldosteronism (IHA)
adrenocortical neoplasm
glucocorticoid-remediable hyperaldosteronism

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15
Q

b/l hyperaldosteronism (IHA)

A

most common cause of primary hyperaldosteronism
older, less severe THn then adrenal neoplasms
familial maybe mutation in KCNJ5 encoding a KCh

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16
Q

adrenocortical neoplasm

A 
adenomas
rare caracinomas
Conn syndrome
if multiple more likely to be carcinoma
also have KCNJ5 mutations
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17
Q

glucocorticoid-remediable hyperaldosteronism

A

uncommon
familial
under control of ACTH so will respond to dexamethasone

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18
Q

aldosterone adenomas morphology

A

solitary, well circumscribed, small
L>R
30-40
BRIGHT YELLOW lipid laden Cx cells resembling fasciulata cells
uniform size and shape
spironolactone bodies after Tx with spirnolactone

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19
Q

b/l idiopathic hyperplasia morphology

A

diffuse focal hyperplasia of glomerulosa

often wedge shaped

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20
Q

hyperaldosterone symptoms

A

HTN
Na retention -> increased fluid volume and CO
hypokalemia

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21
Q

long term effects of hyperaldosteronism

A

CV compromise
strokes
MI

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22
Q

symptoms of hypokalemia

A

weakness
paresthesias
visual disturbances
tetany

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23
Q

Dx of hyperaldosteronism

A

elevated aldosterone: renin ratio

aldosterone suppression test

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24
Q

reticularis secretes

A

DHEA

androstenedione

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25
Q

adrenocortical neoplams

A

androgen-secreting adrenal carcinomas are more common then adenomas
often also associated with hypercortisolism

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26
Q

congenital adrenal hyperplasia

A

severe autosomal recessive inherited metabolic errors d/t enzyme deficiencies

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27
Q

21-hydroxylase deficiency

A 
mutations in CYP21A2
most common 
salt-wasting syndrome
virulizing
non-classical virulism
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28
Q

salt-wasting syndrome

A

total lack of 21-hydroxylase
soon after birth hyponatremia and hyperkalemia -> acidosis -> CV collapse -> death
virulization recognized in females at birth

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29
Q

simple virulizing androgential syndrome w/o salt wasting

A

genital ambiguity

due to increased T

30
Q

non-classical/ late onset adrenal virilism

A

most common pattern
d/t partial deficiency
asymptomatic or mild

31
Q

primary acute adrenocortical insufficiency

A

crisis
rapid withdrawal of meds
massive hemorrhage
waterhouse-friderichsen syndrome

32
Q

crisis

A

chronic adrenochrotical insufficiency precipitated and exasperated by stress

33
Q

massive adrenal hemorrhage

A

newborns post difficult delivery
anticoaglulant therapy
DIC -> waterhouse-friderichsen

34
Q

waterhouse-friderichsen syndrome

A

overwhelming bacterial infection -> hypotensive shock -> DIC -> adrenocortical insufficiency associated with hemorrhage
usually in kids

35
Q

bacterial infections leading to waterhouse-friderichsen

A

nisseria, pseudo, H. influenza, penumo, staph)

36
Q

addisons

A

primary chronic adrenal insufficiency

90% d/t autoimmune, TB, AIDs, or mets

37
Q

autoimmune adrenalitis

A

Abs to several steriodogenic enzymes
APS1
APS2

38
Q

APS1

A

candiasis
ectodermal dystrophy
autoimmune endocrine disorders
AIRE mutations (central T cell tolerance is broken)

39
Q

APS2

A

adrenal insufficiency

autoimmune thyroiditis or DMI

40
Q

TB and other infections

A

usually have active TB infection in lungs and/or GU tract

histo and coccidiodes

41
Q

AIDs

A

MAI
CMV
kaposi

42
Q

METs

A

carcinomas of lungs and breast

usually b/l

43
Q

symptoms of addisons

A

progressive weakness and easy fatigability
GI: anorexia, nausea, vomiting, weight loss, diarrhea
hyperpigmentation of skin
hyperkalemia, hyponatremia, volume depletion, hypotensive

44
Q

secondary adrenocortical insufficency

A

Mets, infections, infarction, or radiation of pituitary
NO hyperpigmentation
normal or near normal aldosterone synthesis

45
Q

familial syndromes with risk of adrenocortical neoplasms

A

LiFraumeni

Beckwith Widemann

46
Q

LiFraumeni

A

TP53 mutation

47
Q

Beckwith Widenmann

A 
epigenetics
macroglossia
macrosomnia
abdominal wall defects
neonatal hypoglycemia
Wilms tumor
48
Q

Functional adenomas of adrenal

A

most commonly associated with hyperaldosteronism and cushings, virulizing are usually caracinomas

49
Q

adrenocoritcal adenomas

A

YELLOW

usually incidentalomas

50
Q

adrenocortial carcinomas

A 
rare
more likely to be functional
large, not well circumscribed
varigated
necrosis, hemorrhage, cysts
invade adrenal v -> IVC
invade lymph
51
Q

adrenal cysts

A

relatively uncommon

may cause abdominal and flank pain

52
Q

adrenal myelolipomas

A

usually benign composed of fat and hematopoietic cells

usually found inceidentally

53
Q

adrenal medulla cells

A

chromaffin- specialized neural crest cells

sustentacular cells- supporting

54
Q

pheochromocytomas

A

neoplasms of chropmaffin cells secreting catecholamines and sometimes peptides

55
Q

pheochromocytoma rule of 10s

A

10% are extra-adrenal (organs of Zuckerkandl and carotid body)
10% of sporadic are b/l
10% are malignant
10% are NOT associated with HTN

56
Q

familial pheochromocytomas

A

younger
b/l
mutations

57
Q

familial mutations of pheochromocytomas

A

enhance GF pathways: RET, NF1

increase HIF1alpha- mutated in VHL syndrome

58
Q

morphology of pheochromocytomas

A

richly vascularized producing lobular pattern
potassium dichromate turns dark brown
Zellballen
only way to determine malignancy is mets

59
Q

MEN general features

A 
tumors at younger age
tumors are in multiple endocrine organs
tumors in single organ are multiple
usually proceeded by asymptomatic stage of hyperplasia
more aggressive and recur
60
Q

MEN-1

A 
aka Wermer syndrome
-parathyroid primary hyperplasia 
-pancreas endocrine tumor
-pituitary adenoma
gastrinomas can also occur in duodenum
germline mutationi n MEN1 -> menin
61
Q

parathyroid primary hyperplasia in MEN-1

A

usually initial MEN manifestation, appears by 40-50

hyperplasia and adenomas

62
Q

pancreas endocrine tumor in MEN-1

A

leading cause of M&M
aggressive with mets
usually functional (PPP, gastrin, insulin)

63
Q

pituitary adenomas in MEN-1

A

usually ant
prolactinoma most common
also somatotrophin secreting

64
Q

MEN-2A

A 
sipple syndrome
pheochromocytoma
parathyroid hyperplasia
medullary carcinoma of thyroid
gain of fnx in RET
65
Q

pheochromocytoma in MEN

A

b/l

extrarenal sites

66
Q

parathyroid hyperplasia in MEN-2A

A

hypercalcemia and renal stones

67
Q

medullary carcinoma of thyroid in MEN-2A

A

in almsot 100%
multifocal
C-cell hyperplasia in adjacent cells
calcitonin

68
Q

MEN-2B

A

pheochromocytomas
medullary carcinomas
neuromas or ganglioneuromas
different RET mutation (point)

69
Q

medullary carcinomas of MEN-2B

A

more aggressive then 2A

70
Q

neuromas and ganglioneuromas of MEN-2B

A

skin, oral mucosa, eyes, respiratory tract, GI tract

marfanoid habitus

71
Q

familial medullary thyroid CA

A

variant of MEN-2A
strong disposition to medullary thyroid CA
develop at older age and are more indolent then MEN-2A

Endo II (15 decks)

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