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adrenals Flashcards

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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
adrenocortical neoplams
androgen-secreting adrenal carcinomas are more common then adenomas often also associated with hypercortisolism
26
congenital adrenal hyperplasia
severe autosomal recessive inherited metabolic errors d/t enzyme deficiencies
27
21-hydroxylase deficiency
``` mutations in CYP21A2 most common salt-wasting syndrome virulizing non-classical virulism ```
28
salt-wasting syndrome
total lack of 21-hydroxylase soon after birth hyponatremia and hyperkalemia -> acidosis -> CV collapse -> death virulization recognized in females at birth
29
simple virulizing androgential syndrome w/o salt wasting
genital ambiguity | due to increased T
30
non-classical/ late onset adrenal virilism
most common pattern d/t partial deficiency asymptomatic or mild
31
primary acute adrenocortical insufficiency
crisis rapid withdrawal of meds massive hemorrhage waterhouse-friderichsen syndrome
32
crisis
chronic adrenochrotical insufficiency precipitated and exasperated by stress
33
massive adrenal hemorrhage
newborns post difficult delivery anticoaglulant therapy DIC -> waterhouse-friderichsen
34
waterhouse-friderichsen syndrome
overwhelming bacterial infection -> hypotensive shock -> DIC -> adrenocortical insufficiency associated with hemorrhage usually in kids
35
bacterial infections leading to waterhouse-friderichsen
nisseria, pseudo, H. influenza, penumo, staph)
36
addisons
primary chronic adrenal insufficiency | 90% d/t autoimmune, TB, AIDs, or mets
37
autoimmune adrenalitis
Abs to several steriodogenic enzymes APS1 APS2
38
APS1
candiasis ectodermal dystrophy autoimmune endocrine disorders AIRE mutations (central T cell tolerance is broken)
39
APS2
adrenal insufficiency | autoimmune thyroiditis or DMI
40
TB and other infections
usually have active TB infection in lungs and/or GU tract | histo and coccidiodes
41
AIDs
MAI CMV kaposi
42
METs
carcinomas of lungs and breast | usually b/l
43
symptoms of addisons
progressive weakness and easy fatigability GI: anorexia, nausea, vomiting, weight loss, diarrhea hyperpigmentation of skin hyperkalemia, hyponatremia, volume depletion, hypotensive
44
secondary adrenocortical insufficency
Mets, infections, infarction, or radiation of pituitary NO hyperpigmentation normal or near normal aldosterone synthesis
45
familial syndromes with risk of adrenocortical neoplasms
LiFraumeni | Beckwith Widemann
46
LiFraumeni
TP53 mutation
47
Beckwith Widenmann
``` epigenetics macroglossia macrosomnia abdominal wall defects neonatal hypoglycemia Wilms tumor ```
48
Functional adenomas of adrenal
most commonly associated with hyperaldosteronism and cushings, virulizing are usually caracinomas
49
adrenocoritcal adenomas
YELLOW | usually incidentalomas
50
adrenocortial carcinomas
``` rare more likely to be functional large, not well circumscribed varigated necrosis, hemorrhage, cysts invade adrenal v -> IVC invade lymph ```
51
adrenal cysts
relatively uncommon | may cause abdominal and flank pain
52
adrenal myelolipomas
usually benign composed of fat and hematopoietic cells | usually found inceidentally
53
adrenal medulla cells
chromaffin- specialized neural crest cells | sustentacular cells- supporting
54
pheochromocytomas
neoplasms of chropmaffin cells secreting catecholamines and sometimes peptides
55
pheochromocytoma rule of 10s
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
familial pheochromocytomas
younger b/l mutations
57
familial mutations of pheochromocytomas
enhance GF pathways: RET, NF1 | increase HIF1alpha- mutated in VHL syndrome
58
morphology of pheochromocytomas
richly vascularized producing lobular pattern potassium dichromate turns dark brown Zellballen only way to determine malignancy is mets
59
MEN general features
``` 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
MEN-1
``` aka Wermer syndrome -parathyroid primary hyperplasia -pancreas endocrine tumor -pituitary adenoma gastrinomas can also occur in duodenum germline mutationi n MEN1 -> menin ```
61
parathyroid primary hyperplasia in MEN-1
usually initial MEN manifestation, appears by 40-50 | hyperplasia and adenomas
62
pancreas endocrine tumor in MEN-1
leading cause of M&M aggressive with mets usually functional (PPP, gastrin, insulin)
63
pituitary adenomas in MEN-1
usually ant prolactinoma most common also somatotrophin secreting
64
MEN-2A
``` sipple syndrome pheochromocytoma parathyroid hyperplasia medullary carcinoma of thyroid gain of fnx in RET ```
65
pheochromocytoma in MEN
b/l | extrarenal sites
66
parathyroid hyperplasia in MEN-2A
hypercalcemia and renal stones
67
medullary carcinoma of thyroid in MEN-2A
in almsot 100% multifocal C-cell hyperplasia in adjacent cells calcitonin
68
MEN-2B
pheochromocytomas medullary carcinomas neuromas or ganglioneuromas different RET mutation (point)
69
medullary carcinomas of MEN-2B
more aggressive then 2A
70
neuromas and ganglioneuromas of MEN-2B
skin, oral mucosa, eyes, respiratory tract, GI tract | marfanoid habitus
71
familial medullary thyroid CA
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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