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30 Cards in this Set

  • Front
  • Back
normal granular, basophilic cytoplasm of the ACTH producing cells inthe anterior pituitary is replaced by homogenous, lightly basophilic material

accumulation of intermediate keratin filaments in the cytoplasm
Crooke hyaline change
Crooke hyaline change

cortical atrophy, diffuse hyperplasia, nodular hyperplasia, or an adenoma

supression of the endogenous ACTH results in bilateral cortical atrophy due to lack of stimulation of zonae faciculata (exogenous); or adrenals are either hyperplastic or contain cortical neoplasm (endogenous)

elevated ACTh
Cushing syndrome
adrenal cortex is diffusely thickened adn yellow due to increase in size and number of lipid rich cells in zona fasciculata adn reticularis
diffuse hyperplasia
Bilateral yellow nodules scattered throughout the cortex, separated by intervening widened cortex
nodular hyperplasia
yellow tumors surrounded by thin or well developed casule and weighing less than 30 gm
adrenal adenoma
larger tumors presenting as unencapsulated masses

contralateral adreal gland is atrophic
Adrenal carcinoma
Central adipose deposition, truncal obesity, moon facies, accumulation of fat in posterior back/neck

selective atrophy fast-twitch myofiberss; decreased muscle mass, proximal limb weakness

secondary diabetes

skin is thin, fragile, easily bruised
Cushing's
solitary, small, well circumscribed lesion more often found on left and in women

bright yellow on cut section; composed of lipid laden cortical cells that closely resemble fasciculata

no evidence of anaplasia

eosinophilic laminated cytoplasmic inclusions (spironolactone bodies) after treatment
aldosterone producing adenoma
Diffuse and focal hyperplasia of cells resembling those of normal zona glomerulosa

wedge-shape
bilateral idiopathic hyperplasia
hypertension, hypokalema

neuromuscular manifestations; expanded ECF
primary hyperaldosteronism
adrenals are bilaterally hyperplastic, sometimes expanding to 10-15 times normal

sustained elevation of ACTH

adrenal cortex is thickened and nodular; brown due to lipid depletion

Hyperplasia of corticotrophs
congenital adrenal hyperplasia
Excessive androgen activity that causes signs of masculinization in females

clitoral hypertrophy, pseudohermaphrodism, oligomenorrhea, hirsutism, acne

enlarged male genetalia, precocious puberty, oligospermia
CAH/21 hydroxylase deficiency
overwhelming bacterial infection (N. meningitidis)

rapidly, progressive hypotension leading to shock

DIC with widespread purpura

massive bilateral adrenal hemorrhage/insufficiency
Waterhous Friderichsen syndrome
Irregularly shrunken glands

scattered residual cortical cells in a collapsed network of connective tissue

variable lymphoid infiltrate
Primary autoimmune adrenalitis
adrenal architecture effaced by a granulomatous inflammatory reaction identical to that encountered in other infectino
tuberculous/fungal disease
adrenals are enlarged; normal architecture obscured by infiltrating neoplasm
metastatic carcinoma
progressive weakness and easy fatigueability

GI disturbances

hyperpigmentation of the skin

hyperkalemia, hyponatremia, volume depletion, hypotension; hypoglycemia occasionally
addison's disease
adrenals may be moderately to markedly reduced in size

small flattened structures that usually retain yellow color

cortex may be reduced to a thin ribbon composed largely of zona granulosa
secondary hypoadrenalism
tumor that is usually silent and encountered incidentally

well circumscribed, nodular lesion up to 2.5 cm in diameter that expand the adrenal

yellow to yellow brown; small neuclei, some degree of pleomorphism may be encountered; eosinophilic to vacuolated
adrenocortical adenoma
ree neoplasm that can occur at any age

often associated with virilism

large, invasive legion that efface the native gland

variegated, poorly demarcated lesions containing areas of necrosis, hemorrhage, cystic change
adrenocortical carcinoma
usually benign lesions composed of mature fat and hematopoietic cells
adrenal myololipomas
masses in asymptomatic individuals or individuals whom presenting complaint is not directly related to adrenal gland
incidentaloma
small circumscribed lesions to large hemorhagic masses

large tumors well demarcated by connective tissue or compressed cortical or medullary tissue; richly vascularized trabiculae

yellow-tan; larger are hemorrhagic, necrotic, and cystic

polygonal to spindle shaped chromaffin cells or chief cells clustered with sustentacular cells into small nests or alveoli

finely granular cytoplasm; salt and pepper chromatin

peripheral sustentacular cells label with S-100
pheochromocytoma
hypertension, tachycardia, palpitations, headache, sweating, tremor, sense of apprehension

sudden release of catecholamines may precipitate CHF, pulmonary edema, MI, Vfib, cerebrovascular accindents
pheochromocytoma
rare heritable disorder

abnormalities of the parathyroid, pancreas, pituitary glands

overproduction of peptide hormones
MEN 1/Wermer syndrome
pheochromocytoma, medullary carcinoma, parathyroid hyperplasia

linked to RET protooncogene on 10q11.2; gain of function
MEN 2A/ sipple syndrome
medullary thyroid carcinomas more aggressive than MEN 2A

no primary hyperthyroidism

neruomas of skin, oral mucosa, eyse, RT, GI

Marfanoid habitus
MEN 2B
variant of MEN 2A with strong predisposition to thyroid cancer but not other manifestations

development at earlier age
Familial medullary thryoid cancer
pineal tumor most frequent in first two decades of life

soft, friable, gray masses punctuated with areas of hemorrhage and necrosis

masses of pleomorphic cells 2-4 x the diameter of RBC

spread via CSF; may cause hydrocephalus
pineoblastoma
pineal tumor occuring mostly in adults; slower growing

well circumscribed, gray, or hemorrhagic masses that compress but don't infiltrate

pineocytes with darkly staining round-to-oval fairly regular nuclei

immunoreactivity to neuro specific enolase adn synaptophysin

pineocytomatous pseudorosettes; lobular growth pattern
pineocytoma