Pathology of pituitary, parathyroid, adrenal glands Flashcards

1
Q

pituitary adenomas

A

10-15% of all intracranial neoplasms, F>M, 3rd to 6th decades,
hormonal secretion: Prolactin is most common (approximately 30%)- lactotrophs, acidophil, Non secreting (null cell) is next (approx 25%), GH ACTH next most common, rarely secrete more than one hormone

Pituitary adenoma is just one color no acidophils

very little reticulin (no lobuleS)

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2
Q

Sheehan syndrome, post partum hypopituitarism

A

Postpartum ischemic necrosis of pituitary gland, pituitary gland enlarges in pregnancy (increased lactotrophs), more susceptible to ischemia, obstetrical hemorrhage or shock, results in hypopituitarism (anterior Not posterior)

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3
Q

Stalk effect

A

slight elevation in prolactin level, result of lack of inhibitory hypothalamic influence on prolactin, caused by a mass/destructive lesion pressing on stalk or hypothalamus- not a prolactin secreting adenoma

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4
Q

Rathke cleft cyst

A

Sella or suprasella location. May produce symptoms or may be asymptomatic found at autopsy

Columnar to cuboidal cells with cilia and occasionally mucin , lining a thin walled cyst, developmental origin (remnant of rathkes cleft pouch)

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5
Q

Cranipharyngioma

A

Benign tumors, usually suprasellar, may be within sella, third ventricle or pineal region

2 age peaks (kids, and old adults)

Presenting symptoms Visualt abnormalities (chiasm), hypopituitarism

Histogenesis is uncertain, misplaced odontogenic epithelium, vestigal remnants of rathkes pouch

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6
Q

Parathyroid development

A

Arise from the pharyngeal pouches, (inferior and thymus- 3rd pharyngeal pouch, superior - fourth pharyngeal pouch), Are normally located in proximity of upper and lower poles of the thyroid gland

May be ectopically located in thymus, anterior mediastinum, carotid sheath

10% of people have only 2 or 3 glands instead of the normal 4

yellow brown, composed primarily of chief cells and some oxyphil cells

In adults there is a large amount of interveneing stromal fat (30-70%), chief cells secrete parathyroid hormones

Chief cells are white with blue nucleus

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7
Q

Parathyroid abnormalities

A

Hyper secretion: Parathyroid hyperplasia, parathyroid adenoma, parathyroid carcinoma

Hypofunction (decreased secretion ofPTH)- Congenital (digeorge syndrome), iatrogenic (surgical), familial, autoimmune

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8
Q

Primary hyperparathyroidism

A

F>M, middle age, adenoma, Primary hyperplasia and parathyroid carcinoma

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9
Q

Bone disease in hyperparathyroidism

A

Osteitis fibrosa cystica (erosion of bone matrix by osteoclasts), grossly thinned cortex, fibrosis of marrow with hemorrhage and cyst formation

Brown tumor- osteoclasts, reactive giant cells, hemorrhage, morphologically identicle to giant cell tumor of bone

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10
Q

Parathyroid adenoma

A

solitary nodule arising in a single parathyroid gland
.5-5 gms
other glands are either normal or atrophic
composed of sheets of chief cells with decrease in stromal fat, oxyphil cells may also be present, may show a rim of normal parathyroid at the periphery

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11
Q

Parathyroid hyperplasia

A

Classically all four glands are involved, might be sparing of 1 or 2

Morphologically there is chief cell hyperplasia just as in adenomas

May be difficult to distinguish histologically from adenoma

diffuse not normal even on edge

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12
Q

Parathyroid carcinm

A

Rare, difficult to distinguish from adenomas, usually not dignosed until they become clearly invasive and/or metastatic

Cellular atypia is not a reliable feature of malignancy, mitotic activity, fibrous bands, and capsular/vascular invasion

difficult to remove from surrounding structures at the time of surgery due to fibrous adhesions

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13
Q

Adrenal gland histology

A

Cortex: zonal glomerulosa (G): mineralocorticoids (aldosterone)- salt. Zona fasciculata (F) glucocorticoids (cortisol- sugar). Zona reticularis (R) sex steroids (estrogens and androgens)- Sex)

MEdulla (M)- Chromaffin cells–> catecholamines (epinephrine)

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14
Q

Adrenocortical hyperplasia

A

Bilateral thickening of the adrenal cortex (Diffuse, nodular)

Predominantly fasciculata cells- clear cells, microscopically resembles adrenocortical adenoma

Largeer zone of clear cells

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15
Q

adrenocortical adenoma

A

yellow, encapsulated, 1-2 cm, <30gm, functional or non- functional (Cannot be determined by histology, most are non functional), Predominantly zona fasciculata cells, like hyperplasia, solitary encapsulated lesion

lots of clear cells

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16
Q

Adrenocortical carcinoma

A

Rare, >200-300 g, usually >5 cm diameter, invasive, with effeacement of normal structures, necrosis and hemorrhage, well to poor differentiated, tendency to invade adrenal vein and vena cava, lymph node metastasis

clear cells like (invasive growth and mets)

Capsular necrosis,

17
Q

Pathology of adrenal cortical hyperfunction

A

Hypercortisolism- depends on cause, exogenous glucocorticoids-> Cortical atrophy
Increased ACTH –> bilateral hyperplasia (pituitary adenoma), ACTH independent hypercortisol–> adrenocortical adenoma or carcinoma

Hyperaldosteronism (usually adrenal cortical adenoma (Conn Syndrome)

Congenital adrenal Hyperplasia (CAH)- bilateral hyperplasia

18
Q

Pheochromocytoma

A

Neoplasms composed of adrenal medullary chromaffin cells, classic triad (headaches, palpitations, diaphoresis), predominantly benign, only reliable indicator of malignancy is mets

Mircoscopically- Zellballen (cell balls)- nests of cells within a rich vascular network, abundant cytoplasm thats granular (basophilic), widely variable cytology varying cytology varying from mature chromaffin cells to highly pleomophic cells

Chromaffin cells are neuroendocrine cells- stain with neuroendocrine markers (chromagranin, synaptophysin)

Deep basophilic

19
Q

Paraganglioma

A

Extra adrenal pheochromocytoma (10%)= paraganglioma

Almost all are non functional
Similar morphology to pheochromocytoma (Zell ballen)

Common sites- jugulotympanic, carotid body, vagal, aorticopulmonary