Path Spring Images

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A, Photomicrograph of normal pituitary. The gland is populated by several distinct cell populations containing a variety of stimulating (tropic) hormones. Each of the hormones has different staining characteristics, resulting in a mixture of cell types in routine histologic preparations.

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A, Photomicrograph of normal pituitary. The gland is populated by several distinct cell populations containing a variety of stimulating (tropic) hormones. Each of the hormones has different staining characteristics, resulting in a mixture of cell types in routine histologic preparations. B, Immunostain for human growth hormone.

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Pituitary adenoma. This massive, nonfunctional adenoma has grown far beyond the confines of the sella turcica and has distorted the overlying brain. Nonfunctional adenomas tend to be larger at the time of diagnosis than those that secrete a hormone.

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Pituitary adenoma. The monomorphism of these cells contrasts markedly with the mixture of cells seen in the normal anterior pituitary. Note also the absence of reticulin network.

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Ultrastructural features of prolactinomas. A, Electron micrograph of a sparsely granulated prolactinoma. The tumor cells contain abundant granular endoplasmic reticulum (indicative of active protein synthesis) and small numbers of electron-dense secretory granules. B, Electron micrograph of densely granulated growth hormone-secreting adenoma. The tumor cells are filled with numerous large, electron-dense secretory granules.

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Adamantinomatous craniopharyngioma, demonstrating characteristic compact, lamellar "wet" keratin (right half of photomicrograph) and cords of squamous epithelium with peripheral palisading on the left.

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A person with hyperthyroidism. A wide-eyed, staring gaze, caused by overactivity of the sympathetic nervous system, is one of the features of this disorder. In Graves disease, one of the most important causes of hyperthyroidism, accumulation of loose connective tissue behind the eyeballs, also adds to the protuberant appearance of the eyes.

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Hashimoto thyroiditis. The thyroid parenchyma contains a dense lymphocytic infiltrate with germinal centers. Residual thyroid follicles lined by deeply eosinophilic Hürthle cells are also seen.

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Granulomatous thyroiditis. The thyroid parenchyma contains a chronic inflammatory infiltrate with a multinucleate giant cell (above left) and a colloid follicle (bottom right).

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Graves disease. A, There is diffuse symmetric enlargement of the gland and a beefy deep red parenchyma. Compare with gross photograph of multinodular goiter in Figure 24-15. B, Diffusely hyperplastic thyroid in a case of Graves' disease. The follicles are lined by tall, columnar epithelium. The crowded, enlarged epithelial cells project into the lumens of the follicles. These cells actively resorb the colloid in the centers of the follicles, resulting in the scalloped appearance of the edges of the colloid.

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A 52-year-old woman with a huge colloid goiter who developed compressive symptoms.

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Multinodular goiter. A, Gross morphology demonstrating a coarsely nodular gland, containing areas of fibrosis and cystic change. B, Photomicrograph of a hyperplastic nodule, with compressed residual thyroid parenchyma on the periphery. Note absence of a prominent capsule, a distinguishing feature from follicular neoplasms.

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Follicular adenoma of the thyroid. A, A solitary, well-circumscribed nodule is seen. B, The photomicrograph shows well-differentiated follicles resembling normal thyroid parenchyma.

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Follicular adenoma of the thyroid. B, The photomicrograph shows well-differentiated follicles resembling normal thyroid parenchyma.

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Hürthle cell (oxyphil) adenoma. A high-power view showing that the tumor is composed of cells with abundant eosinophilic cytoplasm and small regular nuclei.

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Papillary carcinoma of the thyroid. A, The macroscopic appearance of a papillary carcinoma with grossly discernible papillary structures. This particular example contains well-formed papillae

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Papillary carcinoma of the thyroid. A, The macroscopic appearance of a papillary carcinoma with grossly discernible papillary structures. This particular example contains well-formed papillae (B), lined by cells with characteristic empty-appearing nuclei, sometimes called "Orphan Annie eye" nuclei (C).

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Papillary carcinoma of the thyroid.This particular example contains well-formed papillae (B), lined by cells with characteristic empty-appearing nuclei, sometimes called "Orphan Annie eye" nuclei (C).

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Papillary carcinoma of the thyroid. D, Cells obtained by fine-needle aspiration of a papillary carcinoma. Characteristic intranuclear inclusions are visible in some of the aspirated cells.

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Follicular carcinoma. A, Cut surface of a follicular carcinoma with substantial replacement of the lobe of the thyroid. The tumor has a light-tan appearance and contains small foci of hemorrhage. B, A few of the glandular lumens contain recognizable colloid.

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Capsular integrity in follicular neoplasms. In adenomas (A), a fibrous capsule, usually thin but occasionally more prominent, circumferentially surrounds the neoplastic follicles and no capsular invasion is seen (arrows); compressed normal thyroid parenchyma is usually present external to the capsule (top of the panel). In contrast, follicular carcinomas demonstrate capsular invasion (B, arrows) that may be minimal, as in this case, or widespread. The presence of vascular invasion is another feature of follicular carcinomas.

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Medullary carcinoma of thyroid. A, These tumors typically show a solid pattern of growth and do not have connective tissue capsules.

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Medullary carcinoma of thyroid. B, Histology demonstrates abundant deposition of amyloid, visible here as homogeneous extracellular material, derived from calcitonin molecules secreted by the neoplastic cells.

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Electron micrograph of medullary thyroid carcinoma. These cells contain membrane-bound secretory granules that are the sites of storage of calcitonin and other peptides.

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Parathyroid adenomas are almost always solitary lesions. Technetium-99m-sestamibi radionuclide scan demonstrates an area of increased uptake corresponding to the left inferior parathyroid gland (arrow). This person had a parathyroid adenoma. Preoperative scintigraphy is useful in localizing and distinguishing adenomas from parathyroid hyperplasia, where more than one gland would demonstrate increased uptake.

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Parathyroid adenoma. A, Solitary chief cell parathyroid adenoma (low-power photomicrograph) revealing clear delineation from the residual gland below.

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Parathyroid adenoma. B, High-power detail of a chief cell parathyroid adenoma. There is some slight variation in nuclear size but no anaplasia and some slight tendency to follicular formation.

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Hormone production in pancreatic islet cells. Immunoperoxidase staining shows a dark reaction product for insulin in β cells (A), glucagon in α cells (B), and somatostatin in δ cells (C). D, Electron micrograph of a β cell shows the characteristic membrane-bound granules, each containing a dense, often rectangular core and distinct halo. E, Portions of an α cell (left) and a δ cell (right) also show granules, but with closely apportioned membranes. The α-cell granule shows a dense, round center.

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A, Insulitis, shown here from a rat (BB) model of autoimmune diabetes, also seen in type 1 human diabetes.

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B, Amyloidosis of a pancreatic islet in type 2 diabetes.

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Severe renal hyaline arteriolosclerosis. Note a markedly thickened, tortuous afferent arteriole. The amorphous nature of the thickened vascular wall is evident. (PAS stain).

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Renal cortex showing thickening of tubular basement membranes in a diabetic patient (PAS stain).

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Diffuse and nodular diabetic glomerulosclerosis (PAS stain). Note the diffuse increase in mesangial matrix and characteristic acellular PAS-positive nodules.

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Nephrosclerosis in a patient with long-standing diabetes. The kidney has been bisected to demonstrate both diffuse granular transformation of the surface (left) and marked thinning of the cortical tissue (right). Additional features include some irregular depressions, the result of pyelonephritis, and an incidental cortical cyst (far right).

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Diffuse hyperplasia of the adrenal contrasted with normal adrenal gland. In cross-section the adrenal cortex is yellow and thickened, and a subtle nodularity is seen (contrast with Figure 24-46). Both adrenal glands were diffusely hyperplastic in this patient with ACTH-dependent Cushing syndrome.

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A, Primary pigmented nodular adrenocortical disease showing prominent pigmented nodules in the adrenal gland. B, On histologic examination the nodules are composed of cells containing lipofuscin pigment, seen in the right part of the field.

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A patient with Cushing syndrome demonstrating central obesity, "moon facies," and abdominal striae.

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Waterhouse-Friderichsen syndrome in a child. The dark, hemorrhagic adrenal glands are distended with blood.

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Waterhouse-Friderichsen syndrome. At autopsy, the adrenals were grossly hemorrhagic and shrunken; microscopically, little residual cortical architecture is discernible.

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Adrenal cortical adenoma. The adenoma is distinguished from nodular hyperplasia by its solitary, circumscribed nature. The functional status of an adrenal cortical adenoma cannot be predicted from its gross or microscopic appearance.

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Histologic features of an adrenal cortical adenoma. The neoplastic cells are vacuolated because of the presence of intracytoplasmic lipid. There is mild nuclear pleomorphism. Mitotic activity and necrosis are not seen.

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Adrenal carcinoma. The hemorrhagic and necrotic tumor dwarfs the kidney and compresses the upper pole.

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Adrenal carcinoma (A) revealing marked anaplasia, contrasted with normal adrenal cortical cells (B).

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Adrenal carcinoma (A) revealing marked anaplasia, contrasted with normal adrenal cortical cells (B).

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Pheochromocytoma. The tumor is enclosed within an attenuated cortex and demonstrates areas of hemorrhage. The comma-shaped residual adrenal is seen below.

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Pheochromocytoma demonstrating characteristic nests of cells ("zellballen") with abundant cytoplasm. Granules containing catecholamine are not visible in this preparation. It is not uncommon to find bizarre cells even in pheochromocytomas that are biologically benign.

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Life cycle changes. A, Mammograms in young women are typically radiodense or white in appearance, making mass-forming lesions or calcifications (which are also radiodense) difficult to detect. B, The density of a young woman's breast stems from the predominance of fibrous interlobular stroma and the paucity of adipose tissue. Before pregnancy the lobules are small and are invested by loose cellular intralobular stroma. Larger ducts connect lobules. C, During pregnancy, branching of terminal ducts produces more numerous, larger lobules. Luminal cells within lobules undergo lactational change, a precursor to milk formation. D, With increasing age the lobules decrease in size and number, and the interlobular stroma is replaced by adipose tissue. E, Mammograms become more radiolucent with age as a result of the increase in adipose tissue, which facilitates the detection of radiodense mass-forming lesions and calcifications.

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Mammary duct ectasia. Chronic inflammation and fibrosis surround an ectatic duct filled with inspissated debris. The fibrotic response can produce a firm irregular mass that mimics invasive carcinoma on palpation or mammogram.

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Apocrine cysts. A, Clustered, rounded calcifications are seen in a radiograph. B, Gross appearance of typical cysts filled with dark, turbid fluid contents. C, Cysts are lined by apocrine cells with round nuclei and abundant granular cytoplasm. Note the luminal calcifications, which form on secretory debris.

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A, A normal duct or acinus with a single basally located myoepithelial cell layer (cells with dark, compact nuclei and scant cytoplasm) and a single luminal cell layer (cells with larger open nuclei, small nucleoli, and more abundant cytoplasm).

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Breast. B, Epithelial hyperplasia. The lumen is filled by a heterogeneous, mixed population of luminal and myoepithelial cell types. Irregular slitlike fenestrations are prominent at the periphery.

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Sclerosing adenosis. The involved terminal duct lobular unit is enlarged, and the acini are compressed and distorted by dense stroma. Calcifications are present within some of the lumens. Unlike carcinomas, the acini are arranged in a swirling pattern, and the outer border is well circumscribed.

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Radial sclerosing lesion. A, The radiograph shows an irregular central mass with long radiodense projections. B, Grossly the mass appears solid and has irregular borders, but it is not as firm as an invasive carcinoma. C, The mass consists of a central nidus of small tubules entrapped in a densely fibrotic stroma and numerous projections containing epithelium with varying degrees of cyst formation and hyperplasia.

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Intraductal papilloma. A central fibrovascular core extends from the wall of a duct. The papillae arborize within the lumen and are lined by myoepithelial and luminal cells.

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A, Atypical ductal hyperplasia. A duct is filled with a mixed population of cells consisting of oriented columnar cells at the periphery and more rounded cells within the central portion. Although some of the spaces are round and regular, the peripheral spaces are irregular and slitlike. These features are highly atypical, but fall short of a diagnosis of DCIS.

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B, Atypical lobular hyperplasia. A population of monomorphic small, round, loosely cohesive cells partially fill a lobule. Some intracellular lumens can be seen. Although the cells are morphologically identical to the cells of LCIS, the extent of involvement is not sufficient for this diagnosis.

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Noncomedo DCIS. A, Cribriform DCIS composed of cells forming round, regular ("cookie cutter") spaces. The lumens are filled with calcifying secretory material.

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Noncomedo DCIS. B, This solid DCIS has almost completely filled and distorted this lobule with only a few remaining normal luminal cells visible. This type of DCIS is not usually associated with calcifications and may be clinically occult.

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Noncomedo DCIS. A, Papillary DCIS. Delicate fibrovascular cores extend into a duct and are lined by a monomorphic population of tall columnar cells. Myoepithelial cells are absent.

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Noncomedo DCIS. B, Micropapillary DCIS. The papillae are connected to the duct wall by a narrow base and often have bulbous or complex outgrowths. The papillae are solid and lack fibrovascular cores.

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Lobular carcinoma in situ. A, A monomorphic population of small, rounded, loosely cohesive cells fills and expands the acini of a lobule. The underlying lobular architecture can still be recognized. The cells extend into the adjacent lobule by pagetoid spread. B, An immunoperoxidase study shows E-cadherin-positive normal luminal cells that have been undermined by E-cadherin-negative LCIS cells spreading along the basement membrane.

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A, A well-differentiated invasive carcinoma of no special type consists of tubules or a cribriform pattern of cells with small monomorphic nuclei. B, A moderately differentiated carcinoma shows less tubule formation and more solid nests of cells and pleomorphic nuclei. C, This poorly differentiated invasive carcinoma of no special type infiltrates as ragged sheets of pleomorphic cells with numerous mitotic figures and central areas of tumor necrosis.

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Invasive carcinoma variants. A, The specimen radiogram shows a well-circumscribed mass. The majority of such masses are benign, but approximately 6% are carcinomas. B, Grossly, this carcinoma has a pushing border and a fleshy appearance. C, Medullary carcinoma. Note the pushing border, the sheetlike growth of the pleomorphic tumor cells, and the prominent lymphoplasmacytic infiltrate. D, Mucinous (colloid) carcinoma. The malignant cells lie within pools of extracellular mucin. The tumor also has a pushing border and is very deceptively soft in texture.

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Tubular carcinoma. This carcinoma is composed of well-formed angulated tubules lined by a single layer of cells with small uniform nuclei.

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Fibroadenoma. A, The radiogram shows a characteristically well-circumscribed mass. B, Grossly, a rubbery, white, well-circumscribed mass is clearly demarcated from the surrounding yellow adipose tissue. The absence of adipose tissue accounts for the radiodensity of the lesion. C, The proliferation of intralobular stroma surrounds, pushes, and distorts the associated epithelium. The border is sharply delimited from the surrounding tissue.

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Phyllodes tumor. Compared to a fibroadenoma, there is increased stromal cellularity, cytologic atypia, and stromal overgrowth, giving rise to the typical leaflike architecture.

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Gynecomastia. Terminal ducts (without lobule formation) are lined by a multilayered epithelium with small papillary tufts. There is typically surrounding periductal hyalinization and fibrosis.

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Opened ureters showing ureteritis cystica. Note smooth cysts projecting from the mucosa.

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Papillary transitional cell carcinoma extensively involving the ureter

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Exstrophy of the bladder in a newborn boy. The tied umbilical cord is seen above the hyperemic mucosa of the everted bladder. Below is an incompletely formed penis with marked epispadias.

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Cystitis with malacoplakia of bladder showing inflammatory exudate and broad, flat plaques.

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Malacoplakia, periodic acid-Schiff (PAS) stain. Note the large macrophages with granular PAS-positive cytoplasm and several dense, round Michaelis-Gutmann bodies surrounded by artifactual cleared holes in the upper middle field (arrow).

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Cross-section of bladder with upper section showing a large papillary tumor. The lower section demonstrates multifocal smaller papillary neoplasms.

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Papilloma consisting of small papillary fronds lined by normal-appearing urothelium.

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Low-grade papillary urothelial carcinoma with an overall orderly appearance, with a thicker lining than papilloma and scattered hyperchromatic nuclei and mitotic figures (arrows).

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High-grade papillary urothelial carcinoma with marked cytologic atypia.

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A, Normal urothelium with uniform nuclei and well-developed umbrella cell layer (arrow).

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B, Urothelium.
Flat carcinoma in situ with numerous cells having enlarged and pleomorphic nuclei.

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Opened bladder showing a high-grade invasive transitional cell carcinoma at an advanced stage. The aggressive multinodular neoplasm has fungated into the bladder lumen and spread over a wide area. The yellow areas represent areas of ulceration and necrosis.

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Hypertrophy and trabeculation of bladder wall secondary to polypoid hyperplasia of the prostate.

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Carcinoma of urethra with typical fungating growth.

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Condyloma acuminatum of the penis.

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Condyloma acuminatum of the penis. Low magnification reveals the papillary (villous) architecture, and thickening of the epidermis

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Condyloma acuminatum of the penis. The epithelium shows vacuolization (koilocytosis) characteristic of human papillomavirus infection.

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Bowen disease (carcinoma in situ) of the penis. Note the hyperchromatic, dysplastic dyskeratotic epithelial cells with scattered mitoses above the basal layer. The intact basement membrane is not readily seen in this picture.

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Carcinoma of the penis. The glans penis is deformed by a firm, ulcerated, infiltrative mass.

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A, Normal testis shows tubules with active spermatogenesis.

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B, Testicular atrophy in cryptorchidism. The tubules show Sertoli cells but no spermatogenesis. There is thickening of basement membranes and an apparent increase in interstitial Leydig cells.

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Acute epididymitis caused by gonococcal infection. The epididymis is replaced by an abscess. Normal testis is seen on the right.

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Torsion of testis.

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Seminoma of the testis appears as a fairly well-circumscribed, pale, fleshy, homogeneous mass.

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Seminoma. A, Low magnification shows clear seminoma cells divided into poorly demarcated lobules by delicate septa.

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Seminoma. B, Microscopic examination reveals large cells with distinct cell borders, pale nuclei, prominent nucleoli, and a sparse lymphocytic infiltrate.

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Embryonal carcinoma. In contrast to the seminoma illustrated in Figure 21-23, the embryonal carcinoma is a hemorrhagic mass.

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Embryonal carcinoma shows sheets of undifferentiated cells as well as primitive glandular differentiation. The nuclei are large and hyperchromatic.

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Choriocarcinoma shows clear cytotrophoblastic cells (arrowhead) with central nuclei and syncytiotrophoblastic cells (arrow) with multiple dark nuclei embedded in eosinophilic cytoplasm. Hemorrhage and necrosis are seen in the upper right field.

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Teratoma of testis. The variegated cut surface with cysts reflects the multiplicity of tissue found histologically.

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Teratoma of the testis consisting of a disorganized collection of glands, cartilage, smooth muscle, and immature stroma.

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Benign prostate gland with basal cell and secretory cell layer.

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Nodular prostatic hyperplasia. A, Well-defined nodules of BPH compress the urethra into a slitlike lumen.

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Nodular prostatic hyperplasia. B, A microscopic view of a whole mount of the prostate shows nodules of hyperplastic glands on both sides of the urethra.

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Nodular prostatic hyperplasia.
C, Under high power the characteristic dual cell population: the inner columnar and outer flattened basal cell can be seen.

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Adenocarcinoma of the prostate. Carcinomatous tissue is seen on the posterior aspect (lower left). Note solid whiter tissue of cancer in contrast to spongy appearance of benign peripheral zone in the contralateral side.

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Metastatic osteoblastic prostatic carcinoma within vertebral bodies.

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A, Photomicrograph of small focus of adenocarcinoma of the prostate demonstrating small glands crowded in between larger benign glands.

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A, Photomicrograph of small focus of adenocarcinoma of the prostate demonstrating small glands crowded in between larger benign glands. B, Higher magnification shows several small malignant glands with enlarged nuclei, prominent nucleoli, and dark cytoplasm, as compared with larger benign gland (top).

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Carcinoma of prostate showing perineural invasion by malignant glands. Compare to benign gland (left).

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A, Low-grade (Gleason score 1 + 1 = 2) prostate cancer consisting of back-to-back uniform-sized malignant glands. Glands contain eosinophilic intraluminal prostatic crystalloids, a feature more commonly seen in cancer than benign glands and more frequently seen in lower grade than higher grade prostate cancer. B, Needle biopsy of the prostate with variably sized, more widely dispersed glands of moderately differentiated Gleason score 3 + 3 = 6) adenocarcinoma. C, Poorly differentiated (Gleason score 5 + 5 = 10) adenocarcinoma composed of sheets of malignant cells.

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Lesion caused by molluscum contagiosum infection. Arrow points to intracytoplasmic viral inclusions.

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A, Acute salpingo-oophoritis, with tubo-ovarian abscess. The fallopian tubes and ovaries have coalesced into an inflammatory mass adherent to the uterus.

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B, Salpingitis with edematous tubal plicae expanded by inflammatory cell infiltrates.

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Non-neoplastic epithelial vulvar disorders. A, Lichen sclerosus. B, Squamous cell hyperplasia. The main features of the lesions are indicated in the figures.

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A, Numerous condylomas of the vulva encircling the introitus. B, Histopathology of condyloma acuminatum showing acanthosis, hyperkeratosis, and koilocytic atypia with enlarged, atypical nuclei and cytoplasmic vacuolation (center of microphotograph).

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√A, Numerous condylomas of the vulva encircling the introitus. B, Histopathology of condyloma acuminatum showing acanthosis, hyperkeratosis, and koilocytic atypia with enlarged, atypical nuclei and cytoplasmic vacuolation (center of microphotograph).

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A, Histopathology of classic vulvar intraepithelial neoplasia (HPV positive) with diffuse cellular atypia, immaturity, nuclear crowding, and increased mitotic activity.

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B, Differentiated VIN (HPV negative), showing maturation of the superficial layers, hyperkeratosis, and basal cell atypia (arrow).

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A, Basaloid vulvar carcinoma (HPV positive). B, Warty vulvar carcinoma (HPV positive).

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A, Well-differentiated, keratinizing squamous cell carcinoma of the vulva (HPV negative). B, Verrucous carcinoma of the vulva (HPV negative).

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Papillary hidradenoma of the vulva, a well-circumscribed tumor nodule composed of benign papillary projections covered with columnar secretory epithelium and underlying myoepithelial cells.

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Paget disease of the vulva with clusters and single pale tumor cells spreading along the basal portion of the squamous epithelium. There is inflammation in the underlying dermis.

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Paget disease of the vulva with clusters and single pale tumor cells spreading along the basal portion of the squamous epithelium. There is inflammation in the underlying dermis.

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Clear cell adenocarcinoma of the vagina showing vacuolated tumor cells in clusters and glandlike structures.

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Sarcoma botryoides (embryonal rhabdomyosarcoma) of the vagina appearing as a polypoid mass protruding from the vagina.

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Endocervical polyp composed of a dense fibrous stroma covered with endocervical columnar epithelium.

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Cervical squamocolumnar junction showing mature, glycogenized (pale) squamous epithelium, immature (dark pink) squamous metaplastic cells, and columnar endocervical glandular epithelium.

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Spectrum of cervical intraepithelial neoplasia: normal squamous epithelium for comparison; LSIL (CIN I) with koilocytic atypia; HSIL (CIN II) with progressive atypia and expansion of the immature basal cells above the lower third of the epithelial thickness; HSIL (CIN III) with diffuse atypia, loss of maturation, and expansion of the immature basal cells to the epithelial surface.

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A, LSIL-routine H&E staining. B, In situ hybridization test for HPV DNA. The dark granular staining denotes HPV DNA, which is typically most abundant in the koilocytes. C, Diffuse immunostaining for the proliferation marker Ki-67, illustrating abnormal expansion of the proliferating cells from the normal basal location to the superficial layers of the epithelium. D, Up-regulation of p16INK4 (seen as intense brown immunostaining) characterizes high oncogenic risk HPV infections.

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Squamous cell carcinoma of the cervix. A, Microinvasive squamous cell carcinoma with invasive nest breaking through the basement membrane of HSIL. B, Invasive squamous cell carcinoma.

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Squamous cell carcinoma of the cervix. B, Invasive squamous cell carcinoma.

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Adenocarcinoma of the cervix. A, Adenocarcinoma in situ (arrow) showing dark glands adjacent to normal, pale endocervcial glands. B, Invasive adenocarcinoma.

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The cytology of cervical intraepithelial neoplasia as seen on the Papanicolaou smear. Normal cytoplasmic staining in superficial cells (A and B) may be either red or blue. A, Normal exfoliated superficial squamous cells.

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The cytology of cervical intraepithelial neoplasia as seen on the Papanicolaou smear. Normal cytoplasmic staining in superficial cells (A and B) may be either red or blue. B, LSIL-koilocytes.

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The cytology of cervical intraepithelial neoplasia as seen on the Papanicolaou smear. . C, HSIL (CIN II).

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The cytology of cervical intraepithelial neoplasia as seen on the Papanicolaou smear. D, HSIL (CIN III). Note the reduction in cytoplasm and the increase in the nucleus-to-cytoplasm ratio, which occurs as the grade of the lesion increases. This reflects the progressive loss of cellular differentiation on the surface of the lesions from which these cells are exfoliated.

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Histology of the menstrual cycle. A, Proliferative phase with mitoses (arrow).

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Histology of the menstrual cycle. B, Early secretory phase with subnuclear vacuoles (arrow).

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Histology of the menstrual cycle. C, Late secretory exhaustion and predecidual changes (arrow).

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Histology of the menstrual cycle. D, Menstrual endometrium with stromal breakdown (arrow) (see text).

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Common causes of abnormal uterine bleeding. A, The most common is dysfunctional uterine bleeding, seen here as anovulatory endometrium with stromal breakdown. Note breakdown associated with proliferative glands.

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Common causes of abnormal uterine bleeding. B, Chronic endometritis with numerous plasma cells (arrow).

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Common causes of abnormal uterine bleeding. C, Endometrial polyp.

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Common causes of abnormal uterine bleeding.
D, Submucosal leiomyoma with attenuation of the endometrial lining (arrow).

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Endometriosis. A, Endometriosis is present in the mucosa of the colon.

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Endometriosis. B, Higher magnification reveals the presence of both endometrial glands and stroma.

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Adenomyosis. This disorder is characterized by functional endometrial nests within the myometrium, producing foci of hemorrhagic cysts within the uterine wall.

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A, Simple hyperplasia without atypia with architectural abnormalities including mild glandular crowding and cystic glandular dilatation.

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B, Complex hyperplasia without atypia demonstrates increased glandular crowding with areas of back-to-back glands with cytologic features similar to proliferative endometrium.

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C, Complex hyperplasia with atypia has architectural features similar to complex hyperplasia without atypia, but the cytologic features have changed.

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D, High magnification of complex hyperplasia with atypia showing rounded, vesicular nuclei with prominent nucleoli (arrow).

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Type I carcinoma. A, Endometrial adenocarcinoma presenting as a fungating mass in the fundus of the uterus. B, Well-differentiated (grade 1) endometrioid adenocarcinoma with preserved glandular architecture but lack of intervening stroma, distinguishing it from hyperplasia. C, Moderately differentiated (grade 2) endometrioid adenocarcinoma with glandular architecture admixed with solid areas. D, Poorly differentiated (grade 3) endometrioid adenocarcinoma with predominantly solid growth.

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Type II carcinoma. A, Endometrial intraepithelial carcinoma, the precursor to serous carcinoma showing malignant cells (arrow) with morphologic features identical to serous carcinoma lining the surfaces of the endometrial glands without obvious stromal invasion. B, Strong, diffuse expression of p53 as detected by immunohistochemistry in endometrial intraepithelial carcinoma. C, Serous carcinoma of the endometrium with papillary growth pattern consisting of malignant cells with marked cytologic atypia including high nuclear-to-cytoplasmic ratio, atypical mitotic figures, and hyperchromasia. D, As with the previous lesion, there is an accumulation of p53 protein in the nucleus.

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A, Malignant mixed müllerian tumor (MMMT), showing both malignant epithelial and stromal components. B, Lymph node metastasis from a MMMT showing only the epithelial component as is typically seen.

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A, Leiomyomas of the myometrium. The uterus is opened to reveal multiple tumors in submucosal (bulging into the endometrial cavity), intramural, and subserosal locations that display a firm white appearance on sectioning. B, Leiomyoma showing well-differentiated, regular, spindle-shaped smooth muscle cells associated with hyalinization.

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Leiomyosarcoma. A, A large hemorrhagic tumor mass distends the lower corpus and is flanked by two leiomyomas.

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Leiomyosarcoma.
B, The tumor cells are irregular in size and have hyperchromatic nuclei with numerous mitotic figures (arrows).

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Polycystic ovarian disease and cortical stromal hyperplasia. A, The ovarian cortex reveals numerous clear cysts.

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Polycystic ovarian disease and cortical stromal hyperplasia. B, Sectioning of the cortex reveals several subcortical cystic follicles.

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Polycystic ovarian disease and cortical stromal hyperplasia. C, Cystic follicles seen in a low-power microphotograph.

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Polycystic ovarian disease and cortical stromal hyperplasia. D, Cortical stromal hyperplasia manifests as diffuse stromal proliferation with symmetric enlargement of the ovary.

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Cortical inclusion cysts of the ovary. These cysts appear to arise from the overlying mesothelium and are presumed to be the site of origin for many ovarian epithelial neoplasms.

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A, Serous borderline tumor opened to display a cyst cavity lined by delicate papillary tumor growths.

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B, Cystadenocarcinoma. The cyst is opened to reveal a large, bulky tumor mass.

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. B, Cystadenocarcinoma. The cyst is opened to reveal a large, bulky tumor mass.

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C, Another borderline tumor growing on the ovarian surface (lower).

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Serous cystadenomas. A, Papillary serous cystadenoma revealing stromal papillae with a columnar epithelium. B, Borderline serous tumor showing increased architectural complexity and epithelial cell stratification. C, Complex micropapillary growth defines a low-grade "micropapillary" serous carcinoma. D, Papillary serous cystadenocarcinoma of the ovary with invasion of underlying stroma.

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A, A mucinous cystadenoma with its multicystic appearance and delicate septa. Note the presence of glistening mucin within the cysts.

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B, Columnar cell lining of mucinous cystadenoma.

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A, Pseudomyxoma peritonei viewed at laparotomy revealing massive overgrowth of a gelatinous metastatic tumor originating from the appendix. B, Histology of peritoneal implants from an appendiceal tumor, showing mucin-producing epithelium and free mucin (arrow).

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A, Brenner tumor (right) associated with a benign cystic teratoma (left).

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A, Brenner tumor (right) associated with a benign cystic teratoma (left). B, Histologic detail of characteristic epithelial nests within the ovarian stroma.

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Opened mature cystic teratoma (dermoid cyst) of the ovary. Hair (bottom) and a mixture of tissues are evident.

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Benign cystic teratoma. Low-power view of skin (right edge), beneath which there is brain tissue (left edge).

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Immature teratoma of the ovary illustrating primitive neuroepithelium.

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Dysgerminoma showing polyhedral tumor cells with round nuclei and adjacent inflammation.

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A Schiller-Duval body in yolk sac carcinoma.

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Granulosa cell tumor. A, The tumor cells are arranged in sheets punctuated by small follicle-like structures (Call-Exner bodies). B, Strong immunohistochemical positivity with an antibody to inhibin characterizes these tumors.

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A, Thecoma-fibroma composed of plump, differentiated stromal cells with thecal appearance.

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B, Large bisected fibroma of the ovary apparent as a white, firm mass (right). The fallopian tube is attached.

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Sertoli cell tumor. A, Gross photograph illustrating characteristic golden-yellow appearance of the tumor.

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Sertoli cell tumor. B, Photomicrograph showing well-differentiated Sertoli cell tubules.

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A, First-trimester chorionic villi composed of delicate mesh of central stroma surrounded by two discrete layers of epithelium-the outer layer consisting of syncytiotrophoblast (two arrows) and the inner layer consisting of cytotrophoblast (arrow).

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B, Third-trimester chorionic villi composed of stroma with dense network of dilated capillaries surrounded by markedly thinned-out syncytiotrophoblast and cytotrophoblast (same magnification as A.)

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Placental infections derived from ascending and blood-borne routes. Acute chorioamnionitis. A, On gross examination the placenta contains greenish opaque membranes.

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Placental infections derived from ascending and blood-borne routes. Acute chorioamnionitis. B, A photomicrograph illustrates a dense bandlike inflammatory exudate on the amniotic surface (arrow).

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Placental infections derived from ascending and blood-borne routes. Acute chorioamnionitis. C, Acute necrotizing intervillositis, from a fetal-maternal infection by Listeria.

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Acute atherosis of uterine vessels in eclampsia. Note fibrinoid necrosis of the vessel walls, subendothelial macrophages, and perivascular lymphocytic infiltrate.

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Complete hydatidiform mole. Note marked distention of the uterus by vesicular chorionic villi. Adnexa (ovaries and fallopian tubes) are visible on the left and right side of the uterus.

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Complete hydatidiform mole demonstrating marked villous enlargement, edema, and circumferential trophoblast proliferation.

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A, Normal chorionic villi immunostained for p57 exhibit staining in both stromal and cytotrophoblast (arrow) nuclei.

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B, Complete moles lack expression of p57 in the cytotrophoblast (arrow) and villous stroma.

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A, Invasive mole presenting as a hemorrhagic mass adherent to the uterine wall.

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Invasive mole l. B, On cross-section, the tumor invades into the myometrium.

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A, Choriocarcinoma presenting as a bulky hemorrhagic mass invading the uterine wall.

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B, Photomicrograph of choriocarcinoma illustrating both neoplastic cytotrophoblast and syncytiotrophoblast.

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A, Placental-site trophoblastic tumor (PSTT), presenting as a discrete mass in the myometrium. B, Histology of PSTT.

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Astrocytes and their processes. Immunohistochemical staining for GFAP reveals astrocytic perinuclear cytoplasm and well-developed processes (brown).

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Hydrocephalus. Dilated lateral ventricles seen in a coronal section through the midthalamus.

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Duret hemorrhage involving the brainstem at the junction of the pons and midbrain.

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Lissencephaly. The absence of cortical gyri defines this abnormality, seen here in the brain from a full-term infant.

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Agenesis of the corpus callosum. The midsagittal view of the left hemisphere shows the lack of a corpus callosum and cingulate gyrus above the third ventricle.

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Arnold-Chiari malformation. Midsagittal section showing small posterior fossa contents, downward displacement of the cerebellar vermis, and deformity of the medulla (arrows indicate the approximate level of the foramen magnum).

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Multicystic leukoencephalopathy. Numerous cystic spaces representing the consequences of widespread ischemic injury are present.

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A, Multiple contusions involving the inferior surfaces of frontal lobes, anterior temporal lobes, and cerebellum.

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B, Acute contusions are present in both temporal lobes, with areas of hemorrhage and tissue disruption (arrows).

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C, Remote contusions are present on the inferior frontal surface of this brain, with a yellow color (associated with the term plaque jaune).

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Epidural hematoma covering a portion of the dura. Also present are multiple small contusions in the temporal lobe.

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A, Large organizing subdural hematoma attached to the dura. B, Coronal section of the brain showing compression of the hemisphere underlying the subdural hematoma shown in A.

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Cerebral infarction. A, At low magnification it is possible to see the demarcated areas of an acute infarction. In the underlying white matter, the areas of infarction are well shown by the myelin stain. B, Acute ischemic injury causes diffuse eosinophilia of neurons, which are beginning to shrink. C, Infiltration of a cerebral infarct by neutrophils begins at the edges of the lesion where vascular supply has remained intact. D, After about 10 days, an area of infarction is characterized by the presence of macrophages and surrounding reactive gliosis. E, Remote small intracortical infarcts are seen as areas of tissue loss with residual gliosis.

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Cerebral infarction. A, At low magnification it is possible to see the demarcated areas of an acute infarction. In the underlying white matter, the areas of infarction are well shown by the myelin stain. B, Acute ischemic injury causes diffuse eosinophilia of neurons, which are beginning to shrink. C, Infiltration of a cerebral infarct by neutrophils begins at the edges of the lesion where vascular supply has remained intact. D, After about 10 days, an area of infarction is characterized by the presence of macrophages and surrounding reactive gliosis. E, Remote small intracortical infarcts are seen as areas of tissue loss with residual gliosis.

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Widespread white-matter hemorrhages are characteristic of bone marrow embolization.

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A, A hemorrhagic infarction is present in the inferior temporal lobe of the left side of this brain. B, A bland infarct with punctate hemorrhages, consistent with ischemia-reperfusion injury, is present in the temporal lobe.

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Old cystic infarct showing destruction of cortex with cavitation.

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Lacunar infarcts in the caudate and putamen (arrows).

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A, Massive hypertensive hemorrhage rupturing into a lateral ventricle. B, Amyloid deposition in a cortical arteriole in cerebral amyloid angiopathy; inset, Immunohistochemical staining for Aβ shows the deposited material in the vessel wall. C, Electron micrograph shows granular osmophilic material in a case of CADASIL.

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A, View of the base of the brain, dissected to show the circle of Willis with an aneurysm of the anterior cerebral artery (arrow). B, Dissected circle of Willis to show large aneurysm. C, Section through a saccular aneurysm showing the hyalinized fibrous vessel wall (H&E).

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Pyogenic meningitis. A thick layer of suppurative exudate covers the brainstem and cerebellum and thickens the leptomeninges.

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Frontal abscesses (arrows).

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Characteristic findings of viral encephalitis include perivascular cuffs of lymphocytes (A)

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Characteristic findings of viral encephalitis include perivascular cuffs of lymphocytes (A) and microglial nodules (B).

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A, Herpes encephalitis showing extensive destruction of inferior frontal and anterior temporal lobes.

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B, Necrotizing inflammatory process characterizes acute herpes encephalitis.

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The diagnostic histologic finding in rabies is the eosinophilic Negri body, as seen here in a Purkinje cell (arrows).

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HIV encephalitis. Note the microglial nodule and multinucleated giant cells.

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Progressive multifocal leukoencephalopathy. Section stained for myelin showing irregular, poorly defined areas of demyelination, which become confluent in places. Inset, Enlarged oligodendrocyte nucleus represents the effect of viral infection.

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Cryptococcal infection. A, Whole-brain section showing the numerous areas of tissue destruction ("soap bubbles") associated with the spread of organisms in the perivascular spaces.

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Cryptococcal infection. B, At higher magnification it is possible to see the cryptococci in the lesions.

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A, Toxoplasma abscesses in the putamen and thalamus.

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A, Toxoplasma abscesses in the putamen and thalamus. B, Free tachyzoites demonstrated by immunostaining; inset: Toxoplasma pseudocyst with bradyzoites highlighted by immunostaining.

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Necrotizing amebic meningoencephalitis involving the cerebellum (organism highlighted by arrow).

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Prion disease. A, Spongiform change in the cerebral cortex. Inset, High magnification of neuron with vacuoles.

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Prion disease. B, Cerebellar cortex showing kuru plaques (PAS stain) representing aggregated PrPsc.

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Prion disease. C, Cortical plaques surrounded by spongiform change in vCJD.

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Multiple sclerosis. Section of fresh brain showing brown plaque around occipital horn of the lateral ventricle.

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Multiple sclerosis (MS). Unstained regions of demyelination (MS plaques) around the fourth ventricle (Luxol fast blue PAS stain for myelin).

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Multiple sclerosis. A, Myelin-stained section shows the sharp edge of a demyelinated plaque and perivascular lymphocytic cuffs.

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Multiple sclerosis. A, Myelin-stained section shows the sharp edge of a demyelinated plaque and perivascular lymphocytic cuffs.

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Multiple sclerosis. A, Myelin-stained section shows the sharp edge of a demyelinated plaque and perivascular lymphocytic cuffs. B, The same lesion stained for axons shows relative preservation.

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Alzheimer disease with cortical atrophy most evident on the right, where meninges have been removed.

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Alzheimer disease. A, Plaques with dystrophic neurites surrounding amyloid cores are visible (arrows). B, Plaque core and surrounding neuropil are immunoreactive for Aβ. C, Neurofibrillary tangle is present within one neuron, and several extracellular tangles are also present (arrows). D, Silver stain showing a neurofibrillary tangle within the neuronal cytoplasm. E, Tangle (upper left) and neurites around a plaque (lower right) contain tau, demonstrated by immunohistochemistry.

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Pick disease. Pick bodies are round homogeneous neuronal cytoplasmic inclusions that stain intensely with silver stains.

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Parkinson disease. A, Normal substantia nigra.

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Parkinson disease. . B, Depigmented substantia nigra in idiopathic Parkinson disease.

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Parkinson disease. C, Lewy body in a substantia nigra neuron, staining bright pink (arrow).

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Huntington disease. Normal hemisphere on the left, compared with the hemisphere with Huntington disease on the right showing atrophy of the striatum and ventricular dilation.

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Amyotrophic lateral sclerosis. A, Segment of spinal cord viewed from anterior (upper) and posterior (lower) surfaces showing attenuation of anterior (motor) roots compared to posterior (sensory) roots.

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Amyotrophic lateral sclerosis. B, Spinal cord showing loss of myelinated fibers (lack of stain) in corticospinal tracts as well as degeneration of anterior roots.

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Krabbe disease. Much of the white matter is gray/yellow because of the loss of myelin. Inset, "Globoid" cells are the hallmark of the disease.

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Alcoholic cerebellar degeneration. The anterior portion of the vermis (upper portion of figure) is atrophic with widened spaces between the folia.

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Diffuse astrocytoma. A, The right frontal tumor has expanded gyri, which led to flattening (arrows).

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Diffuse astrocytoma. B, There is bilateral expansion of the septum pellucidum by gray, glassy tumor.

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A, Post-contrast T1-weighted coronal MRI shows a large mass in the right parietal lobe with "ring" enhancement.

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B, Glioblastoma appearing as a necrotic, hemorrhagic, infiltrating mass.

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Glioblastoma. Foci of necrosis with pseudopalisading of malignant nuclei and endothelial cell proliferation.

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Pilocytic astrocytoma in the cerebellum with a nodule of tumor in a cyst.

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Oligodendroglioma. Tumor nuclei are round, with cleared cytoplasm forming "halos" and vasculature composed of thin-walled capillaries.

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Ependymoma. A, Tumor growing into the fourth ventricle, distorting, compressing, and infiltrating surrounding structures.

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Ependymoma. B, Microscopic appearance of ependymoma.

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Medulloblastoma. A, Sagittal section of brain showing medulloblastoma destroying the superior midline cerebellum.

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. B, Microscopic appearance of medulloblastoma.

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A, Parasagittal multilobular meningioma attached to the dura with compression of underlying brain.

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B, Meningioma with a whorled pattern of cell growth and psammoma bodies.

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Schwannoma. A, Bilateral eighth-nerve schwannomas.

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Schwannoma. B, Tumor showing cellular areas