GROSS PATH ROBBINS Flashcards
Pressure hypertrophy due to left ventricular outflow obstruction.
The left ventricle is on the lower right in this apical four-chamber view of the heart.
A membranous type ventricular septal defect (arrow) just proximal to the aortic valve.
Dextro-transposition of the great arteries.
Acute myocardial infarct, predominantly of the posterolateral left ventricle, demonstrated histochemically by a lack of staining by triphenyltetrazolium chloride in areas of necrosis (arrow). The staining defect is due to the lactate dehydrogenase leakage that follows cell death. Note the myocardial hemorrhage at one edge of the infarct that was associated with cardiac rupture, and the anterior scar (arrowhead), indicative of an old infarct. The specimen is oriented with the posterior wall at the top.
Consequences of myocardial ischemia followed by reperfusion. Gross (A) and microscopic (B) appearance of myocardium modified by reperfusion. (A) Large, densely hemorrhagic, anterior wall acute myocardial infarction in a patient with left anterior descending artery thrombus treated with streptokinase, a fibrinolytic agent (slice is stained with triphenyl tetrazolium chloride; see Fig. 12.12). Specimen oriented with posterior wall at top.
Complications of myocardial infarction. (A) Anterior myocardial rupture in an acute infarct (arrow). (B) Rupture of the ventricular septum (arrow). (C) Complete rupture of a necrotic papillary muscle.
Complications of myocardial infarction. ( (D) Fibrinous pericarditis, showing a dark, roughened epicardial surface overlying an acute infarct. E, Early expansion of anteroapical infarct with wall thinning (arrow) and mural thrombus. F, Large apical left ventricular aneurysm (arrow). The left ventricle is on the right in this apical four-chamber view of the heart.
Hypertensive heart disease, systemic and pulmonary. (A) Systemic (left-sided) hypertensive heart disease. There is marked concentric thickening of the left ventricular wall causing reduction in lumen size. The left ventricle and left atrium (asterisk) are on the right in this apical four-chamber view of the heart. A pacemaker is present in the right ventricle (arrow).
Hypertensive heart disease, systemic and pulmonary.
(B) Pulmonary (right-sided) hypertensive heart disease (cor pulmonale). The right ventricle is markedly dilated and has a thickened free wall and hypertrophied trabeculae (apical four-chamber view of heart, right ventricle on left). The shape of the left ventricle (to the right) has been distorted by the enlarged right ventricle.
Calcific valvular degeneration. (A) Calcific aortic stenosis of a previously normal valve (viewed from aortic aspect). Nodular masses of calcium are heaped up within the sinuses of Valsalva (arrow). Note that the commissures are not fused, as occurs with postrheumatic aortic valve stenosis (see Fig. 12.22E). (B) Calcific aortic stenosis of a congenitally bicuspid valve. One cusp has a partial fusion at its center, called a raphe (arrow). (C and D) Mitral annular calcification, with calcific nodules at the base (attachment margin) of the anterior mitral leaflet (arrows). (C) Left atrial view. (D) Cut section of myocardium showing the lateral wall with dense calcification that extends into the underlying myocardium (arrow).
Myxomatous degeneration of the mitral valve. (A) Long axis view (left ventricle is on the right) demonstrating hooding with prolapse of the posterior mitral leaflet into the left atrium (arrow). (B) Opened valve, showing pronounced hooding of the posterior mitral leaflet with thrombotic plaques at sites of leaflet-left atrium contact (arrows). (C) Opened valve with pronounced hooding (double arrows) in a patient who died suddenly. Note also mitral annular calcification on the left side (arrowhead). Normal heart valve (D) and myxomatous mitral valve (E). In myxomatous valves, collagen in the fibrosa layer is loose and disorganized, proteoglycan deposition (asterisk) in the central spongiosa layer is markedly expanded, and elastin in the atrialis layer is disorganized.
Acute and chronic rheumatic heart disease. (A) Acute rheumatic mitral valvulitis superimposed on chronic rheumatic heart disease. Small vegetations (verrucae) are visible along the line of closure of the mitral valve leaflet (arrows). Previous episodes of rheumatic valvulitis have caused fibrous thickening and fusion of the chordae tendineae. (B) Microscopic appearance of an Aschoff body in a patient with acute rheumatic carditis. The myocardium exhibits a circumscribed nodule of mixed mononuclear inflammatory cells with associated necrosis; within the inflammation, large activated macrophages show prominent nucleoli, as well as chromatin condensed into long, wavy ribbons (caterpillar cells; arrows). (C and D) Mitral stenosis with diffuse fibrous thickening and distortion of the valve leaflets and commissural fusion (arrows, C), and thickening of the chordae tendineae (D). Note the neovascularization of the anterior mitral leaflet (arrow, D). (E) Surgically resected specimen of rheumatic aortic stenosis, demonstrating thickening and distortion of the cusps with commissural fusion.
Infective (bacterial) endocarditis. (A) Endocarditis of mitral valve (subacute, caused by Streptococcus viridans). The large, friable vegetations are denoted by arrows. (B) Acute endocarditis of congenitally bicuspid aortic valve (caused by Staphylococcus aureus) with extensive cuspal destruction and ring abscess (arrow).
Nonbacterial thrombotic endocarditis (NBTE). (A) Nearly complete row of thrombotic vegetations along the line of closure of the mitral valve leaflets (arrows). (
Carcinoid heart disease. (A) Characteristic endocardial fibrotic lesion involving the right ventricle and tricuspid valve.
Complications of artificial heart valves. (A) Thrombosis of a mechanical prosthetic valve.
Complications of artificial heart valves. (B) Calcification with secondary tearing of a porcine bioprosthetic heart valve, viewed from the inflow aspect.
Dilated cardiomyopathy. (A) Four-chamber dilatation and hypertrophy are evident. There is a mural thrombus (arrow) at the apex of the left ventricle (seen on the right in this apical four-chamber view). The coronary arteries were patent.
Arrhythmogenic cardiomyopathy. (A) Gross photograph, showing dilation of the right ventricle and near-transmural replacement of the right ventricular free-wall by fat and fibrosis. The left ventricle has a virtually normal configuration in this case, but can also be involved by the disease process.
Hypertrophic cardiomyopathy with asymmetric septal hypertrophy. (A) The septal muscle bulges into the left ventricular outflow tract, and the left atrium is enlarged. The anterior mitral leaflet has been reflected away from the septum to reveal a fibrous endocardial plaque (arrow) (see text).
Acute suppurative pericarditis arising from direct extension of an adjacent pneumonia. Extensive purulent exudate is evident.
Atrial myxoma. (A) A large sessile lesion arises from the region of the fossa ovalis and extends into the mitral valve orifice.
(A) Centriacinar emphysema. Central areas show marked emphysematous damage (E) surrounded by relatively spared alveolar spaces. (B) Panacinar emphysema involving the entire pulmonary lobule.
Bullous emphysema. Note the large subpleural bullae (upper left).
Bronchiectasis in a patient with cystic fibrosis, who underwent lung transplantation. Cut surface of lung shows markedly distended peripheral bronchi filled with mucopurulent secretions.
Advanced silicosis. Scarring has contracted the upper lobe into a small dark mass (arrow). Note the dense pleural thickening.
Asbestos-related pleural plaques. Large, discrete fibrocalcific plaques are seen on the pleural surface of the diaphragm.
Large saddle embolus from the femoral vein lying astride the main left and right pulmonary arteries.
Acute hemorrhagic pulmonary infarct.
Vascular changes in pulmonary arterial hypertension. (A) Atheroma-like changes, a finding usually limited to large vessels.
Bronchopneumonia. Section of lung showing patches of consolidation (arrows).
Lobar pneumonia—gray hepatization. The lower lobe is uniformly consolidated.
Cut surface of lung showing two abscesses.
Histoplasmosis. (A) Laminated Histoplasma granuloma of the lung.
Lung carcinoma. The gray-white tumor infiltrates the lung parenchyma. Histologic sections identified this tumor as a squamous cell carcinoma.
Bronchial carcinoid. (A) Carcinoid growing as a spherical mass (arrow) protruding into the lumen of the bronchus.
Numerous metastases to lung from a renal cell carcinoma.
Solitary fibrous tumor. Cut surface is solid with a whorled appearance.
Malignant mesothelioma. Note the thick, firm, white pleural tumor tissue that ensheathes the lung.
Aphthous ulcer. Single ulceration with an erythematous halo surrounding a yellowish fibrinopurulent membrane.
Irritation fibroma. Smooth pink exophytic nodule on the buccal mucosa
Pyogenic granuloma. Erythematous and hemorrhagic exophytic mass arising from the gingival mucosa.
Erythroplakia. (A) Red discoloration of the maxillary gingiva. (B) Red lesion of the mandibular alveolar ridge. Biopsy of both lesions revealed carcinoma in situ.
Leukoplakia. (A) Clinical appearance of leukoplakia is highly variable. In this example, the lesion is relatively smooth and thin with well-demarcated borders.
Keratinizing squamous cell carcinoma. (A) Clinical appearance demonstrating ulceration and induration of the oral mucosa.
Nasopharyngeal carcinoma, nonkeratinizing undifferentiated type. (A) Computed tomography study demonstrating thickening of the nasopharyngeal region (arrow) and an enlarged cervical lymph node (double arrow).
Laryngeal carcinoma. Note the large, ulcerated, fungating lesion involving the right vocal cord and pyriform sinus.
Mucocele. (A) Fluctuant fluid-filled lesion on the lower lip subsequent to trauma.
Pleomorphic adenoma. (A) Slowly enlarging neoplasm in the parotid gland of many years’ duration. (B) Grossly, this representative cross-section of a parotidectomy specimen shows a circumscribed, yellow-white tumor and adjacent normal salivary gland tissue on the left.
Meckel diverticulum. The blind pouch is located on the antimesenteric side of the small bowel.
Hirschsprung disease. (A) Preoperative barium enema study showing constricted rectum (bottom of the image) and dilated sigmoid colon.
Viral esophagitis. (A) Postmortem specimen with multiple, overlapping herpetic ulcers in the distal esophagus.
Esophagitis. (A) Endoscopic view of reflux esophagitis with multiple erosions within the squamous-lined esophagus, a metaplastic zone (Barrett esophagus, discussed later), and distal gastric mucosa. Note the tan islands of metaplastic epithelium within the white squamous mucosa. (B) The “feline” or “ringed” endoscopic appearance of the esophagus is typical of eosinophilic esophagitis.
Esophageal varices.(B) Collapsed varices are present in this postmortem specimen corresponding to the angiogram in (A)
Barrett esophagus. (A) Normal gastroesophageal junction. (B) Barrett esophagus. Note the small islands of residual pale squamous mucosa within the Barrett mucosa.
Esophageal cancer. (A) Adenocarcinoma usually occurs distally and, as in this case, often involves the gastric cardia. (B) Squamous cell carcinoma is most frequently found in the mid-esophagus, where it commonly causes strictures.
Helicobacter pylori gastritis. (A) Spiral-shaped H. pylori are highlighted in this Warthin-Starry silver stain. Organisms are abundant within surface mucus.
Acute gastric perforation in a patient presenting with free air under the diaphragm. (A) Mucosal defect with clean edges.
Ménétrier disease. (A) Marked hypertrophy of rugal folds.
Gastric adenocarcinoma. (A) Intestinal-type adenocarcinoma consisting of an elevated mass with heaped-up borders and central ulceration. Compare to the peptic ulcer in Fig. 17.15A. (B) Infiltrative type (linitis plastica) gastric cancer. The gastric wall is markedly thickened, and rugal folds are partially lost, but there is no dominant mass.
Lymphoma. (B) Disseminated lymphoma within the small intestine with numerous small serosal nodules.
Lymphoma. (C) Large B-cell lymphoma infiltrating the small intestinal wall and producing diffuse thickening.
Neuroendocrine tumor (carcinoid tumor).
A: Gross cross section of a submucosal tumor nodule.
Intestinal obstruction. Portion of bowel incarcerated within an inguinal hernia. Note dusky areas of serosa and associated hemorrhage that indicate ischemic damage.
Ischemic bowel disease. (A) Jejunal resection with dusky serosa of acute ischemia (mesenteric thrombosis). (B) Mucosa is dark colored because of hemorrhage.
Clostridioides (formerly Clostridium) difficile colitis. (A) The colon is coated by tan pseudomembranes composed of neutrophils, dead epithelial cells, and inflammatory debris (endoscopic view)
Clostridioides (formerly Clostridium) difficile colitis. (B) Pseudomembranes are easily appreciated on gross examination.
Gross pathology of Crohn disease. (A) Small intestinal stricture. (B) Linear mucosal ulcers, which impart a cobblestone appearance to the mucosa, and thickened intestinal wall.
Gross pathology of Crohn disease. (C) Perforation and associated serositis. (D) Creeping fat.
Gross pathology of ulcerative colitis. (A) Total colectomy with pancolitis showing active disease, with red, granular mucosa in the cecum (left) and smooth, atrophic mucosa distally (right).
Gross pathology of ulcerative colitis. (B) Sharp demarcation between active ulcerative colitis (right) and normal mucosa (left).
Gross pathology of ulcerative colitis. (C) Inflammatory polyps. (D) Mucosal bridges can join inflammatory polyps.
Sigmoid diverticular disease. (A) Stool-filled diverticula are regularly arranged.
Sigmoid diverticular disease. (B) Cross section showing the outpouching of mucosa through the muscularis propria.
Colonic adenomas. (A) Pedunculated adenoma (endoscopic view).
Colonic adenomas. (B) Adenoma with a velvety surface.
Familial adenomatous polyposis. (A) Hundreds of small polyps are present throughout this colon with a dominant polyp (right).
Colorectal carcinoma. (A) Circumferential, ulcerated rectal cancer. Note the anal mucosa at the bottom of the image.
Colorectal carcinoma. (B) Cancer of the sigmoid colon that has invaded through the muscularis propria and is present within subserosal adipose tissue (left). Areas of chalky necrosis are present within the colon wall (arrow).
Metastatic colorectal carcinoma. (B) Solitary subpleural nodule of colorectal carcinoma metastatic to the lung. (
Metastatic colorectal carcinoma. (C) Liver containing two large and many smaller metastases. Note the central necrosis within metastases.
(A) Massive necrosis, cut section of liver. The liver is small (700 g), bile-stained, soft, and congested.
Cirrhosis resulting from chronic viral hepatitis. Note the depressed areas of dense scar separating bulging regenerative nodules over the liver surface.
Alcoholic cirrhosis. (A) The characteristic diffuse nodularity of the surface is induced by the underlying fibrous scarring. The average nodule size is 3 mm in this close-up view, typical of the “micronodular” cirrhosis of alcoholic liver disease. The greenish tint is caused by cholestasis.
Biliary cirrhosis. (A) Sagittal section through the liver demonstrates the nodularity (most prominent at the right) and bile staining of end-stage biliary cirrhosis.
Hepatolithiasis. A resected, atrophic right hepatic lobe with characteristic findings including markedly dilated and distorted bile ducts containing large pigment stones and broad areas of collapsed liver parenchyma.
Congenital hepatic fibrosis with multiple biliary cysts.
Liver infarct. A thrombus is lodged in a peripheral branch of the hepatic artery (arrow) and compresses the adjacent portal vein; the distal necrotic infarcted tissue has pale margins and multifocal areas of hemorrhage.
Budd-Chiari syndrome. Thrombosis of the major hepatic veins has caused hemorrhagic liver necrosis.
Eclampsia. Subcapsular hematoma dissecting under Glisson capsule in a fatal case.
Focal nodular hyperplasia. (A) Resected specimen showing lobulated contours and a central stellate scar.
Hepatocellular adenoma. (A) Resected specimen showing a well-define tan mass in the liver.
Hepatocellular carcinoma. (A) Liver removed at autopsy showing a unifocal neoplasm replacing most of the right hepatic lobe.
Fibrolamellar carcinoma. (A) Resected specimen showing a well-demarcated nodule.
Cholangiocarcinoma. (A) Multifocal cholangiocarcinoma in a liver from a patient with infestation by the liver fluke Clonorchis sinensis.
Phrygian cap of the gallbladder; the fundus is folded inward.
Cholesterol gallstones. The wall of the gallbladder is thickened and fibrotic due to chronic cholecystitis.
Gallbladder adenocarcinoma. (A) The opened gallbladder contains a large, exophytic tumor that virtually fills the lumen.
The pancreas has been sectioned longitudinally to reveal dark areas of hemorrhage in the head of the pancreas and a focal area of pale fat necrosis in the peripancreatic fat (upper left).
Pancreatic pseudocyst. (A) Cross-section revealing a poorly defined cyst with a necrotic brown-black wall.
Serous cystic neoplasm (serous cystadenoma). (A) Cross-section through a microcystic serous cystic neoplasm. Only a thin rim of normal pancreatic parenchyma remains. The cysts are relatively small and contain clear, straw-colored fluid.
Pancreatic mucinous cystic neoplasm with low-grade dysplasia. (A) Cross-section through a mucinous multiloculated cyst in the tail of the pancreas. The cysts are large and filled with tenacious mucin.
Intraductal papillary mucinous neoplasm. (A) Cross-section through the head of the pancreas showing a prominent papillary neoplasm distending the main pancreatic duct.
Carcinoma of the pancreas. (A) Cross-section through the tail of the pancreas showing normal pancreatic parenchyma and a normal pancreatic duct (left) and a pale mass centered on the duct (right).
Acute pyelonephritis. Cortical surface shows grayish white areas of inflammation and abscess formation.
Papillary necrosis. Areas of pale-gray hemorrhage and necrosis involve the papillae (arrows).
(A) Chronic pyelonephritis. The surface (left) is irregularly scarred. The cut section (right) reveals blunting and loss of several papillae.
Close-up of the gross appearance of the cortical surface in benign nephrosclerosis illustrating the fine, leathery granularity of the surface.
Diffuse cortical necrosis. The pale ischemic necrotic areas are confined to the cortex and columns of Bertin.
(A and B) Autosomal dominant adult polycystic kidney disease (ADPKD) viewed from the external surface and bisected. The kidney is markedly enlarged and contains numerous dilated cysts.
(C) Autosomal recessive childhood PKD, showing smaller cysts and dilated channels at right angles to the cortical surface.
(D) Liver cysts in adult PKD.
Medullary cystic disease. Cut section of kidney showing cysts at the corticomedullary junction and in the medulla.
Multicystic renal dysplasia. (A) Gross appearance.
Hydronephrosis of the kidney, with marked dilation of the pelvis and calyces and thinning of the renal parenchyma.
Nephrolithiasis. A large stone impacted in the renal pelvis.
Renal cell carcinoma. Typical cross-section of yellowish, spherical neoplasm in one pole of the kidney. Note the tumor in the dilated thrombosed renal vein.
Urothelial carcinoma of the renal pelvis. The pelvis has been opened to expose the nodular irregular neoplasm, just proximal to the ureter.
Papillary transitional cell carcinoma extensively involving the ureter.
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.
Malakoplakia. (A) Bladder involved by malakoplakia showing the characteristic yellow-orange mucosal lesions.
Cross-section of bladder with the upper section showing a large papillary tumor. The lower section demonstrates multifocal smaller papillary neoplasms.
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 regions represent areas of ulceration and necrosis.
Hypertrophy and trabeculation of bladder wall secondary to benign prostatic hyperplasia.
Carcinoma of urethra with typical fungating growth pattern (arrow).
Carcinoma of the penis. The glans penis is deformed by a firm, ulcerated, infiltrative mass.
Acute epididymitis caused by gonococcal infection. The epididymis is replaced by an abscess. Normal testis is seen on the right.
Torsion of testis. The dark discoloration is the result of hemorrhage and infarction.
Seminoma of the testis, appearing as a well-circumscribed, pale, fleshy, homogeneous mass on cut surface.
Embryonal carcinoma. In contrast to the seminoma illustrated in Fig. 21.19, as shown here, embryonal carcinoma often produces a hemorrhagic mass.
Teratoma of testis. The variegated cut surface with cysts reflects the presence of multiple tissue types.
Benign prostatic hyperplasia (BPH). (A) Well-defined nodules of BPH compress the urethra into a slit-like lumen.
Adenocarcinoma of the prostate. An area of cancer is present in the posterior aspect (lower left) that has solid gray-white appearance, in contrast to the spongy appearance of benign peripheral zone on the contralateral side.
Metastatic osteoblastic prostatic carcinoma within vertebral bodies.
Sarcoma botryoides (embryonal rhabdomyosarcoma) of the vagina appearing as a polypoid mass protruding from the vagina.
Common causes of abnormal uterine bleeding. (C) Endometrial polyp.
Type I endometrial carcinoma. (A) Endometrial adenocarcinoma presenting as a fungating mass in the fundus of the uterus.
Leiomyomas of the uterine myometrium (A) 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.
Leiomyosarcoma. (A) A large hemorrhagic tumor mass distends the lower corpus and is flanked by two leiomyomas.
Gross appearances of serous tumors of the ovary. (A) Serous borderline tumor opened to display a cyst cavity lined by delicate papillary tumor growths.
Gross appearances of serous tumors of the ovary. (B) Carcinoma. The cyst is opened to reveal a large, bulky tumor mass.
Gross appearances of serous tumors of the ovary. (C) Another borderline tumor growing on the ovarian surface (lower).
Mucinous cystadenoma (A) Note the multicystic appearance, delicate septa, and the presence of glistening mucin within the cysts.
Pseudomyxoma peritonei. (A) View at laparotomy revealing massive overgrowth of a gelatinous metastatic tumor.
Brenner tumor (A) Brenner tumor (right) associated with a benign cystic teratoma (left).
Opened mature cystic teratoma (dermoid cyst) of the ovary. Hair (bottom) and a mixture of tissues are evident.
Sertoli cell tumor. (A) Gross photograph illustrating characteristic golden-yellow appearance of the tumor.
Placental infections derived from ascending and blood-borne routes. Acute chorioamnionitis. (A) On gross examination, the placenta contains greenish opaque membranes.
Complete hydatidiform mole. Note marked distention of the uterus by enlarged, vesicular chorionic villi. Adnexa (ovaries and fallopian tubes) are visible on the left and right side of the uterus.
Choriocarcinoma. (A) Choriocarcinoma presenting as a bulky hemorrhagic mass invading the uterine wall.
Apocrine cysts. (B) Gross appearance of typical cysts filled with dark, turbid fluid contents.
Invasive carcinoma of no special type. The majority of invasive carcinomas have a haphazard pattern of stromal invasion that produces masses with irregular margins on imaging (B). Microscopically, such tumors are marked by an exuberant desmoplastic stromal response
Invasive carcinoma of no special type. The majority of invasive carcinomas have a haphazard pattern of stromal invasion that produces masses with irregular margins on imaging
(E). Microscopically, such cancers typically take on the appearance of expansile masses of cells with pushing borders; stromal response is often limited to a narrow zone of fibrosis at the tumor margin
Invasive carcinoma of no special type. The majority of invasive carcinomas have a haphazard pattern of stromal invasion that produces masses with irregular margins on imaging
(H). Microscopically, tumor cells are found scattered within normal-appearing fibroadipose tissue
Fibroadenoma. (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.
Pituitary adenoma. This massive, nonfunctional adenoma has grown beyond the confines of the sella turcica, distorting the overlying brain. On average, nonfunctional adenomas are larger at time of diagnosis.
A person with hyperthyroidism. A wide-eyed, staring gaze, caused by overactivity of the sympathetic nervous system, is one feature of this disorder. In Graves disease, an important cause of hyperthyroidism, accumulation of loose connective tissue behind the orbit also adds to the protuberant appearance of the eyes.
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 Fig. 24.15.
A 52-year-old woman with a huge colloid goiter who developed compressive symptoms.
Multinodular goiter. (A) Gross morphology demonstrating a coarsely nodular gland containing areas of fibrosis and cystic change.
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).
Diffuse hyperplasia of the adrenal gland contrasted with a normal adrenal gland (top). In cross-section, the hyperplastic adrenal cortex is yellow and thickened, and a subtle nodularity is seen (contrast with Fig. 24.43) in this gland from a patient with ACTH dependent Cushing syndrome.
(A) Micronodular adrenocortical hyperplasia with prominent pigmented nodules in the adrenal gland.
A patient with Cushing syndrome demonstrating central obesity, “moon facies,” and abdominal striae.
Diffuse purpuric rash in a patient with Waterhouse-Friderichsen syndrome.
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.
Adrenal carcinoma. The hemorrhagic and necrotic tumor dwarfs the kidney and compresses the upper pole.
Pheochromocytoma. The tumor is enclosed within an attenuated cortex and demonstrates areas of hemorrhage. The comma-shaped residual adrenal is seen below.
Osteoporotic vertebral body (right) shortened by compression fractures compared with a normal vertebral body (left). Note that the osteoporotic vertebra has a characteristic loss of horizontal trabeculae and thickened vertical trabeculae.
Resected rib, harboring an expansile brown tumor adjacent to the costal cartilage.
Femoral head with a subchondral, wedge-shaped pale area of osteonecrosis. The space between the overlying articular cartilage and bone is caused by trabecular compression fractures without repair.
Resected femur in a person with draining osteomyelitis. The drainage tract in the subperiosteal shell of viable new bone (involucrum) reveals the inner native necrotic cortex (sequestrum).
Osteosarcoma of the proximal tibia. The tan-white tumor fills most of the medullary cavity of the metaphysis and proximal diaphysis. It has infiltrated through the cortex, lifted the periosteum, and formed soft tissue masses on both sides of the bone.
Chondrosarcoma. (A) Nodules of hyaline and myxoid cartilage permeate the medullary cavity, grow through the cortex, and form a relatively well-circumscribed soft tissue mass.
Osteoarthritis. (B) Eburnated articular surface exposing subchondral bone (1), subchondral cysts (2), and residual articular cartilage (3).
Tenosynovial giant cell tumor, diffuse type. (A) Excised synovium with fronds and nodules typical of diffuse tenosynovial giant cell tumor. The color and texture explain the old name of pigmented villonodular synovitis.
(A) Dermatomyositis. Note the heliotrope rash affecting the eyelids.
Hydrocephalus. Dilated lateral ventricles seen in a coronal section through the midthalamus.
Duret hemorrhage. As mass effect displaces the brain downward, there is disruption of the vessels that enter the pons along the midline, leading to hemorrhage.
Myelomeningocele. Both meninges and spinal cord parenchyma are included in the cystlike structure visible just above the buttocks.
Agenesis of the corpus callosum. The midsagittal view of the left hemisphere shows the lack of a corpus callosum and cingulate gyrus.
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).
Chronic stage of periventricular leukomalacia. Large cystic spaces in the periventricular white matter (seen in both hemispheres of this brain) are the long-term sequalae of a severe prenatal or perinatal ischemic injury.
(A) Acute contusions are present in both temporal lobes, with areas of hemorrhage and tissue disruption (arrows).
(B) Remote contusions (arrows) are present on the inferior frontal surface of this brain and have a yellow color (plaque jaune) that reflects hemosiderin accumulation.
Epidural hematoma covering a portion of the dura. Also present are multiple small contusions in the temporal lobe.
(A) Large organizing subdural hematoma attached to the dura.
(B) Coronal section of the brain showing atrophy of the hemisphere compressed by the subdural hematoma shown in A.
(A) An ischemic infarct involves the territory of the middle cerebral artery, including the striatum, on the left side of this brain.
(B) A hemorrhagic infarct with punctate hemorrhages, consistent with ischemia-reperfusion injury, is present in the temporal lobe.
Old cystic infarct showing cavitation from loss of brain parenchyma.
Lacunar infarcts in the caudate and putamen (arrows).
Classic watershed infarct with secondary hemorrhagic transformation (arrow); boundary between anterior and middle cerebral artery circulations.
(A) Massive hypertensive ganglionic hemorrhage rupturing into a lateral ventricle.
(C) Large lobar hemorrhage due to cerebral amyloid angiopathy; it focally dissects into the subarachnoid space.
(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 (hematoxylin and eosin).
Large arteriovenous malformation in the left cerebral hemisphere.
Pyogenic meningitis. A thick layer of suppurative exudate covers the brain surface and thickens the leptomeninges.
Cerebral abscesses (arrows).
(A) Herpes encephalitis showing extensive destruction of inferior frontal and anterior temporal lobes (arrows) and the cingulate gyri (asterisks).
Multiple sclerosis. (A) Section of fresh brain shows gray-brown plaque around occipital horn of the lateral ventricle (arrows).
Alzheimer disease with cortical atrophy most evident on the right, where meninges have been removed.
Parkinson disease. (A) Normal substantia nigra.
(B) Depigmented substantia nigra in idiopathic Parkinson disease.
Multiple system atrophy (MSA). (A) Severe atrophy of the basis pontis in a case of MSA-C.
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.
Amyotrophic lateral sclerosis. (A) Segment of spinal cord viewed from anterior (upper) and posterior (lower) surfaces showing attenuation of anterior (motor) roots compared with posterior (sensory) roots.
Krabbe disease. Much of the white matter is gray/yellow because of the loss of myelin.
Alcoholic cerebellar degeneration. The anterior and superior portion of the vermis (upper portion of figure) is atrophic, with widened spaces between the folia.
Diffuse astrocytoma. (A) On coronal section at autopsy, the left frontal white matter is expanded, and there is blurring of the corticomedullary junction due to infiltrative tumor (circled region).
(B) Glioblastoma appearing as a necrotic, hemorrhagic, infiltrating mass.
Pilocytic astrocytoma. (A) Grossly, this cerebellar tumor forms a mural nodule within a cyst. (
Ependymoma. (A) Tumor of the fourth ventricle, distorting, compressing, and infiltrating surrounding structures.
Medulloblastoma. (A) Sagittal section of brain showing medulloblastoma replacing part of the superior cerebellar vermis.
(A) Resected meningioma specimen showing rounded contour and dural attachment.
The extraocular muscles are greatly distended in this postmortem dissection of tissues from a patient with thyroid (Graves) ophthalmopathy. Note that the tendons of the muscles are spared.
(A, B) Cystic compound nevus of the conjunctiva.
(C, D) Conjunctival malignant melanoma. In C, note the deflection of the beam of the slit lamp over the surface of the lesion, indicative of invasion.
Exogenous panophthalmitis. This eye was removed after a foreign body injury. Note the suppurative inflammation behind the lens that is drawn up to the right of the lens to the cornea, the site of the wound. The central portion of the vitreous humor was extracted surgically (by vitrectomy). Note the adhesions to the surface of the eye at the 8 o’clock position, indicating that the intraocular inflammation has spread through the sclera into the orbit: panophthalmitis.
Uveal melanoma. (A) Fundus photograph from an individual with a relatively flat pigmented lesion of the choroid near the optic disc.
(B) Fundus photograph of the same individual several years later; the tumor has grown and has ruptured through the Bruch membrane.
(C) Gross photograph of a choroidal melanoma that has ruptured the Bruch membrane. The overlying retina is detached.
Cherry-red spot in Tay-Sachs disease. (A) Fundus photograph of the cherry-red spot in Tay-Sachs disease.
Retinoblastoma. (A) Gross photograph of retinoblastoma.
The optic nerve in anterior ischemic optic neuropathy (AION) and papilledema. (A) In the acute phases of AION the optic nerve may be swollen, but it is relatively pale because of decreased perfusion.
The optic nerve in anterior ischemic optic neuropathy (AION) and papilledema. (B) In papilledema secondary to increased intracranial pressure, the optic nerve is typically swollen and hyperemic.
Coagulative necrosis. (A) A wedge-shaped kidney infarct (yellow).
Liquefactive necrosis. An infarct in the brain, showing dissolution of the tissue.
Caseous necrosis. Tuberculosis of the lung, with a large area of caseous necrosis containing yellow-white and “cheesy” appearing debris.
Fat necrosis. The areas of white chalky deposits represent foci of fat necrosis with calcium soap formation (saponification) at sites of lipid breakdown in the mesentery.
Physiologic hypertrophy of the uterus during pregnancy. (A) Gross appearance of a normal uterus (right) and a gravid uterus (removed for postpartum bleeding) (left).
Atrophy. (A) Normal brain of a young adult.
Atrophy. (B) Atrophy of the brain in an 82-year-old man with atherosclerotic cerebrovascular disease, resulting in reduced blood supply. Note that loss of brain substance narrows the gyri and widens the sulci. The meninges have been stripped from the right half of each specimen to reveal the surface of the brain.
Dystrophic calcification of the aortic valve. View looking down onto the unopened aortic valve in a heart with calcific aortic stenosis. It is markedly narrowed (stenosis). The semilunar cusps are thickened and fibrotic, and behind each cusp are irregular masses of piled-up dystrophic calcification.
Fibrinous pericarditis. (A) Deposits of fibrin on the pericardium.
Purulent inflammation. (A) Multiple bacterial abscesses (arrows) in the lung in a case of bronchopneumonia.
The morphology of an ulcer. (A) A chronic duodenal ulcer. (
Chronic wounds illustrating defects in wound healing.
A: External appearance of skin ulcers. Venous leg ulcer.
Chronic wounds illustrating defects in wound healing.
B: External appearance of skin ulcers. Arterial ulcer, with more extensive tissue necrosis.
Chronic wounds illustrating defects in wound healing.
C: External appearance of skin ulcers. Diabetic ulcer.
Chronic wounds illustrating defects in wound healing.
D: External appearance of skin ulcers. Pressure sore.
Clinical examples of excessive scarring and collagen deposition. (A) Hypertrophic scar.
Clinical examples of excessive scarring and collagen deposition. (A) Hypertrophic scar. (B) Keloid.
Liver with chronic passive congestion and hemorrhagic necrosis. (A) Central areas are red and slightly depressed compared with the surrounding tan viable parenchyma, forming a “nutmeg liver” pattern (so-called because it resembles the cut surface of a nutmeg).
(A) Punctate petechial hemorrhages of the colonic mucosa, a consequence of thrombocytopenia.
(B) Fatal intracerebral bleed.
Mural thrombi. (A) Thrombus in the left and right ventricular apices (arrows), overlying a white fibrous scar.
Mural thrombi. (B) Laminated thrombus in a dilated abdominal aortic aneurysm (asterisks). Numerous friable mural thrombi are also superimposed on advanced atherosclerotic lesions of the more proximal aorta (left side of picture).
Embolus from a lower extremity deep venous thrombosis, lodged at a pulmonary artery branchpoint.
Red and white infarcts. (A) Hemorrhagic, roughly wedge-shaped pulmonary red infarct.
Red and white infarcts. (B) Sharply demarcated white infarct in the spleen.
Remote kidney infarct replaced by a large fibrotic scar.
Libman-Sacks endocarditis of the mitral valve in lupus erythematosus. The vegetations attached to the margin of the thickened valve leaflet are indicated by arrows.
Sjögren syndrome. (A) Enlargement of the salivary gland.
Systemic sclerosis. (C) The extensive subcutaneous fibrosis has virtually immobilized the fingers, creating a clawlike flexion deformity. Loss of blood supply has led to cutaneous ulcerations.
IgG4-related disease: representative lesions. (A) Bile duct showing sclerosing cholangitis.
(A) Gross appearance of an opened cystic teratoma of the ovary. Note the presence of hair, sebaceous material, and a tooth.
Fibroadenoma of the breast. (A) The tan-colored, encapsulated small tumor is sharply demarcated from the whiter breast tissue.
Invasive ductal carcinoma of the breast. (A) On cut section, the lesion is retracted and infiltrates the surrounding breast substance and would be stony hard on palpation.
Involvement of omentum by metastatic ovarian carcinoma. Innumerable nodules and more subtle “glazing” are evident due to seeding by carcinoma cells via the peritoneal cavity.
Cancer metastasis. (A) Liver studded with metastatic cancer.
Streptococcal erysipelas.
Membrane of diphtheria (arrow) lying within a transverse bronchus.
Primary pulmonary tuberculosis, Ghon complex. The gray-white parenchymal focus is under the pleura in the lower part of the upper lobe (red arrow). Hilar lymph nodes with caseation are seen on the left (blue arrow).
Secondary pulmonary tuberculosis. The upper parts of both lungs are riddled with gray-white areas of caseation and multiple areas of softening and cavitation.
Miliary tuberculosis of the spleen. The cut surface shows numerous gray-white tubercles.
Syphilitic chancre in the scrotum (see Fig. 8.35 for the histopathology of syphilis).
The morphology of Candida infections. (A) Severe candidiasis of the distal esophagus.
Aspergillus infection. (A) Invasive aspergillosis of the lung in a bone marrow transplant patient. (
Pipe-stem fibrosis of the liver due to chronic Schistosoma japonicum infection.
Massive edema and elephantiasis caused by filariasis of the leg.
Adverse drug reaction. Skin pigmentation caused by minocycline, a long-acting tetracycline derivative. (A) Diffuse blue-gray pigmentation of the forearm.
Extensive mediastinal fibrosis after radiotherapy for carcinoma of the lung. Note the markedly thickened pericardium.
Childhood malnutrition. (A) Marasmus. Note the loss of muscle mass and subcutaneous fat; the head appears to be too large for the emaciated body.
Childhood malnutrition. (B) Kwashiorkor. The infant shows generalized edema, seen as ascites and puffiness of the face, hands, and legs.
Examples of malformations. (A) Polydactyly (one or more extra digits) and syndactyly (fusion of digits) have little functional consequence when they occur in isolation.
Examples of malformations. (B), with or without associated cleft palate, is compatible with life when it occurs as an isolated anomaly; in the present case, however, this neonate had an underlying malformation syndrome (trisomy 13) and died of severe cardiac defects.
Examples of malformations. (C) The stillbirth illustrated represents a severe and essentially lethal malformation, wherein the midface structures are fused or ill-formed; in almost all cases, this degree of external dysmorphogenesis is associated with severe internal anomalies such as maldevelopment of the brain and cardiac defects.
Infant with oligohydramnios sequence. Note the flattened facial features and deformed right foot (talipes equinovarus).
Necrotizing enterocolitis (NEC). (A) Postmortem examination in a severe case of NEC shows the entire small bowel is markedly distended with a perilously thin wall (usually this implies impending perforation).
Necrotizing enterocolitis (NEC). (B) The congested portion of the ileum corresponds to areas of hemorrhagic infarction and transmural necrosis microscopically. Submucosal gas bubbles (pneumatosis intestinalis) can be seen in several areas (arrows).
Hydrops fetalis. (A) There is generalized accumulation of fluid in the fetus.
Hydrops fetalis. (B) Fluid accumulation is particularly prominent in the soft tissues of the neck, and this condition has been termed cystic hygroma. Cystic hygromas are characteristically seen, but not limited to, constitutional chromosomal anomalies such as 45,X karyotypes.
Kernicterus. Note the yellow discoloration of the brain parenchyma due to bilirubin accumulation, which is most prominent in the basal ganglia deep to the ventricles.
Congenital hemangioma at birth (A) and at 2 years of age
Congenital hemangioma at birth (B) after spontaneous regression.
Sacrococcygeal teratoma. Note the size of the lesion compared with that of the stillbirth.
Wilms tumor in the lower pole of the kidney with the characteristic tan-to-gray color and well-circumscribed margins.
Fatty streak, a collection of foamy macrophages in the intima. (A) Aorta with fatty streaks (arrows), associated largely with the ostia of branch vessels.
Gross views of atherosclerosis in the aorta. (A) Mild atherosclerosis composed of fibrous plaques, one of which is denoted by the arrow.
Gross views of atherosclerosis in the aorta. (B) Severe disease with diffuse, complicated lesions including an ulcerated plaque (open arrow) and a lesion with overlying thrombus (closed arrow).
Abdominal aortic aneurysm. (A) External view, gross photograph of a large aortic aneurysm that ruptured (rupture site is indicated by the arrow).
Abdominal aortic aneurysm. (B) Opened view, with the location of the rupture tract indicated by a probe. The wall of the aneurysm is exceedingly thin, and the lumen is filled by a large quantity of layered but largely unorganized thrombus.
Aortic dissection. (A) Gross photograph of an opened aorta with proximal dissection originating from a small, oblique intimal tear (probe), allowing blood to enter the media and creating a retrograde intramural hematoma (thin arrows). Note that the intimal tear has occurred in a region largely free of atherosclerotic plaque and that propagation of the intramural hematoma distally is arrested where atherosclerosis begins (thick arrow). (
Takayasu arteritis. (B) Gross photograph of two cross-sections of the right carotid artery taken at autopsy of the patient shown in (A) demonstrating marked intimal thickening and adventitial fibrosis with minimal residual lumen.
Raynaud phenomenon. (A) Sharply demarcated pallor of the distal fingers resulting from the closure of digital arteries.
Raynaud phenomenon. (B) Cyanosis of the fingertips.
Hemangiomas. (A) Hemangioma of the tongue.
Hemangiomas. (D) Pyogenic granuloma of the lip.
Bacillary angiomatosis. (A) Characteristic cutaneous lesion.
Kaposi sarcoma. (A) Gross photograph illustrating coalescent red-purple macules and plaques of the skin.
Angiosarcoma. (A) Angiosarcoma involving the right ventricle.
Restenosis after angioplasty and stenting. (A) Gross view demonstrating residual yellow atherosclerotic plaque (arrows) and a new, tan-white concentric intimal lesion inside of that plaque. (
