MORPHOLOGICAL FEATURES OF PATHOLOGY POTS AND SLIDES

Disease	Gross features	Histological features	
Aorta: atheroma	•	Fatty streak: multiple yellow flat spots < 1mm in diameter that coalesce into elongated streaks; 1cm or longer.
•	Raised plaques in intima
•	Yellow, yellowish-white, smooth, round.
•	Firm sclerotic surface.
•	Ulcerated with soft exposed grumous material.
•	Fissured, ruptured, haemorrhage. 
•	Confluent with thrombosis.	•	Fatty streak: composed of lipid-filled foam cells with T lymphocytes & extracellular lipid.
•	Early lesion: pale-staining area of thickening in the intima consisting of aggregated myointimal cells containing lipid & fibrous tissue.
•	Foam cells filled with lipid appear as large, pale-staining cells with vacuolated cytoplasm.
•	Non-staining angular clefts of free lipid released by foam cells. 
•	Fibrous cap: smooth muscle cells, macrophages, foam cells, lymphocytes, collagen.
•	Necrotic center: cell debris, cholesterol crystals, foam cells.
•	Collagenization of media. 	
Hyperplastic arteriosclerosis		•	Symmetrical hypertrophy of muscular media.
•	Extensive reduplication of internal elastic lamina.
•	Regular fibrotic thickening of intima.	
Hyaline arteriosclerosis		•	Normal layers of vessel wall become ill-defined.
•	Replaced by homogenous eosinophilic material called hyaline.	
Fibrinoid necrosis		•	Disruption of vessel wall, with leakage of fibrinogen into arteriolar wall.
•	Obliteration of vessel wall by intensely eosinophilic amorphous proteinaceous material.	
Aorta: aneurysm	•	Fusiform dilatation with sharp superior & inferior margins.
•	Saccular dilatations: balloon-like outpouchings may be completely filled with thrombus.
•	Other lesions: atherosclerosis & mural thrombus.		
Aorta: dissecting aneurysm	•	Longitudinal / oblique tear.
•	4 – 6 cm long.
•	Sharp & clean irregular edges.
•	Other lesions: atherosclerosis, hematoma in vessel wall.	•	Laceration of tunica intima leads to tracking of blood into the tunica media.
•	Plane of cleavage is usually between the middle & outer thirds of the media. 
•	Medial hematoma frequently bursts through tunica adventitia. 	
Aortic stenosis	•	Heaped-up, calcified masses at cuspal bases, behind aortic cusps.
•	Cusps are fibrosed & thickened.
•	No commisural fusion.
•	Other lesions: bicuspid aortic valve, rheumatic valvulitis		
Infective endocarditis	•	Irregular, friable, bulky, microbe-laden vegetations attached near lines of closure of leaflets. 
•	Erosion / perforation of underlying valve leaflet.
•	Invasion of adjacent myocardium / aortic wall to produce abscess cavities.
•	Other lesions: mitral valve prolapse, bicuspid aortic valve, prosthetic valve, rheumatic valvulitis.	•	Small colonies of blue-purple-staining bacteria. 
•	Formation of thrombus and large vegetations on valve surface.
	
Chronic rheumatic valvulitis	•	Fibrous thickening of leaflets.
•	Bridging fibrosis across the commissures: fishmouth / buttonhole stenosis.
•	Thickened, fused, and shortened mitral valve chordae.
•	Secondary calcification. 	•	Aschoff bodies: foci of necrosis of collagen with fibrin deposition, surrounded by lymphocytes, macrophages and occasional plump modified histiocytes called Anitschkow cells.	
Right ventricular hypertrophy	•	Dilatation of right ventricle without hypertrophy.
•	Shape: dilated ovoid.
•	Ventricular wall thickens > 1.0cm.		
Left ventricular hypertrophy	•	Concentric thickening of left ventricular to > 1.5cm.
•	No dilatation of left ventricle.		
Myocardial infarct	•	1 – 12hr: None.
•	12 – 24hr: dark mottling.
•	1 – 3 days: mottling with yellow-tan infarct center.
•	3 – 7 days: hyperemic border with central yellow-tan softening.
•	7 – 10 days: maximally yellow-tan and soft, with depressed red-tan margins.
•	10 – 14 days: red-grade depressed infarct borders.
•	2 – 8 weeks: gray-white scar.	•	1 – 12hr: waviness of fibers at border.
•	12 – 24hr: ongoing coagulation necrosis; pyknosis of nuclei; myocyte hypereosinophila; marginal contraction band necrosis.
•	1 – 3 days: coagulation necrosis, with loss of nuclei & striations; interstitial infiltrate of neutrophils.
•	3 – 7 days: disintegration of dead myofibrils; early phagocytosis of dead cells by macrophages at infarct border.
•	7 – 10 days: well-developed phagocytosis of dead cells; early formation of fibrovascular granulation tissue at margins.
•	10 – 14 days: well-established granulation tissue.
•	2 – 8 weeks: dense collagenous scar.	
Pericarditis	•	Pericardium is thickened & organized.
•	Shaggy, necrotic, yellowish loose exudate on surface.
•	Appearance: ‘bread-and-butter’, ‘carpet’ or ‘rug-like’. 
•	Chronic: delicate, stringy adhesions to dense fibrous calcification & obliteration of pericardial space. 		
Brain infarct	•	2 day: tissue becomes pale, soft & swollen & the corticomedullary junction becomes indistinct.
•	2- 10 days: brain becomes gelatinous & friable.
•	10 days – 3 weeks: tissue liquefies, leaving a fluid-filled cavity lined by dark gray tissue.
•	Old: cystic gliotic cavity.	•	12 hrs: ischaemic neuronal change – red neurons and edema.
•	48 hrs: swelling of endothelial cells & astrocytes, neutrophil infiltration. 
•	2 – 3 weeks: phagocytosis of dead neurons by macrophages.
•	Old: astrocyte processes form a dense network of glial fibers admixed with a few perivascular connective tissue fibers & capillaries. 	
Brain haemorrhage	•	Acute: extravasation of blood with compression of the adjacent parenchyma.
•	Old: area of cavitary destruction of brain with a rim of brownish discoloration.	•	Early lesion: a central core of clotted blood surrounded by a rim of brain tissue showing anoxic neuronal & glial changes as well as edema.
•	Old lesion: network of astrocyte processes & connective tissue.	
Bronchopneumonia	•	Patchy consolidation: often multilobar, bilateral & basal because of tendency of secretions to gravitate into the lower lobes. 
•	Lesions are 3 – 4cm in diameter, slightly elevated, dry, granular, gray-red to yellow, & poorly delimited at their margins.
•	Affected areas are firm, airless & have a dark red or gray appearance.
•	Pleural thickening & fibrous adhesions. 	•	Patchy consolidation of alveolar tissues / spaces.
•	Suppurative neutrophil-rich exudates fill the bronchi, bronchioles & alveolar spaces. 	
Lobar pneumonia	•	Red hepatization: lung is heavy, boggy & red, firm & airless with a liver-like consistency.
•	Gray hepatization: grayish brown, dry surface.
•	Resolution: consolidation of entire lobe with gray solid, fibrous, airless material. 
•	Pleuritis: fibrous thickening or permanent adhesions. 	•	Congestion: vascular engorgement, intra-alveolar fluid with few neutrophils.
•	Red hepatization: massive confluent exudate with red cells & neutrophils & fibrin filling the alveolar spaces.
•	Gray hepatization: progressive disintegration of red cells & the persistence of fibrino-suppurative exudate. 
•	Resolution: consolidated exudate undergoes enzymatic digestion to produce a granular, semifluid debris that is resorbed.	
Primary TB complex	•	Ghon focus: 1- to 1.5cm area of gray-white inflammatory consolidation.
•	Ghon complex: combination of subpleural parenchymal lesion & enlarged caseous lymph nodes draining the focus. 
•	Center of focus / complex undergoes caseation necrosis: cheesy-yellow-white lesions with cavitation.  	•	Caseating granulomas with central necrosis.
•	Enclosed within a fibroblastic rim punctuated by lymphocytes. 	
Secondary TB	•	Initial lesion: small focus of consolidation, < 2cm in diameter, located within 1 –2cm of apical pleura.
•	Focus is sharply circumscribed, firm, gray-white to yellow areas with central caseation & peripheral fibrous induration.
•	Fibrocalcific scars depress & pucker pleural surface & cause pleural adhesions & thickening.
•	Cavitation: walls contain ragged white material.
•	Heal lesions are walled off by fibrosis & appear white & hard secondary to dystrophic calcification.
•	Lung may be shrunkened.
•	Bronchiectasis. 	•	Same as above.	
Lung abscess	•	Vary from a few mm to large cavities of 5 – 6 cm.
•	Creamy white lesions, some have cavities filled with necrotic debris.
•	Irregular & shaggy walls.
•	Fibrotic scarring of surrounding tissues. 
•	Multiple, basal & diffusely scattered.
•	May erode into blood vessels or rupture into pleural cavity. 	•	Destruction of pulmonary parenchyma.
•	Exudate of inflammatory cells.
•	Fibrin deposits in between normal lung tissue. 	
Emphysema	•	Lung is hollowy, voluminous, & hyperinflated.
•	Surface: bullae, multiple, coalesced, honey-combed appearance.
•	Involved areas pale due to vessel compression.
•	Black discoloration of walls of spaces.	•	Enlarged air spaces with broken septae in the central portion of the acinus around the terminal bronchiole. 
•	Distortion of pulmonary architecture with deforming & compression of bronchioles & vasculature by the emphysematous distortion of the airspaces.
•	Carbon-laden macrophages may be present.	
Bronchiectasis	•	Dilated bronchi, can be followed to pleural surface, some with saccular outpouchings.
•	Intervening lung tissue reduced & fibrosed.
•	Pleura is fibrotic & thick with dense adhesion to chest wall.
•	Cystic pattern on cut surface.	•	Capillary congestion, interstitial & intraalveolar edema & hemorrhage.
•	Alveolar ducts are dilated & alveoli tend to collapse.
•	Hyaline membranes lining distended alveolar ducts. 
•	Marked distortion of lung parenchyma.
•	Diffuse interstitial fibrosis.	
Squamous cell carcinoma	•	Intraluminal mass arising from bronchial lining, usually a major bronchus.
•	Central fungating lesion.
•	Thickened mucosa.
•	Infiltration into lung parenchyma & paratracheal lymph nodes.
•	Gray-white hard granular neoplasm.
•	Pneumonic consolidation.
•	Necrosis, cavitation & hemorrhage.
•	Direct spread to pleural cavity & pericardium.	•	Cells have large irregular nuclei.
•	Coarse nuclear chromatin with large nucleoli.
•	Cells arranged in sheets.
•	Keratin pearls.
•	Intercellular bridges.	
Small cell carcinoma	•	Perihilar & surround large bronchi.
•	Ill-defined, gray-white or haemorrhagic.	•	Densely cellular resembling ‘millet seeds’.
•	Almost no cytoplasm so nuclei appeared molded to each other.
•	Nuclei are hyperchromatic & irregular.
•	Dense core neurosecretory granules.	
Adenocarcinoma	•	Yellowish-tan with a well-circumscribed lobulated periphery.
•	Involve pleura causing puckering & scarring. 
•	Pleural effusion.
•	Cut surface: glisten & yellow if abundant mucin secretion.	•	Gland forming.
•	Cells show large nuclei with prominent nucleoli.	
Bronchoalveolar carcinoma	•	Peripheral single nodule (coin lesion) or multiple nodules.
•	May fuse into a diffuse involvement of the lung. 	•	Lines pre-existing alveolar septae.
•	Tall columnar cells containing mucin.
•	Columnar cells with extensive atypia & scattered mucin vacuoles. 	
Metastases to lung	•	Multiple, well-circumscribed lesions.
•	Cut section: shaggy, necrotic, cavitations.
•	Lesions more localized to periphery.
•	Pleural surfaces shows multiple, nodular masses underneath with intact pleura.
•	Adjacent vessels compressed. 		
Pulmonary congestion	•	Heavy, red lungs.
•	Ooze bloody fluid on sectioning.
•	Chronic: rusty discoloration. 	•	Dilated blood vessels containing abundant RBCs.
•	Scattered RBCs may be found in the alveoli.
•	Hemosiderin-laden macrophages.
•	Protein-rich edema fluid.	
Esophagus: candidasis	•	White plaques, often multifocal, exudative membranes, erosions & ulcers of increasing depth.
•	Surface may be reddened & hemorrhage can be seen.
•	Elevated balls of debris, fungus & granulation tissue.	•	Intraepithelial proliferation of organisms with pseudohyphae & budding yeast forms.
•	Presence of acute inflammation with necrosis & ulceration.
	
Esophageal varices	•	Linear violaceous / red protrusions into distal esophagus: dilated submucosal veins.
•	Overlying mucosa is intact, but may have erythema.
•	Surface show superficial erosions.
•	Variceal rupture: esophagus is filled with blood; blood clot may be found over site of rupture.
•	Resected surgical specimen: varices collapse & a flattened violaceous linear vascular outline is seen. 	•	Dilated submucosal veins.
•	Overlying esophageal mucosa is normal.
•	Partial thrombosis may be seen in the varices. 	
Esophagus: squamous cell carcinoma	•	Early phase: flat, white, with minimal thickening of mucosa.
•	Exophytic forming an intraluminal mass. 
•	Firm white surface & flaky consistency. 	•	Single cell keratinization.
•	Keratin pearls.
•	Intercellular bridges.
•	Sheet-like growth pattern. 	
Stomach: chronic gastritis	•	Mucosa is reddened & has a coarser texture.
•	Boggy-appearing mucosa with thickened rugal folds. 
•	Atrophic disease: mucosa may be thin and flattened.	•	Lymphocytes & plasma cells present within lamina propria.
•	Presence of neutrophils within glandular & surface epithelial layer.
•	Lymphoid aggregates with germinal centers.	
Stomach: chronic peptic ulcer	•	Round-to-oval, sharply punched-out defect with straight walls.
•	Heaping-up of margins is rare.
•	Base of ulcer is smooth & clean.
•	Scarring may involve entire thickness.
•	Puckering of surrounding mucosa creates mucosal folds, which radiate from the crater in spokelike fashion. 
•	Surrounding mucosa is edematous & reddened.	•	Four zones are demonstrable.
•	Base & margins have a superficial thin layer of necrotic fibrinoid debris.
•	Beneath this layer is the zone of a non-specific inflammatory infiltrate, with neutrophils predominating.
•	In the deeper layers, in the base, there is active granulation tissue infiltrated with mononuclear leukocytes.
•	The granulation tissue rests on a solid fibrous or collagenous scar.
•	Vessel walls within scarred areas are thickened & thrombosed.	
Stomach: adenocarcinoma	•	Exophytic: protrusion of a tumor mass into the lumen.
•	Flat / depressed: there is no obvious tumor mass within mucosa.
•	Excavated: a shallow or deeply erosive crater is present in the wall of the stomach.
•	Cancerous craters: heaped-up, beaded margins & shaggy, necrotic bases, overt neoplastic tissue extending into the surrounding mucosa & wall. 
•	Entire stomach is extensively infiltrated by malignancy, creating a rigid, thickened leather bottle-like stomach – linitis plastica. 	•	Intestinal type: neoplastic intestinal glands permeating gastric wall in an expanding growth pattern.
•	Diffuse type: permeate mucosa & wall as scattered individual cells or small clusters in an infiltrative growth pattern.
•	Signet cells: mucin formation expands malignant cells & pushes nucleus to periphery. 	
Colon: diverticulosis	•	Small, flask-like or spherical outpouchings 0.5 – 1cm in diameter that dissect into appendices epiploicae.
•	Walls are thin, made up of mucosa & submucosa enclosed within fat or an intact peritoneal covering.
•	Hypertrophy of musculature of affected segments.
•	Taenia coli & circular muscle bundles are prominent & most saccules are found penetrating between bundles of circular muscle fibers between the mesenteric & lateral taenia at points where entering arterioles branch out into the submucosa. 
•	Multiple closely adjacent diverticula become inflamed, bowel wall enclosed by fibrous tissue with narrowing of lumen. 
•	Complications: diverticulitis, perforation, sinus, fistula, pericolic abscess.	•	Marked hypertrophy of circular muscle layer.	
Colon: polyposis coli	•	Tubular adenoma: rounded lesions, 0.5 – 2cm in size, red & sit on a stalk of normal mucosa, which has been dragged up by traction of polyp in bowel lumen.
•	Villous adenoma: frond-like lesions, about 0.6cm thick, occupy a broad area of mucosa, 1 – 5cm in diameter, velvety red appearance, composed of finger-like epithelial projections.
•	Tubulovillous adenoma: raised lesioins, 1 – 4cm in size, red & sit on a stalk of normal mucosa, 	•	Adenomatous lesions: composed of neoplastic epithelium which lines glands as a tall, hyperchromatic, disordered epithelium.
•	Carcinomatous invasion into submucosal stalk of polyp: invasive adenocarcinoma.
•	Tubular adenoma: stalk is composed of fibromuscular tissue & blood vessels, covered by normal, non-neoplastic mucosa, branching glands are well separated by lamina propria. 
•	Villous adenoma: frondlike villiform extensions of mucosa, covered by dysplastic disordered columnar epithelium. 
•	Tubulovillous adenoma: intermediate between tubular & villous lesions. 	
Colon: adenocarcinoma	•	Proximal colon: polypoid, exophytic, cauliflower-like masses.
•	Distal colon: annular, encircling lesions producing napkin ring constrictions.
•	Margins of napkin ring: heaped up, beaded & firm, mid-region is ulcerated.
•	Penetration of bowel wall: subserosal & serosal white, firm masses, causing puckering of serosal surface.	•	Tall columnar / undifferentiated anaplastic cells invading submucosa & muscularis propria.
	
Appendicitis	•	Early: edema & telangiectasis of serosal vessels.
•	Late: dilated lumen, thickened wall, dusky discoloration of serosa, fibrinous or fibrinopurulent serosal exudate.
•	Mucosal necrosis with hemorrhage, gangrenous softening of wall, heavy coating of purulent exudate on serosa.
•	Perforation / abscess formation: appendix appear gangrenous & be found in a walled off collection of pus.	•	Early: neutrophil infiltrate of lumen, mucosa & muscularis.
•	Late: mucosal necrosis, fibrinopurulent exudate on serosa.
•	Extensive necrosis of mucosa & muscularis, with microabscesses within the appendiceal wall. 	
Liver: fatty change	•	Enlarged, pale, yellow, greasy.
•	Smooth capsule with no fibrosis.	•	No distortion of architecture of liver parenchyma.
•	Large clear vacuoles in the cytoplasm of hepatocytes, pushing nucleus to periphery.	
Liver: chronic venous congestion	•	Enlarged, deep red and soft.
•	Congested mottled ‘nutmeg appearance’ with alternating pale & dark areas.
•	Capsular surface is smooth. 	•	Distended veins full of blood.
•	Congestion of sinusoids in centrilobular areas.
•	Dark red-brown areas surrounding central veins in lobules with intervening lighter areas. 	
Liver: hemangioma	•		•	Multiple large vascular channels. lined by endothelial cells.
•	Lumen of channels filled with rbcs.
•	Vascular channels are separated by bands / trabeculae / septa of fibrous & connective tissue embedded with fibroblasts. 	
Liver: cirrhosis	•	Tend to be small in size.
•	Capsular surface is intact.
•	Surface: bosselated appearance.
•	Well-circumscribed nodules compressing intervening parenchyma.
•	Cause: fatty change, bile-stained.
•	Complications: malignant change. 	•	Parenchymal nodules varying from < 3mm to several cm in diameter.
•	Bridging fibrous septa in the form of delicate bands / broad scars replacing multiple adjacent lobules.
•	Disruption of architecture of entire liver. 
•	Piecemeal necrosis: lymphocyte infiltration.	
Hepatocellular carcinoma	•	A unifocal large mass with satellite nodules.
•	Multifocal with numerous nodules.
•	A diffusely infiltrative form. 
•	Usually paler than surrounding liver parenchyma. 
•	Invasion of vascular channels. 
•	Liver may be cirrhotic.	•	Well-differentiated: hepatocytes are arranged in trabecular or acinar pseudoglandular patterns.
•	Poorly-differentiated: markedly pleomorphic giant cells; small completely undifferentiated cells.
•	Hepatocytes may contain cytoplasmic inclusions resembling Mallory bodies. 
•	Loss of lobular architecture.
•	Grow in columns resembling normal liver.
•	Functional activity often displayed: bile secretion, fat formation, glycogen storage. 	
Metastases to liver	•	Well-defined multiple nodules.
•	Central necrosis may be present.
•	Background of non-cirrhotic liver. 	•		
Acute cholecystitis	•	Enlarged, edematous, tense & dark colored appearance due to congestion of mucosa & serosa.
•	Purulent exudate on surface.
•	Obstructing stone found in cystic duct or in the neck of gallbladder. 
•	Severe cases: necrosis of sections of walls of gallbladder – gangrenous cholecystitis.	•	Hyperemia.
•	Polymorphonuclear leukocyte infiltration.
•	Edema.
•	Necrosis of the wall. 	
Chronic cholecystitis	•	May be enlarged, normal or shrunken. 
•	Fibrin deposition on serosa with purulent exudate.
•	Thickened wall 2 – 3x normal size due to fibrosis.	•	Infiltration of macrophages, lymphocytes & plasma cells.
•	Outpouchings of mucosa through muscle of gallbladder wall (Rokitansky-Aschoff sinuses).	
Acute haemorrhagic pancreatitis	•	Firm, edematous / soft flabby organ. 
•	Blackened / darkened appearance consisting of small / large patches. 
•	Variegated pattern of blue-back haemorrhages & gray-white necrotic softening alternating with foci of yellow-white chalky fat necrosis.	•	Gray-white necrosis of parenchyma & chalky white fat necrosis.
•	Adipocytes: cells have no nuclei & there are cloudy markings in central regions of cells.
•	Large areas of coagulative necrosis & complete destruction & replacement of pancreatic acina by infiltration of inflammatory cells.
•	Purplish appearance of fat cells due to saponification of fats.	
Pancreas: carcinoma at head	•	Ampullary region is invaded, obstructing outflow of bile.
•	Surrounds & compresses, direct invades the common bile duct or ampulla of Vater. 
•	Ulceration of tumor into duodenal mucosa.
•	Marked distention of gallbladder. 	•	Mucinous or non-mucin secreting.
•	Gland patterns are atypical, irregular & small.
•	Glands are lined by anaplastic cuboidal to columnar epithelial cells.	
Spleen: infarct	•	White / pale infarcts.
•	Wedge shaped.
•	Poorly defined to sharply delimited.	•	Congested capillaries.
•	Infiltration of inflammatory cells.
•	Necrotic tissue is replaced by neutrophils & macrophages. 
•	Formation of granulation tissue and collagenous fibrous scar. 	
Spleen: congestion	•	Acute: tense, cyanotic, modest enlargement.
•	Chronic: dark brown. 	•	Marked sinusoidal dilatation.
•	Foci of hemorrhage. 	
Lymph node: TB		•	Effacement of lymph node architecture.
•	Central caseating necrosis surrounded by a rim of epitheloid macrophages followed by a rim of lymphocytes & fibroblasts.	
Lymph node: metastases from lung SCC		•	Effacement of lymph node architecture with some residual lymph node tissue.
•	Glandular pattern of growth.
•	Keratin pearls & intercellular bridges present.	
Lymph node: Hodgkin’s disease		•	Complete loss of lymph node architecture.
•	Presence of Reed-Sternberg cells: large, binucleate & bilobed.
•	Lymphocytes form extensive sheets within which are scattered few Reed-Sternberg cells. 	
Lymph node: non-Hodgkin’s disease		•	Complete effacement of lymph node architecture.
•	No Reed-Sternberg cells seen. 
•	Diffuse pattern: uniform sheets of neoplastic lymphocytes.
•	Follicular pattern: neoplastic cells are aggregated into irregular follicles. 
•	Lymphocytes are pleomorphic with large number of mitotic figures. 	
Hydronephrosis	•	Enlarged cystic kidney.
•	Distended pelvi-calyceal system.
•	Multi-loculated cystic dilation.
•	Compression & atrophy of surrounding renal parenchyma – almost ‘shell-like’.
•	Renal cortex seen as a very thin layer of fibrous wall. 
•	Obliteration of paillae.
•	Flattening of pyramids.
•	Stone may be present in upper ureter / pelvi-ureteral junction. 
•	Pre-existing pyelonephritis. 	•	Early lesions: tubular dilation, followed by atrophy & fibrous replacement of tubular epithelium with relative sparing of glomeruli.
•	Late: glomeruli become atrophic & disappear, converting entire kidney into a thin shell of fibrous tissue.	
Kidney: infarct	•	Triangular / wedge shaped. 
•	Base at cortical surface & apex pointing towards medulla & occluded artery.
•	Infarct appears pale compared to adjacent parenchyma.
•	Old resolved infarcts: V-shape absence of renal parenchyma. 	•	Hyperemic at periphery.
•	Coagulative necrosis of renal parenchyma: amorphous pale pink mass of glomeruli & renal tubular epithelial cells with no nuclei.
•	Infiltration of neutrophils & macrophages.
•	Granulation tissue & collagenous scars in old infarcts.	
Acute tubular necrosis	•	Kidney is enlarged.
•	Cortex is broad & pale; markings are absent.
•	Pyramids are grossly congested.
•	Cut surface bulges due to edema.	•	Glomeruli are spared.
•	Necrotic tubules have no nuclei & consists of dense eosinophilic amorphous material retaining its outline.
•	Patchy tubular necrosis mostly in straight segments of proximal tubules & ascending limbs of Loop of Henle. 
•	Distal tubules & collecting ducts contain cuts.	
Polycystic kidneys	•	Bilateral enlargement of kidneys.
•	Parenchyma shows innumerable cysts of varying size from barely visible to 4 – 6cm. 
•	Cysts show a variety of colors due to the fluid content which may be clear to reddish brown.
•	Cyst development is found in both cotical & medullary regions. 	•	Most cysts are lined by non-descript, flattened to cuboidal epithelial cells.
•	Tissues between cysts may show unremarkable or atrophic nephron elements.	
Acute pyelonephritis	•	Commonly involves upper & lower poles.
•	Cortical surfaces show suppurative abscesses.
•	Large, wedge-shaped areas of coalescent suppuration. 
•	Dilatation of pelvis & calyces may be present.
•	Congestion of renal parenchyma.
•	Pale streaks with surrounding congestion in medullary rays.
•	Inflammatory foci repaced by scars seen on cortical surface as fibrous depressions. 
•	Pyelonephritic scar: fibrosis & deformation of underlying calyx & pelvis.
•	Look for: calculi, papillary necrosis, pyonephrosis & perinephric abscess.	•	Patches of suppuration in cortex & medulla.
•	Inflammation is mainly interstitial.
•	Glomeruli are usually unaffected. 
•	Tubules are filled with pus cells; some are destroyed with abscess formation.
•	Scars: atrophy of tubules, interstitial fibrosis & lymphocyte infiltrate. 	
Chronic pyelonephritis	•	1 kidney enlarged.
•	Commonly involves upper & lower poles of kidney.
•	Granularities seen on outer cortical surface.
•	Yellow raised discrete surface abscesses, not evenly distributed. 
•	Irregular loss of renal parenchyma: kidneys are diffusely & symmetrically scar.
•	Cut section: obliterated cortico-medullary junction.
•	Hallmark: coarse, discrete, corticomedullary scar overlying a dilated, blunted or deformed calyx. 
•	Parenchyma: diffuse scattered pale suppurative areas alternating with intervening congestion & hemorrhage. 
•	Distortion of associated calyces which appear dilated. 
•	Atrophic kidneys: a lot of pericaliceal & peripelvic fat is seen. 
•	Look for: calculi, papillary necrosis, pyonephrosis & perinephric abscess.	•	Changes involve mainly tubules & interstitium.
•	Tubules show atrophy in some areas & hypertrophy in others or dilatation.
•	Dilated tubules may be filled with colloid casts (thyroidization).
•	Varying degrees of chronic interstitial inflammation & fibrosis in cortex & medulla.
•	Presence of neutrophils in interstitium & pus casts in tubules.
•	Arcuate & interlobular vessels: obliterative endarteritis in scarred areas.
•	Hyaline arteriosclerosis in presence of hypertension. 	
Papillary necrosis	•	Overlying cortical tissue is relatively spared.
•	Dark hemorrhagic areas are necrotic renal papillae.
•	Acute phase: necrotic papillae are pale, soft or hemorrhagic.
•	Late phase: necrotic papillae may become detached from cortical tissues & are therefore absent.
•	Necrotic papillae that are not detached may resolve as amorphous fibrotic scarred tissue. 	•	Necrosis of cellular elements of the papillae.
•	Hemorrhage & inflammatory reactions at the interface with viable areas. 	
End-stage kidney (benign hypertensive nephrosclerosis)	•	Kidneys are small & hard.
•	Symmetrical atrophic thinning of cortex.
•	Finely granular surface.
•	Fine petechial cortical hemorrhages may be present.
•	Malignant hypertension: ‘flea-bitten’ appearance on cortical surface.
•	Cortico-medullary junction & papillae are usually preserved. 
	•	Hyaline arteriolosclerosis: homogenous, pink hyaline thickening with loss of underlying cellular detail & obliteration of glomerular tufts. 
•	Glomeruli develop axial thickening & fibrosis with fibrotic replacement of Bowman’s spaces. 
•	Dilated, hypertrophied or absent tubules.
•	Marked interstitial fibrosis with atrophy & replacement of tubules in cortex.
•	Lymphocytic infiltrates are present in the interstitial tissue.	
Diabetic nephropathy	•	Affected kidney may be normal or shrunken.
•	Overall fine scarring of kidneys.
•	Finely granular cortical surface.
•	Cortico-medullary junction is preserved.
•	May have associated features of pyelonephritis & papillary necrosis.	•	Diffuse thickening of the glomerular capillary basement membrane.
•	Diffuse glomerulosclerosis: diffuse increase in mesangial matrix with mesangial cell proliferation. 
•	Nodular glomerulosclerosis: ball-like deposits of a laminated matrix with mesangial core in periphery of glomerulus – Kimmelstiel-Wilson nodules.
•	Hyaline arteriolosclerosis in afferent arterioles: glassy, homogenous, eosinophilic deposits in parietal layer of Bowman’s capsule. 
•	Features of pyelonephritis & necrotizing papillitis.
•	Glycogen & fatty changes in the tubular epithelium.	
Renal cell adenocarcinoma	•	Kidney enlarged.
•	Cut surface: large spherical tumor involving upper pole. 
•	Multinodular, up to 3 – 4 nodules.
•	Bright-yellow tumor has sharply defined borders & show a variegated cut surface with areas of necrosis & hemorrhage. 
•	Tumor-parenchymal interface is sharp.
•	Distortion of calyces & pelvis: part of calyceal system may be dilated due to obstruction. 
•	Compression of rest of renal parenchyma.
•	Presence of satellite nodules. 
•	Look for invasion into renal veins & adjacent structures – ureter, perirenal fat & adrenal gland. 	•	‘Clear-cell’ pattern: tumor cells have clear cytoplasm due to high content of glycoprotein & lipid.
•	Tubular & papillary carcinoma: epithelial cells with a granular cytoplasm. 
•	Histologic patterns: tubular, trabecular or solid.	
Nephrolithiasis (staghorn calculus)	•	Entire calyceal system & pelvis occupied by a single continuous calculus.
•	Calculus was molded by luminal cavity of pelvis & calyces: staghorn calculus.
•	Hydronephrosis with dilation of renal pelvis & calyces.
•	Thin renal parenchyma between enlarged calyces. 
•	Look for signs of acute pyelonephritis.	•	Atrophy of tubules.
•	Obliteration of glomeruli.	
Kidney: transitional cell carcinoma	•	Involves mucosal surfaces of renal pelvis & calyces & may secondarily invade the renal parenchyma.
•	Tumor has a light tan color & seemingly friable quality.
•	Periphery is ill-defined & not sharply circumscribed.
•	Tumor is papillary or nodular.
•	Tumor involving uretero-pelvic junction may obliterate urine outflow & cause hydronephrosis. 	•	Papillary architecture.
•	Papillae show a central fibrovascular core & are lined by transitional epithelial cells.	
Bladder: transitional cell carcinoma	•	Papillary, flat or nodular tumors.
•	Carcinoma-in-situ: high-grade flat lesion confined to bladder mucosa appearing as an area of mucosal reddening, granularity or thickening. 
•	Lesions are fungating, necrotic & sometimes ulcerative, invading deeply into bladder mucosa.
•	Advanced stages: invasion of adjacent prostate, seminal vesicles, ureters & retroperitoneum.	•	Arise as frond-like papillary outgrowths from the urothelial surface & have a slender connective tissue stroma supporting the layers of neoplastic cells.
•	Tumor extends deeply through bladder submucosa & muscular wall. 	
Breast: fibroadenoma	•	Typically 1 – 4cm in diameter.
•	Firm, rubbery, well-circumscribed, white lesions that are mobile in the breast. 
•	Glistening cut surface & a rough texture with slit-like spaces.	•	Nodule is well circumscribed by a condensation of connective tissue & is composed of both epithelial & fibrous stroma components.
•	Epithelial component: forms gland-like structures lined by duct-type epithelium.
•	Stromal component: loose, cellular fibrous tissue around epithelial areas. 	
Breast: fibrocystic disease	•	Firm, rubbery replacement of breast tissue with cysts.
•	Bilateral single / multifocal cysts.
•	Ill-defined diffuse increase in consistency.
•	Discrete nodularity. 	•	Overgrowth of ducts & acini with fibrosis & cysts. 
•	Cysts: lined by flattened epithelium derived from lobular-ductal unit & are filled with watery fluid. 
•	Apocrine metaplasia: epithelium lining hyperplastic ducts undergoes metaplasia to apocrine glands.
•	Sclerosing adenosis: marked proliferation of stromal tissue & myoepithelial cells, separating & compressing acini & ducts into narrow ribbons of cells.
•	Epithelial hyperplasia within proliferated ducts & lobules in minority of cases – may exhibit papillary proliferation into ducts, forming papillary infoldings. 	
Breast: ductal carcinoma	•	Scirrhous carcinoma: marked increase in dense, fibrous tissue stroma.
•	Fairly sharply delimited nodules of stony-hard consistency 1 – 5cm in diameter.
•	May have infiltrative attachment to surrounding structures with fixation to underlying chest wall, dimpling of skin & retraction of nipple.
•	Small pinpoint foci or streaks of chalky white stroma & calcification within central focus.	•	Extensive proliferation of ductal epithelial cells with marked increase in dense fibrous tissue stroma.
•	Consists of malignant cells disposed in cords, solid cell nests, tubules, anastomosing sheets with bands. 
•	Pattern of growth: radiate from a central area of desmoplasia.
•	Tumor cells have invaded through the basement membrane, infiltrating into surrounding fibrous stroma.
•	Cytology: small cells with hyperchromatic regular nuclei to huge cells with large irregular hyperchromatic nuclei.
•	Invasion of lymphatic & perineural spaces may be evident. 	
Breast: lobular carcinoma	•	Tumor is rubbery & is poorly circumscribed.
•	Dense, lumpy diffuse infiltration.	•	Strands of infiltrating tumor cells, often only one cell in width loosely dispersed throughout fibrous matrix.
•	Lack cohesion without formation of tubules or papillae.
•	Cells are small with little nuclear pleomorphism.
•	Signet-ring cells are common. 	
Cervix: CIN III		•	Marked dysplasia from basal to superficial layer.
•	Atypical cells in entire thickness of cervical epithelium.
•	No morphological differentiation between superficial & deeper layers.
•	Lesion is confined within epithelial layer & basement membrane is intact.
•	Cytology: increased nuclear-cytoplasmic ratio, hyperchromatic nuclei, pleomorphism, mitotic figures & loss of polarity. 	
Cervix: squamous cell carcinoma	•	Fungating tumor: begins as a nodular thickening of the epithelium & eventually as a cauliflower-like mass projecting above surrounding mucosa, encircling external os.
•	Ulcerative form: sloughing of central surface of tumor.
•	Infiltrative: grow downward into underlying stroma.
•	Growth & spread: infiltrate underlying tissue, obliterate external os, grow upward into endocervical canal & lower uterine segment & eventually extend into & through wall of fundus into broad ligaments.	•	Extensive proliferation of abnormal epithelial cells.
•	Breach of basement membrane with sheets, nests of atypical cells invading into subepithelial stroma.
•	Keratin pearls can be seen.	
Uterus: leiomyoma	•	Whorled cut surface.
•	Multiple, sharply circumscribed unencapsulate, firm gray-white masses.
•	Intramural: embedded within myometrium.
•	Subserosal: may become pedunculated.
•	Submucosal: may project as polyps into uterine cavity.
•	Larger leiomyomas can undergo necrosis & cystic degeneration. 	•	Whorling bundles of smooth muscle cells.
•	Foci of fibrosis, calcification, necrosis with hemorrhage may be present.
•	After menopause: smooth muscle cells atrophy & replaced by fibrous tissue.	
Uterus: adenomyosis	•	Uterine enlargement.
•	Irregular thickening of uterine wall.
•	Compression of uterine cavity to a narrow slit.	•	Nests of endometrial stroma or glands, or both, in the myometrium between the muscle bundles.	
Endometrial hyperplasia		•	Marked hyperplasia of endometrium due to proliferation of both glandular & stromal component.
•	Presence of glands of variable shapes & sizes.
•	Majority of glands are dilated, appearing in cyst-like structures.
•	Simple hyperplasia: epithelial lining may be cuboidal, tall columnar or multilayered.
•	Complex hyperplasia: increase in the number & size of endometrial glands which vary in size & irregularity of shape. 
•	Atypical hyperplasia: cellular atypia of hyperplastic epithelium.	
Endometrial carcinoma	•	Infiltrate causing diffuse thickening of affected uterine wall.
•	Exophytic form.
•	Fill endometrial cavity with firm to soft, partially necrotic tumor tissue.
•	Extend through myometrial wall to the serosa. 	•	Adenocarcinoma with squamous differentiation: well-defined gland patterns lined with anaplastic cuboidal to columnar epithelial cells. 	
Ovary: serous cystadenomas	•	May be small: 5 – 10cm in diameter.
•	Most are large, spherical to ovoid, cystic structures: 30 – 40cm in diameter.
•	Serosal covering is smooth & glistening. 
•	Cut section: a single cavity or divided by multiple septa into a multiloculated mass.
•	Cystic spaces are filled with clear serous fluid & mucus.
•	Jutting into cystic cavities are polypoid or papillary projections.	•	Lining epithelium is composed of a single layer of tall, columnar, ciliated epithelial cells with small papillae.
•	Psammoma bodies are common in the tips of papillae.	
Ovary: dermoid cyst	•	< 10cm in diameter.
•	Covered by a glistening serosa.
•	Cut section: a thin cystic wall lined by well-differentiated skin having adnexal glands, including hair.
•	Cystic space is filled with a thick, sebaceous secretion containing matted hair.
•	May contain foci of teeth, both, cartilage, nests of bronchial or gastrointestinal epithelium.		
Ovary: fibroma	•	Solid, spherical, or slightly lobulated, encapsulated, hard, gray-white masses covered by glistening, intact ovarian serosa.	•	Well-differentiated fibroblasts with scant collagenous connective tissue interspersed between the cells. 	
Testes: seminoma	•	Testicular enlargement.
•	Grow rapidly as large, gray-white, fleshy masses.
•	Remained confined within tunica albuginea.	•	Sheets / cords of well-differentiated uniform polygonal cells, with distinct cell membranes, central round nuclei & cleared cytoplasm.	
Testes: teratoma	•	Cut surface: cystic areas & a variegated appearance with foci of cartilage, bone or soft myxomatous tissue.	•	Composed of well-differentiated elements such as neural tissue, muscle, cartilage, fat, bronchial epithelium & bits of intestinal wall.
•	These elements lie helter-skelter with no definite pattern or orientation. 	
Benign prostate hyperplasia	•	Nodules orginate around urethra.
•	Well-demarcated on cros section.
•	Urethra is compressed to a slit-like orifce by nodules on the lateral aspect. 
•	Hyperplastic tissue may project up into the floor of urethra in a hemispheric mass. 	•	Proliferation of glands lined by hypertrophic tall columnar epithelium, thrown into numerous papillary buds & infoldings.
•	Gland formations are well-developed & separated from each other by stroma.
•	Numerous small foci of hyaline concretions, corpora amylacea are nested within these glands.	
Prostate carcinoma	•	Usually begins in peripheral zones of prostate but can arise anywhere in the gland, usually in multiple foci which fuse to form a single mass.
•	Tumor blends imperceptibly into background of gland. 
•	Firm, gritty texture yellower than surrounding tissue.	•	Adenocarcinoma of varying degrees of differentiation.
•	Stroma in between glands is abundant & fibrous.
•	Neoplastic epithelium may be thrown into folds which fuse & give rise to a cribriform pattern. 	
Brain abscess	•	Ill-defined area of swelling, which are congested & soft on cut surface.
•	Central region of liquefactive necrosis & a fibrous capsule surrounded by reactive gliosis.
•	Abscess: rounded cavity, 1 – 2cm in diameter, filled with pus.
•	Abscess wall is produced by fibroblasts from blood vessels that proliferate around margin of necrotic brain. 
•	Marked cerebral edema.		
Tuberculous meningitis	•	Often affects base of brain.
•	Tuberculoma: localized caseous abscess forming a well-circumscribed intraparenchymal mass. 
•	Subarachnoid space: contains a gelatinous / fibrinous exudate of chronic inflammatory cells. 
•	Arteries running through subarachnoid space may show obliterative endarteritis, with inflammatory infiltrates in their walls & marked intimal thickening. 		
Pleomorphic adenoma	•	Well demarcated encapsulated lesion rarely exceeding 6cm in diameter.	•	Epithelial elements forming ducts, acini, tubules, strands or sheets of cells interspersed within a loose myxoid connective tissue storma. 
•	Epithelial cells are small, dark, & range from cuboidal to spindle forms.	
Multinodular goitre	•	Irregular, hyperplastic enlargement of thyroid.
•	Well-circumscribed nodules of varying sizes.
•	Meaty, red-brown parenchyma alternating with pale, gelatinous areas punctuated by small cysts, foci of red-brown hemorrhage & pale fibrotic scars, some with calcification.	•	Same as for follicular adenoma	
Hashimoto’s thyroiditis	•	Gland is modestly enlarged, symmetric, firm, rubbery, & discrete.
•	Sometimes the enlargement is asymmetrical & lobular.
•	Cut surface: normal red-brown, meaty, thyroidal substance is replaced by a pale, gray-white tissue.
•	Thyroid capsule remains intact.	•	Parenchyma is paler than normal.
•	Extensive heavy infiltration of lymphocytes & plasma cells.
•	Lymphoid follicles with germinal centers.
•	Thyroid follicle epithelial cells have abundant eosinophilic granular cytoplasm with lots of mitochondria: Hurthle cell.
•	Scattered areas of fibrosis in stroma.	
Grave’s disease	•	Gland is diffusely & symmetrically enlarged.
•	Red-brown, muscle-like appearance on transection. 	•	Hypertrophy & hyperplasia of follicular epithelium: crowding of columnar cells into irregular papillary folds.
•	Presence of peripheral scalloping colloid at interface of epithelium & colloid.
•	Follicular lining cells are very compact & have tall columnar appearance.
•	Colloid is substantially decreased.
•	Interfollicular parenchyma contains hyperplastic tissue & increased numbers of blood vessels.	
Thyroid: follicular adenoma	•	Spherical, completely encapsulated, seldom > 4cm in diameter.
•	Vary from gray to brown.
•	Central focus of fibrosis & calcification. 
•	Some lesions undergo cystic degeneration. 	•	Well-demarcated solitary lesion occasionally accompanied by fibrosis, hemorrhage or calcification.
•	Sharply demarcated from adjacent parenchyma by a well-defined fibrous capsule. 
•	Compresses surrounding follicles.
•	Follicles are lined by cuboidal & columnar cells.
•	Closely apposed nests & trabeculae to well-developed follicles containing abundant colloid.
•	Hurthle cell adenomas: granular, eosinophilic cells containing abundant mitochondria.	
Thyroid: papillary carcinoma	•	Poorly delineated unencapsulated focal masses located anywhere within the thyroid sometimes with multiple foci.
•	Advanced tumors may penetrate thyroid capsule into surrounding sturctures.
•	Neoplastic foci are gray to brown & firm with furry appearance. 	•	Fibrous capsule is breached by infiltration of tumor into normal thyroid tissue.
•	Form: complex papillary structures, each composed of a narrow stromal core covered with a layer of glandular epithelium. 
•	Stromal cores contain small calcified laminated bodies: psammoma bodies.
•	Hyperchromatic empty nuclei devoid of nucleoli & nuclear grooves with eosinophilic inclusions.	
Thyroid: follicular carcinoma	•	Encapsulated gray-white nodule.
•	Massive, invasive neoplasm with extension into perithyroid structures. 	•	Cells range from well-differentiated to anaplastic.
•	Vascular & capsular invasion may be present. 	
Femur: osteosarcoma	•	Arise in metaphysis cancellous bone.
•	Extends in all directions, eroding cortex & invading adjacent soft tissues, producing an obvious extraosseous mass. 
•	Cut surface: gray-white with areas of hemorrhage & cystic necrosis.	•	Hallmark: formation of osteoid by tumor cells.
•	Anaplastic cells found within lacunae of osteoid. 
•	Cytology: marked hyperchromasia, abnormal mitoses & bizarre-looking giant tumor cells in fibroblastic component.	
Femur: giant cell tumor	•	Tumor is gray-brown, well vascularized & may have areas of hemorrhage, necrosis & cyst formation. 	•	Abundance of mutlinucleate giant cells dispersed throughout a stroma of round to ovoid mononuclear cells. 	
Cranial vault: multiple myeloma	•	Multiple punched-out defects, 1 – 4cm in diameter.	•	Increased number of plasma cells with infiltration, invasion & erosion. 
•	Form: mature to immature forms.