Pathology Slide List – Cardiovascular, Respiratory, Head & Neck, GI, Hepatobiliary
Page 1 of 13
Slide # / Tissue / Pathology / Description5 / Larynx / Squamous Cell Carcinoma
(Neoplasia) / Find normal respiratory mucosa with the ciliated columnar epithelium. Note that it is disrupted by a neoplastic mass of pleomorphic squamous cells. These cells have hyperchromatic and bizarre nuclei with eosinophilic cytoplasm. Note keratinization and intercellular bridges. Lesion penetrates into the muscle layers.
Normally squamous above vocal cords, glandular below. Most common laryngeal tumor is SCC; mostly in 40+ men; associated with smoking and EtOH use.
6 / Liver / Chronic Passive Congestion
(Inflammation) / Center of lobule shows distended sinusoids filled with blood (congestion). Areas of early hemorrhage are present. The dark pigment is artifactual, but the brown pigment is iron. Steatosis is non-specific.
Most often caused by right heart failure. Causes nutmeg liver.
7 / Lung / Adenocarcinoma
(Malignant Neoplasia) / Compare to slides 263, 47. Note formation of glands (acini) The cells are large and not too different from squamous CA. The stroma is fibrous. The tumor is not encapsulated, but infiltrates surrounding lung. Adenocarcinoma with focal bronchoalveolar pattern.
8 / Coronary Artery / Atherosclerosis of coronary artery; Atherosclerosis and thrombus of venous CABG.
(Circulatory) / Cross section of three vessels – two native coronary arteries, one leg vein used in CABG. Differentiate between them. Arterial wall has a media of smooth muscle in a continuous band. The vein has bundles of smooth muscle. The arteries are narrowed by atherosclerotic plaques (pink granular debris, macrophages, cholesterol clefts, collagen, fibrous cap). The vein is occluded similarly. Tiny lumens in the occluding mass are attempts at recanalization.
Grading: 1 (<24% stenotic), 2 (25-50%), 3 (51-74%), 4 (>75% stenotic). Estrogen protects females until menopause. Proximal 1/3 of LAD (left anterior descending) and LCx (left circumflex) and distal 2/3 of RCA (right coronary) arteries most common for grade 4 lesion. Tx with CABG-Coronary Artery Bypass Graft, PTCA-Percutaneous Transluminal Coronary Angiography
CABG generally lasts 10-24yr. Risk of CHF post-MI.
10 / Esophagus / Squamous Cell Carcinoma
(Neoplasia) / Note the region of normal squamous mucosa. Then note the carcinoma arising from surface epithelium and infiltrates the submucosa. Cells are large with moderate amount of pink cytoplasm, hyperchromatic nuclei with prominent nucleoli. In situ component found where cells have not yet proceeded past the epithelium.
Hits men 3:1; related to nitrate consumption; 20% to cervical nodes, 50% to mediastinal nodes, 30% to gastric/celiac nodes; 5-10% 5-year survival rate.
11 / Liver / Metastatic Carcinoma
(Neoplasia – Metastatic) / Primary tumor is lung CA.
Liver is congested and contains one portal nodule of metastatic Adenocarcinoma with numerous small metastatic glands in the sinusoids.
14 / Gallbladder / Chronic Cholecystitis
(Inflammation) / Mild chronic inflammatory infiltrate in the mucosa. Invaginations of the epithelium (Rokitansky-Aschoff sinuses) can bee seen. The amount of chronic inflammation and fibrosis can be variable.
Assoc. with cholelithiasis; bile duct obstruction leads to jaundice, hypercholesterolemia, increased alk. Phos, and hyperbilirubinuria. GB Pain – RUQ / Rt. Shoulder.
15 / Respiratory Mucosa / Nasal Polyp
(Inflammation / Hypersensitivity) / Note the markedly edematous stroma. Numerous eosinophils suggest an allergic etiology. Edema forms blebs that expand into polyps. Glands retain mucous. Note thickened basement membrane.
Polyps are usually bilateral; may be obstructive; epithelium produces excess mucin; seasonal or perennial allergies = sneezing. Eosinophil granules have parasite wall destruction potential due to eosinophil peroxide, major basic proteins, cationic proteins. Involves IgE and mast cells.
20 / Stomach / Adenocarcinoma, diffuse type
(Neoplasia) / Specimen had a rigid, thickened, leather bottle appearance of linitis plastica. The neoplastic cells are scattered individually or in small clusters with a diffusely infiltrative growth pattern. Cells are not forming glands but occasionally have a signet ring appearance due to accumulation of intracellular mucin.
Common in men 50+, blood group A; nitrosamine/ salt/smoke in food, H. pylori; stomach exhibits linea plastica.
25 / Gallbladder / Acute Cholecystitis
(Inflammation) / Note the thickness of the GB wall – thickening due to inflammatory changes. PMN infiltrate, edema of interstitial tissue, vascular congestion, extravasation of RBCs. Changes are transmural, but are prominent near the lumen. Mucosa is intact generally, however there are areas of disruption due to inflammation.
Shock can result from bile accumulation in peritoneum. Less assoc with gallstones than chronic cholecystitis. SSX: nausea, vomiting, fever, leukocytosis, RUQ and Epigastric pain.
28
(Likely) / Gastro-esophageal Junction / Barrett’s Esophagus
(Neoplasia) / Find goblet cells that stain bright blue with this Alcian blue stain – indicates presence of acid mucins. Acid mucins are produced by intestinal goblet cells and not present in normal tissue in the region. Hallmark of intestinal metaplasia.
Barrett’s dysplasia AdenoCA. Varices in lower 1/3 of esophagus can turn to AdenoCA; assoc. with incidence of esophageal CA.
36 / Cardiac / Old Infarct
(Circulatory) / Cross section of LV with broad bands of collagen. Virtually no inflammation because the infarts occurred in the distant past. There is hypertrophy of many of the adjacent myofibers to compensate for the loss of function in infracted regions.
Few dilated vessels remain in infarct scar. Loss of nuclei, no PMNs. Infarcts over 1cm suggest older/aged. Risk with IHD / CAD. Loss of contractility. LV failure favors PaHTN. RV failure favors portal HTN.
38 / Lung / Coal-workers Pneumoconiosis
(Inflammation) / Incidental changes such as acute pneumonia and chronic passive hyperemia are present – disregard these findings. The capillary bed is dilated, representing terminal CHF. Note collections of black pigment and pink collagenous tissue related to small airways. These pigmented nodules are relatively acellular.
Coal mining adds carbon and dust. Progressive form can lead to bronchiatectasis, PaHTN, and death.
43 / Rectum / Adenocarcinoma
(Malignant - Neoplasia) / Moderately differentiated AdenoCA in which abortive glandular structures are formed. Identify the interface between the more normal mucosa and infiltrating tumor. CA invades into smooth muscle of muscularis proper.
AdenoCA accounts for 95% of all malignancy in colon. Produce serum marker CEA and CA 19-1.
47 / Lung / Squamous Cell Carcinoma
(Malignant Neoplasia) / Compare to slides 263, 7. Typical squamous pattern is nests, sheets, and cords. These are big cells with much pink cytoplasm. Nuclei are larger, with clear areas between chromatin. Note intercellular bridges or keratin pearls, and potential squamous epithelium.
Arises from bronchial epithelium. Prevalence favors men. Silent lesions that often metastasize before detection (poor prognosis if pt presents with hoarseness, chest-pain, etc.) Lesions often preceded for years by meta/dysplasia. Cachexia, hypo-resonance, and SOB.
58 / Lung / Acute Bronchopneumonia
(Acute Inflammation) / Alveolar septa are hyperemic but not inflamed. PMNs predominate and a few macrophages are present. Proteinaceous edema fluid and fibrin present in alveolar space. Gram stain may be included – look for gram-positive cocci (tiny blue specks).
Productive cough with sputum that is thick, yellow-gray. SOB, CXR infiltrate. May see a pale purple spleen.
59 / Colon / Ulcerative Colitis
(Inflammation) / Note the superficial ulcers present. The ulcers are shallow and inflammatory infiltrate is confined to the mucosa/submucosa. Glandular epithelium has regenerative changes (mucous cell depletion and irregular glandular contour). Crypt abscesses are rare. Some degree of serositis present; note lack of granulomatous inflammation, full thickness inflammation, fibrosis, or lymphoid follicle formation.
Unknown etiology; ulceration localized to colon and always rectal; pseudopolyps are islands of mucosa surrounded by ulceration; chronic diarrhea with blood; may turn into toxic megacolon, colon perforation, or colon CA; Surgical.
60 / Liver / Hepatocellular Carcinoma [hepatoma] / Malignant neoplasm of liver. Note similar architecture of normal and malignant cells. Malignant cells are more bluish in cytoplasm, mitotic bodies, high N:C ratio, fibrous capsule, larger, and more vesicular (open) nuclear chromatin pattern with very large nucleoli.
Elevated α-FetoProtein AFP. More common in Males. Death within 6mo; GI/Esophageal Variceal Bleeding, Liver Failure. Sudden, worsening ascites, HBV associated.
63 / Liver / Nutritional Cirrhosis ‘Alcoholic Cirrhosis’ / Note connective tissue septa staining blue-gray with criss-cross pattern breaking tissue into regenerative nodules. Steatosis present.
Portal HTN ascites, varices, caput medusa; jaundice, hypoalbuminemia, Clotting factor deficiencies.
64 / Esophagus / Candida Esophagitis
(Inflammation) / Slides stained with PAS for fungus – two slide sets:
1) Mucosa and submucosa may be missing (eroded); replaced by PMNs and lymphocytes. Intermixed with inflammation are fungal elements in the form ob budding yeast pseudohypha. 2) Largely necrotic epithelium; many invading pink stained pseudohypha invading the epithelial surface (inflammatory response was weak due to leucopenia º chemotherapy).
F glycoproteins are stained. ID and Tx of invasive forms crucial. Tx with antifungals. SSx: trouble eating, hemorrhage; assoc. with antibiotic treatment, DM, malignancy, or immunocompromised. Seen as white adherent mucosal patches and painful, difficult swallowing.
66 / Appendix / Benign Carcinoid
(Neoplasia) / Groups of small, uniform cells with a moderate amount of cytoplasm and generally small, uniform, centrally placed nuclei with a salt and pepper quality of chromatin. Note the arrangement of theses cells into cords and insular patterns (looks like islets cells of pancreas).
Invasive but not malignant in this case. Most common site of carcinoid is the appendix; appendix carcinoid rarely mets. Slow growing and low grade malignancy. Caused by elaboration of peptides/amines (serotonin). SSx: cutaneous flushing, watery diarrhea, abd. cramps, bronchospasm, R. heart valve lesions.
71 / Cardiac / Atherosclerosis of Aorta / Note the atherosclerotic lesion that is located in the sub-intima. It has a fibrous cap on the surface, which is largely acellular collagen, with some fibroblasts. Below it is lipid (poorly stained) and calcium deposits. Look for an area of acicular (elongated and pointed at both ends) spaces which represent cholesterol and cholesterol esters that have been washed out of the tissue . Look for ofam cells (macrophages w/ clear/lipid filled cytoplasm).
84 / Colon / Villous Adenoma
(Benign Neoplasia) / Frond-like arrangement of the villous adenoma with slender fibrovascular cores supporting columnar epithelial elements. Nuclei are crowded, elongated, and stratified.
Broad based lesion, may produce mucin. SSx: blood in stool, anemia, detection via colonoscopy, APC GENE; Malignancy risk: much more than tubular adenoma.
91 / Cardiac / Chronic Mitral Valvulitis º Rheumatic
Heart Disease
(Inflammation) / Ventricular myocardium with the base of the mitral valve is present in the slide. Mitral valve appears as large, thick, fibrous mass. Note the vascularity and small number of lymphocytes in the valve tissue. Valve is thickened and should not be vascular or inflamed – due to rheumatic heart disease.
Type III reaction to normal tissue antigen. RHD follows Group A β-hemolytic strep infection. 15-20 million cases world wide annually. Tx with Antibiotics. Long or repeated infections increase risk.
92 / Lung / Coccidioidomycosis
(Inflammation – Chronic) / Many small nodules are visible without microscope. Mature granulomas have well-circumscribed, have fibrosis at periphery, then epithelioid cells and giant cells. Necrosis and PMNs present. Organism is round 20-40micra with thick wall and refractive basophilic internal material.
Caused by spore inhalation; endemic in SW and far west (‘valley fever’); 40% show cough, fever, chills, pleuritic CP; Confirm with skin test and Ab after 1 month.
96 / Lung / Bronchiectasis / Small Airway Disease
(Inflammation) / Large airway disease, as well as some adjacent alveolar lung tissue that has small airways. A large airway should contain cartilage, muscle, and seroumucinous glands, but little are found here. The normal bronchial wall should be quite thick, at least 2mm. This is maybe 0.5mm. The normal wall components have been destroyed. Note the chronic inflammation and fibrosis in the wall. Purulent material is in the lumen. The slides may also show small airway disease, so look for inflammation with dilated small airways; the alveoli look far less diseased.
Always due to infection (Chronic pneumonia). Results from CF and tumors. Copious purulent sputum, hemoptysis; predisposed by chronic sinusitis and bronchial obstruction.
101
(Likely) / Lung / Diffuse Alveolar Damage
(Inflammation) / Pathologic syndrome. Slide is acute interstitial pneumonitis typical of acute viral infection. Inflammatory cells are primarily mononuclear cells (macros). Eosinophilic membranes are present lining some alveolar ducts and show some inflammatory infiltrate. The architecture of the lung is preserved and there is not much interstitial fibrosis. The clinical syndrome is Acute Respiratory Distress Syndrome (ARDS)
Hyaline membrane disease. Unknown etiology may include virus, high levels of inspired oxygen, drugs. ARDS (decreased arterial O2, decreased lung compliance, diffuse pulmonary infiltrate on CXR, lack of Left heart failure). Crackles on auscultation. Diffuse, firm, red lung. 40% of pts recover.
104 / Lung / Sarcoidosis
(Inflammation) / Small nodules of chronic inflammatory cells (epithelioid) and giant cells with rim of lymphocytes. NON-CASEATING granuloma. Reticulonodular pattern on CXR. May progress to looking like slide 242.
Commonly multi-system disease (liver/spleen); pulmonary infiltrates and hilar adenopathy. Unpredictable course. 65-70% recover. Fever, weight loss.
106 / Liver / Hepatitis B Viral Infection / Disruption of normal liver architecture due to massive destruction. HBV may be visible with staining. Note lymphocytes, macrophages, responding to infection and cell necrosis. FEW POLYS. Councilman body (single necrotic/apoptotic cell).
Appears ‘Moth-eaten’. Relatively scant number of inflammatory cells present. Increased number of PMNs in Alcoholic Hepatitis (slide 251).
Need stain for HepB differentiation. Trans via fluid exchange. Ch. liver cell loss and fibrosis cirrhosis.
113 / Liver / Malaria
(Inflammation) / Malaria is a major cause of heptaomegaly in other parts of the world. This is a chronic stage with malaria. Pigments are prominent in the reticuloendothelial (Kupffer) cells. No residual malaria parasite is seen.
Headache, arthralgias, fever; Tx with chloroquine, primaquine, quinine.
117 / Liver / Schistosomiasis
(Inflammation) / Portal mixed inflammation, mostly chronic with large parasites (schistosome ova, large size). Portal fibrosis is prominent, a major global cause for severe portal HTN without cirrhosis.
Tx: portal shunt; assoc with bladder infections; adult
worms lodge in portal veins; Granulomatous response to ova can lead to tissue destruction, fibrosis, portal HTN.
120 / Cardiac / Necrotizing Vasculitis
(Inflammation) / Polyarteritis Nodosa (PAN) from muscle or nerve. Find medium-sized arteries (lumen may be obscured). Look for bright rose-pink ring within the vessel wall. This is fibrinoid necrosis. Karyorectic nuclear debris may be present. In older lsions, there may be an intimal/medial proliferative response of myofibroblast cells. Lymphocytic inflammation may be seen outside of vessel wall.
Myocarditis; neuritis; immune mediated.
127 / Lung / Infarct and Thrombus
(Circulatory) / Notice that the infracted area has become sharply demarcated and diffusely eosinophilic. Note the character of the tissue separating viable lung from infracted – granulation tissue. Adjacent arteries may show thickening and organization. Pleural fibrin is a typical appearance of pleuritis occurring in infarcts.
Macrophages with hemosiderin seen in necrotic area. Visible on XR, angiogram, VQ scan. Tx with heparin. SSx: pain, SOB, PaHTN, Pos D-dimer. Emboli often from leg DVT,
128 / Lung / Hamartoma
(Neoplasia / Chronic / Benign) / One of few benign tumors of the lung. Note diverse cellular elements including cartilage (prominent element usually), fat, loose fibrous tissue, benign glands, and chronic inflammation. The margin is pushing out rather than invading.
Tumor compression leads to visible lesions on CXR. Pt born with hamartoma that begins to grow at 40+yrs. Rare
132 / Pulmonary Artery / Lung / Recent Thrombosis
(Circulatory) / See also slide 127. Embolus shows no tendency of organization. The edge of the embolus shows fibroblasts in the outer portion of the lesion and the arterial walls show some inflammation focally. Probably 1-2 days old.
Formed in areas of active flow; eventually will liquefy and disappear or become organized with fibrous tissue formation. May cause bruits. Angiographic finding. Lines of Zahn present.
138 / Lung / Asthma / Atelectasis
(Inflammatory) / Areas of alveolar collapse (atelectasis) and areas of hyperinflation. The changes of asthma are best recognized in the medium-sized bronchi. Characteristic changes of severe acute asthma are mucous plugging, basement membrane thickening, and infiltrates of eosinophils (bilobed; cytoplasm is more granular than that of PMNs). Note goblet cell hyperplasia of the epithelium and prominence of the muscular wall. Lymphocytes and plasma cells are also numerous.
Note hyperemia and edema. Severe dypsnea / wheezing. Difficulty exhaling with hyperinflation. Acute use of accessory muscles. Tx w/ albuterol, steroids.
139 / Lung / Tuberculosis
(Inflammation – Chronic) / Big caseous granuloma has few giant or epithelioid cells in its walls and a lot of necrosis and cavitation centrally. The small granulomas adjacent to this would be called satellite granulomas.
Strikes overcrowded populations most. Spread by droplets. Positive TB PPD (skin test). Fever, night sweats, hemoptysis.
140 / Lung / Tuberculosis
(Inflammation – Chronic) / Similar to slide 92. Note the distribution of the granulomas and their small uniform size – Miliary. Fibrosis around the granulomas implies heaing.
Spread via droplet inhalation; calcified granulomas may show on CXR; hemoptysis, fever, pleural effusion; often hits apical and posterior segments of upper lobes.
142 / Lung / Complicated Silicosis / Progressive Massive Fibrosis
(Inflammation) / Compare to slide 260. Acellular fibrous nodules of eosinophilic collagenous tissue that appear whorled and laminated appear towards the edge. These nodules fuse together, making it complicated silicosis or PMF. Fibrous tissue containing macrophages filled with black pigment are present between the fibrous nodules and individual alveolar septa are thickened. Many small muscular arteries are in the area and have thick muscular walls. This secondary hypertensive change is due to loss of the capillary vascular bed they were supplying. Some enlarged airspaces have fibrous walls (honeycombing). Thin delicate walls are scar emphysema.