Slide



Slide # |Tissue |Pathology |Description | |

|5 |Larynx |Squamous Cell Carcinoma |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 |

| | |(Neoplasia) |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 |Center of lobule shows distended sinusoids filled with blood (congestion). Areas of|

| | | |early hemorrhage are present. The dark pigment is artifactual, but the brown |

| | |(Inflammation) |pigment is iron. Steatosis is non-specific. |

| | | |Most often caused by right heart failure. Causes nutmeg liver. |

|7 |Lung |Adenocarcinoma |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 |

| | |(Malignant Neoplasia) |encapsulated, but infiltrates surrounding lung. Adenocarcinoma with focal |

| | | |bronchoalveolar pattern. |

|8 |Coronary Artery |Atherosclerosis of coronary |Cross section of three vessels – two native coronary arteries, one leg vein used in |

| | |artery; Atherosclerosis and |CABG. Differentiate between them. Arterial wall has a media of smooth muscle in a |

| | |thrombus of venous CABG. |continuous band. The vein has bundles of smooth muscle. The arteries are narrowed |

| | | |by atherosclerotic plaques (pink granular debris, macrophages, cholesterol clefts, |

| | |(Circulatory) |collagen, fibrous cap). The vein is occluded similarly. Tiny lumens in the |

| | | |occluding mass are attempts at recanalization. |

| | | |Grading: 1 (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 |Note the region of normal squamous mucosa. Then note the carcinoma arising from |

| | | |surface epithelium and infiltrates the submucosa. Cells are large with moderate |

| | |(Neoplasia) |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 |Primary tumor is lung CA. |

| | | |Liver is congested and contains one portal nodule of metastatic Adenocarcinoma with |

| | |(Neoplasia – Metastatic) |numerous small metastatic glands in the sinusoids. |

|14 |Gallbladder |Chronic Cholecystitis |Mild chronic inflammatory infiltrate in the mucosa. Invaginations of the epithelium|

| | | |(Rokitansky-Aschoff sinuses) can bee seen. The amount of chronic inflammation and |

| | |(Inflammation) |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 |Note the markedly edematous stroma. Numerous eosinophils suggest an allergic |

| | | |etiology. Edema forms blebs that expand into polyps. Glands retain mucous. Note |

| | |(Inflammation / |thickened basement membrane. |

| | |Hypersensitivity) |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 |Specimen had a rigid, thickened, leather bottle appearance of linitis plastica. The|

| | | |neoplastic cells are scattered individually or in small clusters with a diffusely |

| | |(Neoplasia) |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 |Note the thickness of the GB wall – thickening due to inflammatory changes. PMN |

| | | |infiltrate, edema of interstitial tissue, vascular congestion, extravasation of |

| | |(Inflammation) |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 |Gastro-esophageal |Barrett’s Esophagus |Find goblet cells that stain bright blue with this Alcian blue stain – indicates |

|(Likely) |Junction | |presence of acid mucins. Acid mucins are produced by intestinal goblet cells and |

| | |(Neoplasia) |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 |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 |

| | |(Circulatory) |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 |Incidental changes such as acute pneumonia and chronic passive hyperemia are present|

| | | |– disregard these findings. The capillary bed is dilated, representing terminal |

| | |(Inflammation) |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 |Moderately differentiated AdenoCA in which abortive glandular structures are formed.|

| | | |Identify the interface between the more normal mucosa and infiltrating tumor. CA |

| | |(Malignant - Neoplasia) |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 |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 |

| | |(Malignant Neoplasia) |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 |Alveolar septa are hyperemic but not inflamed. PMNs predominate and a few |

| | | |macrophages are present. Proteinaceous edema fluid and fibrin present in alveolar |

| | |(Acute Inflammation) |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 |Note the superficial ulcers present. The ulcers are shallow and inflammatory |

| | | |infiltrate is confined to the mucosa/submucosa. Glandular epithelium has |

| | |(Inflammation) |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 |Malignant neoplasm of liver. Note similar architecture of normal and malignant |

| | |[hepatoma] |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 |Note connective tissue septa staining blue-gray with criss-cross pattern breaking |

| | |‘Alcoholic Cirrhosis’ |tissue into regenerative nodules. Steatosis present. |

| | | |Portal HTN ( ascites, varices, caput medusa; jaundice, hypoalbuminemia, Clotting |

| | | |factor deficiencies. |

|64 |Esophagus |Candida Esophagitis |Slides stained with PAS for fungus – two slide sets: |

| | | |1) Mucosa and submucosa may be missing (eroded); replaced by PMNs and lymphocytes. |

| | |(Inflammation) |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 |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.|

| | |(Neoplasia) |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 |Frond-like arrangement of the villous adenoma with slender fibrovascular cores |

| | | |supporting columnar epithelial elements. Nuclei are crowded, elongated, and |

| | |(Benign Neoplasia) |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 |Ventricular myocardium with the base of the mitral valve is present in the slide. |

| | |Rheumatic |Mitral valve appears as large, thick, fibrous mass. Note the vascularity and small |

| | |Heart Disease |number of lymphocytes in the valve tissue. Valve is thickened and should not be |

| | | |vascular or inflamed – due to rheumatic heart disease. |

| | |(Inflammation) |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 |Many small nodules are visible without microscope. Mature granulomas have |

| | | |well-circumscribed, have fibrosis at periphery, then epithelioid cells and giant |

| | |(Inflammation – Chronic) |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 |Large airway disease, as well as some adjacent alveolar lung tissue that has small |

| | |Disease |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 |

| | |(Inflammation) |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 |Lung |Diffuse Alveolar Damage |Pathologic syndrome. Slide is acute interstitial pneumonitis typical of acute viral|

|(Likely) | | |infection. Inflammatory cells are primarily mononuclear cells (macros). |

| | |(Inflammation) |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 |Small nodules of chronic inflammatory cells (epithelioid) and giant cells with rim |

| | | |of lymphocytes. NON-CASEATING granuloma. Reticulonodular pattern on CXR. May |

| | |(Inflammation) |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 |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 |

| | |(Inflammation) |(Kupffer) cells. No residual malaria parasite is seen. |

| | | |Headache, arthralgias, fever; Tx with chloroquine, primaquine, quinine. |

|117 |Liver |Schistosomiasis |Portal mixed inflammation, mostly chronic with large parasites (schistosome ova, |

| | | |large size). Portal fibrosis is prominent, a major global cause for severe portal |

| | |(Inflammation) |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 |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 |

| | |(Inflammation) |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 |Notice that the infracted area has become sharply demarcated and diffusely |

| | | |eosinophilic. Note the character of the tissue separating viable lung from |

| | |(Circulatory) |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 |One of few benign tumors of the lung. Note diverse cellular elements including |

| | | |cartilage (prominent element usually), fat, loose fibrous tissue, benign glands, and|

| | |(Neoplasia / Chronic / Benign) |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 |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 |

| | |(Circulatory) |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 |Areas of alveolar collapse (atelectasis) and areas of hyperinflation. The changes |

| | | |of asthma are best recognized in the medium-sized bronchi. Characteristic changes |

| | |(Inflammatory) |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 |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 |

| | |(Inflammation – Chronic) |called satellite granulomas. |

| | | |Strikes overcrowded populations most. Spread by droplets. Positive TB PPD (skin |

| | | |test). Fever, night sweats, hemoptysis. |

|140 |Lung |Tuberculosis |Similar to slide 92. Note the distribution of the granulomas and their small |

| | | |uniform size – Miliary. Fibrosis around the granulomas implies heaing. |

| | |(Inflammation – Chronic) |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 / |Compare to slide 260. Acellular fibrous nodules of eosinophilic collagenous tissue |

| | |Progressive Massive Fibrosis |that appear whorled and laminated appear towards the edge. These nodules fuse |

| | | |together, making it complicated silicosis or PMF. Fibrous tissue containing |

| | |(Inflammation) |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. |

|144 |Pancreas |Fat Necrosis w/ hemosiderosis |Pancreatitis – identify areas of fat necrosis and pancreatic tissue necrosis. |

| | | |Notice its random, non-vascular distribution and inflammation. Hemosiderosis (brown|

| | |(Endocrine) |pigment within acinar cells) is present. |

| | | |Fat cells lack nuclei; PMN infiltrate; SSx: sharp pain radiating to back / scapula; |

| | | |pancreatic enzymes in blood (amylase/lipase); steatorrhea, tachycardia, |

| | | |hypocalcemia, nausea and vomiting, major cause is trauma and pancreatitis. |

|146 |Lung & Pancreas |Cystic Fibrosis |Portions of both pulmonary and pancreatic tissue. Note marked atrophy of exocrine |

| | | |portion with well preserved endocrine pancreas. Note larger ducts may contain |

| | |(Genetic) |inspissated secretions which plug them and contribute to atrophy. Fibrosis and mild|

| | | |chronic inflammation are seen. |

| | | |CFTR on chromosome 7; sweat/tears have increased salt content (kiss test). |

| | | |Malabsorption and steatorrhea; meconium ileus (bowel clog in newborn); chronic |

| | | |pulmonary disease. |

|148 |Small Intestine |Crohn’s Disease |Note extensive mucosal damage and large ulcer. There are numerous areas of |

| | | |transmural inflammation. Lymphoid aggregates are prominent, scattered throughout |

| | |(Inflammation) |the wall. Non-caseating granulomas present in all tissue layers (may or may not be |

| | | |present, absence is not diagnostic). Fibropurulent exudate present on serosa and |

| | | |pericolic fat. |

|149 |Lung |Amniotic Fluid Embolus |Look in the arteries. The crinkly elongated amphophilic / basophilic membranous |

| | | |structures are squames from fetal skin. Many PMNs are also present in the vessels. |

| | |(Circulatory) |Some bits of stringy basophilic mucous material may also be present. Note the |

| | | |dilation of capillaries, arterioles, and venules. |

| | | |Caused by dysfunctional labor; SSx: respiratory problems (sudden SOB, seizures, |

| | | |coma). 80% maternal mortality. Use up stores of clotting factors. |

|160 |Cardiac |Hypertrophy |This slide depicts myocardial hypertrophy that is seen in systemic hypertension, but|

| | | |the finding is entirely non-specific. Look for nuclei that have irregular profiles |

| | | |in cross section and are hyperchromatic, and in longitudinal section are |

| | | |rectangular/ovoid and enlarged boxcar nuclei. |

| | | |Normal heart weight = 300g, hypertrophied may be 450g. |

| | | |2cm thick myocardium (1cm is normal). Myofibers may appear thick and eosinophilic. |

| | | |LV damage bodes poorly for renal, hepatic, and splenic structures. LV chamber is |

| | | |enlarged (1.5X); chest pain, syncope, palpitations and sudden death. Associated |

| | | |with systemic hypertension. |

| | | |DDX: dilated / restrictive cardiomyopathy. |

|161 |Salivary Gland |Pleomorphic Adenoma |Note the normal rim of salivary gland. Lesion is not well circumscribed – |

| | | |pseudopods extend from the tumor center as it develops. Note duct-like structures |

| | |(Neoplasia) |as well as trabecular arrangement of the epithelial cells. |

| | | |90% benign in parotid gland; 90% malignant in minor glands (but rare). Hard to |

| | | |resect due to 7th Cranial nerve location. Must remove pseudopods of tumor as well, |

| | | |so larger than expected plug must be removed during resection. |

|163 |Cardiac |Dilated Cardiomyopathy |In addition to hypertrophy as seen in 160, there is more interstitial fibrosis, |

| | | |typically around vessels and the hypertrophy is more diffuse. Lymphocyte infiltrate|

| | |(Hypertrophy) |with eosinophils and PMNs are seen around some vessels. Acute myocarditis may |

| | | |evolve into dilated cardiomyopathy and this inflammation may be the residuum of a |

| | | |myocarditis that is now no longer active, but left residual damage. |

| | | |Heavy heart, stretched out ventricles. Heart has low contractility. Lungs may be |

| | | |displaced by encroaching enlarged heart. May be due to EtOH or cocksackie virus. |

|166 |Cardiac |Acute Rheumatic Myocarditis |Look in interstitial areas around arteries and under the endocardium for collections|

| | | |of multinucleate cells with hyperchromatic nuclei and amphophilic (baso and |

| | |(Inflammation) |eosinophilic) cytoplasm. These are Aschoff bodies and when clustered form nodules. |

| | | |Lymphocytes and Anitschkow cells surround nodules. Anitschkow cells are nonspecific|

| | | |cells with elongated nuclei that appears serrated along the edge. Nuclei look like |

| | | |caterpillars. A multinucleate Anitschkow cell is an Aschoff Cell. |

| | | |Necrotic areas may be present. Individual may die if conduction system is affected.|

| | | |Type III Rxn may lead to thrombosis and shock. Tends to localize to high stress |

| | | |areas (valves, posterior L atrial wall. Rubbery vegetations along the leaflets. |

| | | |Mitral (50%) > Aortic > Tricusp > Pulm. |

|178 |Lung |Normal |The two layers of pleura have been separated to show that air can dissect into the |

| | | |pulmonary interstitium, forming a bleb. Bronchioles and terminal bronchioles have a|

| | | |thin wall with muscle and CT, no alveoli, and respiratory epithelium. Respiratory |

| | | |bronchioles have a wall partly like terminal bronchiole, but with alveoli. |

| | | |Atmospheric dirt collects in the centriacinar zones, the pleura, and in lymph nodes.|

|180 |Lung |Acute Abscess |Cavity in the setting of acute alveolar inflammation, i.e. pneumonia. Alveoli are |

| | |and Pneumonia |filled with fibrin, PMNs, Macros, and some hemorrhage. Pneumonia is starting to |

| | | |organize. Near the cavity, PMNs predominate and the lung tissue appears dissolved |

| | |(Inflammation) |away. Shreds of necrotic tissue and PMNs line the cavity. Liquefactive necrosis has |

| | | |occurred leaving an abscess. |

| | | |Caused by bronchial obstruction (esp. CA), aspiration of gastic contents, bacterial |

| | | |(staph, pseudomonas, Klebsiela, or Proteus). Seen in aspiration prone pts. |

|186 |Lung |Metastatic Osteosarcoma |After lymph nodes, the lung is the most common site of metastases because if filters|

| | | |the systemic venous circulation. Malignant cells form irregular pink spicules of |

| | | |osteoid. An organized and fibrinous pleuritis is on the slide. This is |

| | | |non-specific (infection, uremia, trauma, etc) |

| | | |Osteosarcoma is common primary malignant bone tumor (generally located at the knee).|

| | | |Other common sites of metastases is liver and brain. Hits young men (10-20y). |

| | | |Painful to the bone. High levels of serum alk. Phosphatase noted. |

|194 |Lung |Aspergillus |The hyphae are basophilic, segmented and 5-9 micra in diameter. The radial |

| | | |arrangement has been likened to a sunburst. The fungus is growing with minimal host|

| | |(Inflammation) |resistance. Growth into vessels. |

| | | |Hematogenous spread; CXR – fungus ball (surgical resection); Can colonize and invade|

| | | |via skin lesions, eye; can lead to hemoptysis; treat with Amphotericin B |

|195 |Lung |Cytomegalovirus Pneumonia |Lung shows diffuse mild inflammation within alveolar septa and several nodules of |

| | | |pronounced inflammation. Intact and ruptured PMNs are present along with macros, |

| | |(Inflammation) |lymphos, and plasma cells. necrosis is focal. Alveolar lining are enlarged |

| | | |(hyperplastic). Many alveolar lining cells are large with magenta nuclear |

| | | |inclusions surrounded by a clear halo and small granular basophilic cytoplasmic |

| | | |inclusion. Cytoplasmic and nuclear inclusions is diagnostic of CMV. |

| | | |Most common cause of congenital abnormalities in US. Tx via breast milk, |

| | | |x-placenta, and during birth, saliva and sex. Infected fetus – microcephaly, |

| | | |seizures, deafness, jaundice, purpura. Hepatosplenomegaly is common. In healthy |

| | | |CMV can lead to Mononucleosis. No vaccine; acyclovir resistant. |

|197 |Stomach |Adenocarcinoma, intestinal type|Specimen from antrum (no parietal or chief cells). Scan mucosa and identify the |

| | | |ulcer. Under the ulcer, note the growth of neoplastic cells that are generally |

| | |(Neoplasia) |columnar and have large, hyperchromatic nuclei and prominent nucleoli. Note the |

| | | |glandular appearance with central lumen ( intestinal type adenoCA. |

| | | |Incidence decreasing due to lower salt intake; common in men 50+ and blood group A; |

| | | |linked to nitrosamine intake, salt/smoke in food, H. pylori; Stomach CA generally |

| | | |AdenoCA. Antrum commonly hit, fundus rarely. Stomach exhibits linea plastica |

| | | |(rigid tick, wine skin appearance), Met to supraclavicular nodes, ovaries). |

|217 |Stomach |Peptic Ulcer |Surface epithelium has an ulcer that penetrates into muscularis and serosa. Note |

| | | |the surface presence of PMNs mixed with fibrin (fibrinopurulent exudates). Below it|

| | |(Inflammation) |there are numerous dilated capillaries and inflammation and granulation tissue. |

| | | |Note the scar. |

| | | |Bleeding from vessels hit by the ulcer is bad and cause 10% of all hospital deaths. |

| | | |Favors antrum and pre-pyloric areas. Not a CA precursor; not exacerbated by spicy |

| | | |foods; not related to increased gastric acid secretion, but rather to increased |

| | | |mucosal permeability to H+ ions. |

|219 |Colon |Tubular Adenoma |Tubular component is most easily recognized as round glands cut in cross section. |

| | | |Note crowding of nuclei, hyperchromatic, elongated and stratified nuclei. |

| | |(Benign - Neoplasia) |Projects from villous into lumen via stalk. No Mucous. SSx: blood in stool, anemia,|

| | | |detection via colonoscopy, APC GENE; Malignancy risk: 1-3% become malignant. ‘No |

| | | |goblets means trouble for the booty’ – from handout. |

|227 |Lung |Hyaline Membrane Disease |Infant lung with hyaline membrane disease shows acute interstitial injury. Note the|

| | | |bright pink proteinaceous hyaline membranes lining alveolar ducts. The interstitium|

| | |(Inflammation) |looks thick and cellular because the lung is immature. The lung is collapsed |

| | | |because surfactant is absent. This atelectasis is the important pathologic |

| | | |correlate of clinical hypoxia. The membranes are just ‘red herrings’. |

| | | |Hypoxia º atelectasis; stiff, non-compliant lung; Barotrauma can cause iatrogenic |

| | | |dilation of alveoli. DDx: ARDS, DAD. |

|229 |Lung |Tumor Emboli |Look in small arteries for single or small groups of hyperchromatic tumor cells. |

| | | |They don’t look like blood cells. If enough of these emboli block arteries, the |

| | |(Circulatory) |effect is like showers of thromboemboli. |

| | | |May cause sudden death in immobilized or CHF patients. May cause cerebral infarcts,|

| | | |mesenteric infarcts, renal infarcts. |

|235 |Lung |Centriacinar Emphysema |Enlarged air spaces, with a smooth but not thickened wall with few protruding septa,|

|(Likely) | | |that are continuous with adjacent alveolar ducts. Evidence that the lesion is |

| | |(Inflammation) |centriacinar: presence of small artery, black pigment, remnants of a bronchiole. A |

| | | |rim of normal alveoli surround the lesion. |

| | | |99.9% linked to smoking (α1-AT inactivation and attracts PMNs/Macrophages that |

| | | |release elastase). Linked to upper lobes? May coexist with chronic bronchitis. |

| | | |Genetic component possible in the piZ allele on chr 14. Homozygous piZZ state leads|

| | | |to markedly decreased α1-AT function. |

|238 |Lung |Panacinar Emphysema |Great distortion of the pulmonary parenchyma is due to the fact that there is little|

|(Likely) | | |actual alveolar lung tissue left. The pattern of large air spaces without septal |

| | |(Inflammation) |thickening is difficult to capture on glass slide. Notice the blood vessels and the|

| | | |lack of a centriacinar orientation. |

| | | |Dilation of the entire acinus. Often uniformly distributed through lung. Loss of |

| | | |elasticity. See genetic component listed with slide 235. |

|242 |Lung |Usual Interstitial Pneumonia |Chronic stage of interstitial lung injury. Underlying skeleton of the lung is |

| | | |markedly disorganized and a great deal simplified. There are areas of relatively |

| | |(Chronic Inflammation) |normal lung, as well. Some areas show diffuse thickening of alveolar septa with |

| | | |some preservation of architecture. Other areas show large cystic spaces (honeycomb |

| | | |change), and much fibrosis and chronic inflammation. Bits of alveolar and bronchial|

| | | |epithelium become trapped and form small cystic spaces and fill with mucous. |

| | | |Monos>PMNs, pulmonary edema and alveolar exudates. Respiratory difficulty due to |

| | | |poor oxygen diffusion. Hypoxemia and cyanosis in severe disease. Favors males. |

| | | |Hypo-resonance and high respiratory rate. |

|243 |Gallbladder |Adenocarcinoma |Glands have an irregular distribution and vary in size/shape. Some glands are |

| | | |tightly packed with little intervening stroma. Note disordered growth. Cells show |

| | |(Malignant - Neoplasia) |loss of polarity (variable nuclei position), hyperchromatic, variable nuclei, |

| | | |occasional nucleoli. |

| | | |Most common GB tumor; benign tumors are rare; assoc. with gallstones; |

|245 |Pancreas |Adenocarcinoma |Note part is normal, adenoCA is present. Identify the fibrosis (desmoplastic |

| | | |response) which disrupts the parenchyma. Tumor consists of fairly well formed |

| | |(Neoplasia) |gland-like structures of variable size. Cells vary in nuclear size/shape. Rare |

| | | |abnormal mitotic figures are present. |

| | | |Mild inflammation; perineural invasion may cause severe pain. SSx: Painless |

| | | |jaundice, weight loss; low survivability. |

|251 |Liver |Cirrhosis |Chronically inflamed liver from pt with EtOH abuse. Fibrous tissue extends between |

| | | |periportal areas dividing the liver into abnormal nodules. Cirrhosis = fibrosis |

| | | |with regeneration of some cells. Increased PMN infiltrate = acute alcoholic |

| | | |hepatitis. Steatosis. Mallory Bodies. |

| | | |Jaundice, HTN, Hypoalbuminemia, hepatomegaly, micronodular ( ................
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