Labaratory Patho


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Labaratory Patho

  1. 1. 《Slide 1.》Cloudy swelling, Kidney<br />A. Brief Descriptions:<br />Hydropic change or vacuolar degereration. <br />Appears whenever cells are incapable of maintaining ionic and fluid homeostasis. <br />The first manifestation of almost all forms of sell injury. <br />Reversible injury. <br />B. Gross Findings:<br />Pallor, increased turgor, and increased in weight. <br />C. Micro Findings:<br />1.    Cell swelling, cytoplasm contains coarse granules. <br />2.    Nucleus not affected in light microscopy.. <br />3.    Pigmented cast, hyaline cast. <br />D. Others:<br />1.    The first manifestation of cell injury and is reversible. <br />2.    Increasing hydration of the cell due to alteration in ion transport at cell membrane. <br />3.    Cause: infection, physico-chemical injury ( toxic ), ischemia…. <br />E. Reference:<br />Robbins Pathologic Basis of Disease, 6th ed.  P.15.<br /> <br /> <br /> <br />【 Fig. 1-1 (LP)】Cloudy swelling of renal tubules (left third) and normal tubules (right two third).  <br /> <br /> <br /> <br />【 Fig. 1-2 (LP)】Cloudy swelling of the renal tubules. The outline of the tubular lumen is blurred.<br /> <br /> <br /> <br />【 Fig. 1-3 (HP)】Cloudy swelling of the tubules (left two third) and normal tubules (right third).<br /> <br /> <br /> <br />【 Fig. 1-4 (HP)】Pigmented (RBC) cast (red color) and hyaline cast (pink to purple color).<br /> <br /> <br /> <br />【 Fig. 1-10 (HP)】The individual tubular lining cells are enlarged and filled with eosinophilic granules in cytoplasm. Note the normal nucleus.<br /> <br /> <br /> <br />《Slide 2.》Acute hemorrhagic pancreatitis, pancreas<br />A. Brief Descriptions:<br />The ultimate pathogenetic process in acute pancreatitis is the proteolysis, lipolysis, and hemorrhage resulting from the destructive effect of pancreatic enzymes released from acinar cells. <br />B. Gross Findings:<br />1.    Vary from a swollen & edematous but well-preserved organ to a hemorrhagic & necrotic<br />       mass.<br />2.    Yellow plaques & nodules (fatty necrosis) within pancreas, mesentery and peritoneal fat.<br />C. Micro Findings:<br />1.    Autodigestion resulting in destruction of the fat, interstitium & pancreatic parenchyma. <br />2.    Interstitial hemorrhage. <br />3.    Inflammatory cells infiltrate. <br />4.   Amorphous basophilic calcium precipitates. <br />D. Others:<br />1.    Causes: cholelithiasis, alcoholism, viruses, drugs, ischemia, trauma and nutritional. <br />       deficiencies... duct obstruction, acinar cell injury and deranged, intracellular transport <br />       of pancreatic enzymes. <br />2.    Mechanism: activated enzymes. <br />3.    Lesions: interstitial inflammation + proteolysis + fat necrosis + hemorrhage. <br />4.    Clinical manifestations: <br />Acute onset of abdominal pain by increase pancreatic enzymes in blood & urine. <br />Associated with biliary tract diseases, alcoholism, and trauma. <br />Secondary infection with abscess formation, or fibrosis, or pseudocyst formation. <br />E. Reference:<br />Robbins Pathologic Basis of Disease, 6th ed.  P.904-907.<br /> <br /> <br /> <br />【 Fig. 2-1 (LP)】Amorphous basophilic substance deposit within necrotic adipose tissue.<br /> <br /> <br /> <br />【 Fig. 2-2 (HP)】Fat necrosis with blurred cell boundaries and loss of nuclei.<br /> <br /> <br /> <br />【 Fig. 2-3 (HP)】Extravasated red blood cells accumulate in necrotic fat.<br /> <br /> <br /> <br />【 Fig. 2-4 (HP)】Inflammatory cells infilltrate in necrotic adipose tissue<br />《Slide 3.》Necrosis of cerebellum, Cerebellum<br />A. Brief Descriptions:<br />Encephalomalacia: necrosis of the brain following by liquefaction & secondary cavitation. <br />Stages: <br />Cortical pallor with ischemic change in neurons. <br />Softening with granular foamy cells (Gitter cells). <br />Cystic formation & glial scarring. <br />C. Micro Findings:<br />Congestion, hemorrhage, or hemosiderin deposits. <br />Destruction of structure with heavy infiltration by neutrophils, lymphocytes.... <br />Necrosis & granular foamy cells ( from phagocytic microglial cells, Gitter cells ). <br />Gitter cells: vacuolated, eosinphilic or granular cytoplasm with eccentrically located nuclei. <br />D. Reference:<br />Robbins Pathologic Basis of Disease, 6th ed.  P.15-18.<br /> <br /> <br /> <br /> <br />【 Fig. 3-1 (LP)】The necrotic area (right half) is surrounded by granulation tissue in the left.<br /> <br />  <br /> <br />【 Fig. 3-2 (LP)】The granulation tissue is composed of regenerated vasculature, fibroblasts and inflammatory cells.<br /> <br /> <br /> <br />【 Fig. 3-3 (HP)】The necrotic area is composed of cell debris (pinkish color) and nuclear dusts (dark purple or blue color).<br /> <br />   <br />《Slide 4.》Brain abscess, Cerebrum<br />A. Brief Descriptions:<br />Types: <br />Emboli cerebral abscess from infected foci in body 40%. <br />Direct extension of cerebral abscess from adjacent infected foci. <br />Relate to cerebral trauma, 30%. <br />Idiopathic abscess, 20%. <br />Stages : <br />Infected thromboembolus forming a necrotic foci. <br />Acute cerebritis. <br />Liquefaction & purulent exudates. <br />Heavy infiltration (2 days). <br />Granulation at margins (5-7 days). <br />Encapsulation. <br />B. Gross Findings:<br />Discrete lesions with central liquefactive necrosis, surrounding by fibrous, collagenized response and edema. <br />C. Micro Findings:<br />Necrotic, purulent center. <br />Capsule of granulomatous tissue & fibrosis (capillaries proliferation, infiltration, Gitter cells...). <br />Surrounding reactive brain with edema & gliosis.  <br />D. Others:<br />Cerebritis: focal inflammation of brain parenchyma. <br />Myelitis: focal inflammation of spinal cord. <br />Focal pyogenic cerebritis. <br />Emboli suppurative encephalitis. <br />E. Reference:<br />Robbins Pathologic Basis of Disease, 6th ed.  P.349-352.<br /> <br /> <br />【 Fig. 4-1 (LP)】The normal architecture of cerebrum is destructed.<br /> <br /> <br /> <br /> <br />【 Fig. 4-2 (LP)】The necrotic area is in the left, the normal cerebral cortex in the right, and a thick fibrous band lined between them.<br /> <br /> <br /> <br />【 Fig. 4-3 (LP)】The normal cerebral cortex (left) and the fibrous capsule (right) surrounding the necrotic area (not shown here). Note the rather dense and parallel fibrous bundles of the capsule.<br /> <br /> <br /> <br />【 Fig. 4-4 (LP)】The fibrous capsule. Note the more outside of the capsule (left side in this picture), the more thickening of the fibrous bundles.<br /> <br /> <br /> <br />【 Fig. 4-5 (LP)】The necrotic center (right) is surrounded by granulation tissue (left). Note foamy histiocytes (Gitter cells) aggregate in the outermost of the necrotic area.<br /> <br />  <br /> <br />【 Fig. 4-6 (HP)】The necrotic area is composed of cell debris, nuclear dusts, inflammatory cells (most frequently PMNs) and Gitter cells (foamy histiocytes in the CNS).<br />《Slide 203.》Tuberculosis, Lung<br />A. Brief Descriptions:<br />Caused by Mycobacterium tuberculosis. <br />B. Gross Findings:<br />Primary TB – Ghon complex.<br />Secondary TB – in the apex as a small focus of consolidation.<br />C. Micro Findings:<br />Granulomas (tubercles): <br />Central caseation necrosis. <br />Epithelioid histiocytes. <br />Multinucleated Langhans’ giant cells. <br />Fibroblasts and lymphocytes.  <br />E. Reference:<br />Robbins Pathologic Basis of Disease, 6th ed.  P.379-352.<br /> <br /> <br /> <br />【 Fig. 203-1 (LP)】Multiple confluent or separated nodules are seen in lung parenchyma. Note thickened and congested interstitium. The alveoli show emphysematous change.<br /> <br /> <br />【 Fig. 203-2 (LP)】Caseating granuloma (tubercle). The center of the tubercle contains caseous necrotic debris (amorphous eosinophilic substance) and is surrounded by epithelioid histiocytes and lymphocytes.<br /> <br /> <br /> <br />【 Fig. 203-3 (LP)】The center of the tubercle is composed of caseating necrotic debris. Note the elongated epithelioid histiocytes around the caseating center.<br /> <br /> <br />【 Fig. 203-4 (LP)】A caseous granuloma with caseating necrotic center, epithelioid histiocytes and a typical Langhans’ giant cell (middle left). Note the nuclei of the Langhans’ type giant cell lined in horseshoe arrangement.<br /> <br /> <br /> <br /> INCLUDEPICTURE "特殊染色).jpg" * MERGEFORMATINET <br />【 Fig. 203-5 (HP, acid fast stain)】The acid fast stain highlights bacilli of Mycobacterium species (pink color) (Most commonly M. tuberculosis).<br />《Slide 6.》Corrosive gastritis, Stomach<br />A. Brief Descriptions:<br />Ingestion of corrosive agents (lye, acids) with dramatic injury to the esophagus. <br />Grossly, black discoloration of the mucosal surface with edematous change. <br />B. Gross Findings:<br />Blackish discoloration of gastric mucosa, hemorrhage , ulceration, or perforation.<br />C. Micro Findings:<br />Hemorrhage, congestion, coagulative necrosis of mucosa with hemosiderin or carbon deposit. <br />Necrotizing necrosis with inflammatory infiltration. <br />Variant pictures due to agents, amounts & concentration (depth of layers involved). <br />D. Others:<br />Causes :ingestion of corrosive agents (lye, acids) with dramatic injury to the esophagus and stomach. <br />E. Reference:<br />Robbins Pathologic Basis of Disease, 6th ed.  P.789-790.<br /> <br /> <br />【 Fig. 6-1 (LP)】Coagulative necrosis of mucosa and submucosa with relatively preserved muscularis propria.<br /> <br /> <br /> <br /> <br />【 Fig. 6-2 (LP)】Coagulative necrosis of mucosa (upper) and submucosa (lower). Note the relatively preserved contour of mucosal glands with loss of individual nuclei.<br /> <br /> <br /> <br /> <br />【 Fig. 6-3 (LP)】Coagulative necrosi of mucosal glands with relatively preserved glandular contour but without nucleus. A residual gland is seen in the center.<br /> <br /> <br /> <br />【 Fig. 6-4 (LP)】There are many brown to black variable sized particles deposit in coagulative necrotic area.<br /> <br /> <br /> <br />【 Fig. 6-5 (LP)】Congestion and hemorrhage in muscularis propria.<br /> <br /> <br /> <br /> <br />【 Fig. 6-6 (LP)】The serosal surface (left) is coated with fibrinoid substance with inflammatory cells infiltrate. Note diffuse congestion of vessels.<br /> <br /> <br />Steatosis - lipid vessicles (LV) in hepatocytes<br />Myocardial infarction - New Infarct (I) Old Infarct (O) Normal myocardium (N)<br />Normal branching myocardium with central nuclei (N)<br />Dead branching myocardial cells lacking central nuclei<br />Gross - recent cerebral infarct<br />Gross - old cystic cerebral infarct<br />Acute and old cerebral infarcts<br />Acute cerebral infarct with red apoptotic neurons<br />Normal cerebral neurons<br />Cystic formation in old infarction<br />Old cerebral infarct with dead cells and phagocytic cells<br />Slide: Lab 1 (Cellular Injury) -- Case 1.14More: Audio, 640x480 Image, 800x600 Image, 1024x768 ImageDescription: Phagocytic cells in healing cerebral infarct<br />Kupffer cells and hepatocytes with hemosiderin pigment<br />Hemosiderin stained blue in hepatocytes and Kupffer cells<br />