《Slide 1.》Cloudy swelling, Kidney

A. Brief Descriptions：1. Hydropic change or vacuolar degereration.

2. Appears whenever cells are incapable of maintaining ionic and fluid homeostasis.

3. The first manifestation of almost all forms of sell injury.

4. Reversible injury.

B. Gross Findings：1. Pallor, increased turgor, and increased in weight.

C. Micro Findings：

1.    Cell swelling, cytoplasm contains coarse granules.

2.    Nucleus not affected in light microscopy..

3.    Pigmented cast, hyaline cast.

D. Others:

1.    The first manifestation of cell injury and is reversible.

2.    Increasing hydration of the cell due to alteration in ion transport at cell membrane.

3.    Cause: infection, physico-chemical injury ( toxic ), ischemia….

E. Reference：

Robbins Pathologic Basis of Disease, 6th ed.  P.15.

　

 

 

【 Fig. 1-1 (LP)】Cloudy swelling of renal tubules (left third) and normal tubules (right two third). 

　

 

 

【 Fig. 1-2 (LP)】Cloudy swelling of the renal tubules. The outline of the tubular lumen is blurred.

　

 

 

【 Fig. 1-3 (HP)】Cloudy swelling of the tubules (left two third) and normal tubules (right third).

　

 

 

【 Fig. 1-4 (HP)】Pigmented (RBC) cast (red color) and hyaline cast (pink to purple color).

　

 

 

【 Fig. 1-10 (HP)】The individual tubular lining cells are enlarged and filled with eosinophilic granules in cytoplasm. Note the normal nucleus.

　

 

 

《Slide 2.》Acute hemorrhagic pancreatitis, pancreas

A. Brief Descriptions：1. 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.

B. Gross Findings：

1.    Vary from a swollen & edematous but well-preserved organ to a hemorrhagic & necrotic

       mass.

2.    Yellow plaques & nodules (fatty necrosis) within pancreas, mesentery and peritoneal fat.

C. Micro Findings：

1.    Autodigestion resulting in destruction of the fat, interstitium & pancreatic parenchyma.

2.    Interstitial hemorrhage.

3.    Inflammatory cells infiltrate.

4.   Amorphous basophilic calcium precipitates.

D. Others:

1.    Causes: cholelithiasis, alcoholism, viruses, drugs, ischemia, trauma and nutritional.

       deficiencies... duct obstruction, acinar cell injury and deranged, intracellular transport

       of pancreatic enzymes.

2.    Mechanism: activated enzymes.

3.    Lesions: interstitial inflammation + proteolysis + fat necrosis + hemorrhage.

4.    Clinical manifestations:

Acute onset of abdominal pain by increase pancreatic enzymes in blood & urine.

Associated with biliary tract diseases, alcoholism, and trauma.

Secondary infection with abscess formation, or fibrosis, or pseudocyst formation.

E. Reference：

Robbins Pathologic Basis of Disease, 6th ed.  P.904-907.

　

 

 

【 Fig. 2-1 (LP)】Amorphous basophilic substance deposit within necrotic adipose tissue.

　

 

 

【 Fig. 2-2 (HP)】Fat necrosis with blurred cell boundaries and loss of nuclei.

　

 

 

【 Fig. 2-3 (HP)】Extravasated red blood cells accumulate in necrotic fat.

　

 

 

【 Fig. 2-4 (HP)】Inflammatory cells infilltrate in necrotic adipose tissue

《Slide 3.》Necrosis of cerebellum, Cerebellum

A. Brief Descriptions：

1. Encephalomalacia: necrosis of the brain following by liquefaction & secondary cavitation.

2. Stages:

Cortical pallor with ischemic change in neurons.

Softening with granular foamy cells (Gitter cells).

Cystic formation & glial scarring.

C. Micro Findings：

1. Congestion, hemorrhage, or hemosiderin deposits.

2. Destruction of structure with heavy infiltration by neutrophils, lymphocytes....

3. Necrosis & granular foamy cells ( from phagocytic microglial cells, Gitter cells ).

4. Gitter cells: vacuolated, eosinphilic or granular cytoplasm with eccentrically located nuclei.

D. Reference：

1. Robbins Pathologic Basis of Disease, 6th ed.  P.15-18.

 

　

 

 

【 Fig. 3-1 (LP)】The necrotic area (right half) is surrounded by granulation tissue in the left.

　

  

 

【 Fig. 3-2 (LP)】The granulation tissue is composed of regenerated vasculature, fibroblasts and inflammatory cells.

　

 

 

【 Fig. 3-3 (HP)】The necrotic area is composed of cell debris (pinkish color) and nuclear dusts (dark purple or blue color).

　

   

《Slide 4.》Brain abscess, Cerebrum

A. Brief Descriptions：

1. Types:

Emboli cerebral abscess from infected foci in body 40%.

Direct extension of cerebral abscess from adjacent infected foci.

Relate to cerebral trauma, 30%.

Idiopathic abscess, 20%.

2. Stages :

Infected thromboembolus forming a necrotic foci.

Acute cerebritis.

Liquefaction & purulent exudates.

Heavy infiltration (2 days).

Granulation at margins (5-7 days).

Encapsulation.

B. Gross Findings：1. Discrete lesions with central liquefactive necrosis, surrounding by fibrous,

collagenized response and edema.

C. Micro Findings：

1. Necrotic, purulent center.

2. Capsule of granulomatous tissue & fibrosis (capillaries proliferation, infiltration, Gitter cells...).

3. Surrounding reactive brain with edema & gliosis.　

D. Others:

1. Cerebritis: focal inflammation of brain parenchyma.

2. Myelitis: focal inflammation of spinal cord.

3. Focal pyogenic cerebritis.

4. Emboli suppurative encephalitis.

E. Reference：

1. Robbins Pathologic Basis of Disease, 6th ed.  P.349-352.

 

 

【 Fig. 4-1 (LP)】The normal architecture of cerebrum is destructed.

　

 

 

 

【 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.

　

 

 

【 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.

　

 

 

【 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.

　

 

 

【 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.

　

  

 

【 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).

《Slide 203.》Tuberculosis, Lung

A. Brief Descriptions：1. Caused by Mycobacterium tuberculosis.

B. Gross Findings：

1. Primary TB – Ghon complex.

2. Secondary TB – in the apex as a small focus of consolidation.

C. Micro Findings：

1. Granulomas (tubercles):

a. Central caseation necrosis.

b. Epithelioid histiocytes.

c. Multinucleated Langhans’ giant cells.

d. Fibroblasts and lymphocytes.　

E. Reference：

1. Robbins Pathologic Basis of Disease, 6th ed.  P.379-352.

 

 

 

【 Fig. 203-1 (LP)】Multiple confluent or separated nodules are seen in lung parenchyma. Note thickened and congested interstitium. The alveoli show emphysematous change.

　

 

【 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.

　

 

 

【 Fig. 203-3 (LP)】The center of the tubercle is composed of caseating necrotic debris. Note the elongated epithelioid histiocytes around the caseating center.

 

 

【 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.

 

 

 

【 Fig. 203-5 (HP, acid fast stain)】The acid fast stain highlights bacilli of Mycobacterium species (pink color) (Most commonly M. tuberculosis).

《Slide 6.》Corrosive gastritis, Stomach

A. Brief Descriptions：1. Ingestion of corrosive agents (lye, acids) with dramatic injury to the esophagus.

2. Grossly, black discoloration of the mucosal surface with edematous change.

B. Gross Findings：

1. Blackish discoloration of gastric mucosa, hemorrhage , ulceration, or perforation.

C. Micro Findings：

1. Hemorrhage, congestion, coagulative necrosis of mucosa with hemosiderin or carbon deposit.

2. Necrotizing necrosis with inflammatory infiltration.

3. Variant pictures due to agents, amounts & concentration (depth of layers involved).

D. Others:

1. Causes :ingestion of corrosive agents (lye, acids) with dramatic injury to the esophagus and stomach.

E. Reference：

1. Robbins Pathologic Basis of Disease, 6th ed.  P.789-790.

 

 

【 Fig. 6-1 (LP)】Coagulative necrosis of mucosa and submucosa with relatively preserved muscularis propria.

　

 

 

 

【 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.

　

 

 

 

【 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.

　

 

 

【 Fig. 6-4 (LP)】There are many brown to black variable sized particles deposit in coagulative necrotic area.

　

 

 

【 Fig. 6-5 (LP)】Congestion and hemorrhage in muscularis propria.

　

 

 

 

【 Fig. 6-6 (LP)】The serosal surface (left) is coated with fibrinoid substance with inflammatory cells infiltrate. Note diffuse congestion of vessels.

　

 

Steatosis - lipid vessicles (LV) in hepatocytes

Myocardial infarction - New Infarct (I) Old Infarct (O) Normal myocardium (N)

Normal branching myocardium with central nuclei (N)

Dead branching myocardial cells lacking central nuclei

Gross - recent cerebral infarct

Gross - old cystic cerebral infarct

Acute and old cerebral infarcts

Acute cerebral infarct with red apoptotic neurons

Normal cerebral neurons

Cystic formation in old infarction

Old cerebral infarct with dead cells and phagocytic cells

Slide: Lab 1 (Cellular Injury) -- Case 1.14More: Audio, 640x480 Image, 800x600 Image, 1024x768 Image

Description: Phagocytic cells in healing cerebral infarct

Kupffer cells and hepatocytes with hemosiderin pigment

Hemosiderin stained blue in hepatocytes and Kupffer cells