Pathology Cell Adaptation And Necrosis

Front 1

Cellular Swelling of the kidney.
Cytoplasm ranges from finely granular to frankly vauolated.

Back 1

This is an example of?

Front 2

Cellular swelling

Back 2

Note the pattern of changes occurring in the nephron. What is happening?

Front 3

Hypertrophy of Myocardium.

Back 3

Note the range in cell and nuclear size. Where is this? What is occurring?

Front 4

Box-car nucleus of hypertrophied myocyte. Hyertrophy of myocardium.

Back 4

This is an example of what?

Front 5

Fatty changes of the liver

Back 5

This is an example of what?

Front 6

Fatty changes of the liver.

In alcoholic fatty liver, lipid accumulates within the cytoplasm of hepatocytes, creating large clear vacuoles within cells. The nuclei in such cells are compressed to the periphery of the cell. Hepatic steatosis may be associated with slight hepatomegaly and elevations of serum bilirubin and alkaline phosphatase.

Back 6

This is an example of what?

Front 7

Cell Death: Liver Coagulation Necrosis

Preservation of structural outline of dead cells.

Mechanism is the denaturization of enzymes and structural proteins and the inactivation of intracellular enzymes prevent dissolution.

Microscopic features are outlines of cells, absent nuclei, karyolysis

Infarction

Back 7

Where is this?
What do you see?
Mechanism?
Microscopic features?
What causes it?

Front 8

Cell Death: Liver Coagulation Necrosis

Preservation of structural outline of dead cells.

Mechanism is the denaturization of enzymes and structural proteins and the inactivation of intracellular enzymes prevent dissolution.

Microscopic features are outlines of cells, absent nuclei, karyolysis

Infarction

Back 8

What is this?
What do you see?
Mechanism?
Microscopic features?
What causes it?

Front 9

Cell Death: Liver Coagulation Necrosis

Preservation of structural outline of dead cells.

Mechanism is the denaturization of enzymes and structural proteins and the inactivation of intracellular enzymes prevent dissolution.

Microscopic features are outlines of cells, absent nuclei, karyolysis

Infarction

Back 9

What is this?
What do you see?
Mechanism?
Microscopic features?
What causes this?

Front 10

Cell Death: Liver Coagulation Necrosis

Preservation of structural outline of dead cells.

Mechanism is the denaturization of enzymes and structural proteins and the inactivation of intracellular enzymes prevent dissolution.

Microscopic features are outlines of cells, absent nuclei, karyolysis

Infarction

Back 10

What is this?
What do you see?
Mechanism?
Microscopic features?
What causes this?

Front 11

Cell Death: Liver Coagulation Necrosis

Preservation of structural outline of dead cells.

Mechanism is the denaturization of enzymes and structural proteins and the inactivation of intracellular enzymes prevent dissolution.

Microscopic features are outlines of cells, absent nuclei, karyolysis

Infarction

Back 11

What is this?
What do you see?
Mech?
Micro?
Causes?

Front 12

Cell Death: Liver Coagulation Necrosis

Preservation of structural outline of dead cells.

Mechanism is the denaturization of enzymes and structural proteins and the inactivation of intracellular enzymes prevent dissolution.

Microscopic features are outlines of cells, absent nuclei, karyolysis

Infarction

Back 12

What is this?
What do you see?
Mechanism?
Micro features?
Causes?

Front 13

Cell Death: Spleen Coagulation Necrosis

Preservation of structural outline of dead cells.

Mechanism is the denaturization of enzymes and structural proteins and the inactivation of intracellular enzymes prevent dissolution.

Microscopic features are outlines of cells, absent nuclei, karyolysis

Infarction

Back 13

What is this?
What do you see?
Mechanism?
Micro features?
Causes?

Front 14

Cell Death: Spleen Coagulation Necrosis

Preservation of structural outline of dead cells.

Mechanism is the denaturization of enzymes and structural proteins and the inactivation of intracellular enzymes prevent dissolution.

Microscopic features are outlines of cells, absent nuclei, karyolysis

Infarction

Back 14

What is this?

Front 15

Cell Death: Spleen Coagulation Necrosis

Preservation of structural outline of dead cells.

Mechanism is the denaturization of enzymes and structural proteins and the inactivation of intracellular enzymes prevent dissolution.

Microscopic features are outlines of cells, absent nuclei, karyolysis

Infarction

Back 15

Example of:

Front 16

Cell Death: Spleen Coagulation Necrosis

Preservation of structural outline of dead cells.

Mechanism is the denaturization of enzymes and structural proteins and the inactivation of intracellular enzymes prevent dissolution.

Microscopic features are outlines of cells, absent nuclei, karyolysis

Infarction

Back 16

Example of:

Front 17

Cell Death: Spleen Coagulation Necrosis

Preservation of structural outline of dead cells. Bordered by area of hemorrhage and congestion and then viable tissue.

Mechanism is the denaturization of enzymes and structural proteins and the inactivation of intracellular enzymes prevent dissolution.

Microscopic features are outlines of cells, absent nuclei, karyolysis

Infarction

Back 17

Example of:

Front 18

Cell Death: Spleen Coagulation Necrosis

Preservation of structural outline of dead cells.

Mechanism is the denaturization of enzymes and structural proteins and the inactivation of intracellular enzymes prevent dissolution.

Microscopic features are outlines of cells, absent nuclei, karyolysis

Infarction

Back 18

Example of:

Front 19

Cell Death: Kidney Coagulation Necrosis

Preservation of structural outline of dead cells.

Mechanism is the denaturization of enzymes and structural proteins and the inactivation of intracellular enzymes prevent dissolution.

Microscopic features are outlines of cells, absent nuclei, karyolysis

Infarction

Back 19

Example of:

Front 20

Cell Death: Kidney Coagulation Necrosis

Preservation of structural outline of dead cells.

Mechanism is the denaturization of enzymes and structural proteins and the inactivation of intracellular enzymes prevent dissolution.

Microscopic features are outlines of cells, absent nuclei, karyolysis

Infarction

Back 20

Example of:

Front 21

Cell Death: Kidney Coagulation Necrosis

Preservation of structural outline of dead cells.

Mechanism is the denaturization of enzymes and structural proteins and the inactivation of intracellular enzymes prevent dissolution.

Microscopic features are outlines of cells, absent nuclei, karyolysis

Infarction

Back 21

Exmaple of:

Front 22

Cell Death: Kidney Coagulation Necrosis

Preservation of structural outline of dead cells.

Mechanism is the denaturization of enzymes and structural proteins and the inactivation of intracellular enzymes prevent dissolution.

Microscopic features are outlines of cells, absent nuclei, karyolysis

Infarction

Back 22

Example of:

Front 23

Cell Death: Kidney Coagulation Necrosis

Preservation of structural outline of dead cells.

Mechanism is the denaturization of enzymes and structural proteins and the inactivation of intracellular enzymes prevent dissolution.

Microscopic features are outlines of cells, absent nuclei, karyolysis

Infarction

Back 23

Example of:

Front 24

Cell Death: Kidney Coagulation Necrosis

Preservation of structural outline of dead cells.

Mechanism is the denaturization of enzymes and structural proteins and the inactivation of intracellular enzymes prevent dissolution.

Microscopic features are outlines of cells, absent nuclei, karyolysis

Infarction

Back 24

Example of:

Front 25

Cell Death: Pancreatic Fat Necrosis in Acute Pancreatitis

Digested fat appears translucent pink. Purple staining material are calcium "soaps" of fatty acids.

Activation of pancreatic lipase causes hydrolysis of TAGs. Saponification combines FAs and calcium.

Pale outlines of fat cells filled with basophilic calcified areas.

Back 25

Example of:

Front 26

Cell Death: Pancreatic Fat Necrosis in Acute Pancreatitis

Digested fat appears translucent pink. Purple staining material are calcium "soaps" of fatty acids.

Activation of pancreatic lipase causes hydrolysis of TAGs. Saponification combines FAs and calcium.

Pale outlines of fat cells filled with basophilic calcified areas.

Back 26

Example of:

Front 27

Cell Death: Pancreatic Fat Necrosis in Acute Pancreatitis

Digested fat appears translucent pink. Purple staining material are calcium "soaps" of fatty acids.

Activation of pancreatic lipase causes hydrolysis of TAGs. Saponification combines FAs and calcium.

Pale outlines of fat cells filled with basophilic calcified areas.

Back 27

Example of:

Front 28

Cell Death: Pancreatic Fat Necrosis in Acute Pancreatitis

Digested fat appears translucent pink. Purple staining material are calcium "soaps" of fatty acids.

Activation of pancreatic lipase causes hydrolysis of TAGs. Saponification combines FAs and calcium.

Pale outlines of fat cells filled with basophilic calcified areas.

Back 28

Example of:

Front 29

Cell Death: Pancreatic Fat Necrosis in Acute Pancreatitis

Digested fat appears translucent pink. Purple staining material are calcium "soaps" of fatty acids.

Activation of pancreatic lipase causes hydrolysis of TAGs. Saponification combines FAs and calcium.

Pale outlines of fat cells filled with basophilic calcified areas.

Back 29

Example of:

Front 30

Cell Death: Pancreatic Fat Necrosis in Acute Pancreatitis

Digested fat appears translucent pink. Purple staining material are calcium "soaps" of fatty acids.

Activation of pancreatic lipase causes hydrolysis of TAGs. Saponification combines FAs and calcium.

Pale outlines of fat cells filled with basophilic calcified areas.

Back 30

Example of:

Front 31

Cell Death: Pancreatic Fat Necrosis in Acute Pancreatitis

Digested fat appears translucent pink. Purple staining material are calcium "soaps" of fatty acids.

Activation of pancreatic lipase causes hydrolysis of TAGs. Saponification combines FAs and calcium.

Pale outlines of fat cells filled with basophilic calcified areas.

Back 31

Example of:

Front 32

Cell Death: Caseation Necrosis of Spleen

Variant of coagulation necrosis with acellular cheese-like material.

Formed by release of lipid from the cell walls of TB or histoplasma after destruction by macrophages.

Acelleular material contains activated macrophages, CD4s, multinucleated giant cells.

Back 32

Example of:

Front 33

Cell Death: Caseation Necrosis of Spleen

Variant of coagulation necrosis with acellular cheese-like material.

Formed by release of lipid from the cell walls of TB or histoplasma after destruction by macrophages.

Acellular material contains activated macrophages, CD4s, multinucleated giant cells.

Back 33

Example of:

Front 34

Cell Death: Caseation Necrosis of Spleen

Variant of coagulation necrosis with acellular cheese-like material.

Formed by release of lipid from the cell walls of TB or histoplasma after destruction by macrophages.

Acellular material contains activated macrophages, CD4s, multinucleated giant cells.

Back 34

Example of:

Front 35

Cell Death: Caseation Necrosis of Spleen

Variant of coagulation necrosis with acellular cheese-like material.

Formed by release of lipid from the cell walls of TB or histoplasma after destruction by macrophages.

Acellular material contains activated macrophages, CD4s, multinucleated giant cells.

Back 35

Example of:

Front 36

Cell Death: Caseation Necrosis of Spleen

Variant of coagulation necrosis with acellular cheese-like material.

Formed by release of lipid from the cell walls of TB or histoplasma after destruction by macrophages.

Acellular material contains activated macrophages, CD4s, multinucleated giant cells.

Back 36

Example of:

Front 37

Cell Death: Caseation Necrosis of Spleen

Variant of coagulation necrosis with acellular cheese-like material.

Formed by release of lipid from the cell walls of TB or histoplasma after destruction by macrophages.

Acellular material contains activated macrophages, CD4s, multinucleated giant cells.

Back 37

Example of:

Front 38

Cellular Death: Liquefaction Necrosis of Brain

Rapid hydrolysis. Microglial cells, which have phagocyized debris have a foamy, granular cytoplasm, "glitter cells".

Lysosomal enzymes released by necrotic cells or neutrophils cause liquefaction. Autocatalytic effect of hydrolytic enzymes will produce a cystic space.

Back 38

Example of:

Front 39

Cellular Death: Liquefaction Necrosis of Brain

Rapid hydrolysis. Microglial cells, which have phagocyized debris have a foamy, granular cytoplasm, "glitter cells".

Lysosomal enzymes released by necrotic cells or neutrophils cause liquefaction. Autocatalytic effect of hydrolytic enzymes will produce a cystic space.

Back 39

Exmaple of:

Front 40

Cellular Death: Liquefaction Necrosis of Brain

Rapid hydrolysis. Microglial cells, which have phagocyized debris have a foamy, granular cytoplasm, "glitter cells".

Lysosomal enzymes released by necrotic cells or neutrophils cause liquefaction. Autocatalytic effect of hydrolytic enzymes will produce a cystic space.

Back 40

Example of:

Front 41

Cellular Death: Liquefaction Necrosis of Brain

Rapid hydrolysis. Microglial cells, which have phagocyized debris have a foamy, granular cytoplasm, "glitter cells".

Lysosomal enzymes released by necrotic cells or neutrophils cause liquefaction. Autocatalytic effect of hydrolytic enzymes will produce a cystic space.

Back 41

Example of:

Front 42

Cell Injury: Hyalinization

Lumen of arteriosclerotic vessel is reduced. The hyaline material contains foci of dystrophic calcification that stains purple and it also contains cholesterol clefts.

Back 42

Example of:

Front 43

Cell Injury: Hyalinization

Lumen of arteriosclerotic vessel is reduced. The hyaline material contains foci of dystrophic calcification that stains purple and it also contains cholesterol clefts.

Back 43

Example of:

Front 44

Cell Injury: Hyalinization

Lumen of arteriosclerotic vessel is reduced. The hyaline material contains foci of dystrophic calcification that stains purple and it also contains cholesterol clefts.

Back 44

Example of:

Front 45

Cell Injury: Hyalinization

Lumen of arteriosclerotic vessel is reduced. The hyaline material contains foci of dystrophic calcification that stains purple and it also contains cholesterol clefts.

Back 45

Example of:

Front 46

Cell Injury: Hyalinization

Lumen of arteriosclerotic vessel is reduced. The hyaline material contains foci of dystrophic calcification that stains purple and it also contains cholesterol clefts.

Back 46

Example of:

Front 47

Cell Injury: Hyalinization

Lumen of arteriosclerotic vessel is reduced. The hyaline material contains foci of dystrophic calcification that stains purple and it also contains cholesterol clefts.

Back 47

Example of:

Front 48

Cell Injury: Hyalinization

Lumen of arteriosclerotic vessel is reduced. The hyaline material contains foci of dystrophic calcification that stains purple and it also contains cholesterol clefts.

Back 48

Example of:

Front 49

Cell Injury: Hyaline Change of Kidney

Walls of arteries (small and medium) and afferent arterioles are thickened and have amorphous pale pink structureless appearance.

Back 49

Example of:

Front 50

Cell Injury: Hyaline Change of Kidney

Walls of arteries (small and medium) and afferent arterioles are thickened and have amorphous pale pink structureless appearance.

Back 50

Example of:

Front 51

Cell Injury: Hyaline Change of Kidney

Walls of arteries (small and medium) and afferent arterioles are thickened and have amorphous pale pink structureless appearance.

Back 51

Example of:

Front 52

Cell Injury: Fibrinoid Necrosis of Liver

Deeply eosinophilic, smudged, fibrin-like appearance. Deposition of pink-staining proteinaceous material in damaged vessel walls due to basement membranes.

Associated with Immune Vasculitis and Malignant Hypertension

Back 52

Example of:

Front 53

Cell Injury: Fibrinoid Necrosis of Liver

Deeply eosinophilic, smudged, fibrin-like appearance. Deposition of pink-staining proteinaceous material in damaged vessel walls due to basement membranes.

Associated with Immune Vasculitis and Malignant Hypertension

Back 53

Example of:

Front 54

Cell Injury: Fibrinoid Necrosis of Liver

Deeply eosinophilic, smudged, fibrin-like appearance. Deposition of pink-staining proteinaceous material in damaged vessel walls due to basement membranes.

Associated with Immune Vasculitis and Malignant Hypertension

Back 54

Example of:

Front 55

Cell Injury: Fibrinoid Necrosis of Liver

Deeply eosinophilic, smudged, fibrin-like appearance. Deposition of pink-staining proteinaceous material in damaged vessel walls due to basement membranes.

Associated with Immune Vasculitis and Malignant Hypertension

Back 55

Example of:

Front 56

Cell Injury: Fibrinoid Necrosis of Liver

Deeply eosinophilic, smudged, fibrin-like appearance. Deposition of pink-staining proteinaceous material in damaged vessel walls due to basement membranes.

Associated with Immune Vasculitis and Malignant Hypertension

Back 56

Example of:

Front 57

Cell Injury: Fibrinoid Necrosis of Liver

Deeply eosinophilic, smudged, fibrin-like appearance. Deposition of pink-staining proteinaceous material in damaged vessel walls due to basement membranes.

Associated with Immune Vasculitis and Malignant Hypertension

Back 57

Example of:

Front 58

Cell Injury: Fibrinoid Necrosis of Liver

Deeply eosinophilic, smudged, fibrin-like appearance. Deposition of pink-staining proteinaceous material in damaged vessel walls due to basement membranes.

Associated with Immune Vasculitis and Malignant Hypertension

Back 58

Example of:

Front 59

Cell Injury: Fibrinoid Necrosis of Liver

Deeply eosinophilic, smudged, fibrin-like appearance. Deposition of pink-staining proteinaceous material in damaged vessel walls due to basement membranes.

Associated with Immune Vasculitis and Malignant Hypertension

Back 59

Example of:

Front 60

Pulmonary Edema due to Starling pressure (transudate)

BV are engorged with blood. Pink-staining proteinaceous edema transited from capillaries. Macrophages and neutrophils are seen in alveoli. Too recent for "heart failure cells". Bronchioles filled with degenerated neutrophils from tracheobronchitis in addition to pulmonary edema and congestion. Bronchioles have lost their epithelium in the acute inflammation process.

Increased hydrostatic pressure (L heart failure)
Decreased oncotic pressure (nephrotic syndrome, cirrhosis)

Back 60

Example of:

Front 61

Pulmonary Edema due to Starling pressure (transudate)

BV are engorged with blood. Pink-staining proteinaceous edema transited from capillaries. Macrophages and neutrophils are seen in alveoli. Too recent for "heart failure cells". Bronchioles filled with degenerated neutrophils from tracheobronchitis in addition to pulmonary edema and congestion. Bronchioles have lost their epithelium in the acute inflammation process.

Increased hydrostatic pressure (L heart failure)
Decreased oncotic pressure (nephrotic syndrome, cirrhosis)

Back 61

Example of:

Front 62

Pulmonary Edema due to Starling pressure (transudate)

BV are engorged with blood. Pink-staining proteinaceous edema transited from capillaries. Macrophages and neutrophils are seen in alveoli. Too recent for "heart failure cells". Bronchioles filled with degenerated neutrophils from tracheobronchitis in addition to pulmonary edema and congestion. Bronchioles have lost their epithelium in the acute inflammation process.

Increased hydrostatic pressure (L heart failure)
Decreased oncotic pressure (nephrotic syndrome, cirrhosis)

Back 62

Example of:

Front 63

Pulmonary Edema due to Starling pressure (transudate)

BV are engorged with blood. Pink-staining proteinaceous edema transited from capillaries. Macrophages and neutrophils are seen in alveoli. Too recent for "heart failure cells". Bronchioles filled with degenerated neutrophils from tracheobronchitis in addition to pulmonary edema and congestion. Bronchioles have lost their epithelium in the acute inflammation process.

Increased hydrostatic pressure (L heart failure)
Decreased oncotic pressure (nephrotic syndrome, cirrhosis)

Back 63

Example of:

Front 64

Pulmonary Edema due to Starling pressure (transudate)

BV are engorged with blood. Pink-staining proteinaceous edema transited from capillaries. Macrophages and neutrophils are seen in alveoli. Too recent for "heart failure cells". Bronchioles filled with degenerated neutrophils from tracheobronchitis in addition to pulmonary edema and congestion. Bronchioles have lost their epithelium in the acute inflammation process.

Increased hydrostatic pressure (L heart failure)
Decreased oncotic pressure (nephrotic syndrome, cirrhosis)

Back 64

Example of:

Front 65

Pulmonary Edema due to Starling pressure (transudate)

BV are engorged with blood. Pink-staining proteinaceous edema transited from capillaries. Macrophages and neutrophils are seen in alveoli. Too recent for "heart failure cells". Bronchioles filled with degenerated neutrophils from tracheobronchitis in addition to pulmonary edema and congestion. Bronchioles have lost their epithelium in the acute inflammation process.

Increased hydrostatic pressure (L heart failure)
Decreased oncotic pressure (nephrotic syndrome, cirrhosis)

Back 65

Example of:

Front 66

Congestion of Liver

Principally in the central areas of the lobules. Sinusoids are dilated and filled with blood. Finely granular, brown, blood pigments (hemosiderin) found extracellularly and in centro-hepatic and Kupffer cells. Necrosis around central veins, due to anoxia, which may lead to infiltration of PMNLs.a

Back 66

Example of:

Front 67

Congestion of Liver

Principally in the central areas of the lobules. Sinusoids are dilated and filled with blood. Finely granular, brown, blood pigments (hemosiderin) found extracellularly and in centro-hepatic and Kupffer cells. Necrosis around central veins, due to anoxia, which may lead to infiltration of PMNLs.a

Back 67

Example of:

Front 68

Congestion of Liver

Principally in the central areas of the lobules. Sinusoids are dilated and filled with blood. Finely granular, brown, blood pigments (hemosiderin) found extracellularly and in centro-hepatic and Kupffer cells. Necrosis around central veins, due to anoxia, which may lead to infiltration of PMNLs.a

Back 68

Example of:

Front 69

Congestion of Liver

Principally in the central areas of the lobules. Sinusoids are dilated and filled with blood. Finely granular, brown, blood pigments (hemosiderin) found extracellularly and in centro-hepatic and Kupffer cells. Necrosis around central veins, due to anoxia, which may lead to infiltration of PMNLs.a

Back 69

Example of:

Front 70

Congestion of Liver

Principally in the central areas of the lobules. Sinusoids are dilated and filled with blood. Finely granular, brown, blood pigments (hemosiderin) found extracellularly and in centro-hepatic and Kupffer cells. Necrosis around central veins, due to anoxia, which may lead to infiltration of PMNLs.

Back 70

Example of:

Front 71

Congestion of Liver

Principally in the central areas of the lobules. Sinusoids are dilated and filled with blood. Finely granular, brown, blood pigments (hemosiderin) found extracellularly and in centro-hepatic and Kupffer cells. Necrosis around central veins, due to anoxia, which may lead to infiltration of PMNLs.

Back 71

Example of:

Front 72

Congestion of Liver

Principally in the central areas of the lobules. Sinusoids are dilated and filled with blood. Finely granular, brown, blood pigments (hemosiderin) found extracellularly and in centro-hepatic and Kupffer cells. Necrosis around central veins, due to anoxia, which may lead to infiltration of PMNLs.

Back 72

Example of:

Front 73

Edema of lung without congestion.

Alveoli are uniformly filled by homogenous, pale-staining, pink edema fluid. Alveolar capillaries show no distention or congestion. Macrophages laden with black coal dust pigment (anthracosis).

Back 73

Example of:

Front 74

Edema of lung without congestion.

Alveoli are uniformly filled by homogenous, pale-staining, pink edema fluid. Alveolar capillaries show no distention or congestion. Macrophages laden with black coal dust pigment (anthracosis).

Back 74

Example of:

Front 75

Edema of lung without congestion.

Alveoli are uniformly filled by homogenous, pale-staining, pink edema fluid. Alveolar capillaries show no distention or congestion. Macrophages laden with black coal dust pigment (anthracosis).

Back 75

Example of:

Front 76

Edema of lung without congestion.

Alveoli are uniformly filled by homogenous, pale-staining, pink edema fluid. Alveolar capillaries show no distention or congestion. Macrophages laden with black coal dust pigment (anthracosis).

Back 76

Example of:

Front 77

Edema of lung without congestion.

Alveoli are uniformly filled by homogenous, pale-staining, pink edema fluid. Alveolar capillaries show no distention or congestion. Macrophages laden with black coal dust pigment (anthracosis).

Back 77

Example of:

Front 78

Edema of lung without congestion.

Alveoli are uniformly filled by homogenous, pale-staining, pink edema fluid. Alveolar capillaries show no distention or congestion. Macrophages laden with black coal dust pigment (anthracosis).

Back 78

Example of:

Front 79

Edema of lung without congestion.

Alveoli are uniformly filled by homogenous, pale-staining, pink edema fluid. Alveolar capillaries show no distention or congestion. Macrophages laden with black coal dust pigment (anthracosis).

Back 79

Example of:

Front 80

Inflammatory Edema: Acute Bronchopneumonia

Alveolar septa are widened and alveolar spaces contain inflammatory cells, including neutrophils and fluid. Fibrillar material is seen in some spaces, from cleavage of plasma protein fibrinogen.

Dark blue dot-like structures are present within alveoli and admixed with the inflammatory exudate. These are bacteria.

Back 80

Example of:

Front 81

Inflammatory Edema: Acute Bronchopneumonia

Alveolar septa are widened and alveolar spaces contain inflammatory cells, including neutrophils and fluid. Fibrillar material is seen in some spaces, from cleavage of plasma protein fibrinogen.

Dark blue dot-like structures are present within alveoli and admixed with the inflammatory exudate. These are bacteria.

Back 81

Example of:

Front 82

Inflammatory Edema: Acute Bronchopneumonia

Alveolar septa are widened and alveolar spaces contain inflammatory cells, including neutrophils and fluid. Fibrillar material is seen in some spaces, from cleavage of plasma protein fibrinogen.

Dark blue dot-like structures are present within alveoli and admixed with the inflammatory exudate. These are bacteria.

Back 82

Example of:

Front 83

Inflammatory Edema: Acute Bronchopneumonia

Alveolar septa are widened and alveolar spaces contain inflammatory cells, including neutrophils and fluid. Fibrillar material is seen in some spaces, from cleavage of plasma protein fibrinogen.

Dark blue dot-like structures are present within alveoli and admixed with the inflammatory exudate. These are bacteria.

Back 83

Example of:

Front 84

Inflammatory Edema: Acute Bronchopneumonia

Normal areas of lung show relatively empty alveoli, in contrast to areas where alveolar septa are widened and alveolar spaces contain inflammatory cells, including neutrophils and fluid. Fibrillar material is seen in some spaces, from cleavage of plasma protein fibrinogen.

Dark blue dot-like structures are present within alveoli and admixed with the inflammatory exudate. These are bacteria.

Back 84

Example of:

Front 85

Inflammatory Edema: Acute Bronchopneumonia

Alveolar septa are widened and alveolar spaces contain inflammatory cells, including neutrophils and fluid. Fibrillar material is seen in some spaces, from cleavage of plasma protein fibrinogen.

Dark blue dot-like structures are present within alveoli and admixed with the inflammatory exudate. These are bacteria.

Back 85

Example of:

Front 86

Inflammatory Edema: Acute Bronchopneumonia

Some areas appear relatively normal. Adjacent to the bronchiole is an area that appears almost solid.
Alveolar septa are widened and alveolar spaces contain inflammatory cells, including neutrophils and fluid.

Back 86

Example of:

Front 87

Congestion of Spleen

Red pulp is congested. Sinusoids are dilated. Degenerating erythrocytes are present. Lymphoid follicles are small. Trabeculae are prominant, and hyalinized arterioles are present within them. Hyalinization is present in the arterioles of the Malpighian bodies (white pulp, lymph follicles). Hyalin lies in the intima about the lumen of arterioles.

Back 87

Example of:

Front 88

Congestion of Spleen

Red pulp is congested. Sinusoids are dilated. Degenerating erythrocytes are present. Lymphoid follicles are small. Trabeculae are prominant, and hyalinized arterioles are present within them. Hyalinization is present in the arterioles of the Malpighian bodies (white pulp, lymph follicles). Hyalin lies in the intima about the lumen of arterioles.

Back 88

Example of:

Front 89

Congestion of Spleen

Red pulp is congested. Sinusoids are dilated. Degenerating erythrocytes are present. Lymphoid follicles are small. Trabeculae are prominant, and hyalinized arterioles are present within them. Hyalinization is present in the arterioles of the Malpighian bodies (white pulp, lymph follicles). Hyalin lies in the intima about the lumen of arterioles.

Back 89

Example of:

Front 90

Congestion of Spleen

Red pulp is congested. Sinusoids are dilated. Degenerating erythrocytes are present. Lymphoid follicles are small. Trabeculae are prominant, and hyalinized arterioles are present within them. Hyalinization is present in the arterioles of the Malpighian bodies (white pulp, lymph follicles). Hyalin lies in the intima about the lumen of arterioles.

Back 90

Example of:

Front 91

Congestion of Spleen

Red pulp is congested. Sinusoids are dilated. Degenerating erythrocytes are present. Lymphoid follicles are small. Trabeculae are prominant, and hyalinized arterioles are present within them. Hyalinization is present in the arterioles of the Malpighian bodies (white pulp, lymph follicles). Hyalin lies in the intima about the lumen of arterioles.

Back 91

Example of:

Front 92

Congestion of Spleen

Red pulp is congested. Sinusoids are dilated. Degenerating erythrocytes are present. Lymphoid follicles are small. Trabeculae are prominant, and hyalinized arterioles are present within them. Hyalinization is present in the arterioles of the Malpighian bodies (white pulp, lymph follicles). Hyalin lies in the intima about the lumen of arterioles.

Back 92

Example of:

Front 93

Post-mortem clot

Chicken-fat layer- fibrin with enmeshed leukocytes.

Currant-jelly layer- erythrocytes, some leukocytes and fibrin.

Back 93

Example of:

Front 94

Post-mortem clot

Chicken-fat layer- fibrin with enmeshed leukocytes.

Currant-jelly layer- erythrocytes, some leukocytes and fibrin.

Back 94

Example of:

Front 95

Artery has old organized and recanalized thrombus in its lumen. Collagenous tissue containing moderate number of fibrocytes and endothelial-lined vascular channels. The intima, into which the thrombus blends, shows hyaline thickening. The internal elastic lamina is serrated and reduplicated in areas. Media has calcification, as streaks and aggregates of dark blue and purple. Near the zone of calcification there appears to be bone spicules.

Back 95

Example of:

Front 96

Artery has old organized and recanalized thrombus in its lumen. Collagenous tissue containing moderate number of fibrocytes and endothelial-lined vascular channels. The intima, into which the thrombus blends, shows hyaline thickening. The internal elastic lamina is serrated and reduplicated in areas. Media has calcification, as streaks and aggregates of dark blue and purple. Near the zone of calcification there appears to be bone spicules.

Back 96

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Front 97

Artery has old organized and recanalized thrombus in its lumen. Collagenous tissue containing moderate number of fibrocytes and endothelial-lined vascular channels. The intima, into which the thrombus blends, shows hyaline thickening. The internal elastic lamina is serrated and reduplicated in areas. Media has calcification, as streaks and aggregates of dark blue and purple. Near the zone of calcification there appears to be bone spicules.

Back 97

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Front 98

Artery has old organized and recanalized thrombus in its lumen. Collagenous tissue containing moderate number of fibrocytes and endothelial-lined vascular channels. The intima, into which the thrombus blends, shows hyaline thickening. The internal elastic lamina is serrated and reduplicated in areas. Media has calcification, as streaks and aggregates of dark blue and purple. Near the zone of calcification there appears to be bone spicules.

Back 98

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Front 99

Antemortem clot

Clear bands of fibrosis and leukocytes alternating with a layer of RBCs, are "lines of Zahn".

Back 99

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Front 100

Antemortem clot

Clear bands of fibrosis and leukocytes alternating with a layer of RBCs, are "lines of Zahn".

Back 100

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Front 101

Antemortem clot

Clear bands of fibrosis and leukocytes alternating with a layer of RBCs, are "lines of Zahn".

Back 101

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Front 102

Coronary artery atheroma

Lumen is narrowed. Irregular thickening is due to fibrointimal plaque characteristic of atherosclerosis.

Back 102

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Front 103

Coronary artery atheroma

Lumen is narrowed. Irregular thickening is due to fibrointimal plaque characteristic of atherosclerosis.

Back 103

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Front 104

Coronary artery atheroma

Lumen is narrowed. Irregular thickening is due to fibrointimal plaque characteristic of atherosclerosis.

Back 104

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Front 105

Coronary artery atheroma

Lumen is narrowed. Irregular thickening is due to fibrointimal plaque characteristic of atherosclerosis.

Back 105

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Front 106

Myocardial infarct

Myocytes are undergone coagulative necrosis. Outlines of myocytes are retained. Deeply eosinophilic cytoplasm. Loss of nuclei. Interstitial infiltrate of neutrophils. Necrotic myocyutes are disintegrating and are surrounded by dying neutrophils.

Back 106

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Front 107

Myocardial infarct

Myocytes are undergone coagulative necrosis. Outlines of myocytes are retained. Deeply eosinophilic cytoplasm. Loss of nuclei. Interstitial infiltrate of neutrophils. Necrotic myocyutes are disintegrating and are surrounded by dying neutrophils.

Back 107

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Front 108

Myocardial infarct

Myocytes are undergone coagulative necrosis. Outlines of myocytes are retained. Deeply eosinophilic cytoplasm. Loss of nuclei. Interstitial infiltrate of neutrophils. Necrotic myocyutes are disintegrating and are surrounded by dying neutrophils.

Back 108

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Front 109

Renal Infarct

Inside infarct in coagulative necrosis with loss of cellular detail. Chromatin debris and degenerated PMNLs are present in infarct. Edges of infarct have zone of inflammation and hyperemia. Infiltration of PLMNs in interstitial tissue.

Away from infarct the proximal convoluted tubular epithelium shows cloudy swelling, probably due to post mortem autolysis.

Back 109

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Front 110

Renal Infarct

Inside infarct in coagulative necrosis with loss of cellular detail. Chromatin debris and degenerated PMNLs are present in infarct. Edges of infarct have zone of inflammation and hyperemia. Infiltration of PLMNs in interstitial tissue.

Away from infarct the proximal convoluted tubular epithelium shows cloudy swelling, probably due to post mortem autolysis.

Back 110

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Front 111

Renal Infarct

Inside infarct in coagulative necrosis with loss of cellular detail. Chromatin debris and degenerated PMNLs are present in infarct. Edges of infarct have zone of inflammation and hyperemia. Infiltration of PLMNs in interstitial tissue.

Away from infarct the proximal convoluted tubular epithelium shows cloudy swelling, probably due to post mortem autolysis.

Back 111

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Front 112

Renal Infarct

Inside infarct in coagulative necrosis with loss of cellular detail. Chromatin debris and degenerated PMNLs are present in infarct. Edges of infarct have zone of inflammation and hyperemia. Infiltration of PLMNs in interstitial tissue.

Away from infarct the proximal convoluted tubular epithelium shows cloudy swelling, probably due to post mortem autolysis.

Back 112

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Front 113

Renal Infarct

Inside infarct in coagulative necrosis with loss of cellular detail. Chromatin debris and degenerated PMNLs are present in infarct. Edges of infarct have zone of inflammation and hyperemia. Infiltration of PLMNs in interstitial tissue.

Away from infarct the proximal convoluted tubular epithelium shows cloudy swelling, probably due to post mortem autolysis.

Back 113

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Front 114

Pulmonary Infarct
Hemorrhagic Infarct

Distinguished from a simple hemorrhage by the destruction of alveolar walls. The infarct extends to the pleura on one side. Brownish-black pigment is hemosiderin, from breakdown of hemoglobin in degenerated erythrocytes. The segmented nuclei of degenerated neutrophils are scattered about the infarct.

Back 114

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Front 115

Pulmonary Infarct
Hemorrhagic Infarct

Distinguished from a simple hemorrhage by the destruction of alveolar walls. The infarct extends to the pleura on one side. Brownish-black pigment is hemosiderin, from breakdown of hemoglobin in degenerated erythrocytes. The segmented nuclei of degenerated neutrophils are scattered about the infarct.

Back 115

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Front 116

Pulmonary Infarct
Hemorrhagic Infarct

Distinguished from a simple hemorrhage by the destruction of alveolar walls. The infarct extends to the pleura on one side. Brownish-black pigment is hemosiderin, from breakdown of hemoglobin in degenerated erythrocytes. The segmented nuclei of degenerated neutrophils are scattered about the infarct.

Back 116

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Front 117

Pulmonary Infarct
Hemorrhagic Infarct

Distinguished from a simple hemorrhage by the destruction of alveolar walls. The infarct extends to the pleura on one side. Brownish-black pigment is hemosiderin, from breakdown of hemoglobin in degenerated erythrocytes. The segmented nuclei of degenerated neutrophils are scattered about the infarct.

Back 117

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