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By:
Light microscopy or gross examination  detect changes hours to days after injury
 Histochemical or ultrastructural techniques
 detect changes minutes to hours after injury

Patterns of Acute Cell Injury
 Reversible Injury

Cellular swelling: Ultrastructural changes
 plasma membrane blebbing, blunting and distortion of microvilli
 mitochondrial swelling, phospholipid-rich amorphous densities
 dilation of endoplasmic reticulum with detachment of ribosomes and dissociation of polysomes
 disaggregation of granular and fibrillar elements on nucleus

Patterns of Acute Cell Injury
 Reversible Injury
2.
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Fatty change:
Vacuolation of cells due to accumulation of lipid droplets
Results due to disturbance of ribosomal function
The liver is commonly affected
Occurs in hypoxic injury, toxic (alcohol), metabolic
(diabetes mellitus)
Moderate fatty changes are reversible, but sever changes may not be

Patterns of Acute Cell Injury


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Irreversible injury:
Cell death
It is suggested that cell membrane is the central factor in the pathogenesis of irreversible cell injury
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Also due to: sever mitochondrial dysfunction lysosomal rupture
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Two patterns of cell death:
Necrosis
Apoptosis

Patterns of Acute Cell Injury
 Irreversible injury: Cell death
1.
Necrosis:

Definition: sequence of morphologic changes that follow cell death in living tissue
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The morphologic appearance of necrosis is due to:
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Enzymatic digestion of cell:
Autolysis : hydrolytic enzymes are derived from the dead cells themselves
Heterolysis: hydrolytic enzymes are derived from invading inflammatory cells
Denaturation of proteins

Patterns of Acute Cell Injury
 Microscopic appearance of Necrotic dead cells:

Cytoplasmic changes
 eosinophilia (pink) increased  due to eosin binding to denatured proteins

Decreased basophilia (blue) – mainly imparted by RNA

Glassy homogenous cytoplasm
 due to loss of glycogen

Clacification may occur late

Nuclear changes
 due to break down of DNA

Karyolysis : decrease basophilia of chromatin
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Pyknosis : nuclear shrinkage and increased basophilia

Karyorrhexis: fragmentation of pyknotic nucleus

Kidney, necrosis of tubular cells

Patterns of Acute Cell Injury
 Specific Morphologic Patterns of Necrosis

Coagulative necrosis

Liquefactive necrosis
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Gangrenous necrosis
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Caseous necrosis
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Fat necrosis
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Others (fibrinoid necrosis )

1.

Coagulative Necrosis:
Preservation of the structural outline of the dead
( coagulated ) cell for days
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The most common form of necrosis (particularly in myocardium, liver, kidney) characteristic of hypoxic cell death in all tissues except in the brain
Myocardial infarction is a very good example
Mechanism: denaturation of proteins and enzymes
 blocking cellular proteolysis
 preserve cell outline

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Morphology of Coagulative Necrosis:

Gross: pale color, normal firm texture at the beginning
 become soft later due to digestion by macrophages (may lead to rupture of infarcted myocardium)

Microscopic: first few hours
 no abnormalities later
 progressive loss of nuclear staining, with preservation of cell boundaries finally
 damaged cells are removed by macrophages
(the presence of necrotic tissue usually evokes inflammatory response followed by repair)

 Most of necrotic tissue is removed by leukocyte (Phagocytosis) combined with extracellular enzyme digestion
 If necrotic tissue is not eliminated
 it attracts
Ca ++ salts
 dystrophic calcification

Patterns of Acute Cell Injury

(a falling away from)

Definition: Programmed cell death

It is an active (energy-dependant) programmed single cell death to delete the unwanted or defective cells

It has an important role in physiological processes and pathological conditions

Apoptosis

Physiological processes:
 during embryogenesis (implantation, organogenesis, developmental involution, separation of digits in limb development)
 hormone -dependent involution (endometrium during menstruation, lactating
 breast after weaning) cell deletion in proliferating populations
 intestinal crypt epithelium
 deletion of autoreactive T cells in thymus (failure might result in autoimmunity)
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Pathological conditions:
 pathologic atrophy-prostate after castration (hormone -dependent involution)

Cell death in tumors
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Cell death induced by cytotoxic drugs and ionizing radiation

Councilman’s bodies due to viral hepatitis

Apoptosis
Morphology:

Involves single cells or small clusters
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Cells shrink rapidly, retain intact plasma membrane

Formation of cytoplasmic buds

Fragmentation into apoptotic bodies

Apoptotic bodies phagocytosed or rapidly degraded

No inflammatory response

Entire process from 5 to 30 minutes

Apoptosis

Necrosis Vs Apoptosis
Necrosis
 Grp of cells or part of tissue
 passive process

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Always pathologic
Mechanism is ATP depletion, mb damage

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Histology: coagulation.
liquefaction inflammation
Apoptosis:
 Single cell death in living tissue
 Active process
 Physiologic or pathologic
 Endonucleases
 Apoptotic bodies
 No inflammation