Download MORPHOLOGICAL ALTERATIONS

MORPHOLOGICAL ALTERATIONS
IN CELL INJURY
LEARNING OBJECTIVES:
At the end of lecture students should be able to:
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Differentiate between Necrosis and Apoptosis.
Describe the microscopic morphology of Reversible injury.
Describe the nuclear and cytoplasmic features of necrosis.
Define and briefly describe the patterns of Tissue Necrosis including:
Coagulative Necrosis, Liquefactive Necrosis,Gangrenous Necrosis,
Caseous Necrosis, Fat Necrosis and Fibrinoid Necrosis.
Differentiate B/W APOPTOSIS AND NECROSIS
APOPTOSIS
 Chromatin condensation
 Cell shrinkage
 Preservation of organelles
and cell membranes
 Rapid engulfment by
 neighboring cells
 preventing inflammation
 Biochemical hallmark DNA fragmentation
NECROSIS
 Nuclear swelling
 Cell swelling
 Disruption of organelles
 Rupture of cell and
 Release of cellular
contents
 Inflammatory response
MORPHOLOGICAL CHANGES OF REVERSIBLE
INJURY
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Plasma Membrane Alterations.
Mitochondrial Changes.
Dilation of the ER.
Nuclear Alterations.
REVERSIBLE INJURY
Under light microscope
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CELLULAR SWELLING
FATTY CHANGE
CELLULAR SWELLING
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It appears whenever cells are incapable of maintaining ionic and fluid
homeostasis.
Is the result of failure of energy-dependent ion pumps in the plasma
membrane.
FATTY CHANGES
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It occurs in hypoxic injury and various forms of toxic or metabolic injury.
It is manifested by the appearance of lipid vacuoles in the cytoplasm.
It is seen in Hepatocytes and Myocardial Cells.
NECROSIS
• Cell death as the result of injury, disease, or pathological state
• Usually involves large numbers of cells.
• Necrotic cells may spill their contents, causing inflammation and injury to
neighboring cells.
Many types;
• Coagulative necrosis,
• Caseous necrosis
• Liquefactive necrosis
• Fat necrosis
• Fibrinoid necrosis
NECROSIS
MORPHOLOGICAL CHANGES OF NECROSIS
Nuclear Changes appear in one of the three patterns:
• Karyolysis
• Pyknosis
• Karyohexis
Karyolysis
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Loss of DNA because of enzymatic degradation by endonucleases.
PYKNOSIS
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Nuclear shrinkage and increased bosophilia, chromatin condenses into
solid,shrunken basophilic mass.
Karyohexis
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The pyknotic nucleus undergoes fragmentation and with the passage of time
totally disappears.
COAGULATIVE NECROSIS
 Cell outlines remain intact after cell death and can be
observed by light microscopy
 Is typically seen in hypoxic (low-oxygen) environments
Examples
 Infarcts of solid organs,
 Heart, spleen, kidney.
CASEOUS NECROSIS
 Tissues bear soft, granular,
friable appearance.
 Cream-cheesy(caseous) material
 Architecture completely destroyed.
Examples:
 Tuberculosis,
 Some systemic fungal infection
A tuberculous lung with a
large area of caseous necrosis
LIQUEFACTIVE NECROSIS
(COLLIQUATIVE NECROSIS)
Necrotic degradation of tissue that softens and liquify tissues grossly.
Examples
 Infarction of central nervous system
 Abscess in bacterial infection.
FAT NECROSIS
• Results from the action of lipases on fatty tissues
• Chalky yellow white deposits formed
• Basophilic calcified areas
Examples:
• Acute pancreatitis
• Traumatic breast tissue necrosis.
FIBRINOID NECROSIS
• It is marked by deposition of fibrin-like proteinaceous
material in arterial walls.
• Appears smudgy and eosinophilic on light microscopy.
Examples:
• Immune vasculitis
• Malignant hypertension
REFERENCES
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PATHOLOGIC BASIS OF DISEASE BY ROBBINS AND COTRAN Pg 12-17
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