morphological changes of reversible injury

MORPHOLOGICAL ALTERATIONS
IN CELL INJURY
LEARNING OBJECTIVES:
At the end of lecture students should be able to:
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
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
Nuclear swelling
Cell swelling
Disruption of organelles
Rupture of cell and
Release of cellular
contents
Inflammatory response
NECROSIS

CYTOLOGIC FEATURES OF NECROSIS & APOPTOSIS
DIFFERENCE B/W APOPTOSIS AND NECROSIS

MORPHOLOGICAL CHANGES OF REVERSIBLE
INJURY
• Plasma Membrane Alterations.
• Mitochondrial Changes.
• Dilation of the ER.
• Nuclear Alterations.
Under light microscope
• CELLULAR SWELLING
• FATTY CHANGE
REVERSIBLE INJURY
CELLULAR SWELLING
• Incapable of maintaining ionic and fluid homeostasis.
• Result of failure of energy-dependent ion pumps in the plasma membrane.
• Occurs in
• hypoxic injury
• toxic injury
• metabolic injury.
• Manifested by the
• Cytoplasmic lipid vacuoles .
• Seen in
• Hepatocytes
• Myocardial Cells.
FATTY CHANGES

NECROSIS
• Type of cell death associated with loss of membrane integrity & leakage
of cellular contents resulting in dissolution due to enzymatic degradation
• Usually involves large numbers of cells.
• Inflammation and injury to neighboring cells.
Types;
• Coagulative necrosis,
• Caseous necrosis
• Liquefactive necrosis
• Fat necrosis
• Fibrinoid necrosis
MORPHOLOGICAL CHANGES OF NECROSIS
Nuclear Changes appear in one of the three patterns:
• Karyolysis
• Pyknosis
• Karyohexis
Karyolysis
Breakdown of DNA and chromatin because of enzymatic degradation by
endonucleases
PYKNOSIS
• Nuclear shrinkage and increased bosophilia,
• chromatin condenses into solid,shrunken basophilic mass.
• fragmentation of pyknotic nucleus.
Karyohexis

FATES OF NECROTIC CELL
• May persists for sometimes
• Digested by enzymes
• Replaced by myelin figures
• Phagocytosed by other cells
• Further degraded in to fatty acids
• Calcified
NECROSIS: TYPES
Macroscopic
• Coagulative necrosis,
• Caseous necrosis
• Liquefactive necrosis
• Fat necrosis
Microscopic
• Fibrinoid necrosis
COAGULATIVE NECROSIS
“Underlying tissue architecture is preserved for several
days”
can be observed by light microscopy
Is typically seen in hypoxic (low-oxygen) environments
Examples
Infarcts of solid organs such as Heart, spleen, kidney (except
brain).

LIQUEFACTIVE NECROSIS
(COLLIQUATIVE NECROSIS)
“Necrotic degradation, softening and liquifaction of
tissues grossly.”
Examples
Infarction of central nervous system
Abscess in bacterial and fungal infection.
CASEOUS NECROSIS
Caseous = cheese like
Necrotic degradtion with Friable, yellow white tissue appearance
Architecture completely destroyed.
Examples:
Tuberculosis
Some systemic fungal infection
Soft, granular, cream
cheesy tuberculous lung

GRANULOMA
• The necrotic area is enclosed within a distinctive inflammatory border.
• A focus of inflammation.
• Microscopic term.
FAT NECROSIS
“Necrotic degradation resulting from the action of
lipases on fatty tissues.”
• Fat saoponification Chalky yellow white deposits formed.
• Basophilic calcified areas
Examples:
• Acute pancreatitis
• Traumatic breast tissue necrosis.
FIBRINOID NECROSIS
“Necrotic degradation by deposition
of fibrin-like proteinaceous material
in arterial walls.”
• Visible only microscopically
• Appears smudgy and eosinophilic (pink)
Examples:
• Immune mediated diseases
• Malignant hypertension

GANGRENOUS NECROSIS
• Not a distinctive patterns of cell death
• Clinical term
• Usually referring condition of limb, lost blood supply.
CLINICAL IMPLEMENTATION
• Leaked protein of necrotic cells in to the circulation provide a mean of
detecting tissue specific necrosis using blood or serum samples.
e.g.
• Creatinine kinase (cardiac muscles)
• Alkaline phosphatase (hepatic bile duct)
• Transaminase (hepatic cells)
•
REFERENCES
PATHOLOGIC BASIS OF DISEASE BY ROBBINS AND COTRAN Pg. 7 -13
--------------------------------xxxxxxxxxxxxxxxxxxxxxxxxx------------------------------------