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 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

Plasma Membrane Alterations.

Mitochondrial Changes.
Dilation of the ER.
Nuclear Alterations.

REVERSIBLE INJURY
Under light microscope

CELLULAR SWELLING
FATTY CHANGE

CELLULAR SWELLING
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
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
Loss of DNA because of enzymatic degradation by endonucleases.

PYKNOSIS

Nuclear shrinkage and increased bosophilia, chromatin condenses into

solid,shrunken basophilic mass.

Karyohexis
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
PATHOLOGIC BASIS OF DISEASE BY ROBBINS AND COTRAN Pg 12-17

--------------------------------xxxxxxxxxxxxxxxxxxxxxxxxx------------------------------------