Post on 23-Dec-2015
* Light microscopy of irreversible cell injury
• Pyknosis = Shrinkage and darkening of the
nucleus.
• Karyorrhexis = fragmentation and breakdown
of the nucleus, (into "nuclear dust").
• Karyolysis = dissolution of the nucleus.
* Types of cell death:
• Necrosis: local death of a group of cells within
the living body.
• Apoptosis: genetically controlled programmed
single cell death.
* Types of necrosis:
1. Coagulation necrosis.
2. Liquefactive necrosis.
3. Caseation necrosis.
4. Fat necrosis.
5. Fibrinoid necrosis.
Coagulative necrosis* Mechanism:
– Denaturation and coagulation of structural and
enzymatic proteins due to intracellular acidosis.
– Denaturation of lysosomal enzymes by intracellular
acidosis prevents autolysis.
– Preserving cell outlines and tissue architecture.
– Acute ischemia is the most common cause.
Liquefactive necrosis
* Definition: necrosis with complete loss of cell and
tissue structure due to liquefaction by hydrolytic
enzymes.
* Mechanism:
– Enzymes derived from either cell’s own lysosomes
(autolysis) or from Neutrophils and macrophages
(heterolysis).
Caseation necrosis
• It is a combination of coagulative and
liquefaction necrosis. The tissue is firm (grossly)
and without cellular details or tissue outline
(microscopically).
• Most commonly associated with tuberculosis
1. Traumatic fat necrosis Secondary to trauma to fatty tissue.Trauma to fatty tissue acute inflammatory
reaction (neutrophils) healing by fibrous tissue and dystrophic calcification.
Commonly seen in women with pendulous breasts.
Clinical significance:– Scar tissue feels firm, retracts the overlying skin and
shows calcifications on mammography.– “These findings also seen in breast cancer”.
2. Enzymatic fat necrosis
• Focal areas of fat destruction due to the action
of pancreatic enzyme on fatty tissue located
around pancreas.
• Occurs as a complication of Acute pancreatitis.
• Genetically, programmed single cell death.* Morphologically: • The cell membrane does not rupture. • The cell contents are not released into the
extracellular space, and inflammation does not occur.
• May be physiological or pathological.
* Morphologic appearance of apoptotic cells:
1. Cell shrinkage.
2. The cytoplasm becomes deeply esinophilic.
3. The nucleus becomes pyknotic then fragments.
4. Formation of cytoplasmic buds.
5. Each nuclear fragment of go with a cytoplasmic bud and
breaking off to form apoptotic bodies.
6. Phagocytosis of apoptotic bodies by adjacent cells or
macrophages.
7. A lack of inflammatory response.
* Physiologic examples of apoptosis:
1. Embryogenesis.
• Development of lumen within hollow organs (e.g
bowel and heart).
2. Hormone-dependent involution in adults.
– Post-lactational atrophy of breast.
– Prostate atrophy following castration.
3. Involution of Thymus in the adult.
* Pathologic examples of apoptosis:
1. Councilman bodies = dead hepatocytes in viral
hepatitis.
2. Psammoma bodies: apoptosis of neoplastic cell with
subsequent calcification.
3. Tumor cell death by cytotoxic T cells.
4. Neurons that are lost in Alzheimer's disease.
5. HIV-positive T-lymphocytes die by apoptosis.
Intact, may be released in apoptotic bodies.
Enzymatic digestion; may leak out of cell
Cellular contents
Fragmentation
Pyknosis karyorrhexis karyolysis
Nucleus
Reduced (shrinkage)
Enlarged (swelling)
Cell size
Apoptosis Necrosis Feature
Often physiologic, may be pathologic
Always pathologic
Physiologic or pathologic role
NoFrequent Adjacent inflammation
Apoptosis Necrosis Feature