cell injury
Post on 31-Dec-2015
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Liquefaction necrosis * Definition: necrosis with complete loss of cell and tissue structure.* Mechanism: – Destruction of dead cells by hydrolytic enzymes.– Enzymes derived from either: • Cell’s own lysosomes (autolysis) or from• Neutrophils and macrophages (heterolysis).
* Seen in: – Suppurative bacterial infections: characterized by
formation of pus (liquefied tissue debris and neutrophils).
– In ischemic injury to brain tissue: Enzymatic destruction of brain tissue leaves behind a cystic cavity.
* Gross appearance:– Necrotic area: soft and filled with fluid.
* Microscopy:– Structureless tissue debris (no cellular outlines).– Neutrophils.
Caseation necrosis* Definition: a distinct form of necrosis without preservation of cellular outlines and tissue architecture, but firm in consistency.• It is a combination of Coagulative and liquefaction
necrosis.
* Most commonly associated with: – Granulomas like tuberculosis – Fungal infection like histoplasmosis.
* GROSS:– Yellowish white, “cheese-like” material.– Cheese-like appearance • Due to release of lipid from the cell walls of M.
tuberculosis and systemic fungi (histoplasma).• (Latin “caseous” – cheese)
* MICRO: – Eosinophilic material surrounded by activated
macrophages, multinucleated giant cells and helper T cells (= a granuloma).
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.• Acute pancreatitis: – Release of lipases and amylase from pancreas.– Lipases break triglycerides into fatty acids (FA).– FA combine with Ca2+ via the process of
saponification to form chalky white calcified deposits In the pancreas as well as in the omental fat.
Fibrinoid necrosis• Is necrosis of immunologic injury.• Is marked by deposition of Pink staining, fibrin-like
proteinaceous material within tissue.• Examples:– Rheumatic heart disease vegetations on mitral valve.– Inflamed synovial tissue in rheumatoid arthritis.– Malignant hypertension within vessel walls.
Gangrenous necrosis- Most often occurs in lower limbs and bowel
secondary to loss of blood supply.- Two types:1. Dry gangrene: – Is a form of infarction that results from
ischemia.–Characterized primarily by coagulative
necrosis without liquefaction.–Dead tissue has mummified appearance.–Characteristic finding in diabetic foot.
2. Wet gangrene:–Refers to necrosis with superimposed
bacterial infection.– Liquefactive necrosis is the primary type of
necrosis in wet gangrene.
• 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.
* Physiologic examples of apoptosis:
1. Embryogenesis.• Development of lumen within hollow organs (e.g
bowel and heart).2. Hormone-dependent involution in adults.– Endometrial breakdown in menstruation.– Post-lactational atrophy of breast.– Prostate atrophy following castration.
3. Involution of Thymus in the adult.4. Cells that are programmed to die; for
example, 1. The cells of the outer layers of epidermis, 2. Cells in the gut epithelium.
* 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.
* Morphologic appearance of apoptotic cells:
1. Have deeply pink staining cytoplasm.2. Have pyknotic nucleus which fragment.3. Are smaller in size.4. Formation of cytoplasmic buds.5. Breaking off cytoplasmic buds to form apoptotic
bodies.6. Phagocytosis of apoptotic bodies by adjacent cells or
macrophages.7. A lack of inflammatory response.
What if apoptosis is too little or too much!! = dysregulated apoptosis:
• Two groups of disorders:
1. Decreased apoptosis with increased cell survival can give rise to:• Cancers• Autoimmune disorders
2. Increased apoptosis with decreased cell survival:
– Neurodegenerative diseases (Alzheimer’s)– Death of virus infected cells: Lymphocyte depletion
as in AIDS
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
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