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Cell injury By Staff members of pathology 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. Lung Abscesses Necrotic material with loss of cellular architecture Neutrophils Necrotic tissue Coagulative vs. Liquefactive necrosis Coagulative necrosis Focus of liquefactive necrosis 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). Caseous necrosis B Lymph node: histoplasmosis Lung: tuberculosis Caseous necrosis Langhan’s giant cells Granuloma Epithelioid cell Langhan’s giant cell Fat necrosis 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. White nodules on the surface of pancreas Area of necrosis with blue discoloration 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. • Microscopy: fibrinoid material has – Smudgy pink (Eosinophilic) appearance. Fibrinoid Necrosis 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. Dry Gangrene A B 2. Wet gangrene: – Refers to necrosis with superimposed bacterial infection. – Liquefactive necrosis is the primary type of necrosis in wet gangrene. Apoptosis • 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. 2. 3. 4. 5. Have deeply pink staining cytoplasm. Have pyknotic nucleus which fragment. Are smaller in size. Formation of cytoplasmic buds. Breaking off cytoplasmic buds to form apoptotic bodies. 6. Phagocytosis of apoptotic bodies by adjacent cells or macrophages. 7. A lack of inflammatory response. Apoptosis of epidermal cells Apoptotic cell in liver 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 Apoptosis vs. Necrosis Feature Necrosis Apoptosis Cell size Enlarged (swelling) Reduced (shrinkage) Nucleus Pyknosis Fragmentation karyorrhexis karyolysis Cellular contents Enzymatic digestion; may leak out of cell Intact, may be released in apoptotic bodies. Feature Necrosis Apoptosis Adjacent inflammation Frequent No Physiologic or pathologic role Always pathologic Often physiologic, may be pathologic Good luck