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Cellular Injury and Responses to stress Faculty of Medicine Department of Pathology Hussam Telfah, MBBS, FRCPath Cellular Response to Stress • Normal cell needs special conditions “environment” to function properly. Homeo-stasis : similar-standing still. Range of Temperature, PH, Glucose etc Cellular Responses • Adaptation: hypertrophy, hyperplasia, atrophy, metaplasia. • Injury: reversible and irreversible. • Intracellular accumulation; calcification • Cellular aging. Cellular Adaptations • Reversible changes in size, number, phenotype, metabolic activity or function in response to changes in environment. • Adaptation can be both physiologic and pathologic. Hypertrophy • Hypertrophy is an increase in cell size resulting in an increase in the size of the organ. • Alone in nondividing cells or coexisting with hyperplasia in dividing cells. • Physiologic vs pathologic. • Increased functional demand (workload) or stimulation by hormones or growth factors. Hypertrophy • Muscle Hypertrophy • Heart: left ventricle hypertrophy. Hypertrophy • Uterus Hypertrophy • There is a limit for hypertrophy beyond which the muscle is no longer able to compensate for the increased burden. • Some times subcellular organelle may undergo selective hypertrophy. • Example: drugs lead to hypertrophy of smooth endoplasmic reticulum only. Hyperplasia • Increased number of cells resulting in increase of the size of the organ or tissue. • Takes place in cells capable of dividing. • Physiologic vs pathologic. Hyperplasia • Physiological Hyperplasia (hormonal or compensatory), Examples: – Uterine enlargement during pregnancy – Female breast in puberty & lactation – Compensatory hyperplasia in the liver • Pathological – Hyperplasia of the endometrium (excessive hormone stimulation). – Wound healing (Effects of growth factors). – Infection by papillomavirus • Hyperplasia can be a fertile soil for development of neoplasia Hyperplasia Prostate Hyperplasia Endometrium Atrophy • Reduced size of an organ or tissue as a result from a decrease in cell size and number. • Physiologic : Embryonic development. • Pathologic: Decreased workload (Disuse atrophy) Loss of innervation (Denervation atrophy) Diminished blood supply. Inadequate nutrition. Loss of endocrine stimulation. Pressure. Metaplasia • Metaplasia is a “reversible” change in which one differentiated cell type (epithelial or mesenchymal) is replaced by another cell type. • New epithelium is better in dealing with the current stress or irritation. • Persistence of factors causing metaplasia may lead to progression into malignant transformation. • Examples: respiratory , GIT, cervix, muscle. Metaplasia • Replacement of ciliated columnar epithelium with stratified squamous epithelium in the respiratory tract of a smoker. Causes of Cell Injury • • • • • • Oxygen Deprivation: hypoxia and ischemia Chemical agents & Drugs. Physical agents: mechanical trauma, changing T⁰. Infection Agents: viruses to worms. Immunological reactions: autoimmune. Genetic derangement: chromosomal to single amino acid defect • Nutritional Imbalances: Deficiency vs excess. Morphologic alterations in cell injury Reversible injury • Generalized swelling of the cell: failure of energy-dependent ion pumps in the plasma membrane result in disturbances in ionic and fluid homeostasis. It is usually the first manifestatioin. Another names hydropic change or vacuolar degeneration. • Plasma membrane alterations: blebs, blunting or loss of villi and loosening of intercellular attachments. Morphologic alterations in cell injury Reversible injury • Mitochondrial changes: swelling and appearance of small amorphus densities. • Dilatation of ER and detachment of polysomes (ribosomes) with possibility of myelin figure formation. • Nuclear alterations: nuclear chromatin clumping. Kidney tubules Downloaded from: StudentConsult (on 24 September 2011 08:38 PM) © 2005 Elsevier Figure 1-8 Schematic illustration of the morphologic changes in cell injury culminating in necrosis or apoptosis. Downloaded from: StudentConsult (on 24 September 2011 08:56 PM) © 2005 Elsevier Morphologic alterations in cell injury irreversible injury (Necrosis) • Result from denaturation of intracellular proteins and enzymatic digestion of cells. • Loss of membrane integrity. • Digestion enzymes: lysosomes of dying cells and leukocytes. Morphologic alterations in cell injury irreversible injury (Necrosis) • Increased eosinophilia in H&E stain. • Vacuolation due to digestion of cytoplasmic organelles. • Myelin figures: aggregates of damaged cell membranes (phospholipids). Then they are either phagocytosed by other cells or further degraded into fatty acids and calcify. • Plasma and organelle membrane discontinuities. Morphologic alterations in cell injury irreversible injury (Necrosis) • Marked dilatation of mitochondria and appearance of large densities. • Nuclear changes: breakdown of DNA - Karyolysis: loss of DNA, fade of basophilia. - Pyknosis: nuclear shrinkage and increased basophilia. - Karyorhexis: fragmentation of the pyknotic nucleus. - Disappearance of the nucleus. Patterns of tissue necrosis • Coagulative necrosis: preservation of the architecture of dead tissue for at least some days. • Denaturation of structural proteins and enzymes. • Eosiniphilic anucleated cells • Cells are removed by inflammatory leukocytes. Patterns of tissue necrosis • Ischemia in any organ except the brain may lead to coagulative necrosis. • Infarction: localised area of coagulative necrosis. Patterns of tissue necrosis • Liquifactive necrosis: digestion of the dead cells resulting into a liquid jelly-like mass. • In focal bacterial or fungal infections and in hypoxic death in central nervous system. • Creamy yellow due to accumulation of dead leukocytes (pus).