Cell Injury (W1 Tutorial 1) PDF

Cell Injury Prepared by Dr. Nourhan Elfar, Ph.D CELL INJURY 1-Hypoxia: due to ischemia (deficient blood supply), inadequate oxygenation and anemia. 2- Physical agents: including trauma, heat, cold, radiation, and electric shock. 3- Chemical agents and drugs: including therapeutic drugs, pois...

Cell Injury Prepared by Dr. Nourhan Elfar, Ph.D CELL INJURY 1-Hypoxia: due to ischemia (deficient blood supply), inadequate oxygenation and anemia. 2- Physical agents: including trauma, heat, cold, radiation, and electric shock. 3- Chemical agents and drugs: including therapeutic drugs, poisons, environmental pollutants and alcohol 4- Infectious agents: viruses, bacteria, fungi, and parasites. 5- Immunologic reactions: including autoimmune diseases 6- Genetic derangements 7- Nutritional imbalances: including protein–calorie deficiency or lack of specific vitamins, as well as nutritional excesses. Morphologic Alternations in cell injury 1- Reversible injury (degeneration): q Cloudy swelling (water) q Hydropic (water) change q Fatty (fat) change II- Irreversible injury: q Necrosis (coagulative, liquefactive, caseation, fat necrosis) q Apoptosis (programmed cell death) Morphologic Alternations in cell injury I- (Reversible cell injury) Degeneration : 1-CLOUDY SWELLING : qOne of the earliest changes in injury. q Accumulation of sodium and water inside the cell>> swollen. qIt is seen in liver cells and myocardial cells. 2- Hydropic, ballooning or vacular change : qSame mechanism as cloudy swelling but more advanced. qThe cells are swollen due to excess water accumulation. The cytoplasm is pale and shows multiple vacuoles 3- Fatty change : qFatty change occurs in hypoxic and toxic injury. qIt is seen in cells involved in or dependent on fat metabolism, such as liver cells and myocardial cells. qLipid appears as empty vacuoles in the cytoplasm. II- (IRREVERSIBLE CELL INJURY) 1- NECROSIS: Definition: — Necrosis is death of a group of cells within a living body and the surrounding tissue showing inflammation. Morphology: 1- Nuclear changes: – Pyknosis: Nuclear shrinkage followed by karyorrhexis. – Karyorrhexis: Destructive nuclear fragmentation. – Karyolysis: Fading of nuclear basophilia. – Eventually the nucleus disappears completely 2- Cytoplasmic changes: qThere is loss of cell border qLater the necrotic tissue appears structureless. Types of necrosis: 1- Coagulative necrosis: q It occurs as a result of acute ischemia (sudden decrease in blood supply) q Necrotic tissues appear firm and dry. q Microscopic examination: loss of cellular details and appears structureless 2- Liquefactive necrosis: q Necrotic area appears ad liquid. q In case of CNS infarction, the cause of liquefaction is the high lipid and fluid content q In case of pyogenic abscess, the cause of liquefaction is the lysosomal enzymes released from dead polymorphs [pus cells]. 3- Caseation necrosis: q appears semi-solid, yellowish and cheese-like (casein). q Begins as coagulative necrosis followed by slow partial liquefaction q loss of cellular details followed by loss of cell structure. q This occurs mainly in tuberculosis. 4- Fat necrosis: of two types: I. Traumatic fat necrosis: Trauma to adipose tissue leads to release of intracellular fat provokes an inflammatory response then lead to fibrosis. A common site is the breast where it results in a palpable mass. II. Enzymatic fat necrosis: In acute pancreatitis, there is leakage of pancreatic lipase, which acts on fat cells, splitting it into glycerol and fatty acid. Glycerol is absorbed and fatty acids combine with Ca+ and deposited as white paths >>> fibrosis. coagulative liquefactive Caseative Fat necrosis II- (IRREVERSIBLE CELL INJURY) 2- APOPTOSIS: Definition: q It is a programmed cell death which is energy dependent. q It is a form of cell death which leads to the deletion of individual cells, It is sometimes referred to as cell suicide. Morphological changes: 1- The cell shrinks, retaining an intact plasma membrane. 2- The nucleus shrinks and fragments. 3- Apoptotic cells show surface blebs which later fragment into apoptotic bodies. 4- Apoptotic cells and apoptotic bodies are removed by adjacent cells or macrophages. 5-No inflammation in the surrounding tissues. Causes of apoptosis: Physiological conditions: Normal cell turn over. Programmed cell death during embryonic development. Endocrine-dependent tissue involution: menstrual cycle Pathological conditions: 1. Radiation cell injury. 2. Cell death by cytotoxic lymphocytes 3. Liver cells in viral hepatitis. 4. Pathological atrophy Cell Injury