reversible and irreversible cell injury

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Slide 1 :

REVERSIBLE AND IRREVERSIBLE CELL INJURY SPOKESPERSON- Dr Suchitra Sahoo ( PG STUDENT; DEPT OF PATHOLOGY; VSS MEDICAL COLLEGE,BURLA) MODERATOR-Dr Alaka Sahu ASST PROF, DEPT OF PATHOLOGY; VSS MEDICAL COLLEGE,BURLA

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LEARNING OBJECTIVES Definition Of Cell Injury Injurious Stimuli & Causes Cellular Responses To Injury Types Of Cell Injury Mechanisms Of Cell Injury Reversible cell injury & its morphology Irreversible cell injury & its morphology

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WHAT IS CELL INJURY ????? Crossing the Limits of adaptive responses Exposure to injurious agents or stress Deprivation of essential nutrients Mutations affecting essential cellular constituents CELL INJURY

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INJURIOUS STIMULI O2 Imbalance > hypoxia >hyperoxia Physical Agents > trauma > radiation > burn & cold > electric shock Chemical Agents & Drugs > arsenic, cyanide > acetamenophen, alcohol Infectious Agents Immunologic Mediators & Processes > autoimmune reactions > hypersensitivity reactions Genetic Derangements > down’s syndrome Nutritional Imbalances > deficiency(pem) > excess(obesity,atherosclerosis)

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CELLULAR RESPONSES TO INJURY

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TYPES OF CELL INJURY Irreversible injury iirreversible

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Factors Determining Injury Consequences INJURY

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MECHANISMS OF CELL INJURY

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DEPLETION OF ATP HOW ATP IS PRODUCED ? Site – mitochondria mechanism –oxidative phosphorylation pathway - electron transfer system(ets) HOW ATP IS DEPLETED ?

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Depletion of ATP Contd…….. CONSEQUENCES OF ATP DEPLETION 1.reduced sodium pump activity ER swelling loss of microvilli Blebs formation 2.increased anaerobic glycolysis Lactic acidosis chromatin clumping 3. ribosomal detachment Lipid deposition 4. misfolding of proteins Cell death 5.mitochondrial & lysosomal damage Cell death

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MITOCHONDRIAL DAMAGE MITOCHONDRIAL KILLERS 1. Increased Cytosolic Calcium Ions 2.Reactive Oxygen Species (ROS) 3. Lipid Peroxidation MITOCHONDRIAL MEMBRANE DAMAGE Inability to generate ATP Release of pro-apoptotic proteins Necrosis Apoptosis

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INFLUX OF CALCIUM & LOSS OF ITS HOEMEOSTASIS

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OXIDATIVE STRESS cell injury induced by free radicals ,particularly by reactive oxygen species (ROS) Free radicals – have single unpaired electron, unstable,initiate autocatalysis ROS – oxygen derived free radical, e.g-superoxide anion, hydroxyl ions FREE RADICAL GENERATION FENTON REACTION (Fe2+) SUPEROXIDE DISMUTASE

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PATHOLOGIC EFFECTS OF FREE RADICALS

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REVERSIBLE CELL INJURY WHAT DO I UNDERSTAND ? > The injury does not cause significant damage to the cells and they remain viable throughout the process of being injured. > The functional and morphologic changes are reversible if the damaging stimulus is removed . MORPHOLOGIC ALTERATIONS a. Light microscopic changes b. Ultrastructural changes

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LIGHT MICROSCOPIC CHANGES 1. cellular swelling (hydrropic changes) – enlargement of cell and its organelles - slightly enlarged pale cytoplasm -normally located nucleus ,Sometmes enlarged 2. Fatty change (steatosis) -accumulation of excess fat in cytoplasm - liver , heart &kidney usually affected - 2 types; micro & macro vesicular microvesicular – numerous small fat vacuoles in cytoplasm - centrally placed nucleus macrovesicular- single large vacuole in cytoplasm - cytoplasm appears as a ring - nucleus peripherally placed - signet ring appearance of cell

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Normal kidney tubule Hydropic change Necrosis

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FATTY CHANGE Large fat vacuole, cytoplasm at periphery of vacuole, Nucleus pushed to corner, signet ring appearance

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ULTRASTRUCTURAL CHANGES; Plasma Membrane Alterations- Blebbing - Loss of microvlli Mitochondrial changes -swelling -small amorphous densities Endoplasmic reticulum changes – dilatation -detachment of polysomes Nuclear changes - disaggreations of granular and fibrillar elements

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NORMAL INJURED MITOCHONDRIAL SWELLING

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IRREVERSIBLE INJURY WHERE TO USE THIS TERM ? >with continuing damage, cell cannot recover and it dies. CHARACTERIZED BY MAINLY: >inability to reverse mitochondrial dysfunction >profound disturbances in membrane function TYPES: 1.Necrosis 2.Apoptosis

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NECROSIS HOW TO DEFINE IT… Morphologic changes following cell death in living tissue, resulting from progressive degradative action of enzymes on lethally injured cells. MORPHOLOGIC ALTERATIONS: 1. Cytoplasmic changes 2. Nuclear changes 3. Inflammatory infiltration

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CYTOPLASMIC CHANGES: - increased eosinophilia - glassy homogenous appearance - mitochondrial dilatation with large amorphous densities - myelin figures - moth eaten appearance NUCLEAR CHANGES: - pyknosis - karyorrhexis - karyolysis

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Dilated mitochondria Large amorphous densities Glassy homogenous Increased eosinophillic cytoplasm

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Morphologic variants of necrosis Coagulative necrosis Liquefactive necrosis Caseous necrosis Fat necrosis Fibrinoid necrosis Gangrenous necrosis

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COAGULATIVE NECROSIS Ghost outlines Necrotic cell Inflammatory cells Opaque, yellow , firm Intensly eosinophilic cytoplasm, indistinct nucleus

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LIQUEFACTIVE NECROSIS Necrotic area Soft , liquified, creamy yellow Cystic space Necrotic cell debris, Proliferating capillaries

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CASEOUS NECROSIS Lymph nodes C N Caseous necrosis CN Yellow white Sharply circumscribed Dry cheese like Amorphous ,eosinophilic, granular foci

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FAT NECROSIS F N F N Pale outline of cell , Amorphous ,faintly basophilic material in cytoplasm

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FIBRINOID NECROSIS Necrotic area

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Gangrenous necrosis Types : > dry gangrene > wet gangrene DRY GANGRENE

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APOPTOSIS An active self-destructive cellular process. MORPHOLOGIC ALTERATIONS: 1. Cell shrinkage – dense cytoplasm 2. Chromatin condensation – most characteristic - aggregated peripherally 3. Cytoplasmic blebs and apoptotic bodies formation 4.Phagocytosis of apoptotic bodies MICROSCOPIC APPEARANCE: - Cytoplasm intensely eosiniphilic - Nuclei with dense nuclear chromatin

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Apoptotic cell >intensely eosinophilic cytoplasm > Condensed nucleus Nuclei-peripheral crescents of chromatin APOPTOTIC CELLS

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APOPTOTIC DISORDERS EXCESS APOPTOSIS Neurodegenerative diseases ischemic heart disease stroke DEFECTIVE APOPTOSIS Autoimmune disorders Malignancies

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SUMMARY When various stimuli injure a cell beyond its adaptive limits; they trigger multiple complex intracellular processes, the end result of which can either be irreversible i.e cell death or reversible i.e transient morphologic and functional alteration, depending upon the severity of injury and resistance power of the cell. The ensuing necrosis is always pathological indicating advanced stage of a disease that can be identified by both gross and microscopic examinations whereas, apoptosis is mostly a physiological, programmed self destruction of a cell, whose dysregulation leads to several diseases and its morphologic changes are identifiable only under microscope.

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CONCLUSION Avoid stress & anxiety Use antioxidants Dietary Calorie restriction Life style modifications

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THANK YOU

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