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    Necrosis

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    Dr. Ashish Jawarkar
    this is a series of notes on general pathology, useful for undergraduate and post graduate pathology students

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    Necrosis

    Uploaded by

    Dr. Ashish Jawarkar
    223 views6 pages
    this is a series of notes on general pathology, useful for undergraduate and post graduate pathology students

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    PDF, TXT or read online from Scribd

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    this is a series of notes on general pathology, useful for undergraduate and post graduate pathology students

    Copyright:

    Attribution Non-Commercial (BY-NC)
    Download as PDF, TXT or read online from Scribd
    Download as pdf or txt
    223 views6 pages

    Necrosis

    Uploaded by

    Dr. Ashish Jawarkar
    this is a series of notes on general pathology, useful for undergraduate and post graduate pathology students

    Copyright:

    Attribution Non-Commercial (BY-NC)
    Download as PDF, TXT or read online from Scribd
    Download as pdf or txt
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    The key takeaways are the different types of cell injury including reversible and irreversible injury, causes of cell injury, timeline of injury, mechanisms of necrosis, and morphology of necrosis.

    The different types of cell injury are reversible injury, irreversible injury which includes necrosis and apoptosis.

    The mechanisms of cell injury leading to necrosis include damage to membranes, failure of calcium pumps, accumulation of free radicals, mitochondrial membrane damage and depletion of ATP.

    1

    General Pathology Notes (Robbins)


    By Dr. Ashish Jawarkar Chapter 1 : CELLULAR RESPONES TO STRESS AND TOXIC INSULTS: ADAPTATION, INJURY AND CELL DEATH

    TOPIC 2. CELL INJURY AND NECROSIS Overview 1. definition 2. types reversible, irreversible (necrosis,apoptosis) 3. causes 4. timeline 5. Mechanisms of cell injury (necrosis) 6. morphology 7. necrosis vs apoptosis 8. patterns of necrosis 9. molecular basis

    *definition and types Cells exposed to stress

    Adaptation (hypertrophy/hyperplasia/atrophy/metaplasia)

    Continued stress, no more adaptation possible

    Cell injury

    Reversible cell injury

    Irreversible cell injury (necrosis & apoptosis)

    Notes on General Pathology Apoptosis.By Dr. Ashish V. Jawarkar Contact: pathologybasics@gmail.com Website: pathologybasics.wix.com/notes

    *Causes of cell injury 1. O2 deprivation, nutritional imbalances 2. Physical agents trauma, heat, cold, UV light, shock 3. Chemical agents cyanide, arsenic, pollutants 4. Infectious agents 5. Deranged immunity *Timeline

    Reversible Injury
    cell function
    effect

    irreversible cell injury


    Biochemical alterations Days Light Microscopic Changes

    Minutes Ultrastructural changes

    Gross Morphologic Changes

    *Mechanisms of Cell injury (Necrosis) 1. Damage to membranes (plasma, lysosomal,mitochondrial) 2. Failure of calcium pump 3. Accumulation of free radicals 4. Mitochondrial membrane damage and depletion of ATP 5. Protein misfolding and DNA damage 1. Damage to membranes Plasma membrane damage Lysosomal membrane damage

    Osmotic imbalance Leakage of metabolites

    leakage of (DNAases, RNAases, Proteases etc.)

    Notes on General Pathology Apoptosis.By Dr. Ashish V. Jawarkar Contact: pathologybasics@gmail.com Website: pathologybasics.wix.com/notes

    2. Failure of Ca2+ pump

    Calcium influx

    Activation of leaked enzymes (DNAases, RNAases)

    Alteration of mitochrondrial Membrane permeability

    3. Accumulation of free radicals Generation of free radicals ROS


    1. Redox rns in Normal metabol 2. Radiation 3. Inflammn 4. CCl4 5. Transition metals (Fenton rn#) 6. NO

    O2Super Oxide

    SOD

    H2O2 Hydrogen Peroxide

    fenton rn +Fe2+

    OH Hydroxyl Radical

    FENTON RN H202 + Fe2+

    Fe3+ + OH + OH-

    MITOCHONDRIA

    Removal of free radicals done by 1. SOD (superoxide dismutase) mitochondria 2. Glutathione peroxidase mitochondria 3. Catalase peroxisome Pathologic effects of ROS 1. Fatty acid oxidation and disruption of membranes, organelles 2. Protein oxidation and loss of enzyme activity, protein misfolding 3. DNA oxidation and mutations and breaks

    Notes on General Pathology Apoptosis.By Dr. Ashish V. Jawarkar Contact: pathologybasics@gmail.com Website: pathologybasics.wix.com/notes

    4. Mitochondrial membrane damage and depletion of ATP Mitochondrial membrane damaged by 1. increased cytosolic calcium 2. ROS 3. hypoxia 4. mutations in mito genes Activation of caspases (apoptosis) Due to leakage of cyto c

    Alteration of mitochondrial membrane permeability Due to leakage of H+

    H+ leakage and Loss of membrane potential

    Decreased Oxidative Phosphorylation

    Decreased ATP generation

    Detachment of Ribosomes

    Failure of Na+ pump

    Increased anaerobic Glycolysis

    Decreased protein synthesis

    Influx of Na +, Ca2+ H2O Cellular swelling ER swelling

    Lactic acidosis

    Increased lipid deposition

    Clumping of nuclear chromatin

    Notes on General Pathology Apoptosis.By Dr. Ashish V. Jawarkar Contact: pathologybasics@gmail.com Website: pathologybasics.wix.com/notes

    *Morphology

    GROSS

    Light Microscopy

    REVERSIBLE INJURY 1. Pallor 2. Turgor 3. Increased weight 1. Cellular swelling 2. vacuolar degeneration/hydropic change clear vacuoles in cytoplasm that represent pinched off segments of ER

    NECROSIS

    1. Cytoplasm a. eosinophilia due to loss of cytoplasmic RNA b. Glassy appearance due to loss of glycogen particles c. Moth eaten app due to vacuolation 2. Cell membrane a. Myelin figures membrane fragments collect in cytoplasm b. Calicification of myelin figures Nucleus Karyoloysis lysis of chromatin Pyknosis nuclear shrinkage Karyorrhexis chromatin condenses into solid shrunken basophilic mass Plasma membrane discontinuities Cytoplasm Myelin figures 3. a. b. c.

    Ultra structure

    Plasma membrane blebs, loss of microvilli Nucleus disaggregation of granular and fibrillar elements ER dilatation and detachment of ribosomes Mitochondria amorphous densities

    Mitochondria - Large amorphous densities

    *Patterns of tissue necrosis 1. COAGULATIVE NECROSIS Gross: The tissue is firm. Eg of localized coagulative necrosis is infarct. Microscopy: preserved cell outlines, loss of nuclei, inflammatory infiltrate 2. CASEOUS NECROSIS (cheese like, in TB) Gross: friable white app of necrotic area
    Notes on General Pathology Apoptosis.By Dr. Ashish V. Jawarkar Contact: pathologybasics@gmail.com Website: pathologybasics.wix.com/notes

    Microscopy: Granuloma central necrosis with lysed cells forming amorphous debris, surrounded by inflammatory cells and epithelioid cells 3. LIQUEFACTIVE NECROSIS (necrosis in CNS) Characterized by digestion of dead tissue transformation into liquid viscous mass Gross: Abscess cavity formation with ragged margins Microscopy: Necrotic material is creamy yellow containing dead leucocytes 4. GANGRENOUS NECROSIS 1. coagulative necrosis occurring in a limb that has lost its blood supply 2. occurs in multiple tissue planes 3. superimposed bacterial infection causes liquifactive necrosis wet gangrene 5. FAT NECROSIS Refers to focal areas of fat destruction occurring due to release of pancreatic enzymes into substance of pancreas and peritoneal cavity Seen in acute pancreatitis Gross: Pancreatic enzymes liquefy membranes of fat cells in peritoneum, split triglycerides, produce saponification and deposition of calcium, chalky white areas Microscopy: shadowy outlines of fat cells, basophilic calcium deposits, inflammatory reaction 6. FIBRINOID NECROSIS Seen in immune reactions like SLE and other vasculitic syndromes Seen in the wall of blood vessels Microscopy: The wall of the vessels show circumferential bright pink areas of necrosis and inflammation. Its basically immune complex deposition with extravasated fibrin.

    Notes on General Pathology Apoptosis.By Dr. Ashish V. Jawarkar Contact: pathologybasics@gmail.com Website: pathologybasics.wix.com/notes

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