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    Necrosis

    PresentedBy

    Ahmed El-RashedyProfessor & Previous Head

    of Pathology DepartmentAl-Azhar University

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    NecrosisDef.: An irreversiblemorphological changes in a living

    tissue or cells on exposure to a lethalirritant.N.B.:Autolysis is complete cessation of energy productionand anabolic activities with continuation of the

    catabolic and lytic activities of the releasedlysosomal enzymes.

    Differences between Necrosis and Autolysis

    AutolysisNecrosisPost-mortem.Ante-mortem.1. Duration

    Whole body.Localized area of a living body.2. Location

    Absent.Present (In the surrounding tissue).3. Inflammation

    Prof. Dr. Ahmed Elrashedy

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    Pathogenesis:

    Two essential processes:

    1.Enzymatic digestion of the cell by one of these factors:

    A. Lysosomes of the dead cells themselves.

    B. Lysosomes of the surrounding immigrant inflammatory

    leukocytes (Heterolysis).

    2. Denaturation of the cell proteins.

    Pathology (Morphological changes):

    I)Cytoplasmic changes:

    1) Increased eosinophilia (due to increased affinity of the

    denatured proteins for eosin stain).2) Vacuolated(due to enzymatic digestion of its organelles).

    3) Calcification of the dead cells (dystrophic calcification;

    deposition of calcium salts in the serum onto the dead cells).

    4) Loss of striations: in the sarcoplasm of necrotic muscles.

    Prof. Dr. Ahmed Elrashedy

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    II)Nuclear changes:

    1. Early (reversible):

    Clumping of the chromatin into large aggregatesattached to the nuclear membrane & to the

    nucleolus

    2. Later (Irreversible):1) Pyknosis: Small densely stained nucleus.

    2) Karyorrhexis (Chromatorrhexis): Fragmented

    nucleus.3) Karyolysis (Chromatolysis): Progressive

    dissolution and fading of the nucleus (due to the

    hydrolytic action of lysosomal DNases).

    Prof. Dr. Ahmed Elrashedy

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    Types of Necrosis:

    1) Coagulative necrosis e.g. any organ infarction except

    the brain.2) Liquefactive necrosis e.g. brain infarction & abscess.

    3) Caseous necrosis e.g. secondary tuberculosis.

    4) Fat necrosis:

    A. Traumatic fat necrosis: e.g. trauma to the female

    breast.

    B. Enzymatic fat necrosis: e.g. Acute hemorrhagic

    pancreatitis.5) Gangrenous necrosis:

    A. Dry gangrene: e.g. in exposed areas as in limbs.

    B. Moist or Wet gangrene:in internal organs as intestine.

    Prof. Dr. Ahmed Elrashedy

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    I) Coagulative Necrosis

    Incidence:

    The most common type of necrosis.

    Pathogenesis:Sudden severe ischemia Denaturation of

    cellular proteins that blocks the proteolysis

    of these dead cells Removal of the

    necrotic cells either by fragmentation &phagocytosis of the cellular debris by

    phagocytic leukocytes.

    Pathology:

    A. Gross: The necrotic tissue appears:1.Firm.

    2.Pale.

    3.Triangular with base towards the capsule

    of the organ.

    Prof. Dr. Ahmed Elrashedy

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    B.L/M (City of Ghosts): This means:

    1) Preserved general outline of the cells.

    2) Loss of fine cellular details.

    3) Loss or fragmentation of the cellular nuclei.

    Examples:

    1) Myocardial infarction.

    2) Renal infarction.

    3) Splenic infarction.

    4) Pulmonary infarction.

    5) Suprarenal infarction.

    Complications:

    1) Gangrene (due to invasion of the necrotic

    tissue by saprophytic bacteria).

    2) Loss of function of the necrotic area.

    3) Dystrophic calcification of the necrotic area.

    Pulmonary infarction

    (Darker pink area)

    Myocardial infarction

    Prof. Dr. Ahmed Elrashedy

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    II) Liquefactive Necrosis

    Pathogenesis:

    Ischemia proteolysis (by the action of powerful

    hydrolytic enzymes) that is more prominent (rapidliquefaction) than denaturation of cellular proteins

    Pathology:

    A. Gross: The necrotic tissue appears:

    1.Soft.2.Liquefied & forms a cyst filled with fluid &

    debris.

    B. L/M:

    Like coagulative but with a cystic structure.

    Site:

    Fat-rich tissues as nervous tissue.

    Examples:

    1.Cerebral infarction.

    2.Abscessin any organ particularly brain & breast.

    Cerebral infarction

    Prof. Dr. Ahmed Elrashedy

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    III) Caseous Necrosis

    Pathogenesis:

    Denaturation of the cellular proteins with slow

    liquefaction i.e. it is a combination of coagulative &liquefactive necrosis.

    Pathology:

    A. Gross: The necrotic tissue appears

    1) Soft.

    2) Friable.3) Cheesy yellowish gray poultaciouslike debris,

    hence, the name caseous necrosis.

    B. L/M:

    Homogenous structureless pink material surrounded by

    a chronic inflammatory granulomatous reaction formed

    of lymphocytes, plasma cells, histiocytes, giant cells

    (Langhans)& fibroblasts.

    Example:

    Secondary T.B.

    2ry Pulmonary T.B.

    2ry T.B. Encephalitis

    Prof. Dr. Ahmed Elrashedy

    f h d El h d

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    IV) Gangrenous Necrosis

    Pathogenesis:

    1. Sudden ischemia Denaturationof cellular proteins together with

    liquefaction of the dead tissue by

    the bacteria & recruited

    inflammatory leucocytes

    (heterolysis).

    2. When denaturation is more

    prominent, the process is termeddry gangrene but when liquefaction

    is more pronounced, the process is

    termed wet or moist gangrene.

    Moist or Wet gangrene inintestine

    Dry gangrene in lower limb

    Prof. Dr. Ahmed Elrashedy

    P f D Ah d El h d

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    IV) Gangrenous Necrosis

    Examples & Pathology:

    1) Dry gangrene in lower limbs:

    Occlusion of the artery with opening of

    both venous & lymphatic drainage

    adequate drainage of the offensive

    gangrenous fluid through these opened

    vessels dry shriveled gangrenous part.

    2) Moist or Wet gangrene in internal

    organs as intestine:

    There is obstruction of both venousdrainage & accompanied artery ,thus, no

    drainage of the offensive gangrenous

    fluid that accumulates in the affected part

    causing its swelling & enlargement.

    Moist or Wet gangrene in

    intestine

    Prof. Dr. Ahmed Elrashedy

    Dry gangrene in lower limb

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    V) Fat Necrosis

    Pathogenesis:

    Increased lipolysis in fat rich organs

    occurring by trauma or release & activation of

    lipase by damage of the pancreatic duct.

    Examples:

    1.Traumatic fat necrosis:

    e.g. Trauma to a female breast.

    Pathology:

    Trauma activates lipolysis that liquefies fatty

    tissue which is surrounded by a granulomatous

    reaction formed of lipid-laden or foamy

    macrophages (phagocytic cells eating liquefied

    lipid) together with lymphocytes, plasma cells,

    foreign body giant cells & fibroblasts.

    Traumatic fat necrosis in

    breast

    Prof. Dr. Ahmed Elrashedy

    P f D Ah d El h d

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    V) Fat Necrosis

    2) Enzymatic fat necrosis: e.g. Acute

    hemorrhagic pancreatitis (Acute

    pancreatic necrosis):

    This is accompanied with a release &

    activation of pancreatic lipase destruction

    & lysis of the pancreatic tissue as well asthe fat depots throughout the abdomen

    (Omentum & fat about the pancreas)

    causing Disintegration of the neutral

    fat into free fatty acids which combineswith intestinal calcium forming

    calcium soaps (Chalky white deposits on

    the intestine).

    Prof. Dr. Ahmed Elrashedy

    P f D Ah d El h d

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    2) Enzymatic fat necrosis

    Pathology:

    Gross: The affected intestine is:1. Firm.

    2. Shows chalky white foci.

    L/M:1) Shadow of lipolyzed necrotic tissue

    surrounded by an inflammatory reaction

    formed of lipid-laden macrophages,lymphocytes , plasma cells & giant cells.

    2) Amorphous bluish calcified areas

    (stained black by Van Kossa stain).

    Prof. Dr. Ahmed Elrashedy

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    Prof. Dr. Ahmed Elrashedy