Normal cells that are subject to a damaging stimulus may become sublethally damaged. If the stimulus abates, cells recover but if it continues, cells die and undergo necrosis. Massively damaging stimuli, e.g. great heat or strong acids, cause immediate - PowerPoint PPT Presentation

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Normal cells that are subject to a damaging stimulus may become sublethally damaged. If the stimulus abates, cells recover but if it continues, cells die and undergo necrosis. Massively damaging stimuli, e.g. great heat or strong acids, cause immediate

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Title: Normal cells that are subject to a damaging stimulus may become sublethally damaged. If the stimulus abates, cells recover but if it continues, cells die and undergo necrosis. Massively damaging stimuli, e.g. great heat or strong acids, cause immediate


1
Normal cells that are subject to a damaging
stimulus may become sublethally damaged. If the
stimulus abates, cells recover but if it
continues, cells die and undergo necrosis.
Massively damaging stimuli, e.g. great heat or
strong acids, cause immediate death of
cells without any sublethal damage. Certain
special stimuli can cause pathological
cell death by switching on apoptosis (see
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Cell death,
  • is one of the most crucial events in the
    evolution of disease of any tissue or organ.

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Causes of cell injury
  • External causes
  • gross physical violence of an automobile accident
    to
  • internal endogenous causes,
  • a subtle genetic mutation causing lack of a vital
    enzyme that impairs normal metabolic function.

5
Physical Agents.
  • Prick of a thorn
  • mechanical trauma,
  • extremes of temperature (burns and deep cold),
  • sudden changes in atmospheric pressure,
  • radiation,
  • electric shock

6
Chemical Agents and Drugs
  • Simple chemicals such as glucose or salt in
    hypertonic concentrations may cause cell injury
    directly or by deranging electrolyte balance
  • Even oxygen, in high concentrations, is severely
    toxic.
  • Trace amounts of agents known as poisons, such as
    arsenic, cyanide, or mercuric salts, may destroy
    sufficient numbers of cells within minutes to
    hours to cause death.

7
Chemical Agents and Drugs
  • environmental and air pollutants,
  • insecticides, and herbicides
  • industrial and occupational hazards, such as
    carbon monoxide and asbestos
  • social stimuli, such as alcohol and narcotic
    drugs
  • variety of therapeutic drugs.

8
Infectious Agents.
  • viruses
  • tapeworms. rickettsiae,
  • bacteria,
  • fungi,

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Immunologic Reactions.
  • immune system serves an essential function in
    defense against infectious pathogens,
  • immune reactions may, in fact, cause cell
    injury.
  • The anaphylactic reaction to a foreign protein or
    a drug is a prime example,
  • reactions to endogenous self-antigens are
    responsible for a number of autoimmune disease

10
Oxygen Deprivation.
  • Hypoxia is a deficiency of oxygen, which causes
    cell injury by reducing aerobic oxidative
    respiration.
  • Hypoxia is an extremely important and common
    cause of cell injury and cell death.

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hypoxia is inadequate oxygenation
  • cardiorespiratory failure.
  • Loss of the oxygen-carrying capacity of the
    blood, as in anemia or
  • carbon monoxide poisoning (producing a stable
    carbon monoxyhemoglobin that blocks oxygen
    carriage),
  • Depending on the severity of the hypoxic state,
    cells may adapt, undergo injury, or die.
  • if the femoral artery is narrowed, the skeletal
    muscle cells of the leg may shrink in size
    (atrophy).
  • a balance between metabolic needs and the
    available oxygen supply may be achieved. More
    severe hypoxia induces injury and cell death.

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ischemia
  • loss of blood supply from impeded arterial flow
    or reduced venous drainage in a tissue.
  • Ischemia compromises the supply not only of
    oxygen, but also of metabolic substrates,
    including glucose (normally provided by flowing
    blood).
  • ischemic tissues are injured more rapidly and
    severely than are hypoxic tissues.

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Genetic Derangements.
  • genetic injury may result in a defect as severe
    as the congenital malformations associated with
    Down syndrome, caused by a chromosomal
    abnormality,
  • subtle as the decreased life of red blood cells
    caused by a single amino acid substitution in
    hemoglobin S in sickle cell anemia.
  • Variations in the genetic makeup can also
    influence the susceptibility of cells to injury
    by chemicals and other environmental insults.

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Nutritional Imbalances.
  • Protein-calorie deficiencies
  • Deficiencies of specific vitamins
  • Nutritional problems can be self-imposed
  • as in anorexia nervosa or
  • self-induced starvation.
  • nutritional excesses have also become important
    causes of cell injury.

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Nutritional Imbalances.
  • Excesses of lipids predispose to atherosclerosis,
  • obesity is a manifestation of the overloading of
    some cells in the body with fats.
  • In addition to the problems of under nutrition
    and over nutrition, the composition of the diet
    makes a significant contribution to a number of
    diseases.
  • Metabolic diseases such as diabetes also cause
    severe cell injury.

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Reversible injury
  • generalized swelling of the cell and its
    organelles
  • blebbing of the plasma membrane
  • detachment of ribosomes from the endoplasmic
    reticulum
  • and clumping of nuclear chromatin.
  • Laminated structures (myelin figures) derived
    from damaged membranes of organelles and the
    plasma membrane appear

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irreversible injury
  • increasing swelling of the cell
  • disruption of cellular membranes
  • swelling and disruption of lysosomes
  • presence of large amorphous densities in swollen
    mitochondria
  • and profound nuclear changes.
  • The latter include nuclear codensation
    (pyknosis),
  • followed by fragmentation (karyorrhexis)
  • and dissolution of the nucleus (karyolysis).
  • Laminated structures (myelin figures) become
    more pronounced in irreversibly damaged cells.

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Proverb of this week
Necessity is the mother of invention
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There are two principal patterns of cell death,
necrosis and apoptosis.
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cell death the morphological pattern of which is
called necrosis occurs after such abnormal
stresses as ischemia and chemical injury, and it
is always pathological.
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Apoptosis occurs when a cell dies through
activation of an internally controlled suicide
program.
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Physiological
  • It is designed to eliminate unwanted cells during
    embryogenesis
  • and in various physiologic processes, such as
    involution of hormone-responsive tissues upon
    withdrawal of the hormone.

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Pathological apoptosis
  • Immunological injuries

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9 The sequential ultrastructural changes seen in
necrosis (left) and apoptosis (right). In
apoptosis, the initial changes consist of nuclear
chromatin condensation and fragmentation,
followed by cytoplasmic budding and phagocytosis
of the extruded apoptotic bodies.
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Feature Necrosis Apoptosis
Cell size Enlarged (swelling) Reduced (shrinkage)
Nucleus Pyknosis ? karyorrhexis ? karyolysis Fragmentation into nucleosome size fragments
Plasma membrane Disrupted Intact altered structure, especially orientation of lipids
Cellular contents Enzymatic digestion may leak out of cell Intact may be released in apoptotic bodies
Adjacent inflammation Frequent No
Physiologic or pathologic role Invariably pathologic (culmination of irreversible cell injury) Often physiologic, means of eliminating unwanted cells may be pathologic after some forms of cell injury, especially DNA damage
Table 1-2. Features of Necrosis and Apoptosis
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Mechanism of injury
  • The cellular response to injurious stimuli
    depends on
  • the type of injury,
  • its duration, and
  • its severity
  • depend on
  • the type,
  • state,
  • and adaptability of the injured cell.
  • The cell's nutritional and hormonal status
  • and its metabolic needs.

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Mechanism of injury
  • How vulnerable is a cell, for example, to loss of
    blood supply and hypoxia?
  • The striated muscle cell is less vulnerable to
    deprivation of its blood supply not so the
    striated muscle of the heart.
  • Exposure of two individuals to identical
    concentrations of a toxin, such as carbon
    tetrachloride, may produce no effect in one and
    cell death in the other.
  • This may be due to genetic variations affecting
    the amount and activity of hepatic enzymes that
    convert carbon tetrachloride to toxic byproducts

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targets of injury
  • aerobic respiration involving mitochondrial
    oxidative phosphorylation and production of ATP
  • the integrity of cell membranes, on which the
    ionic and osmotic homeostasis of the cell and its
    organelles depends
  • protein synthesis
  • the integrity of the genetic apparatus of the
    cell

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Cellular and biochemical sites of damage in cell
injury
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Mechanism of injury
  • DEPLETION OF ATP
  • MITOCHONDRIAL DAMAGE
  • INFLUX OF CALCIUM AND LOSS OF CALCIUM HOMEOSTASIS
  • ACCUMULATION OF OXYGEN-DERIVED FREE RADICALS
    (OXIDATIVE STRESS)
  • DEFECTS IN MEMBRANE PERMEABILITY

35
DEPLETION OF ATP
Functional and morphologic consequences of
decreased intracellular ATP during cell injury.
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INFLUX OF CALCIUM AND LOSS OF CALCIUM HOMEOSTASIS

37
INFLUX OF INTRACELLULAR CALCIUM AND LOSS OF
CALCIUM HOMEOSTASIS
Sources and consequences of increased cytosolic
calcium in cell injury. ATP, adenosine
triphosphate.
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ACCUMULATION OF OXYGEN-DERIVED FREE RADICALS
(OXIDATIVE STRESS)
39
Reversible vs. irreversible cell injury
  • there are clearly many ways to injure a cell,
  • the "point of no return," at which irreversible
    damage has occurred, is still largely
    undetermined
  • thus, we have no precise cut-off point
  • dissolution of the injured cell is characteristic
    of necrosis, one of the recognized patterns of
    cell death.
  • There is also widespread leakage of potentially
    destructive cellular enzymes into the
    extracellular space, with damage to adjacent
    tissues

40
Reversible vs. irreversible cell injury
  • leakage of intracellular proteins across the
    degraded cell membrane into the peripheral
    circulation provides a means of detecting
    tissue-specific cellular injury and death using
    blood serum samples.
  • Cardiac muscle, for example, contains a specific
    isoform of the enzyme creatine kinase and of the
    contractile protein troponin
  • liver (and specifically bile duct epithelium)
    contains a temperature-resistant isoenzyme of the
    enzyme alkaline phosphatase
  • and hepatocytes contain transaminases.
  • Irreversible injury and cell death in these
    tissues are consequently reflected in increased
    levels of such proteins in the blood.

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Nuclear changes in necrosis
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Necrosis
  • Necrosis refers to a spectrum of morphologic
    changes that follow cell death in living tissue,
  • resulting from the progressive degradative action
    of enzymes on the lethally injured cell (cells
    placed immediately in fixative are dead but not
    necrotic
  • Necrotic cells are unable to maintain membrane
    integrity and their contents often leak out.
  • This may elicit inflammation in the surrounding
    tissue.

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Necrosis
  • The morphologic appearance of necrosis is the
    result of
  • denaturation of intracellular proteins and
  • enzymatic digestion of the cell.
  • The enzymes are derived either from the lysosomes
    of the dead cells themselves, in which case the
    enzymatic digestion is referred to as autolysis,
  • or from the lysosomes of immigrant leukocytes,
    during inflammatory reactions.
  • These processes require hours to develop, and so
    there would be no detectable changes in cells ,

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for example, a myocardial infarct caused sudden
death.
  • The only telling evidence might be occlusion of a
    coronary artery.
  • The earliest histologic evidence of myocardial
    necrosis does not become manifest until 4 to 12
    hours later,
  • but cardiac-specific enzymes and proteins that
    are released from necrotic muscle can be detected
    in the blood as early as 2 hours after myocardial
    cell death.

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Necrosis
  • Necrotic cells show increased eosinophilia
  • Loss of ribosomes responsible for the of the
    normal basophilia imparted by the RNA in the
    cytoplasm
  • increased binding of eosin to denatured
    intracytoplasmic proteins
  • The necrotic cell may have a more glassy
    homogeneous appearance than that of normal cells,
  • mainly as a result of the loss of glycogen
    particles.
  • the cytoplasm becomes vacuolated and appears
    moth-eaten.
  • enzymes have digested the cytoplasmic organelles,
  • Finally, calcification of the dead cells may
    occur.

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Necrosis
  • myelin figures
  • Dead cells may ultimately be replaced by large,
    whorled phospholipid masses
  • These phospholipid precipitates are then either
    phagocytosed by other cells or further degraded
    into fatty acids
  • calcification of such fatty acid residues
    results in the generation of calcium soaps.

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Necrosis
  • Nuclear changes appear in the form of one of
    three patterns,
  • due to nonspecific breakdown of DNA
  • A pattern (also seen in apoptotic cell death) is
    pyknosis, characterized by nuclear shrinkage and
    increased basophilia.
  • A pattern, known as karyorrhexis, the pyknotic or
    partially pyknotic nucleus undergoes
    fragmentation.
  • A pattern The basophilia of the chromatin may
    fade (karyolysis), a change that presumably
    reflects DNase activity.
  • With the passage of time (a day or two), the
    nucleus in the necrotic cell totally disappears.

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Once the necrotic cells have undergone the early
alterations, the mass of necrotic cells may have
several morphologic patterns.
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Necrosis
  • . coagulative necrosis When denaturation is
    the primary pattern
  • liquefactive necrosis
  • dominant enzyme digestion,
  • caseous necrosis
  • fat necrosis
  • in special circumstances,

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Coagulative necrosis
  • preservation of the basic outline of the
    coagulated cell for a span of at least some days
  • The affected tissues exhibit a firm texture.
  • the injury or the subsequent increasing
    intracellular acidosis has denatured not only
    structural proteins but also enzymes
  • Blocking of the proteolysis of the cell.

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Coagulative necrosis
  • The heart is an excellent example
  • acidophilic, coagulated, anucleate cells may
    persist for weeks.
  • the necrotic myocardial cells are removed by
    fragmentation and phagocytosis of the cellular
    debris
  • scavenger leukocytes and by the action of
    proteolytic lysosomal enzymes brought in by the
    immigrant white cells.
  • The process of coagulative necrosis, with
    preservation of the general tissue architecture,
    is characteristic of hypoxic death of cells in
    all tissues except the brain

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Micrograph shows a section of liver damaged
by the poison paraquat. Normal liver cells
contrast with injured cells, which are
swollen, pale and vacuolated.
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The normal Cells cell cytoplasm is pink with
a a decrease of purple, the purple coloration
(basophilia) being due to ribosomes, mainly on
the RER
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Damaged cells . With swelling of ER, ribosomes
become detached and reduced in number, so the
normal purple cytoplasmic tint is reduced.

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  • Apoptosis is a more orderly process of cell death
    in which there is individual cell necrosis, not
    necrosis of large numbers of cells. liver cells
    are dying individually (arrows) from injury by
    viral hepatitis. The cells are pink and without
    nuclei.

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  • Here is myocardium in which the cells are dying.
    The nuclei of the myocardial fibers are being
    lost. The cytoplasm is losing its structure,
    because no well-defined cross-striations are
    seen.

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  • This is an example of coagulative necrosis. This
    is the typical pattern with ischemia and
    infarction (loss of blood supply and resultant
    tissue anoxia). Here, there is a wedge-shaped
    pale area of coagulative necrosis (infarction) in
    the renal cortex of the kidney.

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  • Microscopically, the renal cortex has undergone
    anoxic injury at the left so that the cells
    appear pale and ghost-like. There is a
    hemorrhagic zone in the middle where the cells
    are dying or have not quite died, and then normal
    renal parenchyma at the far right. This is an
    example of coagulative necrosis

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Figure 1-19 Coagulative. A, Kidney infarct
exhibiting coagulative necrosis, with loss of
nuclei and clumping of cytoplasm but with
preservation of basic outlines of glomerular and
tubular architecture.
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  • Two large infarctions (areas of coagulative
    necrosis) are seen in this sectioned spleen.
    etiology of coagulative necrosis is usually
    vascular with loss of blood supply,
  • the infarct occurs in a vascular distribution.
  • Thus, infarcts are often wedge-shaped with a base
    on the organ capsule.

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Cell Injury                                     
                                                  
                                        
  • The contrast between normal adrenal cortex and
    the small pale infarct is good. The area just
    under the capsule is spared because of blood
    supply from capsular arterial branches. This is
    an odd place for an infarct, but it illustrates
    the shape and appearance of an ischemic (pale)
    infarct well

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Liquefactive necrosis
  • is characteristic of focal bacterial or,
    occasionally, fungal infections, because microbes
    stimulate the accumulation of inflammatory cells
  • For obscure reasons, hypoxic death of cells
    within the central nervous system often evokes
    liquefactive necrosis.
  • Whatever the pathogenesis, liquefaction
    completely digests the dead cells.
  • The end result is transformation of the tissue
    into a liquid viscous mass.
  • If the process was initiated by acute
    inflammation the material is frequently creamy
    yellow because of the presence of dead white
    cells and is called pus.

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A focus of liquefactive necrosis in the kidney
caused by fungal infection. T he focus is filled
with white cells and cellular debris, creating a
renal abscess that obliterates the normal
architecture. liquefactive necrosis in the
kidney caused by fungal infection. The focus is
filled with white cells and cellular debris,
creating a renal abscess that obliterates the
normal architecture.
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  • The liver shows a small abscess here filled with
    many neutrophils. This abscess is an example of
    liquefactive necrosis.

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  • Grossly, the cerebral infarction at the upper
    left here demonstrates liquefactive necrosis.
    Eventually, the removal of the dead tissue leaves
    behind a cavity.

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  • As this infarct in the brain is organizing and
    being resolved, the liquefactive necrosis leads
    to resolution with cystic spaces.

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  • This is liquefactive necrosis in the brain in a
    patient who suffered a "stroke" with focal loss
    of blood supply to a portion of cerebrum. This
    type of infarction is marked by loss of neurons
    and neuroglial cells and the formation of a clear
    space at the center left.

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gangrenous necrosis
  • It is usually applied to a limb, generally the
    lower leg, that has lost its blood supply and has
    undergone coagulative necrosis.

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  • This is gangrene, or necrosis of many tissues in
    a body part. In this case, the toes were involved
    in a frostbite injury. This is an example of
    "dry" gangrene in which there is mainly
    coagulative necrosis from the anoxic injury.

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wet gangrene).
  • When bacterial infection is superimposed,
    coagulative necrosis is modified by the
    liquefactive action of the bacteria and the
    attracted leukocytes

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  • This is gangrene of the lower extremity. In this
    case the term "wet" gangrene is more applicable
    because of the liquefactive component from
    superimposed infection in addition to the
    coagulative necrosis from loss of blood supply.
    This patient had diabetes mellitus.

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Caseous necrosis
  • a distinctive form of coagulative necrosis,
    encountered most often in foci of tuberculous
    infection
  • caseous is derived from the cheesy white gross
    appearance of the area of necrosis

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A tuberculous lung with a large area of caseous
necrosis. The caseous debris is yellow-white and
cheesy.
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  • This is the gross appearance of caseous necrosis
    in a hilar lymp node infected with tuberculosis.
    The node has a cheesy tan to white appearance.
    Caseous necrosis is really just a combination of
    coagulative and liquefactive necrosis that is
    most characteristic of granulomatous inflammation.

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  • This is more extensive caseous necrosis, with
    confluent cheesy tan granulomas in the upper
    portion of this lung in a patient with
    tuberculosis. The tissue destruction is so
    extensive that there are areas of cavitation
    (cystic spaces) being formed as the necrotic
    (mainly liquefied) debris drains out via the
    bronchi.

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  • Microscopically, caseous necrosis is
    characterized by acellular pink areas of
    necrosis, as seen here at the upper right,
    surrounded by a granulomatous inflammatory
    process.

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microscopic examination,
  • the necrotic focus appears as amorphous granular
    material
  • looks like composed of fragmented, coagulated
    cells
  • amorphous granular debris enclosed within a
    distinctive inflammatory border known as a
    granulomatous reaction
  • Unlike coagulative necrosis, the tissue
    architecture is completely obliterated.

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Fat necrosis
  • acute pancreatitis
  • activated pancreatic enzymes escape from acinar
    cells and ducts,
  • the activated enzymes liquefy fat cell membranes,
  • the activated lipases split the triglyceride
    contained within fat cells.
  • The released fatty acids combine with calcium to
    produce grossly visible chalky white areas (fat
    saponification),

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  • This is fat necrosis of the pancreas. Cellular
    injury to the pancreatic acini leads to release
    of powerful enzymes which damage fat by the
    production of soaps, and these appear grossly as
    the soft, chalky white areas seen here on the cut
    surfaces.

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Foci of fat necrosis with saponification in the
mesentery. The areas of white chalky deposits
represent calcium soap formation at sites of
lipid breakdown.
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Fat necrosis
  • the surgeon and the pathologist can identify the
    lesions
  • focal areas of fat destruction, typically
    occurring as a result of release of activated
    pancreatic lipases into the substance of the
    pancreas and the peritoneal cavity.

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  • Microscopically, fat necrosis is seen here.
    Though the cellular outlines vaguely remain, the
    fat cells have lost their peripheral nuclei and
    their cytoplasm has become a pink amorphous mass
    of necrotic material.

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Fat necrosis/ On histologic examination,
  • the necrosis takes the form of foci of shadowy
    outlines of necrotic fat cells,
  • with basophilic calcium deposits,
  • surrounded by an inflammatory reaction.

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Final outcome
  • in the living patient, most necrotic cells and
    their debris disappear
  • enzymatic digestion
  • fragmentation,
  • phagocytosis of the particulate debris by
    leukocytes.
  • If necrotic cells and cellular debris are not
    promptly destroyed and reabsorbed, they tend to
    attract calcium salts and other minerals and to
    become calcified.
  • This phenomenon, called dystrophic calcification,

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Fibrinoid necrosis
  • is a term used to describe the
  • histological appearance of arteries in cases
    of vasculitis
  • (primary inflammation of vessels) and
    hypertension,
  • when fibrin is deposited in the damaged
    necrotic vessel wall

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  • The small intestine is infarcted. The dark red to
    grey infarcted bowel contrasts with the pale pink
    normal bowel at the bottom. Some organs such as
    bowel with anastomosing blood supplies, or liver
    with a dual blood suppy, are hard to infarct.
    This bowel was caught in a hernia and the
    mesenteric blood supply was constricted by the
    small opening to the hernia sac.

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Haemorrhagic necrosis
  • describes dead tissues that are suffused with
    extravasated red cells.
  • This pattern is
  • seen particularly when cell death is due to
    blockage of
  • the venous drainage of a tissue, leading to
    massive congestion by blood and to subsequent
    arterial failure of perfusion

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Gummatous necrosis
  • tissue is firm and rubbery. As in caseous
    necrosis the dead
  • cells form an amorphous proteinaceous mass
  • no original architecture can be seen
    histologically.
  • However, the gummatous pattern is restricted
    to describing necrosis in the spirochaetal
    infection
  • syphilis

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Patterns of reversible cell injury
  • cellular swelling
  • fatty change.

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Cellular swelling
  • Cellular swelling appears whenever cells are
    incapable of maintaining ionic and fluid
    homeostasis
  • and is the result of loss of function of plasma
    membrane energy-dependent ion pumps.

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Fatty change
  • Fatty change occurs in hypoxic injury and various
    forms of toxic or metabolic injury.
  • It is manifested by the appearance of small or
    large lipid vacuoles in the cytoplasm and occurs
    in hypoxic and various forms of toxic injury.
  • It is principally encountered in cells involved
    in and dependent on fat metabolism, such as the
    hepatocyte and myocardial cell.

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3 Reactive oxygen metabolites damage cells
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