week 8 necrosis.pdf
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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
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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.
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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).
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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.
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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.
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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
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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
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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
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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
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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
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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).
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Prof. Dr. Ahmed Elrashedy