week 8 necrosis.pdf

8/10/2019 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

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.



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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


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


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


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


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).


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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week 8 necrosis.pdf

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