Page 32 - Concise Pathology for Exam Preparation ( PDFDrive )

1 Cell Injury and Cell Death 17

TABLE 1.4. Differences between coagulative and liquefactive necrosis

Features Coagulative necrosis Liquefactive necrosis
Cause Hypoxic/ischaemic injury in all tissues ex- • Bacterial and fungal infections
cept in brain, eg, myocardial, renal or • Hypoxic injury in brain
placental infarction
Tissue architecture Tissue architecture is preserved; the basic Both cell outline and intracellular details are
outline of cell is intact, although cytoplas- lost; tissue architecture is not preserved
mic and nuclear details are lost
Pathogenesis Due to intracellular acidosis, structural as Hydrolytic enzymes from bacteria and fungi
well as enzymatic proteins are denatured as well as inflammatory cells cause com-
and proteolysis is blocked; dead cells plete digestion of dead cells and forma-
are removed by fragmentation and phago- tion of pus (lysis)
cytosis
Morphology Conversion of cells into acidophilic, coagu- No cellular outline/tissue architecture recog-
lated, anucleate units nized

Q. Differentiate between coagulative and caseous necrosis.

Ans. Differences between coagulative and caseous necrosis are shown in Table 1.5.

TABLE 1.5. Differences between coagulative and caseous necrosis

Features Coagulative necrosis Caseous necrosis
Cause Hypoxia Tuberculous infection of lymph nodes,
lungs, skin, etc.
Pathogenesis Due to intracellular acidosis, structural as Delayed hypersensitivity reaction to myco-
well as enzymatic proteins are denatured bacterial capsular antigens
and proteolysis is blocked
Gross Affected tissue is firm in texture Cheesy white appearance
Tissue architecture Preserved Completely obliterated

Q. Differentiate between dry and wet gangrene.

Ans. Differences between dry and wet gangrene are shown in Table 1.6.

TABLE 1.6. Differences between dry and wet gangrene
Features Dry gangrene Wet gangrene
Cause Mainly arterial occlusion (coagulative ne- More in venous occlusion; obstruction in-
crosis) variably followed by secondary bacterial
infection (liquefactive necrosis)
Distribution Limbs More common in bowel
Gross appearance Organ is dry, shrunken and black Moist, soft, swollen
Line of demarcation Present at junction between healthy and Not clear
gangrenous parts
Putrefaction Limited (no infection and less blood supply) Marked
Presence of bacteria Absent, little or no septicaemia Overwhelming septicaemia present
Prognosis Better Poor

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