Necrosis


Necrosis is a spectrum of morphological changes following cell death in a living tissue or organ, resulting from progressive degradation of lethally injured cells by enzymes.

Changes of necrosis may be due to: i) enzymatic digestion; ii) denaturation of proteins.

Enzymatic digestion may be of two types:

i) Autolysis: enzymes are derived from the lysosomes of the dead cells themselves.

ii) Heterolysis: enzymes are derived from immigrant leukocytes.

Nuclear changes seen in necrosis:

i) Pyknosis: condensation of chromatin. (Shrunken mass.)

ii) Karyorrhexis: fragmentation of chromatin.

iii) Karyolysis: dissolution of chromatin by DNAases. (Fading.)

iv) Loss of the nucleus in dead cells. (Takes 1-2 days.)

Types of Necrosis

1.Coagulative Necrosis: Necrosis with the preservation of cellular and tissue architecture.

The nucleus, cytoplasm, and cellular outlines remain intact because it is a slower process.

It occurs in solid organs.

Coagulative Necrosis in Kidney

Coagulative Necrosis

2.Liquefactive Necrosis: Necrosis secondary to focal bacterial infections, which attract polymorphonuclear leukocytes (neutrophils) which release enzymes that fight bacteria but also dissolve (liquefy) nearby tissues.

There is an accumulation of pus (i.e. a mixture of dead and dying polymorphs along with amorphous debris.)

It occurs in soft tissues.

Liquefactive Necrosis in Brain

Liquefactive Necrosis

3.Fat Necrosis: Necrosis caused either by the release of pancreatic enzymes (enzymatic fat necrosis) or due to trauma to fat by a physical blow or by surgery (traumatic fat necrosis.)

Lipases release free fatty acids which combine with calcium to produce detergents (soapy deposits in tissue.)

Macrophages may be found in fat-necrosed tissue.

Enzymatic Fat Necrosis in Pancreas

Enzymatic Fat Necrosis

Traumatic Fat Necrosis of Breast

Traumatic Fat Necrosis

4.Caseous Necrosis: Coagulative necrosis seen in mycobacterial infections or in tumor necrosis; however, coagulated tissue no longer resembles cells but becomes chunks of unrecognizable debris.

A giant cell or granulomatous reaction is often associated with caseous necrosis.

Caseous Necrosis in Lung

Caseous Necrosis

5.Gangrenous Necrosis: Putrefactive coagulative necrosis, which is grossly visible and advanced.

It may be dry gangrene (blackening of tissue) or wet (bacteria infect tissue and cause cells to swell) or gas gangrene (bacteria infect and destroy tissue, producing gas.)

6.Fibrinoid Necrosis: Necrosis in the walls of injured and drying blood vessels, characterized by insudation (leaking) of fibrin from the lumen, across the endothelium, and into the intima and muscle layers.

Possible Outcomes of Necrosis:

i) Autolysis, apoptosis.

ii) Phagocytosis

iii) Organization and fibrous repair.

iv) Dystrophic calcification.

Best Examples of Major Types of Necrosis

Type Example
Coagulative Necrosis Kidney necrosis following blockage of renal artery
Liquefactive Necrosis Necrosis of brain tissue following focal infection
Enzymatic Fat Necrosis Necrosis following acute pancreatitis
Traumatic Fat Necrosis Necrotic breast lump after traumatic injury
Caseous Necrosis Necrosis of lung following Tuberculosis infection
Gangrenous Necrosis ‘Diabetic foot’ necrosis of diabetic patient
Fibrinoid Necrosis Necrosis following vasculitis

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  1. Pingback: Curso de Electrocardiograma | Medicina Familiar

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