NECROSIS - PATHOLOGY - EASYMEDNOTES 2021

NECROSIS

Any Disturbances from external environment beyond the limits of homeostasis can lead to premature cell death, known as necrosis. 
Necrosis may be caused by ischaemia, infection, poisoning etc.


Types


The types of necrosis include:

• Coagulative necrosis

• Liquefactive necrosis

• Fat necrosis

• Caseous necrosis

• Gangrenous necrosis

Coagulative Necrosis


  •  It is the common type of necrosis and it is caused by ischaemic injury which results in hypoxic death of cells in all tissues except the brain.
  •  On gross examination, the affected tissue will be pale in colour and firm in texture.
  • Microscopically, increased eosinophilia of the cytoplasm and decreased basophilia of the nucleus are seen.

Liquefactive Necrosis 

  • This occurs in situations in which enzymatic breakdown is more prominent than protein denaturation unlike coagulative necrosis.
  •  It is usually associated with bacterial or fungal infections because microbes stimulate the accumulation of leukocytes and liberation of enzymes from these cells.
  •  The tissue is digested and is converted into a liquefied mass, which look like creamy yellow in colour and it is called ‘pus’.
  • Liquefactive necrosis is most commonly seen in organs that have a high-fat and low-protein content like the brain, or those with a high-enzymatic content like the pancreas, and typically causes gangrene of intestine and limbs and hypoxic death in brain.

Gangrenous Necrosis


• Dry gangrene is similar to coagulative necrosis.

• Wet gangrene is similar to liquefactive necrosis.


Caseous Necrosis


  • It is associated with tuberculous infection.
  •  It is also seen in syphilis and coccidioidomycosis
  •  It is a combination of coagulative and liquefactive necrosis.
  • Necrotic material will look like cheese.

Enzymatic fat necrosis


  • Destruction of fat that converts adipocytes into necrotic cells 
  • Shadowy outlines and basophilic calcium deposits are seen.
  • It is seen in acute pancreatitis and traumatic fat necrosis of breast.


Necrosis occurs by the following mechanisms


A. Hypoxia

B. Free radical-induced cell injury

C. Cell membrane damage

D. Increased intracellular calcium level

A. Hypoxia


Hypoxia is decreased oxygen supply to tissues. 
It can be caused by:

1. Ischemia

Ischemia is decreased blood flow to the organ. 
Ischemia can be caused by obstruction of arterial blood flow.
Occurs in cardiac failure, hypotension, & shock.

2. Anemia

Anemia is the reduction in number of oxygen-carrying red blood cells.

3. Carbon monoxide poisoning

CO decreases the oxygen-capacity of red blood cells.

4. Due to the pulmonary diseases, poor oxygenation is seen.

The cell injury that results following hypoxia can be divided into early & late stages:

1. Early-reversible stages of hypoxic cell injury

  • In this stage, hypoxia results in decreased oxidative phosphorylation & ATP synthesis. Decreased ATP leads to: Failure of the cell membrane Na – K pump, which leads to increased intracellular Na & water, which cause cellular  swelling. 
  • Cellular swelling (hydropic change) is characterized by the presence of large vacuoles in the cytoplasm. The endoplasmic reticulum also swells.
  • The mitochondria show a low amplitude swelling.
  • All of the above changes are reversible if the hypoxia is altered.
  •  Disaggregation of ribosomes & failure of protein synthesis.

2. Late-irreversible stages of hypoxic cell injury.

  • It is caused by severe or prolonged injury. 
  • It is caused by massive calcium influx & very low pH, which lead to activation of enzymes and damage the cell membrane & organelle membranes. 
  • Irreversible damage to the mitochondria, cell membranes, & the nucleus mark the point of no return for the cell, that is after this stage, the cell will die.
  • Release of aspartate aminotransferase (AST), creatine phosphokinase(CPK), & lactate dehydrogenase (LDH) into the blood is an important indicator of irreversible injury to heart muscle following myocardial infarction.

B. Free radical-induced injury

  • Free radical is a molecule with a single unpaired electron in the outer orbital. 
  • Examples include superoxide & the hydroxyl radicals. 
  • Free radicals are formed by normal metabolism, oxygen toxicity, ionizing radiation, & drugs & chemicals, & reperfusion injury. 
  • They are degraded by spontaneous decay, intracellular enzymes such as glutathione peroxidase, catalase, or superoxide dismutase, & endogenous substances such as ceruloplasmin or transferrin. 
  • When the production of free radicals exceeds their degradation, the excess free radicals cause membrane pump damage, ATP depletion, & DNA damage. These can cause cell injury & cell death.

C. Cell membrane damage

Direct damage to the cell membrane, as in extremes of temperature, toxins, or viruses,

Or indirect cell membrane damage as of hypoxia can lead to cell death by disrupting the homeostasis of the cell.

D. Increased intracellular calcium level

  • Increased intracellular calcium level is a common pathway via which different causes of cell injury operate. 
  • For example, the cell membrane damage leads to increased intracellular calcium level. The increased cytosolic calcium, activates enzymes in the presence of low pH. 
  • The activated enzymes will degrade the cellular organelles.

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