In Necrosis, excess fluid enters the cell, swells it, and ruptures its membrane which kills it. After the cell has died, intracellular degradative reactions occur within a living organism. Necrosis does not occur in dead organisms. In dead organisms, autolysis and heterolysis take place.
Apoptosis is the death of single cells within clusters of other cells. (Note that necrosis causes the death of clusters of cells.) In apoptosis, the cell shows shrinkage and increased acidophilic staining of the cell. This is followed by fragmentation of the cells. These fragments are called apoptotic bodies
Necrosis occurs by the following mechanisms:
A. Hypoxia
Hypoxia is decreased oxygen supply to tissues. It can be caused by: Ischemia. Ischemia is decreased blood flow to or from an organ. Ischemia can be caused by obstruction of arterial blood flow the most common cause, or by decreased perfusion of tissues by oxygen-carrying blood as occurs in cardiac failure, hypotension, and shock. Anemia: Anemia is a reduction in the number of oxygen-carrying red blood cells. Carbon monoxide poisoning: CO decreases the oxygen-capacity of red blood cells by chemical alteration of hemoglobin. Poor oxygenation of blood due to pulmonary disease.
B. Free radical-induced cell injury
Free radical is any molecule with a single unpaired electron in the outer orbital. Examples include superoxide and the hydroxyl radicals. Free radicals are formed by normal metabolism, oxygen toxicity, ionizing radiation, and drugs and chemicals, and reperfusion injury. They are degraded by spontaneous decay, intracellular enzymes such as glutathione peroxidase, catalase, or superoxide dismutase, and 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, and DNA damage
C. Cell membrane damage
Direct cell membrane damage as in extremes of temperature, toxins, or viruses, or indirect cell membrane damage as in the case 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, in turn, activates enzymes in the presence of low pH. The activated enzymes will degrade the cellular organelles.
The types of necrosis include:
1. Coagulative necrosis
Cogulative necrosis most often results from sudden interruption of blood supply to an organ, especially to the heart. It is, in early stages, characterized by general preservation of tissue architecture. It is marked by the following nuclear changes: Pyknosis (which is chromatin clumping and shrinking with increased basophilia), karyorrhexis (fragmentation of chromatin), and karyolysis (fading of the chromatin material).
2. Liquefactive necrosis
Liquefactive necrosis is characterized by digestion of tissue. It shows softening and liquefaction of tissue. It characteristically results from ischemic injury to the CNS. It also occurs in suppurative infections characterized by formation of pus.
3. Fat necrosis
Fat necrosis can be caused by trauma to tissue with high fat content, such as the breast or it can also be caused by acute hemorrhagic pancreatitis in which pancreatic enzymes diffuse into the inflamed pancreatic tissue and digest it. The fatty acids released from the digestion form calcium salts (soap formation or dystrophic calcification). In addition, the elastase enzyme digests the blood vessels and cause the hemorrhage inside the pancreas, hence the name hemorrhagic pancreatitis
4. Caseous necrosis
Caseous necrosis has a cheese-like (caseous, white) appearance to the naked eye. And it appears as an amorphous eosinophilic material on microscopic examination. Caseous necrosis is typical of tuberculosis.
5. Gangrenous necrosis
This is due to vascular occlusion and most often affects the lower extremities and the bowel. It is called wet gangrene if it is complicated by bacterial infection which leads to superimposed liquefactive necrosis. Whereas it is called dry gangrene if there is only coagulative necrosis without liquefactive necrosis.
