How cell injury happens and what is the result?

A normal cell has a general organization at a chemical level that involves atoms, molecules moving around in complex fashion that ultimately is critical to the way we live. The cell membrane and various organelles such as the mitochondria all have vital roles to play.

At the cellular level, injury is a result of three basic causes: deficiency, intoxication, or trauma. A deficiency is when the cell lacks a compound of a sort that causes interference with function such as when there’s a dietary deficiency of B vitamins. Intoxication is when a compound present actually poisons the cell, interfering with function such as when a biological infection, or toxic product in the cell like barbiturates. Trauma is when there is actual physical injury to the cell, causing loss of cell integrity such as hypothermia causing ice crystals or hyperthermia causing denaturation of cellular proteins.

The cell can respond in various ways by adapting with reversible (functional or structural) and, sometimes, irreversible (structural or deadly) changes.

The reversible may include alternative metabolisms such as in hypoxia when the cell changes from oxidative phosphorylation to glycolysis, or with altered size as in hypertrophy when demand increases. Reversible changes also include apoptosis that reduces cell numbers, production of cell-stress proteins (like heat stress or heat shock proteins) or organelle changes to make certain enzymes available as in detoxification.

There are also fatty changes as in the liver, residual bodies that are derived from phagosomes when lysosomes aren’t enough, and hyaline changes when proteins accumulate in a cell.

Structural reversible changes include blebs that project out of a cell and myelin figures that are membrane structural abnormalities.

Irreversible injury to cells involve unrecoverable structural changes to the cell membrane causing increased permeability or spillage. It can also involve similar changes to mitochondrial membranes or the structure of other organelles.

Cell death is an irreversible injury called necrosis. Unlike apoptosis, it’s not programmed. It can happen due to coagulation, when proteins are denatured quickly because of acid, heat or enzymes. Caseous necrosis happens as a type of coagulation necrosis in tuberculosis causing a cheeselike appearance. Gangrenous necrosis is another kind that happens when toxic metabolites of bacteria cause reduced blood flow and produce putrefaction.

If coagulation doesn’t occur, and tissue breaks down quickly because of lysosomal enzymes then liquefaction necrosis has resulted.

Calcification is a deposition of calcium crystals at sites of necrosis. It occurs when cell injury allows calcium into the cell condensing in mitochondria and causing death. The calcium crystals can start out tiny, but become large masses in a process called dystrophic calcification.

And, when calcium is deposited only as a result of excessive calcium, as in hypercalcemia, then metastatic calcification has occurred. Generally, metatstatic calcium deposits are not severe, but can interfere with lung or kidney function.

Reference

Nowak TJ, Hanfod AG. Pathophysiology: Concepts and applications for health care professionals, 3rd ed. 2004. New York, McGraw-Hill.

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