After discussing cellular adaptation, Cellular Injury, and Cellular Damage, today I will be discussing cellular death. I said that our cells have the ability to adapt to a certain level of stress using mechanisms that can be hyperplasia, hypertrophy, or metaplasia, but when this stress becomes too much and the threshold of the cell is exceeded, cellular injury is experienced. This damage can be either in the reversible stage or in the irreversible stage. In the reversible stage, the cells can swell up as a result of sodium, potassium, and ATP pumps not functioning. If the stress is removed, reversible cell injuries can go back to a normal state. The irreversible damage is a result of cellular and membrane damage and this will lead to cell death.
The mophological hallmark of cell death is the loss of the cell's nucleus which is the main component of the cell. For the nucleus to die, it starts shrinking in size, a process known as pyknosis. Once the nucleus shrinks, it starts to break into smaller pieces known as Karyorrhexis followed by karyolysis where the cell is degraded leaving the cell empty and the cell is dead. Cell death can be caused by necrosis or apoptosis. Necrosis is when there is a large-scale type of cell death. This cell death happens in large percentages due to uncontrolled cellular degradation. With cellular necrosis, enzymes responsible for controlled death are inactivated. The cell dies even when the cell doesn't intend to die but an external effect leads to the death. Cell Necrosis occurs by releasing intracellular components when the cell membrane bursts, and since the death is not a controlled type of death, it usually leads to inflammation since the process is not physiological rather it is pathological and the body tries to fight the process. Apoptosis on the other hand is different. It doesn't have to do with the non-physiological types of death. This type of death is controlled by the cell and it is known as programmed cell death. This process requires ATP and other genes to kill the cell. When a cell isn't working properly, it can be killed by the white blood cell and an example of apoptosis is cell-mediated cell death (CD8+T-cells) Let's explain Cell Necrosis properly.
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Cellular Necrosis has to do with cell death on a large scale caused by exogenous cell injury thereby causing uncontrolled cellular injury and cell death. This death is usually a result of an underlying factor such as infection. There are several different types of cell Necrosis, and they include Coagulative, Liquefactive, Caseous, Gangrenous, fat, and fibrinoid types of Necrosis.
Coagulative necrosis occurs in firm tissues or organs like the kidney, or liver. When these cells die, they coagulate their cell protein to preserve their shape. Coagulative necrosis occurs as a result of Ischemic infarction (where there is not enough blood supply going into the organ or a region of the organ) and this leaves the region pale and the organ having a wedge-shape. Coagulative Necrosis leads to the denaturing of the enzymes in the region, and proteolysis blockage. This type of death preserves the cellular architecture, although its nucleus is dead. This death leads to an increase in the cytoplasmic binding of eosin stain.
Liquefactive Necrosis is another cellular necrosis that occurs in soft tissues such as the brain. This is a result of the enzymatic lysis of cells and the proteins around the cells. These can happen in brain infarction, Abscesses, and pancreatitis. This condition is an enzyme-mediated condition.
Caseous Necrosis are necrosis of solid orgams and it is a combination of coagulative and liquefactive necrosis which occurs as a result of infections such histoplasma capsulatum, and nocardia. With this necrosis, the macrophages tries to wall off the infesting organism causing granular debris which looks like cottage-cheese.
Gangrenous necrosis are necrosis that occur at the tissues of extremities, the Gastrointestinal tract, and this necrosis can be either coagulative or liquefactive, and it is often found in diabetic patient. This necrosis can be dry gangrene or wet gangrene where dry gangrenes are associated with coagulative necrosis, and it is not associated with infection, while wet gangrene are assosiated with liquefactive necrosis and associated with infection.
Fat Necrosis is associated with fat tissues. This is when the fat tissue becomes necrotic causing the fat tissue to become a hard mass as the dead cells release lipase which breaks down triglycerides releasing fatty acid which binds with calcium making the tissues hard. This necrosis occurs in the breast and in the pancrease.
Fibrinoid necrosis occurs when tissues in the blood wall become necrotic which is usually as a result of proteins leaking from the blood vessels as a result of hypertension, polyarteritis nodosa, or pre-eclampsia. The immune complexes combines with fibrin which leads to vessel wall damage. This will cause the blood vessels to be thick.
https://www.ncbi.nlm.nih.gov/books/NBK430935/
https://www.ncbi.nlm.nih.gov/books/NBK557627/
https://scialert.net/fulltext/?doi=ajava.2015.646.668
https://www.ncbi.nlm.nih.gov/books/NBK560552/
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC500549/pdf/jclinpath00243-0079.pdf
https://study.com/academy/lesson/fibrinoid-necrosis-definition-symptoms-treatment.html