Discuss how a cell will change or alter itself in response to stress. Address different types of adaptation or change along with what might be the reason that brings about the changes.
A cell will change depending on the stress causing it. Stress to a cell can be caused by changes in temperature, oxygen levels, and toxins (Braun and Anderson, 2006). Cellular responses include a reduction in number, change in size and structure. The different adaptations are addressed below.
Atrophy
This refers to a decrease in the cell size. This may result from a decrease in the number of functions a particular cell produces (Braun and Anderson, 2006). For instance, a scenario where a limb is immobilized in a cast resulting to the impairment of muscle movement. Reduction in oxygen supply also causes a reduction in cell size (Rubin and Strayer, 2011).
Hypertrophy
This refers to an increase in the size of the cell (Braun and Anderson, 2006). The increase in cell size is due to an increase in the functional demands of the cell (Rubin and Strayer, 2011). For example, according to Braun and Anderson (2006), strength-building exercise results to an increase in muscle cell size.
Hyperplasia
According to Braun and Anderson (2006), hyperplasia as a cell-adaption technique refers to an increase in the number of cells. An increase in work activity may result to an increase in the number of cells. In high altitudes, an increase in pressure cause an increase in production of the red blood cells to increase the production of oxygen levels.
Metaplasia
This refers to the changing of one cell type to another (Braun and Anderson, 2006). For example, persistent use of cigarette smoke can cause such a cell change. The persistent smoke causes the columnar cells to change into squamous cells in a process of trying to survive the exposure to the toxins (Braun and Anderson, 2006).
Dysplasia
This is the definite change in cell size, arrangement, uniformity and structure (Braun and Anderson, 2006). This change is caused by abnormal differentiation of cell division. Dysplasia is a cells response to a persistent stressor.
Cell Injury types
Cellular Swelling
Cellular swelling results from an imbalance in the ionic content of the cells (Porth, 2010). The increase in ionic content of the cell results in water accumulating in the cells. Treatment includes reduce the limiting water or increasing sodium intake (Braun and Anderson, 2006).
Fatty Changes
This is the intracellular accumulation of fat (Porth, 2010). This type of cellular injury is more severe than the cellular swelling. Fatty changes arise because of an increase in fats, which the normal cells to handle since injured cells are unable to perform metabolism. Reduction in the consumption of fats helps to change the situation to normal.
Association of recent research to the Pathologic concept of Cellular Injury
Cellular injury is as a result of stress upon cells to perform their actions. According to Samuel and Sitirin (2008), studies conducted in animals have revealed that Vitamin D secosteroids inhibit the growth of many cancers. The vitamin D reduces the cell cycle progression of the cancerous cells. According to Dowd and Stafford (2012), Vitamin D increases the cells resistance. The vitamin D increases release of insulin in the pancreas, which is very critical in preventing diabetes (Dowd and Strafford, 2012). The presence of vitamin D increases the metabolism of fats whose accumulating nay cause cell injury.
Inflammation/Cell Proliferation/Tissue Repair and Regeneration
Labile Cells
Stabile Cells
Permanent cells
These cells are located in tissues that are in a constant state of renewal. Tissues that are composed of labile cells regenerate after injury provide that there are enough stem cells.
Normally found in tissues that are renewed slowly. According to Brooks (2010), these cells have long life spans and only divide rapidly after a tissue injury.
These cells have no ability to regenerate (McConnell, 2006). These cells have to last a lifetime due to their inability to regenerate.
Concepts of Tissue repair for a 79-year-Old woman with type 1 diabetes, with cerebral vascular accident, paralysis and a stage 3 decubitus ulcer of her coccyx region
The type 1 diabetes affects her pancreas cells, which will regenerate slowly. Based on her age, the ability of cells to regenerate is highly reduced, especially for the labia cells that are affected by the amputation (McConnel, 2006). The cerebral vascular accident and paralysis has affected the brain cells, which are permanent cells that cannot regenerate. Cells affected by the ulcers in the coccyx region will regenerate. The stage 3 decubitus ulcer may fail to heal because most of the labial cells in this region have aged and died (Rodashi and Kowalski, 2007).
Oncogenesis
A woman has breast cancer. The doctor had cells from her tumor tested and discovered that they have very high levels of estrogen receptors. How would each of the following therapies work on this cancer?
Tamofixen
Tamoxifen is effective when the breast cancer cells are well-differentiated (Pasqualini, 2002). Based on the high levels of estrogen receptors the cancer cells are well differentiated hence the use of tamoxifen will be effective.
An antibody to the tumor cells with a toxin attached to it
The presence of the toxin in the antibody tends to stimulate the immune system to attack effectively the cancer by attaching itself on the growth-promoting protein (Ko and Dollinger, 2008).
Lumpectomy followed by local radiation
Lumpectomy will involve the removal of only the part of the breast that has the cancerous cells. Local radiation therapy will ensure that any lumps left after the lumpectomy are completely removed. This ensures that the cancer cells do not spread (Carlson, Eisenstat, and Ziporyn, 2004).
A second woman has breast cancer, but her tumor cells have normal levels of estrogen receptors. Instead, they have G proteins that are constantly active, producing high levels of the second messenger cyclic AMP. How could this cause the cells to grow?
The proteins have an estrogen receptor that that promotes the proliferative effects of estrogen in breast cancer cells (Ignatov, 2011). The tamoxifen therapy will not work effectively since it will stimulate cell growth. The decline in p53 levels indicate that the estrogen levels have gone up. The p53 has anti-proliferative mechanisms that inhibit the growth of cancer cells. The third woman is more likely to have primary cancers elsewhere in the body. The p53, responsible for inhibition are reduced.
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