The Oesophagus Structure And Illnesses Effecting It Biology Essay

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Barrett's oesophagus is a complicated chronic gastroesophageal reflux disease. Barrette's oesophagus is an example of metaplasia. Metaplasia is a reversible change in which an epithelial cell is replaced by another epithelial cell. When the normal squamous lining cells of the oesophagus cannot withstand adverse environments, they are replaced by columnar cells which can adapt to the environment, but the replaced cells are not always capable of carrying the job that the original cells did. The reason why the cells are replaced is so that the body can respond to irritation and protect itself, but the more cells are damaged and replaced the higher the chance of them gathering all the genetic changes that can turn it into a cancer cell.

With gastroesophageal reflux disease (GERD), acid and food splash up into the oesophagus repeatedly. It is possible for stomach acid to damage some of the cells in the tissue of the oesophagus. Sometimes the damaged cells turn into another type of cells. This process is called metaplasia. When metaplasia occurs in the oesophagus this condition is called Barrette's Oesophagus. When this happens, the normally smooth tiles of the oesophagus lining look more like shagged carpeting. The barrette's lining always joins the stomach and extends upward towards the mouth in various lengths, when lining is short (1.3inches), this is called a Short segment Barrette's Oesophagus, but when it extends further up it is called Long segment oesophagus. The region where the normal squamous oesophageal lining joins the normal columnar stomach lining is called squamocolumnar junction. The cells involved in Barrette's oesophagus are not cancerous when they first appear, but over time they may become abnormal and are typical glandular cacinomas.

Metaplasia is a cellular replacement process.

The diaphragm is a muscle that separates the chest from the abdomen, and it helps one to breathe.

Food enters the oesophagus, contractions called peristalsis push food down the oesophagus. At the bottom of the oesophagus food passes through a muscular valve called the LES (lower oesophageal sphincter) and into the stomach. The digestive juices secreted by the stomach are very acidic, when a stomach contracts to move the food into the intestine, the LES closes tightly to prevent the acid from moving back into the oesophagus in order for it not to cause any damage.

Normally the diaphragm has a opening for the oesophagus to pass through where it connects to the stomach. A hiatal hernia occurs when a part of the stomach pushes upwards through the small opening. The hiatal hernia can cause discomfort with symptoms such as heartburn, belching, difficulty swallowing and chest pain.

2. How does metaplasia differ from dysplasia?

Metaplasia is a common cause of oesophageal carcinoma, it is when one type of tissue changes in form and transforms into another specialisedtype of tissue.Dysplasia is pre-cancer,it is a condition of deranged cell growth in which the cells are structurally malformed in size, shape and appearance from the original cell type.

Metaplasia and dysplasia are in actual fact two different conditions. Metaplasia is carcinogenic by nature unlike in dysplasia,it is an indication of a premature neo-plastic progression.

Metaplasia is a condition in which the lining of the lower part of the oesophagus changes from one cell type into another. The cell type changes from a multi-layered tissue which is known as stratified squamous epithelium into a single cell layer which has features of a intestinal type of epithelium.

A metaplastic response often takes place when there is a chronic irritation and inflammation. The irritation and inflammation is caused by the reflux of acid and bile from the stomach and duodenum into the oesophagus, however it has also been stated that bile and pancreatic enzymes combined with the acid could be more injurious than acid alone.

As the original cells are unable to survive under the circumstances, they die out. They are then replaced by tissues that are more resistant to the peripheral stress (external stimulus) as they are more capable of survival. The cellular changes naturally result in a loss of function which was performed by the original cells that died and were replaced.

Dysplasiaconsists of the increased growth of immature cells with a synchronised reduction in the growth of mature cells, their numbers and their site of growth. It is a indication of a premature neo-plastic progression and it directly indicates a state when the cellular defect are constrained within the tissue origin.

A frequent feature of dysplastic cells is that the dysplastic cells have a mitotic rate higher than the predecessor normal cells and the nuclei are larger than normal.

Dysplasia is commonly caused by infection and irritation, in many cases dysplasia can be reversed if the stress is removed and normal cells return, in other cases dysplasia can become permanent and represent a precancerous change.

An example of dysplasia is cervical cancer whichis mainly caused by smoking or sexual behaviour.

Cervical cancer could be limited by carrying out a screening examination at early stages. The areas which is targeted at are the bronchi in the region of the trachea.

Cervical dysplasia is a condition in which irregular cells are developed on the uterine cervix.

3. What kinds of stimuli can produce metaplasia? Give two other

examples of metaplasia that can occur in different areas of the body.

Metaplasia in

Keratinizing metaplasia is a condition distressing the epithelial surfaces of the body, it is caused by vitamin A deficiency (retinoic acid) andthe squamous metaplasia in the respiratory epithelium gets induced while it strongly overpowers keratinization. It is a dietary deficiency of a fat-soluble vitamin that is usually found in fats, milk and leafy vegetables. In this example, the more rugged stratified squamous epithelium is able to survive under circumstance in which the more fragile specialised columnar epithelium would have most likely surrendered. Even though the metaplastic squamous cells in the respiratory tract are capable of surviving, an important mechanism is lost (mucus secretion). Although epithelial metaplasia is reversible, in most cases it could represent an undesirable change. However the influences that affect metaplasia and is persistent, this may induce malignant transformation in metaplastic epithelium. The common form of cancer in the respiratory tract is made up of squamous cells, which will then arise in the areas of metaplasia of the normal columnar epithelium into squamous cells.

Metaplastic breast cancer is when the cancer forms in the milk ducts of the breast and moves into other parts of the tissue in and around the breast, this is a form of invasive ductal cancer. This type of cancer is not found inside the breast such as the skin (squamous) or the bone (osseous cells). This is known as carcinoma with metaplasia, this means that the cancer has spread from its original sites to other areas (it has changed or moved place). Cancer often occurs when cells start to divide uncontrollably, even when new cells are not needed. In order from cells to change from normal to cancerous gene alteration is required, uncontrolled growth and altered genes may lead to tumours. These tumours can be either cancerous (malignant) or not cancerous (benign). Malignant tumours invade, damage and destroy nearby tissues and could possibly spread whereas benign tumours do not spread but can damage the tissues surrounding it. Cancer spreads throughout the body when cancer cells break away from malignant tumours and enter the blood stream. Cancer cells that form breast cancer are usually found in the lymph nodes under the arm when it spreads. When the cancer cells continue to spread to the others parts of the body, it still remains as breast cancer (for example if the breast cancer spreads to your lungs, it will still be called 'breast cancer').

4. What is necrosis? How does it differ from apoptosis?

Necrosis is caused by a physical disruption to the cell through injury, infection, cancer, infarction, poisons and inflammation. Necrosis is the death of cells or a group of cells which are still part of a living organism. Tissue necrosis as a result of reduced blood supply and anoxia, this term is called infarction. The stimuli for necrosis is pathologic and the consequences are irreversible cell injury and cell death.

Bacteria can secrete toxins that disrupt cellular structure and function. This leads to an influx of extracellular fluid. The cell loses functional control which leads the organelles, the chromatin clumps and mitochondria to swell and leads the cells to eventually burst. The cytotoxic cellular components which include proteolytic enzymes, cationic proteins and oxidizing molecules spill out from the membrane causing extensive tissue damage resulting in an extreme inflammatory response.

Cells that die because of necrosis do not send the same chemical signals to the immune system like the cells that go through apoptosis do. This averts nearby cells phagocytes from establishing and engulfing the dead cells, leading to a accumulation of dead tissue and cell debris at the site of the cell death. It is essential to remove the necrotic tissue surgically before it spreads to other parts of the body, this process is called debridement.

Most eukaryotic cells are genetically programmed for cell death (apoptosis). Apoptosis is an organised way removing a non-functioning cell that is no longer draining nutrients or spreading infections. The stimuli for apoptosis is physiological, it is genetically regulated in the response of a pathogen that the body reacts to (eg.antibody).

Molecular signals continually inhibit or promote this process. Bcl-2 protein which is on the outer mitochondrial membrane plays a major role in inhibiting apoptosis. Deactivating bcl-2 initiates apoptosis through a well controlled chain of enzymatic reactions. Catabolic processes begin throughout the cell. Enzymes digest cytosolic components and fragment the nuclear DNA. Specialised cysteine proteases which is called caspases target specific proteins in the nuclear lamina and cytoskeleton. The cell is 're-packaged' for safe removal. The chromatic condenses, the cell shrinks and fragments into small membrane-bound apoptotic bodies. Then the compacted cell is phagocytised by adjoining cells.

Necrosis and apoptosis are two key processes leading to cell death. Apoptosis is not fatal, whereas necrosis can be a lethal and can lead to fatal conditions such as gangrene. Gangrene is often caused by damage from the cold. Gangrene is caused by frostbite, frostbite is a condition caused by long-lasting exposure to extreme cold. The skins blood vessels narrow which provides greater blood flow to the rest of the body (organs), lessened blood flow to the skin means less oxygen which can lead to cell death in the skin.

Apoptosis is a way to remove unwanted cells, cellular contents are not released and inflammation does not occur during apoptosis as this is a controlled cell death. Apoptosis is a termination of an individual cell. In other hand necrosis is not a controlled cell death and is caused by a physical disruption. Necrosis causes death to a group of cells in an area. In apoptosis, programmed cell death is needed to destroy cells that represent a treat to the integrity of the organism. For example cancer cells, radiation and chemicals are used in cancer therapy inducing apoptosis in some types of cancel cells.

Necrosis typically causes inflammation and can be very harmful, it has a disorderly DNA fragmentation and is caused by lack of ATP. Whereas apoptosis does not cause inflammation and often provides a beneficial effect, it requires ATP and has an orderly DNA fragmentation.

In apoptosis cells shrink and try to defend themselves against infection, this is called phagocytosis. In necrosis cells swell and bursts decaying tissue in a particular part of the body, this is called necrotic.