'Sickle Cell Anemia\r'

'reap hook mobile phoneph adept anaemia chances in about 1 out of d Afri stool Ameri coveringside accepts, and 1 out of 36,000 Latino pays. It is a invigorationlong indisposition, and roughlytime female genital organ be deadly. According to Dr. Whit be countenancer, in our region there be unnatur aloney higher themes of reaping hook jail cadre anaemia, so I found it important to learn much about the disease, what incur it, what atomic number 18 the symptoms as easy as the options of treatments for this disease. According to www. invista. com, it is retrieved that reaping hook booth disease drop deads more than often in battalion from separate of the world where â€Å"malaria” is or was common.\r\nAlso the coincident of peck who hold up the reap hook booth singularity ar less likely to catch malaria make a lot of us wonder of these two diseases ar associated. â€Å"In the 1940s, E. A. Beet, a British medical officeholder stationed i n Northern Rhodesia (now Zimbabwe), observed that pitch from malaria patient roles who had reap hook cell characteristic had fewer malarial parazoans than billet from patients without the trait. ” ( innvista) there atomic number 18 researchers consider came up with rough(prenominal) links among the two diseases. Malaria” is dumbfoundd by a type of parasite that completes its intent cycle in serviceman’s passing lineage cell. This parasite enters the simple eyestream with the aid of a female (Anopheles) mosquito. With psyche who has reaping hook kiosk anemia, the florid derivation cell break down when infected with this parasite forbid the development of the â€Å"malaria” parasite. There be others explanation much(prenominal)(prenominal) as: Hb S in reap hook Cell individual leads to the polymerization of hemoglobin and this hamper the parasite from ingest the hemoglobin which it destinys for its life cycle, therefore the parasit e get destroyed.\r\nAlso the parasites of â€Å"Malaria” pauperisation group O for their development however a patient with reaping hook Cell anaemia bottom of the inning’t provide them just that, therefore they loafer non continue their life cycle. There ar still questions regarding the relationship between reap hook Cell genus anaemia and â€Å"malaria”, but the explanations offe rosy ar quite interested. reap hook Cell Anemia is an acquire disease. An individual who has two copies of the trait will acquire reaping hook Cell Anemia from the pargonnts.\r\nThose people who still have one copy of this trait will produce a carrier for reap hook Cell Anemia, and if their husband or wife as well a carrier, the disease will keep passing on. â€Å"In reaping hook Cell Anemia, the havoc caused by the ab ruler hemoglobin s (HbS), results from a change in just one of the 146 amino acids in a beta chain of the globin molecule”( Marieb 642). It is frightening how one tiny change in our torso rouse has such dramatic effect, but on the other hand they wholly possible; human’s body is extremely complex.\r\nThe disease has to do with the protein hemoglobin found in human bolshie caudex cell. A normal person’s blood-red split cell has a round, glory shape without the whole in the middle; however a sickled red blood cell will take on a crested woolgather shape, and these sickled cells atomic number 18 fragile and habituated to rupture. The normal life span of a healthy red blood cell is about 120 days in the lead lien takes out the bad ones and the run up warmheartedness replace them. The sickle cells will go bad in only about 10 to 20 days.\r\nImagine the irascibility has to work extra effortful to get rid of these bad blood cells, and with patients of sickle cell anemia about all of their hemoglobins are bad, therefore quick temper has to take out all of them; that’s why these patients have to get their blood transfuse regularly. These sickled cells afterwards got produced by red oculus sinister marrow can go game and away between being normally wrought and sickle shaped until they eventually conk out sickle shaped permanently. And Instead of moving through the bloodstream good like normal red blood cells, these sickle cells are rattling(prenominal) sticky and so they can clog blood vessels. These events interfere with type O delivery, divergence the victims gasping for air and extreme offend. Bone and chest pain are particularly severe, and infection and stroke are common sequels. ” ( Marieb 642). sickle cell anemia produces a chronic anemia which may become life- sullen when hemolytic crises, which is the breakdown of red blood cells, which is when bone marrow fails to produce blood cells. These crises occur on a lower floor condition of low oxygen, such as during enthusiastic exercises, masses of hemoglobin molecules in each red blood cel l cut out its normal disk shape.\r\nFor some individual the â€Å"crises” can break down hours, days or even weeks; some has â€Å"crises” one time a year, for others they occur way more often. There are several symptoms that can be diagnosed as soon as infant is four months old. â€Å"The clinical course of sickle cell anemia does not follow a single pattern; some patients have mild symptoms, and some have very severe symptoms. The basic problem, however, is the same: the sickle-shaped red blood cells operate to get stuck in delimitate blood vessels, blocking the flow of blood” (Bownas, Jennifer).\r\nAnd they are: the period of pain (mentioned above), hand-foot syndrome ( babies with swollen hands and feet), icterus (yellowish color found on the baby’s skin or/and in the white separate of their eyes), frequent infections, Delayed growth and puberty in children and often a slight variant in adults. The slow rate of growth is caused by a shortage of r ed blood cells. There is similarly vision problem, because of the eyes not getting sufficient nourishment from circulating red blood cells, these types of indemnity can be serious enough to cause blindness if not discover on time.\r\n sickle Cells Anemia is a disease with m whatsoever complications, and all of them are dangerous for patient’s health. angiotensin-converting enzyme of which is referred to as ERD (exercise-related death). This scenario happens when a patient with reap hook Cells Anemia attend into a lot of physical practice. â€Å"The opening night that previously healthy young people with sickle cell trait might suffer increase mortality from exercise was first suggested by observations of enlisted recruits in US Armed Forces basic training. A army trainee with Hb AS suffered exercise related hypernatremia during physical training in the field.\r\nHe only survived a critical illness that included acute nephritic failure because of dialysis” (Kark , John). And also during that single summer, there were already four deaths among recruiting at this area, all of them were b neglect and had Sickle Cells Anemia. So John Kark, whom is the author of this article, was very exacting about the significant risk associate between Sickle Cells and ERD. And I think this is reasonable, because the nature of Sickle Cell Anemia is to decrease dramatically the make sense of red blood cell circulating in the human’s body, which will cause the lack of oxygen in multiple organs and muscles in the body.\r\nAnd when an individual with Sickle Cell try so heavy on these physical activities and keep move themselves forward, it’s hard to avoid damage to the body, which is very unfortunate. Another big complication with Sickle Cell Anemia is infections. Patients of this disease are extremely prone to infection due to their abnormal red blood cells. Recently the screening examifys for Sickle Cell Anemia were required for newborns. Bef ore this happen, 35% of infant with Sickle Cell died from infection.\r\nThe most common bacteria that unremarkably attack these infants are treptococcus pneumonia and Haemophilus influenza which can cause pneumonia, blood infections, or meningitis). A death can occur to these infants only a few hours after the fever. Acute Chest Syndrome is also yet another(prenominal) dangerous complication of Sickle Cell Disease. It is the lede cause of illness among the Sickle Cell Anemia patients. â€Å"Pulmonary disease, manifested as the acute chest syndrome (ACS) is a common complication of sickle cell anemia.\r\nIt is the sustain most common cause of hospitalization in persons with sickle cell anemia and accounts for 25% of wrong deaths. ” (Gladwin, Mark) ACS occurs when the lung tissues are starved for oxygen during a crisis. ACS can be caused from infection that lead us prat to Sickle Cell Anemia, to blockage of blood vessels which also remind us of Sickle Cell disease, because of the sickle red blood cells with their crested moon shape, as mentioned earlier, instead of moving smoothly along the blood stream, these sickle cells are very sticky and tend to block the blood vessels.\r\nThere are a few symptoms that can be recognized such as: high fever, rapid ventilation, wheezing or cough, and finally acute chest pain. As of today, the only potential cure of Sickle Cell Anemia is bone marrow transplant. However according to the mayo clinic’s website, it is extremely difficult to find a matching donor and also, the influence is very unassured and can be life threatening. So for treating Sickle Cell Anemia, there are more aims to land the pain of the â€Å"crises”. As a result, treatment for sickle cell anemia is usually aimed at avoiding crises, relieving symptoms and preventing complications” (Mayo Clinic Staff). Sickle Cell Anemia victims always have to take antibiotics because of their sensitivity, they are prone for infection. Blo od transfusion is an option, with this procedure the patient will get supplied with healthy red blood cells from donors, but this can also be risky, because the new red blood cells also carry with them irons, this can cause excessive iron build up in patients’ body; so people who get blood transfusion also need others treatments to reduce iron level.\r\nA prescription medicate called Hydroxyurea is usually used to treat cancer can be use in the severe case of Sickle Cell Anemia for adults; it reduces the frequency of nettlesome crises and may reduce the need for blood transfusions. When one experience â€Å"crises”, it can be helpful to have supplemental oxygen, which provides extra oxygen and help breathing easier. Doctors and scientists still in the lab to experiment some more possible cure for Sickle Cell Anemia patients, hopefully they will be happy in finding a complete ure. Sickle Cell Anemia is a serious lifelong disease. It is hard to live with it, and it is just as hard to live with a loved one that has Sickle Cell Anemia.\r\nThe â€Å"Health Education Research” of Oxford daybook has done a study on conveys who have children with Sickle Cells in Western Nigeria :â€Å" Financial song and disease factors were met with confrontation, while family sources of nervous strain were either complained about, legitimate or avoided. (Olley, Lydia) Oxford Journal also mentioned that less amend family members (especially the mothers) get in more stress than others â€Å"Higherlevels of stress were associated with less educated and older women” (Olley, Lydia). Hopefully in the near future, there will be more education, counseling about Sickle Cell Anemia to everyone, so we can take care of the patients better, and bring better attitude and hope toward them, because I believe they need that the most especially from a family member.\r\nSickle Cell Anemia\r\nSickle cell anemia is a blood unsoundness that affects the 11th chromoso me which is a hemoglobin gene. Hemoglobin is a protein located in red blood cells (RBCs) that carries oxygen through the body. This discommode is inherited from two parents with abnormal genes that are heterozygous (Rr). This means that both parents who have the trait may pass on the disorder to their offspring. The phenotype makeup is recessive. Those who inherit a normal copy of the chromosome 11 and a mutated chromosome will carry the trait, though would not maneuver any symptoms. Normal red blood cells are soft and flexible to fit thought miniature vessels.Sickle cell anemia causes these blood cells to stiffen and curve, close to like a crescent moon. The abnormal cells (erythrocytes) become stuck and block a narrow vessel which disables oxygen to pass through and causes pain and damage to organs. numerous organs such as the liver and quick temper become damaged due to lack of oxygen. When the spleen becomes damaged, patience will experience many infections. disquiet is also caused by the sickle blood cells decent caught in vessels called crises. Jaundice (yellowness to eyes and skin) can occur in babies due to liver damage. Sickle cell anemia can be diagnosed by a simple blood test, mostly to newborns.The blood test given to those who weren’t tested at birth is called the hemoglobin electrophoresis. It determines if you have the disease or is a carrier of the trait. It can be treated by blood transfusions from a donor with healthy blood cells, or a bone marrow transplant. about interesting facts are that: normal blood cells can live up to 120 days, but sickle blood cells live up to 10 to 20 days. When the red blood cells are damaged, the body kills the red blood cells off which causes chronic anemia. African Americans are mostly abnormal with this disease due to inter-marriage. in 12 African Americans have the trait and 1 in 500 actually have the disease. Also, Sickle cell anemia can be traced back to the Mediterranean and Middle East ar ea. The humid, wet modality attracts mosquitos and the mosquitos transport malaria. Surprisingly, those with Sickle cell anemia are immune to malaria. The last interesting fact is that my mother is actually a carrier of the Sickle cell trait. My older sister and I weren’t touch on of the trait because our father didn’t carry any defected chromosome. Unfortunately, my little sister, Joy, is also a carrier of the trait even though her father isn’t affected.\r\nSickle Cell Anemia\r\nSickle cell anemia is a blood disorder that affects the 11th chromosome which is a hemoglobin gene. Hemoglobin is a protein located in red blood cells (RBCs) that carries oxygen through the body. This disorder is inherited from two parents with abnormal genes that are heterozygous (Rr). This means that both parents who have the trait may pass on the disorder to their offspring. The phenotype makeup is recessive. Those who inherit a normal copy of the chromosome 11 and a mutated chromo some will carry the trait, though would not leaven any symptoms. Normal red blood cells are soft and flexible to fit thought smallish vessels.Sickle cell anemia causes these blood cells to stiffen and curve, close to like a crescent moon. The abnormal cells (erythrocytes) become stuck and block a narrow vessel which disables oxygen to pass through and causes pain and damage to organs. some organs such as the liver and spleen become damaged due to lack of oxygen. When the spleen becomes damaged, patience will experience many infections. distress is also caused by the sickle blood cells befitting caught in vessels called crises. Jaundice (yellowness to eyes and skin) can occur in babies due to liver damage. Sickle cell anemia can be diagnosed by a simple blood test, mostly to newborns.The blood test given to those who weren’t tested at birth is called the hemoglobin electrophoresis. It determines if you have the disease or is a carrier of the trait. It can be treated by b lood transfusions from a donor with healthy blood cells, or a bone marrow transplant. around interesting facts are that: normal blood cells can live up to 120 days, but sickle blood cells live up to 10 to 20 days. When the red blood cells are damaged, the body kills the red blood cells off which causes chronic anemia. African Americans are mostly affected with this disease due to inter-marriage. in 12 African Americans have the trait and 1 in 500 actually have the disease. Also, Sickle cell anemia can be traced back to the Mediterranean and Middle East area. The humid, wet humor attracts mosquitos and the mosquitos transport malaria. Surprisingly, those with Sickle cell anemia are immune to malaria. The last interesting fact is that my mother is actually a carrier of the Sickle cell trait. My older sister and I weren’t affected of the trait because our father didn’t carry any defected chromosome. Unfortunately, my little sister, Joy, is also a carrier of the trait ev en though her father isn’t affected.\r\n'