Sickle Cell Disorder Essay Example

Introduction

Sickle cell disease is a disorder that is inherited through blood characterization when abnormal hemoglobin molecules form in the red blood cells. Also known as Sickle Cell Disease, the condition takes place when Hemoglobin (protein-like component responsible for oxygen transportation) changes its form and becomes abnormal (Al-Salem 226). While the atypical hemoglobin molecules present in RBC's causes Sickle Cell disorder, they also change their shape to a sickle or crescent shape. This essay will elaborate more on sickle cell disease, the formation, and diagnosis.

Is your time best spent reading someone else’s essay? Get a 100% original essay FROM A CERTIFIED WRITER!

Save 25%

Sickle cell disorder is also caused by fraction and ischemia where the blood-cells changed to the cresent-shape blocks the blood and restricts its flow to other tissues or organs of the body (Al-Salem 228). As described, the diagram demonstrates how blood is blocked when the red blood cells develop the crescent shapes.

This diagram was retrieved from http://thenurseszone.com/a-19-year-old-man-with-sickle-cell-disease-presenting-with-spinal-infarction-a-case-report/0210502500One primary symptom of the Sickle cell disorder is Hemolytic anemia primarily known for its deficiency due to the break down of the red sickle cells. Several organs, in this case, are usually damaged when this condition forms (Al-Salem 234). Some of them include The kidneys, liver, spleen and bone marrow. The lung is sometimes affected and causes serious complications and problems also known as pulmonary hypertension (also known as high blood pressure) which if not treated can cause the heart to fail.

When sickle cell disease is said to be in the hemolytic-state, then the red bone marrow is usually found in unusual place in the human body (Al-Salem 247). Based on the diagram, the red bone marrow has combine cells of the white blood, red ad hematopoietic stem. cells.

This photo is borrowed from HYPERLINK "https://sicklecellanemianews.com/2016/06/08/new-approach-make-bone-marrow-transplants-safer/" https://sicklecellanemianews.com/2016/06/08/new-approach-make-bone-marrow-transplants-safer/

Patients that have sickle cell disease go through a complicated procedure to retain their marrow through a process called the marrow hyperplasia (Caplice 957). This process leads to bone trabeculae thinning which leads to bone osteoporosis and weakness. Patients that carry the sickle cell gene are always known to have the sickle cell trait. This type of condition as discovered by scientists does not cause any health challenges. In fact, the situation is known to protect a person from malaria which is an illness caused by blood-borne caused by the mosquito's bite (Caplice 948).

0000Pace et al., (p.1045), did a research and discovered that the genetic mutation of the sickle cell disease existed a thousand years ago. When a person, in this case, has the sickle cell condition, their genetic variation changes its structure.

This image is borrowed from https://evolution.berkeley.edu/evolibrary/article/mutations_06Coincidentally, the increase of mutation in a person usually carries genes that make patients refrain from malaria. The gene is also passed to their young ones and traits of malaria prevention is established in areas where the disease is prevalent (Pace et al., 1067). In Africa America for instance, research revealed that one in 12 citizens have the attributes of sickle cell. Around the globe, it has also been established that one out of 250,000 infants born every year have the sickle cell disease (Benjamin 1006). Primarily this disorder affects people of the Middle East, Africa, Asian Indian and the Mediterranean ancestry. In the U.S, the disease mostly affects the African Americans who for every 400 kids born, they are usually carriers of the disease (Benjamin 1014). Individuals from different ethnic backgrounds have also been known to have sickle cell disease more profound the Latino Americans, in particular, those of Central American, Caribbean, and the South American ancestry. Almost 1000-1400 of Latino babies are born carriers of the sickle cell condition (Benjamin 1022).

The formation of Sickle cell AnemiaEvery person that does not have the sickle cell disease have several hemoglobin proteins that make oxygen transportation faster. Every development stage in an individual determines whether the person makes primarily fetal, embryonic or adult hemoglobins. Each hemoglobin, in this case, consists of three components: alpha globin (alpha-like), beta-globin (beta-like) or beta (Steinberg 52). When there is a genetic change in the beta, then the sickle hemoglobin is formed as a normal adult hemoglobin. At chromosome 11, the beta-globin gene then locates its elf and forms the beta-globin gene which is usually from the substitution of the single DNA generic or nucleotide building block (Steinberg 54). The change from thymine to adenine of the beta-globin gene is then inserted into the amino acid valine, which is similar to the position of the global beta protein.

Diagnosis of Sickle Cell disease

The traits of this disease cannot be prevented from being inherited, but can easily be predicted. One way of discovering this condition is through screening, especially in high-risk populations (Nottage & Hankins 399). Africa America, the Latino Americans, and the United States, in this case, are known to have the highest risk either to the traits or the disease. Sickle cell is also common to people of the Middle East, Eastern Indian, and the Mediterranean descents (Benjamin 1032). Blood transfusion is also another way of treating the sickle cell disease, particularly those that have severe and frequent painful events. In some cases, blood transfusion is also done if the patient has any risks of getting a stroke. However, when the damage is too much, then sickle cell disease can be prevented through the administration of medication known as deferoxamine (Nottage & Hankins 417). This process assists in the elimination of excess iron that passes through the urine.

Works Cited

Al-Salem, Ahmed. "The Hand-Foot Syndrome in Patients with Sickle Cell Anemia." Medical and Surgical Complications of Sickle Cell Anemia, 2015, pp. 225-244., doi:10.1007/978-3-319-24762-5_11.

Benjamin, Georges C. "Sickle-Cell Anemia." The Cambridge World History of Human Disease, 2010, pp. 1006-1047., doi:10.1017/chol9780521332866.189.

Caplice, N. M. "Role of Vessel Wall and Bone Marrow Syndecan-4 in Neointimal Hyperplasia: The Plot Thickens." Arteriosclerosis, Thrombosis, and Vascular Biology, vol. 31, no. 5, 2011, pp. 952-967., doi:10.1161/atvbaha.111.225557.

Nottage, Kerri, and Jane Hankins. "Future Perspectives for the Treatment of Sickle Cell Anemia." Sickle Cell Anemia, 2016, pp. 399-429., doi:10.1007/978-3-319-06713-1_16.

Pace, Betty S., et al. "Precision Medicine for Sickle Cell Disease: Discovery of Genetic Targets for Drug Development." Sickle Cell Disease - Pain and Common Chronic Complications, Oct. 2016, pp. 1044-1078., doi:10.5772/64817.

Steinberg, Martin H. "Overview of Sickle Cell Anemia Pathophysiology." Sickle Cell Anemia, 2016, pp. 49-73., doi:10.1007/978-3-319-06713-1_3.