The MSC differs significantly from cohorts based in the USA, UK or Jamaica due to the near 100% of

This paper outlines the etiology of sickle cell anemia and the nutrition considerations that is needed to maintain this disease. It also provides a five day menu plan that will greatly provide nutrition needs to prevent having a sickle cell crisis.

Conferring to the case study 1 of Ms. A, who is suffering from iron deficiency anemia. “People who experience iron deficiency anemia lack adequate iron required to produce hemoglobin. Hemoglobin supports red blood cells in carrying oxygen all through the body” (Mayo Clinic, 2014). In this presentation, the writer will provide rationales where Ms. A is presenting signs and symptoms of Iron Deficiency Anemia.

In high-income countries like the United States, the life expectancy of a person with SCD is now about 40–60 years. In 1973, the average lifespan of a person with SCD in the United States was only 14 years. Advances in the diagnosis and care of SCD have made this improvement possible. Sickle Cell disease affects mostly African, Mediterranean and related ancestries it is passed on through generational traits and common related blood type. Sickle Cell disease is a disease that causes painful attacks called crises; which causes throbbing in their bones and backs. Sickle cell is caused by a protein that is abnormal called hemoglobin S which causes the shape of red blood cells to change into a sickle or crescent type shape. (George Buchanan, 2010) Cells in tissues need a steady supply of oxygen to work well. Normally, hemoglobin in red blood cells takes up oxygen in the lungs and carries it to all the tissues of the body. Red blood cells that contain normal hemoglobin are disc shaped (like a doughnut without a hole). This shape allows the cells to be flexible so that they can move through large and small blood vessels to deliver oxygen. Sickle hemoglobin is not like normal hemoglobin. Sickle-shaped cells are not flexible and can stick to vessel walls, causing a blockage that slows or stops the flow of blood. When this happens, oxygen can’t reach nearby

Sickle cell disease, also known as SCD, is a hereditary blood disorder that takes place due to mutation in the hemoglobin gene that is found in red blood cells. While it is said to have originated in Africa and is mostly predominant in African Americans, sickle cell disease is now common among different ethnic groups all over the world. Sickle cell anemia (HbSS) infects “an estimated 70,000 to 100,000 Americans”(Housman) and accounts for approximately 70% of anemia in the United States. Hemoglobin functions as an oxygen carrying protein as it carries oxygen from the lungs through the arteries and to the rest of the body. In sickle cell disease,

The term sickle cell disease (SCD) involves a range of disorders characterized by the occurrence of at least one haemoglobin S (Hb S) allele and a second abnormal allele allowing abnormal haemoglobin polymerization leading to a symptomatic disorder. Most patients often are healthy at early stages in their life and become symptomatic later on in their life time. Fetal haemoglobin levels decrease and haemoglobin s levels increase. Sickle cell disease is determined at conception, when a person acquires his/her genes from the parents. Sickle cell disease cannot be caught, acquired, or otherwise transmitted.

Essentially, there is an incorrect base- pair change when the Deoxyribonucleic Acid strand are being duplicated, exchanging the “the sixth amino acid from glutamic acid to valine causing the mutated hemoglobin (HbS) to polymerize” or change the shape of each cell (Adams1). The most severe form of Sickle Cell Disease is Hemoglobin SS, in which both parents are carriers of Sickle Cell gene, “SS”, and ultimately reproduce a child that has SCD. In Hemoglobin SC, one parent has the gene “S” while the other has the trait “C”, thus having a milder form of Sickle Cell Disease (Stuart7). Sickle Cell Anemia or Hemoglobin S beta thalassemia is another form of SCD, where one parent has the “S” gene while the other parent has an additional form of anemia or thalassemia (CDC5). Due to the constricting shape of the erythrocytes, the blood cells began to die at an alarming rate causing the body to be deprived of oxygen, creating a number of other health complications. Stroke, neurocognitive functions, infections and the increased risk of death can occur if left untreated. Amongst individuals with SCD, the risk of having a stroke is increased, especially in children (Adams1). Stroke is said to be caused by the constriction of blood vessels and lack of oxygen in the brain that is associated with Sickle Cell Disease. However, because of the stroke increase in

I was surgery last month. After surgery, my doctor told me I had an amount of blood. So, I felt very tired. I become more interested in anemia. Accordingly, I had picked iron deficiency anemia. According to the Health line, anemia occurs when I have a level of red blood cells (RBCs) in my blood that is lower than normal. They explained iron deficiency anemia that is the most common type of anemia, and it occurs when my body do not have enough of the mineral iron. My body needs iron to make a protein called hemoglobin. This protein is responsible for carrying oxygen to my body’s tissues, which is essential form my tissues and muscles to function effectively. When there is not enough iron in my blood stream, the rest of my body cannot get the

Final Question: In patients with non-dialysis-dependent (NDD) Chronic Kidney Disease (CKD) who have iron-deficiency anemia, how efficacious is intravenous (IV) ferric carboxymaltose in increasing hemoglobin levels and reducing treatment-related adverse events compared to IV iron sucrose?

Sickle cell anemia is a genetic blood disorder that is caused from the abnormal function of hemoglobin. In the case of sickle cells anemia, the hemoglobin molecule in red blood cells is sickle- shaped leading to the blockage of blood flow to blood vessel of the lungs and other organs and therefore a very slow transportation of oxygen. It mostly affects people with African descents with an affected population of 0.25% in African Americans. It results from a mutation at the sixth codon of the beta globin gene (HBB gene) in which the amino acid glutamic acid is substituted for valine, leading to the production of an altered form of hemoglobin S (hbS). Griffiths AJF, Miller JH, Suzuki DT, et al

SCD begins with a mutation of the genetic makeup of the hemoglobin, a protein contained by red blood cells (RBCs) that deliver oxygen throughout the body. Hemoglobin is made up of two alpha and two beta polypeptide chains made up of amino acids. Normal hemoglobin allows RBCs to take on a biconcave or doughnut like shape and is able to squeeze or alter its shape in order to travel through different sized blood vessels. Hemoglobin has a high affinity for oxygen, is oxygenated in the lungs and delivers the oxygen to the body’s tissues. Once deoxygenated, hemoglobin returns to the lungs to return carbon dioxide and become re-oxygenated.

1) Sickle Cell Disease (SCD) (Sickle Cell Crisis): Sickle cell disease is a hereditary disease. The majority of individuals affected by SCD are those of African descent (Yawn & John-Sowah, 2015). SCD develops hereditarily by an individual being homozygous for sickle hemoglobin (HbSS) (Yawn & John-Sowah, 2015). Individuals will also have another abnormal hemoglobin gene, such as HbSC (Yawn & John-Sowah, 2015). The red blood cells (RBCs) in SCD lose oxygen and become sickled (Yawn & John-Sowah, 2015). The RBCs loose flexibility and shape; sickled cells have been described as having a crescent moon shape (Yawn & John-Sowah, 2015). Organ and tissue damage is due to the sickled RBCs (Rees & Gibson, 2011). Without flexibility, the sickled cells cause vaso-occlusions which lead to tissue infarction and inflammation (Rees & Gibson, 2011). Vasoocclusive crisis (VOC) is a common complication of SCD that will be sudden and severe causing severe pain (Yawn & John-Sowah, 2015). Individuals must be monitored for infection, pain, renal failure, cerebrovascular disease, and acute chest syndrome (Rees & Gibson, 2011). Individuals with SCD are at a high risk for stroke (Yawn & John-Sowah, 2015).

Hemochromatosis is the most common form of iron overload disease. This disease causes the body to absorb more iron then what it needs; too much iron results in an iron overload or hemochromatosis. Although the body needs iron, too much of it becomes dangerous to the body. The body doesn’t remove iron naturally; instead it stores it in organs which cause damages to them if left untreated. Organs included are the liver, the heart and the pancreas. There are three types if hemochromatosis; primary hemochromatosis, secondary hemochromatosis and neonatal hemochromatosis.

Early histological and biochemical studies into the pathophysiology in patient’s samples revealed that dysregulation of iron metabolism is a key feature of the disease, mainly characterised by mitochondrial iron accumulation and cytoplasmic iron deficiency. In consistence with our previous study21, we found that IRP2 is upregulated and ferritin is

Nutrition is an essential component in the complex development of infants, mainly because of their rapid growth in one year. One of the most prevalent nutrition problems among young children in the United States is iron deficiency anemia.1 Anemia is defined as a reduction below normal in the number of red blood cells per cubic millimeter in the quantity of hemoglobin, or in the volume of packed red blood cells per 100 milliliters of blood.1 This reduction occurs when the balance between blood loss and blood production is disturbed.1 Iron deficiency can be defined as absent bone marrow iron stores, an increase in hemoglobin concentration of less than 1.0 g/dL after treatment with iron, or other abnormal values.1 Iron deficiency is found to be more common among low-income children and among African American and Mexican American children.1 The consequences of iron deficiency anemia include poor cognitive and motor development. The purpose of this paper is to present four research studies all focusing on the occurrence of iron-deficiency anemia in newborns in developing countries. The first study will focus on the behavior of infants with iron-deficiency anemia2 in Costa Rica. The following study will exhibit anemia in pregnancy3 and the impact on weight and in the development of anemia in the newborn3 in Brazil. The third study will present the effect of maternal iron deficiency anemia on the iron store of newborns in Ethiopia.4 Lastly, the fourth study is a prospective study

A 14 year old boy presented to the Accident and Emergency department of the Kingston Public Hospital with a history of acute left sided weakness. He was known to have sickle cell disease with the HbSS genotype. He had previously presented with a stroke and had residual right sided weakness. There was no history of headaches fever, vomiting, chest or joint pain. He was admitted to the medical ward where treatment was instituted. On admission he had a Glasgow Coma Score (GCS) of 15 with grade 2 power (MRC) in the upper limbs and grade 3 (MRC) in the lower limbs. Radiological investigations were