Punctuality and Correct Medical Aid Essay Example for Free

Punctuality and Correct Medical Aid Essay The saying which goes A stitch in time saves nine is very true!!!Punctuality is no doubt a virtue no man can afford to lack. It is the simplest and easiest to acquire but at the same time really needed to succeed in life. Punctuality is the habit of doing things in time. It is a disciplinary force which contributes to the efficiency and success of both an individual and organization. A punctual person is always a step ahead of others . He is able to complete his assignments and keep commitments which wins him the command and respect of all those who work with him .He becomes an asset and support in any field of life. He will be a sought after member of any organization for the respect he has earned by his reliability and sense of discipline. Lessons of punctuality are introduced from the very birth of a child. Feeds are given punctually and so are medications. Schools , colleges also implement and enforce these in every possible way .Time tables, classes ,examinations all demand punctuality. A company which fails to deliver goods or services in time or is unpunctual in collecting dues is also bound to fail one day or the other. In hospitals on some occassions punctuality may make all the difference between life and death . Forgetting to give a medicine or injection on time may take a life! On the other hand bringing a patient and giving him the correct medical aid in time will save a precious life!History also shows how punctuality plays such an important role even in war. General Neys unpunctuality ruined Napoleon and changed the course of European history. If we study the lives of some great people we find that punctuality was one of the pillars of their success. Professionals like lawyers , doctors, teachers who have reached success are further respected when they keep their appointments and timely commitments . If we look around we shall see that sense of order and punctuality is seen in Nature too. The sun rises in the day , planets move in orbits, seasons keep their cycle teaching us the significance of time and punctuality in life. Today we live in a modern complex society where so many things are interdependent. It is essential for the smooth functioning that people recognise the need for punctuality. If trains and flights do not keep punctuality it can create such a mess and sometimes cause havoc and disaster or even accidents. In the age of rockets and moonlandings the importance of punctuality is felt even more. To organize events meetings and make them successful it is essential that all participants keep time and are punctual. Could big events like the Olympics be a success without punctualityWe should make a humble beginning and start incorporating punctuality in our lives in our day to day activities. Bed time and waking time , meal times if adhered to will help discipline us and tune our minds towards punctuality in other areas also. Once disciplined and punctual a very different future welcomes you. One would surely realise that punctuality is the key to success and greatness in life. One step at a time but always on time..!!!!

Hemoglobin Malaria Haemoglobinopathies

Hemoglobin Malaria Haemoglobinopathies Despite major advances in the understanding of the molecular pathophysiology and control and management of the inherited disorders of hemoglobin (haemoglobinopathies), thousands of infants and children with this disease are dying. As a result in heterozygote advantage against malaria the inherited hemoglobin disorders are the commonest monogenic disease. Population migrations have ensured that haemoglobinopathies are now encountered in most countries including the UK. Haemoglobinopathies have spread from areas in the Mediterranean, Africa and Asia and are now endemic throughout Europe, the Americas and Australia. This review examines the available literature to find out more about the prevalence of haemoglobinopathies in the UK. The data on the demographics and prevalence of the gene variants of haemoglobinopathies was extracted from books, journals, reference sources, online databases and published review articles from the WHO. Introduction It has been estimated that approximately 7% of the world population are carriers of such disorders and that 3000 000 4000 000 babies with severe forms of haemoglobinopathies. Haemoglobinopathy disorders occur at their highest frequency in tropical regions and population migrations have ensured that they are now encountered in most countries. Because of this, haemoglobinopathies have become a global endemic, so the World Health Organization published journals and reviews with recommendations on screening programmes and management of haemoglobinopathies. The programmes are tailored to specific socioeconomic and cultural contexts and aimed at reducing the incidence, morbidity and mortality associated with these diseases. www.who.int/en/ The WHO Executive Board wrote a review on haemoglobinopathies. In this article, the WHO Executive Board recognized that the prevalence of haemoglobinopathies varies between communities, and that insufficiency of relevant epidemiological data may hamper effective and equitable management of haemoglobinopathies. On this note England implemented the LIVE programmes. The Executive Board also recognizes that haemoglobinopathies are not yet officially recognized as priorities in Public Health Sector. This raised an issue about awareness of haemoglobinopathies. The WHO Executive Boards advice for prevention and management of haemoglobinopathies was to design, implement and reinforce in a systematic equitable and effective manner, comprehensive national, integrated programs for prevention and management of haemoglobinopathies, including surveillance, dissemination, such programs being tailored to specific socioeconomic and cultural contexts and aimed at reducing the incidence, morbidity and mortality associated with these diseases. www.who.int/en/ With immigration in the UK on its highest, the prevalence of haemoglobinopathies is expected to increase. The NHS has implemented programmes for individuals with haemoglobinopathies by implementation of LIVE program (NHS Plan, 2000). LIVE program is set-up to implement variant screening in the whole of UK by the year 2007. LIVE program started as early as January 2004 in high prevalence. The NHS Trusts involved are to offer variant screening by end of 2004/5 (NHS Plan, 2000). Low prevalence Trust are expected to have implemented the screening program by January 2008 and so far 86 out of 90 Trusts have successfully implemented the program. Antenatal and Newborn Screening programs have compiled a training pack to assist Low Prevalence Trusts with the implementation of haemoglobinopathies screening programmes. The NHS Plan (2000) made a commitment to implement effective and appropriate screening programs for women and children including a new national linked Antenatal and Newborn screen ing programs for haemoglobinopathies. The NHS Plan (2000) recommends that all pregnant women living in high prevalence areas are offered screening for haemoglobinopathies. All pregnant women living in low prevalence areas are offered screening for haemoglobinopathies. If a woman is identified as being at increased risk using the family origin questionnaire, she will then be offered screening for haemoglobinopathies (NHS Plan, 2000). The Low Prevalence Trust is where the fetal prevalence of sickle cell disease is less than 1.5 per 10 000 pregnancies. Low prevalence trusts are to offer screening for variants based on an assessment of risk determine by a question to women about their babys fathers family origin by the end of 2005/6 (NHS Plan, 2000). Background on Haemoglobinopathies Haemoglobin: is the oxygen carrying capacity of the blood and it is also a protein. Haem is iron containing pigment, while globin is made up of chains which are a globular tetrameric protein which accounts for 97.4% of the mass of the haemoglobin molecule (Tortora et.al., 2006) . The globin tetramer consists of four polypeptides which are two alpha (ÃŽ ±) chains and two non-alpha chains. The synthesis of ÃŽ ¶ and ÃŽ µ chains is done during the first 10 to 12 weeks of fetal life. Within the fourth to the fifth week of intrauterine life ÃŽ ± and ÃŽ ² chains are synthesized. The non-alpha is beta (ÃŽ ²), gamma (ÃŽ ³), delta (ÃŽ ´), epsilon (ÃŽ µ) zeta (ÃŽ ¶) chains. Haemoglobin transports oxygen from the lungs to all parts of the body and it gives blood its red colour (Fleming, 1982) Haemoglobin synthesis Haem and globin synthesis occur separately but in a carefully coordinated fashion. Globin synthesis is under the genetic control of eight functional genes arranged in two clusters, the ÃŽ ± globin gene cluster on chromosome 16 and the ÃŽ ² globin gene cluster on chromosome 11. The major haemoglobin in the foetus is HbF (ÃŽ ±ÃŽ ²) 2 and in adults HbA (ÃŽ ±ÃŽ ²) 2 (Fleming, 1982). Haemoglobin Structure The primary structure of haemoglobin is made-up of amino acid sequence of globin. And the secondary structure comprise of nine non-helical sections joined by eight helices; tertiary structure describes globin chain folding to form a sphere and the quaternary structure of haemoglobin describes the tetrahedral arrangements of the four globin subunits ( Fleming, 1982). The external surface of each folded globin is hydrophilic and the inner surface is hydrophobic, this protects the haem from oxidation, which is also why each haem chain sits in a protective hydrophobic pocket. In haemoglobin A, ÃŽ ± ÃŽ ² dimmers are held together strongly at the ÃŽ ±1 ÃŽ ²1 or ÃŽ ±2ÃŽ ²2 junction. The tetramer is held together much less tightly at the ÃŽ ±1 ÃŽ ²2 and ÃŽ ±2 ÃŽ ²1 contact areas (Fleming, 1982). Haemoglobin function Each haemoglobin molecule can carry four oxygen molecules. Oxygenation and deoxygenation are accompanied by molecular expansion and contraction via haem haem interaction (Bienz, 2007). Under physiological conditions, blood in the aorta carries about 19.5ml of oxygen per 100ml of blood. Upon entering the tissues about 4.5ml of oxygen are donated per 100ml of blood. 2,3-DPG is an important modulator of haemoglobin A oxygen affinity in red cells (Fleming, 1982). Haemoglobin disorder (haemoglobinopathies) Haemoglobinopathies is a hematological disorder due to alteration of a genetically defect, that results in abnormal structure of one of the globin chains of the haemoglobin molecule (Bienz, 2007). Haemoglobinopathies are any of a group of diseases characterized by abnormalities, both quantitative and qualitative in the synthesis of haemoglobin (Hb) (Bienz, 2007). Qualitative affecting the quality of haemoglobin e.g. Sickle cell disorder and quantitative affecting the amount of haemoglobin produced e.g. Thalassaemias. Most of them are genetically inherited but occasionally they can be caused by a spontaneous mutation. Haemoglobinopathies are the worlds most common monogenic autonomic and recessive disease in humans (Anionwu et.al., 2001). 2.1Haemoglobinopathies fall into two main types; There are two categories of haemoglobinopathies. The two categories are: qualitative and quantitative; Qualitative affecting the quality of the haemoglobin e.g. Sickle cell disorder. In this disease the globin structure is abnormal. Quantitative the haemoglobin structure is normal but the amount of haemoglobin produced is affected. e.g. alpha and beta thalassaemias (Bienz, 2007). History of haemoglobinopathies In 1910 Herrick wrote an article in it he used the term â€Å"sickle† to describe the shape of the red blood cells of a 20 year old medical student from Grenada. This student had consulted Dr Herrick in 1994 complaining of a cough, fever and Feeling weak and dizzy. He constantly had anaemia episodes, jaundice, chest complications as well as recurring leg ulcers on both ankles. When his blood was examined, his red blood cells showed a large number of thin, elongated, sickle shaped and crescent- shaped forms (Herrick, 1990). The name thalassaemia was coined by the eminent haematologist George Whipple in 1936 as an alternative to the eponymous ‘Cooleys anaemia. He wanted a name that would convey the sense of an anaemia which is prevalent in the region of the Mediterranean Sea, since most of the early cases originated there. Thalassaemia is derived by contraction of thalassic anaemia (from the Greek thalassa -sea, an none and anemia blood) (Fleming,1982). Origins and Geographic distribution of haemoglobinopathies Carriers are found in all parts of the world: people from the North Mediterranean (South Europe) coast are 1-19% carriers. People of Arab origin are over 3% carriers. In Central Asia 4-10% and in South East Asia, the Indian subcontinent and China 1-40% carriers (the very high rates in this part of the world are due to HbE). In the Americas, North Europe, Australia and South Africa the local population has very low carrier rates but thalassaemia is still present because of the significant immigration from high prevalence area (Anionwu et.al.; 2001). Sickle cell and thalassaemia disorder mainly affect individual who are descended from families where one or more members originated from parts of the world where falciparum malaria was, or is still endemic. Population with such ancestry include those from many parts of Africa, the Caribbean the Mediterranean (including southern Italy, Northern Greece and Southern Turkey), Southeast Asia and thalassaemia gene is much wider now due to the hi storical movements of at-risk populations to North and South America, the Caribbean and Western Europe (Livingstone 1985). The geographic distribution of the thalassaemias overlaps with that of sickles cell disease. This is because carriage of these abnormal genes affords some protection against malaria. Thus, being heterozygous for one of these conditions offers a selective survival advantage and increases the opportunity for these genes to be passed on (Campbell et.al.,2004) 4Types and terminology of sickle cell and thalassaemia There are various types of sickle cell and thalassaemia disorders. The thalassaemia syndromes include alpha and beta thalassaemia major as well as beta thalassaemia intermedia. Sickle cell disorders (or Fickle cell disease include sickle cell anaemia (Hb SS), Sickle haemoglobin C disease (Hb SC) ÃŽ ² disease and E beta thalassaemia (www.sickle-thalassaemia.org/sickle.cel.htm) 4.1Sickle Cell Disorder: affects the normal oxygen carrying capacity of the red blood cells. The red blood cell forms a crescent or a sickled shape when it is deoxygenated. The ‘sickled cells are unable to pass freely through capillaries; the sickle cells also get stuck in blood vessels forming clusters which block the blood vessels and the blood flow. They dont last as long as normal, round red blood cells, which leads to anemia. This results in a lack of oxygen to the tissues in the affected area, resulting in hypoxia and pain (sickle cell crisis). Other symptoms include severe anaemia, damage to major organs and infection (NHS Antenatal and Newborn; 2006). There are several types of Sickle cell disease. The most common are: sickle cell anemia (SS), sickle hemoglobin C disease (SC), sickle beta plus thalassaemia and sickle beta zero thalassaemia. Each of these can cause pain episodes and complications. HbSS sickle is due to two sickle cell genes (â€Å"S†), one from each parent. This is commonly called sickle cell anemia. An individual with sickles cell anemia have a variation in the ÃŽ ²-chain gene, which then causes a change in the properties of hemoglobin which results in sickling of red blood cells (www.sickle-thalassaemia.org/sickle.cel.htm) HbSc inherited one sickle cell gene and one gene from an abnormal type of haemoglobin called â€Å"C†. It is due to the variation in the ÃŽ ²-chain gene. An individual with this variant suffers from mild chronic haemolytic anaemia. (NHS Antenatal and Newborn; 2006). HbS beta thalassaeamia: This form of sickle is due to inherited one sickle cell gene and one gene for beta. 4.2Thalassaemias: is a term used for the description of a globin gene disorders that results from a diminished rate of synthesis of one or more globin chains and a consequently reduced rate of synthesis of the haemoglobin or haemoglobins of which that chain constitutes a part ; ÃŽ ± thalassaemia indicates a reduced rate of synthesis of the ÃŽ ± globin chain, similarly, ÃŽ ², ÃŽ ´, ÃŽ ´ ÃŽ ² and ÃŽ µ ÃŽ ³ ÃŽ ´ ÃŽ ² thalassaemia indicate a reduced rate of synthesis of the h, ÃŽ ´, ÃŽ ´, +ÃŽ ² and ÃŽ µ + ÃŽ ³ + ÃŽ ´ + ÃŽ ² chains, respectively (Modell et.al, 2001). Thalassaemia is the most common single gene disorder known. It is autosomal recessive syndromes, which is divided into ÃŽ ±- and ÃŽ ² thalassaemia. Types of thalassaemia There are two types of thalassaemia: (i)Thalassaemia minor (thalassaemia trait) (ii)Thalassaemia major Thalassaemia minor is when a person inherits one thalassaemia gene, while thalassaemia major is a severe form of anaemia if a person inherits two thalassaemia genes, one from each parent (Bienz, 2007). Subtypes of thalassaemia Alpha (ÃŽ ±) thalassaemia results from inadequate production of ÃŽ ± chains, which are normally controlled by two pairs of chromosomes. If one or two are malfunctioning, then there is a healthy carrier state. If three are non- functional then anaemia results, known as HbH Disease, which can be quite severe but usually does not need blood transfusions and is compatible with a normal life span (Anionwu et al, 2001). If all four genes are non functional then the result is severe anaemia of the unborn child, leading to heart failure and death (miscarriage). This condition is known as hydrops felalis (Fleming, 1982). Beta (ÃŽ ²) Thalassaemia is caused by the bodys inability to produce normal haemoglobin, leading to a life threatening anaemia (Bienz, 2007). The severity of illness depends on whether one or both genes are affected and the nature of the abnormality. If both genes are affected, anemia can range from moderate to severe. Beta thalassaemia results from inadequate or lack of production of ÃŽ ² chains (Anionwu et.a.l, 2001). Homozygous, ÃŽ ² thalassaemia has two forms: major, in which the patient can survive only with regular transfusions of blood and intermedia in which the patient can survive with occasional or even with no transfusions at all. The condition requires frequent blood transfusions and treatment to prevent complications from iron overload, such as diabetes and other endocrine disorders (Anionwu et.a.l, 2001). Both of these conditions can restrict a child or adults ability to conduct their normal daily activities and can have profound psychological affects on individuals a nd their families This form of thalassaemia is the most important and constitutes a major public health problem in many parts of the world, because of the high frequency of carriers and the demanding treatment that must be followed (Fleming, 1985). Association of Haemoglobinopathies with Malaria Malariais a vector borne infectious disease caused by protozoan parasites. It is widespread in tropical and subtropical regions, including parts of the Americans, Mediterranean, Asia and Africa. It causes diseases in approximately 515 million people and kills between one and three million people, the majority of whom are young children. Malaria parasites are transmitted by female Anopheles mosquitoes. The parasites multiply within red blood cells, causing symptoms that include symptoms of anemia (Campbell et al, 2004). Sickle cell developed as a by product of human defense mechanisms against malaria. The most severe form of malaria, falciparum malaria, leads to very high death rate in young infants. This is particularly a problem between the time immediately after birth, when they are protected by immunity from the mother, and the time when they are old enough to acquire their own immunity. Malaria is a parasite which lives within the red blood cells and feeds off the protein that is contained within those red cells, haemoglobin (Campbell et al, 2004). When the malarial parasite enters the blood stream through a mosquito bite, it penetrates the red blood cells by attaching to the outside membrane or envelope of the red blood cell and gaining entry (Franklin, 1990). Once in the red blood cell, the malarial parasites use the haemoglobin as a source of energy, so that they multiply within the red cells. The parasites multiple filling-up the red blood cells and once they are filled-up the red cells bur st, thereby releasing the multiple parasites in the blood. Each new young parasite enters a single cell again and multiplies again, thereby causing a disease or infection. Whenever the parasites burst out of the cells they cause illness and fever in patients. Malaria can be severe by causing death; death is believed to be caused by red cells not being able to pass through the narrow gaps in the smallest blood vessels and by blockage of tissues when so many parasites are in the red blood cell (Campbell et al, 2004). Over the years human genes developed ways to prevent malaria becoming serious and potentially lethal, the developments were to prevent malarial parasites from spreading and multiplying (Tortora et.al,2006). The most changes were changes (mutation) in the type of haemoglobin (haemoglobin S) within the red blood cell which would in turn slow down the multiplying of the parasite (Campbell et al, 2004). The individuals with haemoglobin S are known to have a sickle cell trait or being carriers of sickle cell haemoglobin. When sickle-cell haemoglobin has given up its oxygen in the cells, the red cells stick together to form crystalline groupings of haemoglobin known as polymers. The red blood cells become deformed into sickle shapes and the presence of these crystalline polymers within the red cells inhibits the growth of the malarial parasite (Beinz, 2007). Even though individuals with haemoglobin S stills suffer from malaria, they are protected from the most severe effects of malaria (Li vingstone, 1985). Diagnosis Diagnosis for sickle cell disease The most used diagnose test for sickle cell is the haemoglobin electrophoresis. HbS and HbC amino acid substitutions change the electrical charge of the protein, the migration pattern of the haemoglobin with electrophoresis or isoelectric focusing results in diagnostic patterns with each of the different haemoglobin variants. HbSBeta-thal requires careful evaluation of red blood cell count and mean corpuscular red cell volume (MCV) and specifically quantifying HbA, S, A2 and F. In emergency setting, the presence of HbS is detected using a five minute solubility test called sickledex. Sickledex test does not differentiate sickle syndromes from the benign carrier state (HbAS or a sickle trait (NHS Antenatal and Newborn; 2006). Diagnosis for thalassaemias When testing for thalassaemias, a blood test is the simplest and most effective test for diagnosis and also the use of a test called Haemoglobin Electrophoresis. The blood of individuals with thalassaemias tend to be microcytic (smaller in size) and hypochromic (paler in colour) (NHS Antenatal and Newborn; 2006). 7 Pathophysiology 7.1Sickle-cell Sickle-cell anemia is caused by changes (mutation) in the structure of the ÃŽ ² -globin chain of the haemoglobin replacing the amino acid glutamic acid with the less polar amino acid valine at the sixth position of the ÃŽ ² chain. When two wild type ÃŽ ±-globin subunits associate with two mutant ÃŽ ²-globin subunits forms hemoglobin S. Haemoglobin S polymerizes under low oxygen conditions, which causes distortion of red blood cells and also causes red blood cells to lose their elasticity, resulting in red blood cells forming an irreversible sickle shape (Fleming,1982). Very often a cycle occurs, as the cells sickle they cause a region of low oxygen concentration which causes more red blood cells to sickle. Repeated occurrence of sickling causes cells to not return to normal even when oxygen levels are normal. The deformation of cells makes it difficult for the cells to pass through capillaries resulting in vessel occlusion, severe anemia, ischemia and other problems (Beinz, 2007). 7.2Thalassaemias The pathophysiologic effects of the thalassaemias range from mild microcytosis to death in uterus. The anaemia manifestation of thalassaemia is microcytic hypochromic haemolytic anaemia (Belcher, 1993). The haemoglobin abnormality is caused by substitution of a single amino acid for another; or substitution of two amino acids, also amino acid deletion or fusion (point of mutation) and the synthesis of elongated chains. In alpha trait, one of the genes that form the alpha chain is defective (Beinz, 2007). In alpha-thalassaemia minor, two genes are defective and in haemoglobin H disorder, three genes are defective. Alpha-thalassaemia major is most fatal thalassaemia disorder; this is because four of the chains forming genes are defective. Without alpha chains, oxygen cannot be released to the tissues (Belcher, 1993). In beta-thalassaemia haemoglobin abnormality is due to the uncoupling of alpha and beta-chain synthesis. This causes a depression in beta-chain synthesis, resulting in er ythrocytes with a reduced amount of haemoglobin and accumulation of free alpha chains, which are unstable and easily precipitate the in cell (Bienz, 2007). 8.Causes Genetic control of haemoglobin synthesis The synthesis of structurally normal haemoglobin chains is determined by allelic genes situated on the autosomal chromosome (Beniz, 2007). Haemoglobinopathies occur due to an inheritance of one or more faulty copy of gene(s) that contain the information for the cells to make the globin chains. The gene may result in abnormality in the production or structure of the haemoglobin protein causing haemoglobinopathies (Franklin, 1990). Thalassaemia is an inherited autosomal recessive blood disorder. Genetic defects in Thalassaemia results in reduced synthesis of one of the globin chains which make up haemoglobin. Reduced synthesis of one of the globin chains causes the formation of abnormal haemoglobin molecules, which in turn causes anaemia. Anaemia is a symptom of the Thalassaemias. It is caused by under production of globin proteins, often through mutations in regulatory genes (Franklin, 1990). Inheritance of Haemoglobin Disorder Due to haemoglobin mutation, individuals who had haemoglobin trait had a resistance to dying from malaria, therefore passed on their haemoglobin trait gene to their children (Campbell et.al,2004). As time went on more individuals with the trait were born and eventually individuals who had haemoglobin trait had children together (Franklin, 1990). In that satiation (partnership), if both parents carry the trait gene, there is a one in four chance that any one child will receive the haemoglobin trait gene from one parent and also from the other, thereby having a haemoglobin disorder(Franklin, 1990) . Clinical Manifestations 9.1Thalassaemias clinical manifestations Individuals who inherited the alpha trait are usually asymptomatic, with possible mild microctyosis. Alpha- thalassaemia minor has signs and symptoms almost identical to those of beta-thalassaemia; mild microcytic hypochronic anemia, enlargement of the liver and spleen, and bone marrow hyperplasia (Belcher, 1993). Alpha- thalassaemia major cause hydrops fetalis and fulminana intrauterine congestive heart and liver, edema and massive ascites. The disorder usually is diagnosed post mortem (Bienz, 2007). Beta-thalassaemia minor causes mild to moderate microcytic-hypochronic anemia, mild splenomegaly, bronze coloring of the skin, and hyperplasia of the bone marrow. Skeletal changes depend on the degree of reticulocytosis, which in turn depends on the severity of the anaemia (Bienz, 2007). People who have beta-thalassaemia minor usually are asymptomatic, whereas those with beta- thalassaemia major the anemia is severe, resulting in a great cardiovascular burden, with high output congestive heart failure (Belcher, 1993). Blood transfusions can increase the persons life span by a decade or two. Individuals with beta-thalassaemia major have an enlarged liver and spleen, and growth and maturation are retarded (Belcher, 1993). A characteristic deformity develops on the face as the bones expand to accommodate hyperplastic marrow (Belcher, 1993). Both and beta thalassaemias major are life threatening. Children with thalassaemia major usually are week, fail to thrive, how poor development and experience cardiovascular compromise with high-output failure; if the condition goes untreated, these children die by 6 years of age (Modell et.al., 2001) Blood transfusions can return haemoglobin and hematocrit to normal levels, alleviating the anaemia induced cardiac failure. Iron overload and hemochromatosis, which are complications of transfusion therapy, are treated with chelating agents (Bienz, 2007). . 9.2.Sickle-cell clinical manifestations The severity of sickle cell disorder depends on the amount of haemoglobin S and the clinical manifestations, which are signs and symptoms of the individuals with sickle-cell (Belcher, 1993) . Manifestations of the sickling are those of hemolytic anemia; pallor, jaundice, fatigue and irritability. Extensive sickling can precipitate four types of crises: vaso-occlusive or thrombotic crises and a plastic crisis (Belcher, 1993). A vaso-occlusive crises begins with red blood cells sickling in the microcirculation. Vasospasm brings a log-jam effect causing blood flow to stop flowing in the vessels and this will lead to thrombosis (blood clot formation) and infarction of local tissue occur, resulting in ischemia, pain and organ damage (Modell et.al.,2001). Vaso-occlusive crisis is believed to be extremely painful and lasts an average of 4 to 6 days. This crisis may develop spontaneously or may be precipitated by localized hypoxemia (low PO2) exposure to cold, dehydration, acidosis (low pH), or infection. In infancy, sickle-cells first manifestation is the symmetric painful swelling of the hands (see Fig 3) and feet, but in older children and adults, the large joints and surrounding tissues become swollen and painful. Individuals with the sickle-cell disorder suffer from severe abdominal pain caused by infarction in abdominal structures (Belcher, 1993). Any cerebral vascular accidents may cause paralysis or othe r central nervous system deficits, and if penile veins are obstructed priapism may occur. Studies have shown that bone, especially weight- bearing bones, are also a common target of vaso-occlusive damage, this is due to bone ischemia (Bienz, 2007). The spleen of individuals with sickle-cell disorder is frequently affected due to its narrow vessels, functions in clearing defective red blood cells and this results in a sequestration crisis (Belcher,1993). A sequestration crises, is occurrence of large amounts of blood pool in the liver and spleen. It only occurs in young children and death results from cardiovascular collapse (NHS Antenatal and Newborn,2006). An aplastic crisis develops when a compensatory increase in erythropoiesis is compromised; this then results in profound anemia (Belcher,1993). A hyperhemolytic crisis is rare but may occur with certain drugs or infections. G-6-PD deficiency, when also present, contributes to this type of crisis (Belcher,1993). Clinical manifestations of sickle cell disease do not usually appear until an infant is at least 6 months old. The most cause of death in individuals with sickle-cell anemia is infections, but it is major problem at all ages. Infections are due to splenic dysfunction from sickle damage (Belcher,1993). This occurs from a few months of age especially with certain bacteria e.g. pneumococcal sepsis. Infection tends to rapidly overwhelm the immune system (NHS Antenatal and Newborn,2006) . Sickle-cell haemoglobin C is known to be milder, with symptoms related to vaso-occlusive crises resulting from higher hematocrit and blood viscosity. Obstructive crises cause sickle cell retinopathy is most common in older children, and this include renal necrosis, and aseptic necrosis of the femoral head (Belcher, 1993). The mildest of sickle-cell is the sickle-cell thalassaemia the individuals with this form of sickle-cell tend to be microcytic and hypochromic, which makes the cells less likely to clog the microcirculation even when sickling (Belcher, 1993). Severe hypoxia can be seen in individuals with the sickle cell trait and may cause vaso-occlusive episodes. The cells in these people form an ivy shape (Belcher, 1993). Recent studies have shown that stroke is co-exiting with Sickle cell disease. At least 1% of patients with sickle cell disorder suffer from stroke and those individuals result in physical disability, IQ reduction, Learning difficulties, TIAs and seizures (Beinz, 2007). Treatment of haemoglobinopathies. 10.1Treatment in Sickle-cell anemia. Febrile illness: Children with fever are screened (a full blood count, reticulocyte count and blood culture taken) for bacteremia. In young children the fever is treated with intravenous antibiotics, the children would be admitted at the hospital so that they can be monitored (Belcher, 1993).. But older children with reassuring white blood cell counts are managed at home with oral antibiotics, but if the older children have a history of bacteremia episodes, they get a hospital admission. (Modell et al, 2001) Zn administration: is when zinc is given to stabilize the cell membrane (Beinz, 2007). Painful (vaso-occlusive) crises: individuals with sickle cell disorder experiences painful episodes called vaso-occlusive crises. Vaso-occlusive crises is often treated symptomatically with analgesics (Beinz,2007). Pain management requires opioid administration at regular intervals until the crises has gone. The frequency, severity and duration of these crises episodes vary tremendously form episodes to episode or from person to person (Belcher,1993). Individuals who suffer from milder vaso-occlusive crises manage their pain on NSAIDs e.g. diclofenac or naproxen. And if the crises is severe, individuals require inpatient management, where intravenous opioids. Diphenhydramine is used to stop the itchiness associated with the opioids (Modell et al, 2001). Acute chest crises management is similar to vaso-occlusive crises treatment with the addition of antibiotics, oxygen supplementation for hypoxia, and close observation. If the pulmonary infiltrate worsen or the oxygen requirements increase,

Custom Term Papers: Hamlet’s Heroine, Ophelia -- GCSE English Literatu

Hamlet’s Heroine, Ophelia In Shakespeare’s tragedy Hamlet there is, technically, no heroine. But the female character who comes closest to qualifying for the role is not Gertrude, whose sinful past precludes this, but rather Ophelia, the â€Å"universal victim† of the drama. She is truly a good, upright person although she is victimized by her father, brother and boyfriend. Harry Levin, in the General Introduction to The Riverside Shakespeare, elaborates on the special kind of prose which the dramatist uses with Ophelia when she suffers her madness: Though there is no invariable rule, the comic scenes are frequently in prose, whereas the tragic scenes are usually in verse. Yet some of the most tragic, notably Ophelia’s made scenes and the sleep-walking scene of Lady Macbeth, are in that special kind of distracted prose which Shakespeare reserved for moments of mental distraction, when the fragments of suppressed emotion well up from the unconscious. (11) Shakespeare’s use of distinctive language is one consideration concerning Ophelia. Another is her victimization. Gunnar Boklund in â€Å"Hamlet† performs a partial-analysis on the character of Ophelia in Shakespeare’s tragedy, Hamlet: The only character who is presented almost entirely as a victim is Ophelia, a victim of the King’s fear and curiosity, her father’s servility and fundamental indifference to her, Hamlet’s misunderstanding of the situation and brutal treatment of her, and finally his fatal thrust through the arras in the closet scene. Her madness is, as I see it, a purely pathetic element in the play. In the world where Hamlet has been forced to act, there appears to be no room for passive and obedient innocence. It is crushed, and perishes. (123) The p... ...: Madness Her Only Safe Haven.† Readings on Hamlet. Ed. Don Nardo. San Diego: Greenhaven Press, 1999. Rpt. from â€Å"Hamlet†: A User’s Guide. New York: Limelight Editions, 1996. Pitt, Angela. â€Å"Women in Shakespeare’s Tragedies.† Readings on The Tragedies. Ed. Clarice Swisher. San Diego: Greenhaven Press, 1996. Excerpted from Shakespeare’s Women. N.p.: n.p., 1981. Shakespeare, William. The Tragedy of Hamlet, Prince of Denmark. Massachusetts Institute of Technology. 1995. http://www.chemicool.com/Shakespeare/hamlet/full.html Ward & Trent, et al. The Cambridge History of English and American Literature. New York: G.P. Putnam’s Sons, 1907–21; New York: Bartleby.com, 2000 http://www.bartleby.com/215/0816.html Wilkie, Brian and James Hurt. â€Å"Shakespeare.† Literature of the Western World. Ed. Brian Wilkie and James Hurt. New York: Macmillan Publishing Co., 1992.

Shakespeares Othello - Desdemona the Ideal Essay -- Othello essays

Desdemona the Ideal  Ã‚        Ã‚  Ã‚   What wife can compare to the ideal wife which the Bard of Avon has painted for us in his tragedy Othello? She is appreciated by everyone except the villain.    Angela Pitt in â€Å"Women in Shakespeare’s Tragedies† comments on Desdemona as the ideal wife:    Handbooks of the period explain in some detail what is required of the ideal wife, and Desdemona seems to fulfill even the most conservative expectation. She is beautiful and also humble:    A maiden never bold Of spirit so still and quiet that her motion Blushed at herself. (I.iii.)    Her concern for Cassio shows her generosity, for she will intercede for him with Othello. She is wise, and also a ‘true and loving’ wife – ‘the sweetest innocent that e’er did lift up eye’. (44-45)    David Bevington in William Shakespeare: Four Tragedies describes the depth of virtue within this tragic heroine:    We believe her [Desdemona] when she says that she does not even know what it means to be unfaithful; the word â€Å"whore† is not in her vocabulary. She is defenseless against the charges brought against her because she does not even comprehend them, cannot believe that anyone would imagine such things. Her love, both erotic and chaste, is of that transcendent wholesomeness common to several late Shakespearean heroines [. . .]. Her â€Å"preferring† Othello to her father, like Cordelia’s placing her duty to a husband before that to a father, is not ungrateful but natural and proper. (221)    Blanche Coles in Shakespeare’s Four Giants interprets the protagonist’s very meaningful four-word greeting to Desdemona which he utters upon disembarking in Cyprus:    Othello’s four words, â€Å"O, my soul’s joy,† tel... ...mind behind the murder results in Iago’s murder of her. Gullible Othello, grief-stricken by remorse for the tragic mistake he has made, stabs himself and dies on the bed next to his wife, his sorrow being as deep as his love for Desdemona prior to Iago’s machinations.    WORKS CITED    Bevington, David, ed. William Shakespeare: Four Tragedies. New York: Bantam Books, 1980.    Coles, Blanche. Shakespeare’s Four Giants. Rindge, New Hampshire: Richard Smith Publisher, 1957.    Pitt, Angela. â€Å"Women in Shakespeare’s Tragedies.† Readings on The Tragedies. Ed. Clarice Swisher. San Diego: Greenhaven Press, 1996. Reprint from Shakespeare’s Women. N.p.: n.p., 1981.    Shakespeare, William. Othello. In The Electric Shakespeare. Princeton University. 1996. http://www.eiu.edu/~multilit/studyabroad/othello/othello_all.html No line nos.      

The Cultural Invasion of Kenya Essay -- American Culture Traditions Es

The Cultural Invasion of Kenya A screeching yell ripped through the house that Wednesday evening, "Ahhhhh, we're being invaded!". My mother rushed into the living room. I pointed to the flickering television screen. "Look," I whispered in disbelief. A few seconds of silence followed. There they were, the words I never thought would appear on our 29 inch Sony screen: "Sizzlin' Hot Country". The appearance of American country music on the Kenyan airwaves was the latest sign that American culture had penetrated the borders of my country. The airing of Garth Brooks and Dolly Parton on the local television station is not the only evidence of the rapid spread of American culture in Kenya. One look at a large portion of its youth and this cultural invasion will become apparent. Baggy pants, Nike, pop music and malls, symbols of American youth culture can now be associated with the Kenyan teenagers. The Nike phenomenon hit Kenya several years ago. My classmates in primary school were obsessed with the American brand name that had rocked the global shoe industry. Their school desks had the Nike name and logo painted on in every color imaginable. Not being able to afford some of the merchandise, many resorted to drawing the logo on bags, clothes, shoes and other visible possessions. Turning up to a class party with the trademark tick appearing on one's footwear simply made one the center of attention. My favorite pair of shoes, I have to admit, were a pair of black Nikes which raised many brows and turned just as many heads. Secondary school had its fair share of examples of the cultural invasion. In most schools in Kenya, students dress in uniforms. For example, in my school it was compulsory to wear a white shirt, gra... ...ols of success. While hip hop and baggy pants may not epitomize American success, Kenyan youth adopt this aspect of American culture perhaps because of the common roots and racial background the majority share with African Americans. Wearing Nike shoes or sagging one's pants may seem to be meaningless gestures. However, wearing shoes that many popular, rich American sporting icons don or sagging pants like the famous hip hop artists makes one different from the rest. It allows one to adopt an American identity, one defined by success and importance. While some would argue that such a spread of American culture would be beneficial because it would, in a sense, create a global village, I think this cultural invasion creates more harm than good. It would result in the demise of local cultures and languages. And this is certainly not a good thing.

Ethics and Morality Essay

There is an inherent question on the basis of morality and whether or not it is a man-made, almost religious invention or if it is intrinsic to our beings as humans. I think that the rope that is the argument between is too complicated and tightly knotted to have a short conversation about, but by fraying the ends of the rope we can inevitably decide that morality is innate and that religion may have a part in building upon it, but not in creating it. The curiosity behind the topic of morality is normally fashioned by religious arguments for the assumption that a deity endowed us as humans with some sort of moral compass. However, by searching the brain for its different functions and activities during moral dilemmas and religious interactions, along with historical clues and a little knowledge of sociology, determining that morality is not created, only built upon, is inevitable. Morality is defined as normatively to refer to a code of conduct that, given specified conditions, would be put forward by all rational persons (Stanford). With this as a definition, the first question to rises is the following: What is one moral action that a believer can do that a non-believer cannot do? There are few answers to the inverse, if any, but non-believers do not pose that they have any stronger of a moral compass than believers, while believers do. It is incredibly important to think about an answer to this question because if there truly is no answer to this challenge, then a road has been paved toward an objective that we can already see, which is that being ethical and moral is not necessarily a religious view, so such claims can immediately be cast off and the topic can stay on a strictly scientific road. Now the consideration lies upon what is deemed as an ethical person. Is the president ethical in his decisions? Is a doctor ethical in his decisions? Of course, there is an ethical code in these circles, but does that immediately mean that any decisions outside of the codes are immoral? A moral person is normally described as somebody who takes into account the possible consequences of his or her actions and rationally decides on a choice based on how it may affect those around him. We call these people morally good because their contributions to whomever they are around are normally well thought-out, harmless contributions to the topic. However, this is simply a definition, and the person is simply his or her self. Take into account the thoughts of those around the subject. A religiously-convicted man would say that his religion is the reason for his good nature, while one not necessarily supporting religion would say that he is simply a good person. As an aside, there are multiple people who would take the chance to point out many historically immoral figures, such as Mao Zedong, Stalin, Pol Pot, who were atheistic. While it is true that these figures were indeed non-believers, it is important to distinguish the reasons for their immorality. It was not based on religion, but rather by social constructs and a greed for power that caused them to act out. Some may cite Hitler as an atheist as well, but they’d be digging their own grave. Hitler, in Mein Kampf, even gives credit to the Christian god, and had religious inscriptions on every Nazi-uniform belt. To get back to the previous point, it is important to take into account what those around the subject would perceive, and although the religiously-convicted man might have millions of people around the world following his train of thought, research done Dr. Pyssiainen and Dr. Hauser from the departments of Psychology and Human Evolutionary Biology at Harvard University offers an interesting perspective on the topic: â€Å"†¦Despite differences in, or even an absence of, religious backgrounds, individuals show no difference in moral judgments for unfamiliar moral dilemmas. The research suggests that intuitive judgments of right and wrong seem to operate independently of explicit religious commitments. † Pyssiainen’s and Hauser’s study grants us that although religious backgrounds may indeed build upon moral constructs, as good religion is only positively influential to a good person, a complete lack of religious background is perfectly plausible if an individual wishes to be moral because moral judgments are not linked to religious commitments. This finding is absolutely crucial to determining whether or not morality is man-made or inherent to humans because it breaks the perceived bond between belief and morality. So their contribution to the topic has been seen through and accepted as a welcome source of reference. However, it is essential to look at the other side of the argument. Which studies show that seem to show that religion is a key factor in morality? Unfortunately, they are found few and far between. As a matter of fact, there are literally no scientific studies that show religion is crucial in the formation of morality. It’s widely granted that religion, in some aspects, can further construct upon morality and cause others to be exceedingly altruistic and generous, and that is conceded by Paul Bloom of Yale University, but it is not a formative agent. In his paper, â€Å"Religion, Morality, Evolution,† he accepts that religion can be a guiding influence on a positive path. However, he points out that it is by no means the reason for morality, and that religion itself may just be an accident by which humans needed an answer to questions that they couldn’t fathom without the help of a deity. Necessity dictates that there should be some rather fueled individuals on a topic as flammable as the topic of morality and religion. Speaking as an outsider looking in, I cannot very well use the words of Christopher Hitchens, though I would love to dearly, because he was so against religion. While he was indeed logical in most of his claims, he was a self-described anti-theist, meaning that he was against a spectating deity who watched over each individual. Thus, his words would seem rather biased. However, Richard Dawkins, an evolutionary biologist, and Sam Harris, a well-known neuroscientist, are individuals who speak strictly through logical and provable means. Richard Dawkins posed the same point as Paul Bloom that religion is most likely an accident through evolution that was used as a possible answer to the world’s greatest questions, and Harris poses multiple reasonable points. The most relevant, though, is that if the bible were the only book in the world, it would be rational to use it as a basis for morality. However, because the bible is not the only book in the world and society is far more civilized now than it was when the bible was conceived, it is reasonable to assume that the bible is not the best book for building a moral compass. To end on a rather short note, there are few, if any, scientific studies arguing that religion is the factory that builds moral compasses. However, there are studies being conducted which follow Pyssiainen’s and Hauser’s and should end up corroborating their finds that morality works independently of religious constructs and confines. Thus, it is both rational and reasonable to assume that, after looking through history at the reasons for extreme wrongdoings and the social situations that facilitated them, and the evidence against opposing claims, morality is indeed intrinsic to our human nature and that it is simply augmented by outside forces, such as good religion. References Bloom, Paul, Religion, Morality, Evolution (January 2012). Annual Review of Psychology, Vol. 63, pp. 179-199, 2012. Available at SSRN: http://ssrn. com/abstract=1982949 or http://dx. doi. org/10. 1146/annurev-psych-120710-100334 Cell Press (2010, February 9). Morality research sheds light on the origins of religion. ScienceDaily. Retrieved May 12, 2013, from http://www. sciencedaily. com /releases/2010/02/100208123625. htm Harris, Sam. Letter to a Christian Nation. New York: Random House, Print. Harris, Sam. The End of Faith: Religion, Terror, and the Future of Reason. New York: W. W. Norton, Print. Pyysiainen, Hauser et al. The origins of religion Q1 : evolved adaptation or by-product? Trends in Cognitive Sciences, February 8, 2010 â€Å"The Nature of Morality and Moral Theories. † Morality and Moral Theories. University of San Diego. Web. 12 May 2013. .

Nina

childrens needs February 2012 | | |Assignment 1: | |Explain what constitutes the physical and psychological needs of a three year old child. Explain how you would ensure that these physical and | |psychological needs can ideally be met in a setting/nursery which the 3 year old child attends from 8 am to 6 pm, 5 days a week. Reading for your assignment. Though we provide some recommended books and chapters, (see below) you need to read around the subject as much as possible and not limit yourself to just the recommended readings. Recommended reading from your prescribed text books:- Macleod-Brudenell, I,& Kay, J (2008, Second Ed) Advanced Early Years for Foundation Degrees & Level 4/5 Harlow: Heinemann Chapters 4, 5 and 9 Montessori Centre International (MCI) (undated a) Module 2 Child Development London: MCI Chapters 1 and 3 (pg 39 – 42) Montessori Centre International (MCI) (undated b) Module 4 Contemporary Issues London: MCIChapters 1, 3, 4 and 5 Montessori Centre Internat ional (MCI) (undated c) Module 5 Childcare and Health London: MCI Additional reading to consider for this assignment:- Montessori International (Issue 94, January – March) (Various articles in this issue of the magazine are relevant) Unicef (2008) Convention on the Rights of the Child, available from http://www. unicef. org/crc/ This assignment focuses on the importance of supporting the child’s well-being. Although, you will be given guidelines and additional reading material to assist you in the writing of this assignment, it is important for you to read as widely as you can.You will also need to consider the specific requirements within your own country. In these tutorial guidelines, the assignment question will be broken down into sections, giving you some pointers to consider when preparing your answer for submission. In order to enable you to focus on the different aspects of the questions, each has been given a weighting. These are the maximum marks that can be awarded for this part of the answer. The other 25% of the marks cover structure, expression and presentation (Take note of the marking table on the assessment sheet that you have received). WORKING ON THIS ASSIGNMENTBegin by:- †¢ Work through the recommended chapters listed above, making notes as you did for your Study Skills assignment. Please note that you are not limited to these chapters – You may also find it useful to do some independent research in your local library or on the internet. Be careful to limit your reading to academically sound sources – Wikipedia is not a safe site to use and should be avoided. (Remember to keep a record of the source document for later referencing and bibliography). †¢ Go through the extended guidelines below, and begin to gather information for your answer. Make note of any questions you have regarding this assignment and send them through to me. These questions and their answers will then form the second half of this f irst tutorial (the Q&A) which will be emailed to you so that you can take the information into consideration before finalising your essay for submission. Start to work on your answer:- 0 Study skills recap – †¢ Organise your information and thoughts into a logical, structured argument, addressing each of the important / main bullet points. Ensure that there is an overall flow to the information, and that each section links back to the question posed. Begin with an introduction that will state what you are going to cover in the main body of the essay. The introduction should be  ± 5-10% of the total length of the essay. Draw your argument to a conclusion at the end. †¢ Reference each time you paraphrase ideas you have read during your research for the essay, as well as the first time you include specific terminology in any one essay. In this essay you should ensure that you are quoting from academically sound sources. †¢ Find three or four relevant quotes that will support your argument.Use MCI protocol when referencing and quoting. CONTENT GUIDELINES FOR THIS ASSIGNMENT Identify and define the specific physical needs of a three year old child – including exercise and rest, diet, health and safety. (10) †¢ Briefly define what is meant by physical needs, including exercise and rest, diet, health and safety . †¢ Identify the specific physical needs of a three year old. Give a full explanation of how these physical needs should ideally be met by an early years setting/nursery which offers care from 8am to 6pm five days a week. (17. ) – Consider for example, how you could provide for gross and fine motor skills. Also think about safety issues (such as appropriate clothing for specific weather conditions), access to fresh air and ventilation in the classrooms, opportunities for rest, etc. – Give practical examples of what a setting would do to ensure the child’s well being as an essential pre-requisite to effective learning. Identify and define the psychological needs of a three year old child – focus on emotional and social needs. (10) †¢ Briefly define what is meant by psychological needs, focus on emotional and social needs.Your definition should briefly consider the needs for survival, participation and belonging. †¢ Identify the specific psychological needs of a three year old. Give a full explanation of how the psychological needs should ideally be met in an early years setting/nursery which offers care from 8am to 6pm five days a week. (17. 5) – Explain how the three year old’s emotional and social needs can be met. Here you should be looking at consistency, predictability and availability of care. – Explain how the children’s well-being and sense of belonging are promoted. Focus on settling in procedures and transitions, availability of a key person and liaison with parents. – Give practical examples of how you could make a three year old comfortable, settled, at ease and ready to actively participate in the daily life of the nursery. Having discussed the physical and psychological needs of a three year old relate these to relevant articles in the UNCRC (United Nations Convention on the Rights of the Child) which inform the statutory requirements for best practice in early years settings/nurseries in your country (20) –Briefly explore the general underlying principles (especially that of survival, protection and participation) which underpin the relevant articles of the UNCRC. (supplied with this tutorial) – Link these principles to the child’s needs. 0 Study skills recap – †¢ Your conclusion should summarise what you have said, without adding or introducing anything new. †¢ The word count includes references and quotes, but excludes bibliography †¢ Remember to use double line spacing and to number the pages of your document Finalising your answer:- †¢ R ead through your essay, checking your spelling, grammar and referencing format. Make sure your argument has a logical flow, and that you have answered each aspect of the question fully, in your own words. †¢ Fill in the cover sheet, including all necessary details. Check that your word count is within the accepted limit. †¢ Compile or finalise your bibliography using the correct format. (Follow the MCI protocol as outlined in your Student Handbook. ) 0 Study skills recap – Your bibliography must include full entries for all sources that you have referred to in your essay, as well as other books, articles, websites etc that you have read or consulted in preparation for this assignment.Bibliography:- Macleod-Brudenell, I, & Kay, J (2008, Second Ed) Advanced Early Years for Foundation Degrees & Level 4/5 Harlow: Heinemann Montessori Centre International (MCI) (undated a) Module 2 Child Development London: MCI Montessori Centre International (MCI) (undated b) Module 4 C ontemporary Issues London: MCI Montessori Centre International (MCI) (undated c) Module 5 Childcare and Health London: MCI