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Slow-Onset Disaster
Slow-Onset Disaster
Name of Student
Institution
Slow Onset Disaster
William Gunn (2012, P. 39) defines a slow-onset disaster, otherwise known as a chronic disaster as one associated with an insidious beginning and gradual progression. As such, it becomes eminent when it inflicts damage and suffering to large numbers, demanding an emergency response. Alabala-Bertand (2000, P. 215) describes a chronic disaster as a ‘complex humanitarian emergency’ which comes about as a result of the failure of institutional-based compensatory measures by the society and the social system. An example of a slow-onset disaster is a drought, which sets in slowly, but affects a large number of people, and whose response is an emergency. A specific example is the 2011-Horn of Africa drought that saw almost a million victims migrate from Somalia to neighboring countries like Kenya and Ethiopia. Kuman (2000, P. 67) observes that the nature of a chronic disaster is that it can be discerned in the pre-disaster phase, and a humanitarian crisis prevented if measures are implemented on time.
Disaster response managers face a huge challenge in regard to the management of chronic disasters. As LaPlante and Kroll-Smith (1989, P. 144) note, the potential to act and the knowledge of what needs to be done are two main challenges for disaster response managers in chronic disasters. Due to their nature, chronic disasters require government-coordinated policies, especially in the pre-disaster phase in order to ensure adequate management. Coordination of different levels of government becomes a challenge. The need for government policy limits the ability of disaster response managers, even in the instances where they know what to do. On the other hand, the body of research about chronic disasters is limited, as compared to rapid-onset disasters. As such, knowledge of solutions may pose a big challenge.
References
Alabala-Bertrand, J.M. (2000). “Responses to complex humanitarian emergencies andnatural disasters: an analytical comparison” Third World Quarterly, 21: 215-227.
Gunn, W.S. (2012). Dictionary of disaster medicine and humanitarian relief. New York, NY: Springer Science & Business Media.
Kuman, G.S. (2000). “Disaster Management and Social Development” International Journal of Sociology and Social Policy, 20:66-81.
LaPlante, M.J., & Kroll-Smith, S.J. (1989). Coordinated emergency management: The challenge of the chronic technological disaster. International Journal of Mass Emergencies and Disasters, 7(2), 134-150. <https://training.fema.gov/hiedu/downloads/ijems/articles/coordinated%20emergency%20nmanagement%20the%20challenge%20of%20the%20chron.pdf>
Sickle Cell Disease (SCD)
Sickle Cell Disease (SCD)
Student’s name
Institution
Course
Date
Sickle cell disease (SCD) was discovered in 1910. It represents a common inherited blood disorder. Sickle cell disease is a serious condition that can cause labour complications, organ damage and even death. People with sickle cell live a short life and have children with the same condition. Anyone with SCD has an abnormal haemoglobin molecule which causes red blood cells to become rigid and shaped like a sickle when they move through the body’s circulatory system. This condition can cause complications such as stroke and other problems with the brain and heart, resulting in severe cases (Sickle Cell Anemia) or improper oxygen delivery to parts of your body that need it most (such as your brain) (Sundd et al., 2019).
Defecting haemoglobin causes red blood cells to become rigid and sickle-shaped and reduced in number. The symptoms of SCD include fatigue, pain and episodes of destruction (hemolysis) of the red blood cells. The disease often results in severe, disabling lifelong complications such as chronic pain, damage to internal organs, stroke and acute chest syndrome (ACS). Inf underdeveloped blood vessels or organs can have sickle cell anaemia problems during or after birth. These problems can include infections, anaemia and feeding difficulties (Sundd et al., 2019).
Sickle Cell Disease is inherited in an autosomal recessive pattern. This means that each of your parents must be a carrier to pass the disease on to their child. The sickle cell trait (SCQ) is a genetic trait that produces an atypical haemoglobin molecule inherited by the heterozygous state (a single autosomal recessive gene). Individuals with SCQ have a 50% chance of expressing the symptomatic disease and only 25% for milder cases. Therefore, having two carriers for both genes will result in a 75% risk of expressing SCD.
A mutation in the beta-globin chain of the haemoglobin molecule causes sickle cell disease (SCD). This mutation results in sickle haemoglobin, which is less soluble and more rigid than normal haemoglobin. This abnormal haemoglobin causes the red blood cells to be malformed, becoming sickle-shaped. The sickle cells cannot travel easily through small capillaries, thus depriving areas of oxygen, leading to the aetiology of SCD.
This condition is inherited as an autosomal recessive trait. This means it is passed on from carrier parents to the offspring having a 25% chance of passing each of the genes to their offspring. The sickle cell gene is located on one of two copies (one copy inherited from each parent) in most heterozygous people and is dominant over normal haemoglobin in homozygous people. There are two major types of SCD: type I and type II sickle cells. The gene that causes a severe form of SCD (type II) is also called thalassemias. The gene responsible for milder (type I) SCD is called sickle cell trait.
The symptoms of SCD include high fever, jaundice, frequent infections and pain in bones, which can progress to bone necrosis or death. The severity of these symptoms varies from patient to patient and from time to time.
Regarding pathophysiology, red blood cells that are affected by the sickle cell gene are less elastic than normal ones and, as such, do not pass easily through the capillaries, leading to microvascular occlusion. This occurs because there is a decrease in blood flow in circulation due to blockage of vessels. There are three main categories of SCD, i.e. pulmonary, intestinal and hepatic manifestations. In the pulmonary phase, there is a defect in the formation or retention of alveoli and lung micro vascularization. The patient will have pneumonia due to the red blood cells settling in the alveoli due to reduced or delayed oxygen uptake. In this phase, patients will also have pleural effusion (accumulation of liquid) and ascites (accumulation of fluid). In liver pathology, there is involvement with microvascular injury and hepatomegaly due to the accumulation of red blood cells at the cellular level in hepatocytes (Orhurhu et al., 2020).
Hydroxyurea (HU): HU was approved by FDA in 2000 for the treatment of SCD. It is a cytotoxic agent that works to stimulate the production of an enzyme capable of stopping blood cells from abnormally clumping together (Ndefo et al., 2008). HU is typically taken 3x per week for 12 weeks at a time and then taken less often as needed depending on the patient’s symptoms, which may decrease with time or have unsuccessful outcomes after ten years if not continued therapy. However, some doctors will prescribe it for indefinite periods due to low side effects.
A care plan and patient education on Sickle Cell Disease are vital in managing the disorder. The various goals of such a plan are to care for individuals with SCD, monitor their disease status, and provide supportive care. A typical plan will include a prescription of the proper treatment, follow-up visits with the clinician, and education regarding symptom management. It is equally important that individuals understand their condition and its effects on their everyday life to take advantage of preventive measures when possible (Matthie et al., 2015). It is also important that they know what symptoms to watch out for to get appropriate care immediately.
To ensure that individuals with SCD are properly caring for themselves, education and guidance (palliative) are also important components of the management plan. Palliative care goals include early recognition of and prompt intervention in complications of SCD so that the individual can undergo surgery for organ damage when possible. Education about the disorder’s presentation, risk factors, diagnosis and treatment will allow the individual to be proactive in managing their disease (Matthie et al., 2015).
References
Matthie, N., Jenerette, C., & McMillan, S. (2015). Role of self-care in sickle cell disease. Pain Management Nursing, 16(3), 257-266.
Ndefo, U. A., Maxwell, A. E., Nguyen, H., & Chiobi, T. L. (2008). Pharmacological management of sickle cell disease. P & T : a peer-reviewed journal for formulary management, 33(4), 238–243.
Orhurhu, M. S., Chu, R., Claus, L., Roberts, J., Salisu, B., Urits, I., … & Orhurhu, V. (2020). Neuropathic pain and sickle cell disease: a review of pharmacologic management. Current Pain and Headache Reports, 24(9), 1-14.
Sundd, P., Gladwin, M. T., & Novelli, E. M. (2019). Pathophysiology of sickle cell disease. Annual review of pathology, 14, 263.
Reckhow maintains
School District Funding
Student’s name
Institutional affiliation
Reckhow maintains that foundations employ two major strategies in deciding which school districts to give funding to. To begin with, foundations need to have shared interests with the school district. Common interest helps the foundations to amplify their voice. This makes it easy for big foundations to join hands and raise more funding and this way. The foundations can work together as partners. Additionally, foundations only target specific school districts instead of spreading funding in many areas across the country. When they concentrate their funding in one area, they are better placed to achieve their plans and strategies than when they scatter the funding across many locations. Essentially, attaining goals becomes easier because each school is allocated enough funding because they are concentrated in one place. These influences should be of concern because they dictate whether the schools will receive funding and can potentially lock out deserving schools from accessing the funding.
What concerns me the most about contemporary issues affecting urban education has to do with how some schools are likely to be left out in funding while some schools continue getting all the funding. There is a chance that the schools that do not meet the criteria to receive funding will be locked out of funding each time (Mudrazija & Blagg, 2019). This disproportionately affects the performance outcomes of the students and, by extension, the school. This increases the poverty gap between well-to-do schools and schools that do not often meet the criteria for funding from foundations. Schools that qualify for foundations are likely to have more resources, including updated facilities such as libraries that play a critical role in ensuring students attain the highest possible educational qualification. This excludes and marginalizes the students from other schools that do not qualify for loans from foundations.
Student response
I couldn’t agree with you less on this matter. I think that foundations tend to think about what they stand to gain by funding a particular school than the good deeds that the funds will be used to execute. Sadly, the political climate dictates if and when a particular school will receive funding from a foundation.
References
Mudrazija, S., & Blagg, K. (2019). School District Funding in Texas.