Sickle Tissue: A Case Study

The dosage was to high for the patient because the chart started going over the regular normal level

NH hospitalization record reveals a medical history of a non-injurious stroke, numerous episodes of sickle cell crisis, acute chest syndrome and chronic asthma. NH is prescribed a daily regimen of medications including a daily dose of 15,00 mg hydroxyurea, 1 mg folic acid for his SCD and 44 mcg of inhaled fluticasone for his asthma. Currently, while suffering from sickle cell crisis, NH is prescribed oxycodone 5mg, Toradol 21 mg IV solution, acetaminophen, and morphine as well as a continuous IV drip of D5 ½ NS, KCL. Due to the opioids and level of pain NH has endured the last 4 days (since beginning of crisis) he is exhausted and considered a fall risk due to his fatigue and reports that he naps off and on throughout the day and only gets out of bed to use the

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.

Per office visit notes dated 8/7/2016, patient presents for a follow up for neck pain, left elbow pain and bilateral wrist pain. Current medications include Naprosyn EC 500 mg, Tramadol 50 mg, Lyrica 50 mg and Levora-28 0.15/0.03 mg. Patient was recommended retrial of Celexa for her depressed mood related to her chronic

Vaso-occlusive events are moments of severe pain common in sickle cell patients; it is a result of the adhesion of cells to the endothelial lining. While leukocytes play a role in vaso-occlusive events, erythrocyte activity plays an even bigger role. It was discovered that the receptors on the erythrocytes and the endothelial cell were responsible for the mediation of the adhesion of erythrocytes to the endothelial lining (Stuart; Nagel, 2004). The adhesions of these cells to the cell wall is what leads to inflammatory disease, and certain types of acute chest syndrome.

Sickle cell anemia is one of the disease out there in the world that cannot be cured. The only thing people suffering from sickle cell can do is get treatments for the symptoms they are suffering from. Not only are there treatments, but there are also things that can be done that can prevent some of the symptoms. Some of the treatments available are different kinds of medications, vaccines, and experimental treatments. When a child suffers from sickle anemia their life could be put on line when catching an infection that may not be life threating to some who may not have that disease, so it is important for children to take antibiotics. From the antibiotics a person can take painkillers to relieve the suffer pain. A drug that is

She also uses Acetaminophen 500 mg tablet. Beside that resident takes Actonel DR 35 mg tablet, which is equivalent to Risedrontate, which are bisphosphonates medication use in the prevention or the treatment of Osteoporosis. Resident also takes Escitalopram 10 mg tablet, which are antidepressant medicines uses for general anxiety disorder. Another medicine that the resident takes is Furosemide, it is equivalent to Lasix, and it is loop diuretic medication uses for edema with cognitive heart failure however, asses the resident input and output daily to determine the fluid loss. Resident takes potassium chloride for the treatment or the prevention of hypokalemia. Trazodone is another medication resident takes which is for her depression. Resident takes Ipratropium and use for chronic obstructive pulmonary disease. Pulmicort is also another medicine this resident takes and is use to prevent asthma attacks. Last, is Salbutamol and is use for prevention of exercise –including acute

Most of the medication the patient will have to stay on for the rest of their life, because the medications reduce mortality, reduce risk of another MI from occurring, and also decrease the risk of another

In this essay I will be talking about sickle cell anemia. Well I was diagnosed with the disease at birth. I have what they call SS, which means I have the full illness. The reason I do is because both of my parents have a trait. This is my story.

This is a 50 year-old male who required inpatient hospitalization due to dizziness, abdominal pain, headache, and nausea after taking atenolol. Mr. A came to the Emergency Department with complaints of some dizziness two-day prior to admission and collapsed several times. For the past 2 weeks, he had not been taking his blood pressure medications due to financial reasons. He was given clonidine and atenolol from his dialysis center while he was unable to afford his normal hypertension medication. He was dialyzed three times a week through his arteriovenous fistula and had not missed any sessions. He also had increased dyspnea on exertion over the past 3 weeks, orthopnea and usually sleeps on several pillows which worsened between his dialysis. His medical history is significant for hypertension, diabetes mellitus type II, morbid obesity and end stage renal disease on dialysis.

It is interesting to know the relationship between race and body structure, skin color, other visible characteristics, enzymatic and genetic variations, susceptibility to diseases and nutritional preferences varies among certain racial groups (Giger, 2013). There are marked intra individual and inter individual inconsistency in SCD. Medical heterogeneity of the disease has been clarified by both genetic and environmental factors. Identified genetic causes adding to differences in clinical severity of the disease include the pattern of sickle cell inheritance. Other modulators of the disease include environmental factors such as access to optimal health care, ambient living conditions, and availability of finance. Proper training of healthcare

Imagine living a life with misleading information about a younger sibling's death. Many wonder why God took them, but not myself. For the simple fact the morning of Madison’s passing God told me everything would be okay. Experiencing this at such young age makes thou think of the extreme; however, it makes thee stronger. The idea of this paper is to break down the information and show everyone how Sepsis breaks down the body. Along, with linking Sepsis with Sickle Cell Trait when the body is already weak and cannot fight off the infection.

The patient needs a certain level of the drug in their blood to get the proper effect but some medications are harmful if the level goes up too high and they do not work if the levels are too low. For that reason it is necessary to monitor the amount of the drug that is in the blood of the patient. This allows the health care provider to make sure that drug levels are in the proper range. Tests can also be done to determine how well the patient's body breaks the drug or how it

Sickle Cell Anemia is a genetic disease that causes some red blood cells to take the form of a sickle this form is more easily destroyed which can lead to anemia. The disease is caused by defective hemoglobin. There are different types of hemoglobin, but Hemoglobin A is the primary hemoglobin affected by sickle cell. Hemoglobin A is made up of 2 alpha globin chains and 2 beta globin chains. The beta globin chain becomes misshapen due to a mutation. The mutation in the beta globin chain occurs when the sixth amino acid is valine instead of glutamic acid. Valine is Hydrophobic which has different properties than glutamic acid which is Hydrophilic. When the cell is deoxygenated it combinates with other cells that have the mutation

Madsen et al. developed this classification to asthmatic, cardiac, lymphatic, and sickle cell-related disease states(10, 13, 14). Madsen et al.(10, 13) defined this classification depending on the analysis of prior case studies. Cardiac patients mentioned by them consist of eight Fontan patients, one Glenn shunt patient and three Blalock–Taussig shunt patients. The casts can be immediately expectorated and sometimes patients will cough up large amount from their tracheobronchial tree(14). If the patients do not expectorate, it may delay the diagnosis(14). Patients often need bronchoscopy for the expulsion of cast(14). It is a rare condition that is mentioned in asthma and sickle cell disease patients and has higher mortality in patients with congenital heart disease(10, 13) and death is not unusual due to the occlusion of airway from a cast(14). The pathophysiology and management of plastic bronchitis is not clear due to insufficient clinical data. Over the years, plastic bronchitis has been labeled by various names as Hoffman's bronchitis, cast bronchitis, fibrinous