Case Study # 85 Acute Lymphoblastic Leukemia (ALL)Order DescriptionCase Study # 85 Acute Lymphoblastic Leukemia (ALL)Start out with a BRIEF description of your case (a maximum 9 sentences). Everyone has the text book, so do not just repeat information. Summarize you patient, the problem, and any SIGNIFICANT findings (please do not list all medical history or every single lab result) only those pertaining to the problem.Please answer the following questions pertaining to this CASE STUDYAnswer Questions: 1, 2, 3, 4, 5, 6, 7, 8Write out each question before answering itPlease answer in detail pertaining to this patient and use some outside resources total number of 3 no older than 5 years as references (I provided 1 of the 3 references needed) APA format.Case Study # 85 Acute Lymphoblastic Leukemia (ALL)Start out with a BRIEF description of your case (a maximum 9 sentences). Everyone has the text book, so do not just repeat information. Summarize you patient, the problem, and any SIGNIFICANT findings (please do not list all medical history or every single lab result) only those pertaining to the problem.Example of Summary:J.T. 61-year-old Caucasian male reports to the emergency department (ED) with the following complaint “ I’ve been having trouble breathing, my cough has gotten worst in the last three days and my ankles are swollen.” He further reports cough has gotten progressively worst especially in the morning upon awaking. The patient’s medical history shows he has smoked for the last 37 years 2 packs of cigarettes daily. Patient reports cutting back to 5 cigarettes a day since being diagnosed with COPD six years ago.On examination his respiratory status yielded few breathe sounds on auscultation; patient was short of breath (SOB) with exertion, and unable to speak in full sentences. Patient is currently prescribed Albuterol 180mcg MDI 2 QID PRN and Ipratropium 35mcg MDI QID for his COPD. Patient reports respiratory distress continue after several uses of his Albuterol inhaler prior to his arrival to the ED. His vital signs were as follows: Respiratory rate 32bpm and labored, heart rate 110 BPM, blood pressure 165/95 mmHg, height 5’10”, and 120lbs.Please answer the following questions pertaining to this CASE STUDYAnswer Questions: 1, 2, 3, 4, 5, 6, 7, 8Please answer in detail pertaining to this patient and use some outside resources total number of 3 no older than 5 years as references (I provided 1 of the 3 references needed) APA format.In the paper: Write out each question as the title before answering it and indicate the question number.Here Is a Reference you can use for 1 of 3 Needed (Below)Bruyere, H. (2010). 100 case studies in pathophysiology. Philadelphia: PA: Lippincott,Williams.DS85-4 Case Study 85 ¦ Acute Lymphoblastic LeukemiaSignificanceApproximately 1,460 deaths (800 males and 660 females) due to ALL are expected in theUnited States in 2008. ALL is the most common cancer of childhood, representing nearlyone third of all cases of pediatric cancer, 80% of all acute leukemias in children, and approximately73% of all leukemia cases in individuals younger than age 20 years.Causes and Risk FactorsAlthough a small percentage of cases are associated with inherited genetic syndromes, thecause of ALL remains largely unknown. Many environmental factors (e.g., exposure to ionizingradiation or benzene) have been investigated as potential risk factors, but none have beenshown to definitively cause ALL. Furthermore, a number of anti-cancer agents (especially procarbazine,melphalan, and etoposide) are believed to be leukemogenic, and leukemia mayoccur as a second cancer following aggressive chemotherapy for other cancers.Because a significant number of cases of leukemia have been reported in identical twins,a genetic predisposition to ALL is suggested. An identical twin of a person with acuteleukemia has a 25% probability of developing the disease, particularly during the first yearafter the initial diagnosis of ALL. After approximately 7 years, however, the risk to the unaffectedtwin returns to the same risk as that of the general population. The incidence ofleukemia in siblings of leukemic children is four-fold greater than in the general population.Leukemia is also frequently associated with congenital chromosomal abnormalities such asDown syndrome, Klinefelter syndrome, and Turner syndrome.Advances in cytogenetics have made it increasingly evident that many forms of leukemiaare associated with non-random chromosomal abnormalities. In many cases, these chromosomalaberrations disappear with remission of the disease but reappear with relapse. Theunderlying cause of these chromosomal changes is unknown.PathophysiologyIn ALL, a lymphoid progenitor cell (or stem cell) becomes genetically altered by carcinogens(i.e., cancer-causing agents) and subsequently undergoes uncontrolled proliferation and cellpopulation expansion. In most cases, the pathophysiology of these transformed cells reflectsthe altered expression of genes and gene products that contribute to the normal developmentof B and T lymphocytes. It has long been thought that cancerous lymphoblasts resulted froman inhibition of differentiation or maturation at distinct stages of lymphocyte development.Recent data challenge this theory and suggest that leukemia instead arises from a stem cellthat acquires features of more differentiated cells. While this may appear to be a subtle andinsignificant difference, it is very important because it suggests the need to eradicate bothstem cells and lymphoblasts to achieve a cure for the disease. Because leukemic cells areimmature, they are capable of cell division but cannot perform the functions of matureWBCs and ward off infections.ALL is generally believed to originate in the bone marrow. However, since the disease isa type of cancer, malignant lymphoblasts often spread through the blood and lymphatics tothe thymus gland, liver, spleen, lymph nodes, testes, and central nervous system (CNS). Thisis known as metastasis. Cells continue to divide in their new locations and cause cell injuryand cell death by depriving metastatic tissues of oxygen and important nutrients.Diagnosis: Clinical Manifestationsand Laboratory TestsAcute leukemias usually have a sudden and dramatic onset. Patients typically have had symptomsfor only 1 week before diagnosis. Children with ALL generally present with clinical manifestationsthat reflect a massive overload of leukemic lymphoblasts in the bone marrow. As aresult, patients show signs of bone marrow failure—anemia, thrombocytopenia (i.e., subnormalplatelet count), and neutropenia (i.e., subnormal neutrophil count). Anemia manifests withfatigue and paleness, thrombocytopenia with small hemorrhages (i.e., petechiae) and both