Advanced pathophysiology - Case Study Example

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What is the pathophysiology basis for the signs/symptoms and lab results that are seen in this case? The patient has a white blood cell count of 250 000 which higher than the normal of 3500-10500cells/mcL…
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Advanced pathophysiology
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Download file to see previous pages The elevated WBC is from the proliferation of immature WBC which continue to increase, however do not mature (Harrison, 2011). The accumulation of immature white blood cells in the bone marrow and blood leads to the replacement of normal cells such as thrombocytes, which leads to thrombocytopenia and a disruption of blood clotting (Harrison, 2011). Therefore, this patient presents with gum bleeding and easy bruising. In addition, decreased levels of leucocytes also increase the patient’s vulnerability to bruising. The replacement of cells also leads to a decrease in the number of red blood cells which are responsible for oxygen transport. This in turn is the reason why the patient developed fatigue and shortness of breath may also have been present (Harrison, 2011). The splenomegaly occurs as a result of extamedullary hematopoiesis as the bone marrow becomes less competent. The reduction of red blood cells due to replacement also leads to paleness. Upper abdominal tenderness could be attributed to splenomegaly. Opportunistic infections that occur as a result of the comprised immune system may lead to arthalgia. Describe pathophysiology of ALL. Compare it with other leukemia forms in children The development of ALL is assumed to occur as a result of alteration of a progenitor cell responsible for continuous clonal expansion (Bassan & Hoelzer, 2011). This event can occur in cells of T of B cell lineage which give rise to different types of acute lymphoblastic leukemia. These subtypes are based on the stage of cell development which the transformation occurred. Approximately 80% of ALL cases have been found to originate from B lymphocyte precursors (Onciu, 2009). Several factors have been found to influence the development of this cancer and these include radiation exposure, genetics, chemical exposure and some viral infections such as HTLV-1 (Onciu, 2009). As mentioned above the alteration of the precursor cells leads to an arrest in development. This then leads to the proliferation of immature white blood cells in the bone marrow which replace its physiological components. Therefore, there is a marked decrease in the formation of several blood elements. This may lead to other complications such as thrombocytopenia, anemia and neutropenia (Pui, Relling & Downing, 2004). In addition, the disruption of bone marrow function leads to extramedullary hematopoiesis which occurs in the spleen, liver and lymph nodes (Pui, Relling & Downing, 2004).These organs will then increase in size resulting in hepatomegaly and splenomegaly. This leukemia is different from AML which involves the myeloid blast cells whilst ALL involves lymphoblasts. In the pathogenesis of Acute Myeloid Leukemia, the pathological defect will involve numerous precursor cells which will develop immature (Pui, Relling & Downing, 2004). Meanwhile in Acute Lymphoblastic Leukemia, the effect is on a precursor cell that that will proliferate and produce several immature cells. The etiological factors between the two types of leukemia are also different. AML often occurs as a result of certain preleukemic blood disorders whilst ALL often associated with genetic factors and a prolonged exposure to radioactive substances (Pui, Relling & Downing, 2004). What is the purpose of chemotherapy in ALL? What is a common side effect of Therapy? Chemotherapy is necessary in this condition as the drugs are injected intravenously and can be used to treat cancerous cells that have ...Download file to see next pagesRead More
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