The study seeks to analyze the changes of the typical mechanical, physical and biochemical function caused by myelodysplastic syndrome from an abnormal syndrome. The disease is caused by myeloid lineage accountable for the inefficient hematopoiesis (Keel et al. 2016). It affects the bone marrow of an individual where the evolution gets identified by the worsening cytopenias (Keel et al. 2016). The disease begins to form the altered function of the cell stem of hematopoiesis cell lineage leading to failure of bone marrow functioning mechanism in the body. It causes a hypercellular bone marrow with a large number of abnormal cells (Keel et al. 2016). For instance, there is an increase in apoptosis, resulting in futile cycling of the blood cells with reduced production of mature blood cells.
The primary physical examination and diagnostic findings of the problem is the failure of the bone marrow of the patient due to toxic exposure (Elnair, Sethi, Hassouna & Galal, 2018). The patient may experience pallor and fatigue due to anaemiaand further bruising and petechiae. The other common finding is the low presence of the haemoglobin, platelets, and neutrophils, which also varies broadly (Elnair et al. 2018). The diagnostic results of the disease are a bone marrow aspiration, the peripheral blood smear examination, and biopsy. It will help identify the presence of features of anaemia, dysgranulopoiesis with distinctive hypo pigmentation in neutrophils (Elnair et al. 2018). Also, the blood test is appropriate to figure out the immune-related mechanisms.
The evidential treatment plan is first to identify the toxic substance that leads to the disease (Vivot et al. 2017). The patient should undergo assessment strategies to identify features such as hepatosplenomegaly predominates in juvenile myelomonocytic leukaemia(Vivot et al. 2017). In this case, the patient undergoes immunosuppressive therapy for the acute myeloid leukaemia.The initial treatment plan also involves the transfusion therapy where it identifies the erythropoiesis agents(Vivot et al. 2017). Chemotherapy is another treatment that is suitable for the plan, which should get accompanied by the cell transplant(Vivot et al. 2017).
References
Elnair, R., Sethi, P., Hassouna, T., & Galal, A. (2018). Sclerosing mesenteritis as a presentation of myelodysplastic syndrome (MDS) with improvement following treatment targeted at MDS. Annals of haematology, 97(3), 547-549.
Keel, S. B., Scott, A., Sanchez-Bonilla, M., Ho, P. A., Gulsuner, S., Pritchard, C. C., ... & Shimamura, A. (2016). Genetic features of myelodysplastic syndrome and aplastic anaemia in pediatric and young adult patients. Haematologica, 101(11), 1343-1350.
Vivot, A., Boutron, I., Beraud-Chaulet, G., Zeitoun, J. D., Ravaud, P., &Porcher, R. (2017). Evidence for treatment-by-biomarker interaction for FDA-approved oncology drugs with required pharmacogenomic biomarker testing. Scientific reports, 7(1), 6882.
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