NURS 6501 Knowledge Check Concepts Of Pediatrics
Walden University NURS 6501 Knowledge Check Concepts Of Pediatrics-Step-By-Step Guide
This guide will demonstrate how to complete the Walden University NURS 6501 Knowledge Check Concepts Of Pediatrics assignment based on general principles of academic writing. Here, we will show you the A, B, Cs of completing an academic paper, irrespective of the instructions. After guiding you through what to do, the guide will leave one or two sample essays at the end to highlight the various sections discussed below.
How to Research and Prepare for NURS 6501 Knowledge Check Concepts Of Pediatrics
Whether one passes or fails an academic assignment such as the Walden University NURS 6501 Knowledge Check Concepts Of Pediatrics depends on the preparation done beforehand. The first thing to do once you receive an assignment is to quickly skim through the requirements. Once that is done, start going through the instructions one by one to clearly understand what the instructor wants. The most important thing here is to understand the required format—whether it is APA, MLA, Chicago, etc.
After understanding the requirements of the paper, the next phase is to gather relevant materials. The first place to start the research process is the weekly resources. Go through the resources provided in the instructions to determine which ones fit the assignment. After reviewing the provided resources, use the university library to search for additional resources. After gathering sufficient and necessary resources, you are now ready to start drafting your paper.
How to Write the Introduction for NURS 6501 Knowledge Check Concepts Of Pediatrics
The introduction for the Walden University NURS 6501 Knowledge Check Concepts Of Pediatrics is where you tell the instructor what your paper will encompass. In three to four statements, highlight the important points that will form the basis of your paper. Here, you can include statistics to show the importance of the topic you will be discussing. At the end of the introduction, write a clear purpose statement outlining what exactly will be contained in the paper. This statement will start with “The purpose of this paper…” and then proceed to outline the various sections of the instructions.
How to Write the Body for NURS 6501 Knowledge Check Concepts Of Pediatrics
After the introduction, move into the main part of the NURS 6501 Knowledge Check Concepts Of Pediatrics assignment, which is the body. Given that the paper you will be writing is not experimental, the way you organize the headings and subheadings of your paper is critically important. In some cases, you might have to use more subheadings to properly organize the assignment. The organization will depend on the rubric provided. Carefully examine the rubric, as it will contain all the detailed requirements of the assignment. Sometimes, the rubric will have information that the normal instructions lack.
Another important factor to consider at this point is how to do citations. In-text citations are fundamental as they support the arguments and points you make in the paper. At this point, the resources gathered at the beginning will come in handy. Integrating the ideas of the authors with your own will ensure that you produce a comprehensive paper. Also, follow the given citation format. In most cases, APA 7 is the preferred format for nursing assignments.
How to Write the Conclusion for NURS 6501 Knowledge Check Concepts Of Pediatrics
After completing the main sections, write the conclusion of your paper. The conclusion is a summary of the main points you made in your paper. However, you need to rewrite the points and not simply copy and paste them. By restating the points from each subheading, you will provide a nuanced overview of the assignment to the reader.
How to Format the References List for NURS 6501 Knowledge Check Concepts Of Pediatrics
The very last part of your paper involves listing the sources used in your paper. These sources should be listed in alphabetical order and double-spaced. Additionally, use a hanging indent for each source that appears in this list. Lastly, only the sources cited within the body of the paper should appear here.
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QUESTION 1
Scenario 1: Acute Lymphoblastic Leukemia (ALL)
An 11-year-old boy is brought to the clinic by his parents who states that the boy has not been eating and listless. The mother also notes that he has been easily bruising without trauma as he says he is too tired to go out and play. He says his bones hurt sometimes. Mother states the child has had intermittent fevers that respond to acetaminophen.
Maternal history negative for pre, intra, or post-partum problems.
PMH: Negative. Easily reached developmental milestones.
PE: reveals a thin, very pale child who has bruises on his arms and legs in no particular pattern.
LABS: CBC revealed Hemoglobin of 6.9/dl, hematocrit of 19%, and platelet count of 80,000/mm3. The CMP demonstrated a blood urea nitrogen (BUN) of 34m g/dl and creatinine of 2.9 mg/dl.
DIAGNOSIS: acute leukemia and renal failure and immediately refers the patient to the Emergency Room where a pediatric hematologist has been consulted and is waiting for the boy and his parents.
CONFIRMED DX: acute lymphoblastic leukemia (ALL) was made after extensive testing.
Question
- Explain what ALL is?
ALL is a malignant transformation and proliferation of lymphoid progenitor cells in the blood, bone marrow, and extramedullary sites. It occurs following an abnormal proliferation and differentiation of a clonal population of lymphoid cells. Factors that predispose an individual to ALL include exposure to pesticides, ionizing radiation, certain solvents, and viruses like Epstein-Barr Virus and HIV (Malard & Mohty, 2020). Clinical manifestations of ALL include spontaneous bruising/bleeding, fatigue, and infections. Some patients can have fever, night sweats, and unintentional weight loss. In addition, most adults with ALL have hepatomegaly, splenomegaly, and lymphadenopathy.
QUESTION 2
Scenario 1: Acute Lymphoblastic Leukemia (ALL)
An 11-year-old boy is brought to the clinic by his parents who states that the boy has not been eating and listless. The mother also notes that he has been easily bruising without trauma as he says he is too tired to go out and play. He says his bones hurt sometimes. Mother states the child has had intermittent fevers that respond to acetaminophen.
Maternal history negative for pre, intra, or post-partum problems.
PMH: Negative. Easily reached developmental milestones.
PE: reveals a thin, very pale child who has bruises on his arms and legs in no particular pattern.
LABS: CBC revealed Hemoglobin of 6.9/dl, hematocrit of 19%, and platelet count of 80,000/mm3. The CMP demonstrated a blood urea nitrogen (BUN) of 34m g/dl and creatinine of 2.9 mg/dl.
DIAGNOSIS: acute leukemia and renal failure and immediately refers the patient to the Emergency Room where a pediatric hematologist has been consulted and is waiting for the boy and his parents.
CONFIRMED DX: acute lymphoblastic leukemia (ALL) was made after extensive testing.
| Correct Answer: |
Renal failure as a result of hyperuricemia can be associated with ALL, particularly at diagnosis or during active treatment. Uric levels rise as an end product of purine metabolism from cellular destruction. Because the major excretory pathway is through the kidneys, urates can precipitate |
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Question
- Why does ARF occur in some patients with ALL?
ARF is a known renal complication of ALL associated with treatment-related side effects like the use of nephrotoxic drugs, tumor lysis syndrome, sepsis, hyperuricemia, and hypercalcemia. Hyperuricemia is an established complication of tumor lysis syndrome, and in most cases, it develops after starting chemotherapy (Patil et al., 2020). However, ARF as an initial presenting feature of ALL is rare. Leukemic infiltrates develop due to uric acid nephropathy causing renal enlargement and eventually ARF. Infiltration has to be bilateral and renal enlargement is normally uniform. Nevertheless, the degree and location of infiltration usually influence prognosis (Patil et al., 2020). Interstitial infiltration is related to ARF, unlike glomerular infiltration, which causes glomerulopathy.
QUESTION 3
Scenario 2: Sickle Cell Disease (SCD)
A 15-year-old male with known sickle cell disease (SCD) present to the ER in sickle cell crisis. The patient is crying with pain and states this is the third acute episode he has had in the last 10-months. Both parents are present and appear very anxious and teary eyed. A diagnosis of acute sickle cell crisis was made.
Question
- Explain the pathophysiology of acute SCD crisis. Why is pain the predominate feature of acute crises?
SCD crises occur intermittently and are precipitated by fever, viral infection, and local trauma. Vaso-occlusive or pain crisis is the most common type of SCD crisis. It is caused by tissue hypoxia, causing ischemia and infarction, primarily in the bones, as well as in the lungs, spleen, or kidneys (Inusa et al., 2019). A plastic SCD crisis occurs when bone marrow erythropoiesis delays during acute infection secondary to human parvovirus, during which an acute erythroblastopenia can occur. A painful vaso-occlusive crisis causes excruciating pain in long bones, hands, feet, back, and joints. Hip pain can be caused by avascular necrosis of the femoral head (Inusa et al., 2019).
QUESTION 4
Scenario 2: Sickle Cell Disease (SCD)
A 15-year-old male with known sickle cell disease (SCD) present to the ER in sickle cell crisis. The patient is crying with pain and states this is the third acute episode he has had in the last 10-months. Both parents are present and appear very anxious and teary eyed. A diagnosis of acute sickle cell crisis was made.
Question
- Discuss the genetic basis for SCD.
SCD is a genetic disease that is inherited through an autosomal recessive pattern. SCD represents all genotypes having at least one sickle gene, in which HbS makes up at least half the hemoglobin present. A patient with SCD usually has two HbS gene alleles, one inherited from each parent (Inusa et al., 2019). This results in 80-100% of the total hemoglobin being HbS. If a person with SCD gets children, each child inherits one of the two abnormal gene alleles and has a sickle cell trait. As a result, individuals with the sickle cell trait have one normal and one abnormal gene allele for hemoglobin, which are inherited (Inusa et al., 2019). Consequently, half of the hemoglobin chains they produce are abnormal.
QUESTION 5
Scenario 3: Hemophilia
8-month infant is brought into the office due to a swollen right knee and excessive bruising. The parents have noticed bruising about a month ago but thought the bruising was due to the attempts to crawl. They became concerned when the baby woke up with a swollen knee. Infant up to date on all immunizations, has not had any medical problems since birth and has met all developmental milestones.
FH: negative for any history of bleeding disorders or other major genetic diseases.
PE: within normal limits except for obvious bruising on the extremities and right knee. Knee is swollen but no warmth appreciated. Range of motion of knee limited due to the swelling.
DIAGNOSIS: hemophilia A.
Question
- What is the pathophysiology of Hemophilia
Hemophilia is a hereditary bleeding disorder caused by deficiencies of clotting factor VIII or IX. It is attributed to deletions, mutations, or inversions affecting the factor VIII or IX gene (Castaman & Matino, 2019). Since these genes are located on the X chromosome, hemophilia primarily affects males. The severity of hemophilia is grouped according to the plasma level of factor VIII or factor IX activity. The severe form of hemophilia is described as a factor level <1% of normal, the moderate form is a factor level of 1-5%, and the mild form is a factor level of 5-40% (Castaman & Matino, 2019). Persons with severe hemophilia often develop hemorrhages into muscles, joints, or soft tissues without obvious causes.
References
Castaman, G., & Matino, D. (2019). Hemophilia A and B: molecular and clinical similarities and differences. Haematologica, 104(9), 1702–1709. https://doi.org/10.3324/haematol.2019.221093
Inusa, B., Hsu, L. L., Kohli, N., Patel, A., Ominu-Evbota, K., Anie, K. A., & Atoyebi, W. (2019). Sickle Cell Disease-Genetics, Pathophysiology, Clinical Presentation and Treatment. International Journal of Neonatal Screening, 5(2), 20. https://doi.org/10.3390/ijns5020020
Malard, F., & Mohty, M. (2020). Acute lymphoblastic leukaemia. Lancet (London, England), 395(10230), 1146–1162. https://doi.org/10.1016/S0140-6736(19)33018-1
Patil, A., Deshpande, R., Dash, S., Bhat, G., & Mehta, S. (2020). Non-oliguric renal failure with nephromegaly as the presenting manifestation of acute lymphoblastic leukemia in a young adult: an unusual case report. Nephrol Renal Dis, 5.