Sample Answer for NURS 6501 Knowledge Check Pediatrics Included After Question
In this exercise, you will complete a 10- to 20-essay type question Knowledge Check to gauge your understanding of this module’s content.
Possible topics covered in this Knowledge Check include:
Growth and development
Normal growth patterns
Scoliosis (ortho)
Kawasaki
Alterations in children
Congenital (heart syndrome)
PDAs
Sudden Infant Death Syndrome (SIDS)
Asthma
Lead poisoning and effects on neurological functioning
Sickle cell
Hemophilia
Photo Credit: laflor / E+ / Getty Images
(Note: It is strongly recommended that you take the Knowledge Check at least 48 hours before taking the Final Exam.)
Complete the Knowledge Check By Day 5 of Week 11
To complete this Knowledge Check:
Module 8 Knowledge Check
Final Exam
This 101-question exam is a test of your knowledge in preparation for your certification exam. No outside resources, including books, notes, websites, or any other type of resource, are to be used to complete this exam. You are expected to comply with Walden University’s Code of Conduct.
This exam will be on topics covered in Weeks 7, 8, 9, 10, and 11. Prior to starting the exam, you should review all of your materials. This exam is timed with a limit of 2 hours for completion. When time is up, your exam will automatically submit.
(Note: It is strongly recommended that you take the Knowledge Check at least 48 hours before taking the Final Exam.)
Photo Credit: Getty Images
By Day 7 of Week 11
Complete and submit your Final Exam.
To complete your exam:
Final Exam
A Sample Answer For the Assignment: NURS 6501 Knowledge Check Pediatrics
Title: NURS 6501 Knowledge Check Pediatrics
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.
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
1.Explain what ALL is?
Selected Answer:
Acute lymphocytic leukemia (ALL) is also called acute lymphoblastic leukemia. Acute means that leukemia can progress quickly and, if not treated, would probably be fatal within a few months. Lymphocytic means it develops from immature forms of lymphocytes, a type of white blood cell. ALL is a malignant, clonal disease of the bone marrow in which early lymphoid precursors proliferate and replace the normal hematopoietic cells of the marrow. In most cases, the leukemia cells invade the blood quickly. They can also sometimes spread to other parts of the body, including the lymph nodes, liver, spleen, central nervous system, and testicles (in males). Acute lymphocytic leukemia is the most common type of cancer in children, and treatments result in a good chance of a cure. Acute lymphocytic leukemia can also occur in adults, though the chance of a cure is greatly reduced. Signs and symptoms of acute lymphocytic leukemia may include: bleeding from the gums, bone pain, fever, frequent infections, frequent or severe nosebleeds, lumps caused by swollen lymph nodes in and around the neck, armpits, abdomen or groin, pale skin, shortness of breath, weakness, fatigue or a general decrease in energy.
Correct Answer:
Acute lymphoblastic leukemia (ALL) is a malignant (clonal) disease of the bone marrow in which early lymphoid precursors proliferate and replace the normal hematopoietic cells of the marrow. ALL is the most common type of cancer and leukemia in children in the United States. The malignant cells of acute lymphoblastic leukemia (ALL) are lymphoid precursor cells (ie, lymphoblasts) that are arrested in an early stage of development. This arrest is caused by an abnormal expression of genes, often as a result of chromosomal translocations or abnormalities of chromosome number. These aberrant lymphoblasts proliferate, reducing the number of the normal marrow elements that produce other blood cell lines (red blood cells, platelets, and neutrophils). Consequently, anemia, thrombocytopenia, and neutropenia occur, although typically to a lesser degree than is seen in acute myeloid leukemia. Lymphoblasts can also infiltrate outside the marrow, particularly in the liver, spleen, and lymph nodes, resulting in enlargement of the latter organs.
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.
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
1.Why does ARF occur in some patients with ALL?
Selected Answer:
Renal injury in ALL is common and can occur through many different mechanisms, including prerenal acute kidney injury, acute tubular necrosis, reno-vascular disease, obstruction, glomerulonephritis, and parenchymal infiltration of tumor cells. Although renal involvement is not uncommon in ALL, renal failure is rarely a presenting symptom in ALL and is thought to be a poor prognosis indicator. Leukemic may lead to significant impairment of renal function if it is bilateral and diffuse, particularly involving the cortical region. Acute renal failure in patients with acute leukemia is usually a consequence of a chemotherapeutic regimen, leading to tumor lysis syndrome—the tumor lysis syndrome results in acute uric acid and calcium phosphate nephropathy. The most common form of kidney injury in leukemia is related to prerenal AKI in the setting of volume depletion. When infiltration is suspected, kidney biopsy is typically recommended as the extent of infiltration can give prognostic information regarding the malignancy as the rate of infiltration parallels the stage and grade of the disease
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
Response Feedback:
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· Question 3
A Sample Answer For the Assignment: NURS 6501 Knowledge Check Pediatrics
Title: NURS 6501 Knowledge Check Pediatrics
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
1.Explain the pathophysiology of acute SCD crisis. Why is pain the predominate feature of acute crises?
Selected Answer:
The term “sickle cell crisis” describes several acute conditions such as the vaso- occlusive crisis (acute painful crisis), aplastic crisis, splenic sequestration crisis, hyperhemolytic crisis, hepatic crisis, dactylitis, and acute chest syndrome. Sickle cell disease is an autosomal recessive disorder of a gene mutation. On chromosome 11, nucleotide mutation substitutes glutamic acid for valine at position six on the beta-globin subunit. A sickle cell crisis occurs when sickle-shaped red blood cells clump together and block small blood vessels that carry blood to certain organs, muscles, and bones. This causes mild to severe pain. The pain can last from hours to days. “Painful event” and “painful crisis” are other terms used to describe these episodes. Some people with sickle cell disease have many painful events, while others have few or none. The pain can happen in any part of the body.
Nevertheless, the most common areas include the: bones of the spine, arms, and legs; chest; and abdomen. Inflammatory mediators such as plasma cytokines lead to a pro-inflammatory state, causing further complications of vaso-occlusion. It is postulated that the intestinal microbiome may be a potential trigger for the vaso-occlusive crisis. While some triggers (cold temperature, dehydration, low humidity, stress) for pain are identifiable, most episodes do not have an identifiable cause.
These reactions further promote sickled erythrocytes to be come arrested during movement through the microvascular. The sluggish and stagnant red cells within the inflamed vascular vessels result in extended exposure to low oxygen tension, sickling, and vascular obstruction. Lysed sickle erythrocytes release hemoglobin and free hemoglobin can bind and inactivate nitic oxide (NO), which is a powerful vasodilator and inhibitor of platelet aggregation. Decreased blood pH reduces hemoglobin affinity for oxygen leading to an increasing fraction of deoxygenated HbS at any oxygen tension and predisposition to sickling. As less oxygen is taken up by hemoglobin in the lungs, the PO2 drops promoting additional sickling. The intense pain of an acute crisis is due to lack of oxygen to major organs and bones. The lack of oxygen leads to ischemia and organ death.
