NURS 6501 Explain what ALL is?

NURS 6501 Explain what ALL is?

NURS 6501 Explain what ALL is?

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.


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.
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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

What’s Coming Up?

Congratulations! After you have finished all of the assignments for this week, you have completed the course. Please submit your Course Evaluation by the end of the week.

Week 11: Concepts of Pediatrics

Pediatric disorders can present unique challenges to patients, families, and healthcare providers. Disorders in these areas areNURS 6501 Explain what ALL is complicated by the fact that young patients can have difficulties communicating symptoms. Furthermore, the manner in which disease and disorders manifest in children may be unique.

APRNs working to support these patients and their loved ones must demonstrate not only support and compassion, but expertise to

communicate and guide understanding of diagnoses and treatment plans. This includes an understanding of disease and disorders at the pediatric level.

This week, you examine pathophysiology in pediatrics. You apply key terms, concepts, and principles in this area to demonstrate an understanding of the impact they have on altered physiology in children.

Click here to ORDER an A++ paper from our Verified MASTERS and DOCTORATE WRITERS: NURS 6501 Explain what ALL is?

Learning Objectives

Students will:

  • Analyze concepts and principles of pathophysiology across the lifespan

Learning Resources

Required Readings (click to expand/reduce)

McCance, K. L. & Huether, S. E. (2019). Pathophysiology: The biologic basis for disease in adults and children (8th ed.). St. Louis, MO: Mosby/Elsevier.

  • Chapter 14: Cancer in Children, including Summary Review
  • Chapter 20: Alterations of Neurologic Function in Children (stop at Childhood tumors); Summary Review
  • Chapter 34: Alterations of Cardiovascular Function in Children (stop at Defects decreasing pulmonary blood flow); Summary Review
  • Chapter 37: Alterations of Pulmonary Function in Children (stop at Congenital malformations); Summary Review
  • Chapter 40: Alterations of Renal and Urinary Tract Function in Children, including Summary Review
  • Chapter 43: Alterations of Digestive Function in Children, including Summary Review
  • Chapter 46: Alterations of Musculoskeletal Function in Children (stop at Avascular diseases); (start at Cerebral palsy) (musculoskeletal tumors in children); Summary Review
  • Chapter 48: Alterations of the Integument in Children, including Summary Review
  • Chapter 50: Shock, Multiple Organ Dysfunction Syndrome, and Burns in Children, including Summary Review

U.S. National Library of Medicine. (2019). Normal growth and development. Retrieved from

Document: NURS 6501 Final Exam Review (PDF document) 


Note: Use this document to help you as you review for your Final Exam in Week 11.

Module 8 Overview with Dr. Tara Harris

Dr. Tara Harris reviews the structure of Module 8 as well as the expectations for the module. Consider how you will manage your time as you review your media and Learning Resources throughout the module to prepare for your Knowledge Check and your Final Exam. (3m)

Pediatrics – Week 11 (14m)

Wyatt, K. (2018, February 4). Pediatrics – Growth and development milestones review  [Video file]. Retrieved from

Note: The approximate length of the media program is 34 minutes.

Online Media from Pathophysiology: The Biologic Basis for Disease in Adults and Children

In addition to this week’s media, it is highly recommended that you access and view the resources included with the course text, Pathophysiology: The Biologic Basis for Disease in Adults and Children. Focus on the videos and animations in Chapter 20, 34, 37, 40, 43, and 46 that relate to alterations in hematological function in children. Refer to the Learning Resources in Week 1 for registration instructions. If you have already registered, you may access the resources at

Question 4

4 out of 4 points

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.


1.     Discuss the genetic basis for SCD.

Selected Answer: Sickle Cell Disease is inherited and involves an autosomal recessive pattern which means both copies of the gene in each cell have mutations. The parents of an individual with an autosomal recessive condition carry one copy of the mutated gene, but they typically do not show signs and symptoms. Hemoglobin (Hb), a gene that determines how red blood cells are made and how they work, is inherited from both parents. Each birth parent provides one hemoglobin (Hb) gene. Normal hemoglobin is called HbA. HbS is a change to the normal Hb gene. An abnormal HbS gene causes red blood cells to become sickle-shaped, limiting the amount of oxygen the red blood cells can carry through the body.
Correct Answer: SCD denotes all genotypes containing at least one sickle gene, in which HbS makes up at least half the hemoglobin present. Major sickle genotypes described so far include the following: • HbSS disease or sickle cell anemia (the most common form) – Homozygote for the S globin with usually a severe or moderately severe phenotype and with the shortest survival • HbS/b-0 thalassemia – Double heterozygote for HbS and b-0 thalassemia; clinically indistinguishable from sickle cell anemia (SCA) • HbS/b+ thalassemia – Mild-to-moderate severity with variability in different ethnicities • HbSC disease – Double heterozygote for HbS and HbC characterized by moderate clinical severity • HbS/hereditary persistence of fetal Hb (S/HPHP) – Very mild or asymptomatic phenotype Sickle cell trait or the carrier state is the heterozygous form characterized by the presence of around 40% HbS, absence of anemia, inability to concentrate urine (isosthenuria), and hematuria. Under conditions leading to hypoxia, it may become a © 2020 Walden University 4 pathologic risk factor. Sickle cell disease produces illness, while sickle cell trait usually does not. People who inherit two genes for sickle hemoglobin (one from each parent) have sickle cell disease. With a few exceptions, a child can inherit sickle cell disease only if both parents have one gene for sickle cell hemoglobin
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·  Question 5

4 out of 4 points

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.


1.     What is the pathophysiology of Hemophilia 

Selected Answer: Hemophilia is the most prevalent severe hereditary bleeding disorder and is characterized by the inability to form thrombi in response to injury, resulting in continuous bleeding. Both hemophilia A and B result from mutations in the F8 gene and F9 gene. Changes or mutations of the genes result in deficiency or dysfunction of clotting factors VIII and IX, respectively. Specifically, “inversions in introns 1 and 22 of the factor VIII gene are the most frequently observed mutations and account for most severe cases of hemophilia A” . Another type of mutation that may result in hemophilia is a point mutation. In this instance, a single nucleotide in the DNA is added, deleted, or changed. When these alterations take place, the amino acid chain is typically destroyed. Otherwise, the protein chain can disrupt protein function, inhibit intracellular processing, or result in protein clearance.
Correct Answer: Hemophilia A is caused by an inherited or acquired genetic mutation that results in dysfunction or deficiency of factor VIII, or by an acquired inhibitor that binds © 2020 Walden University 5 factor VIII. Of genetic cases, up to approximately one third are the result of de novo mutations not present in the mother’s X chromosome. Inadequate factor VIII results in the insufficient generation of thrombin by the FIXa and FVIIIa complex by means of the intrinsic pathway of the coagulation cascade. This mechanism, in combination with the effect of the tissue-factor pathway inhibitor, creates an extraordinary tendency for impaired clotting in response to trauma and, especially in persons with severe hemophilia, with spontaneous bleeding.
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