NURS 6501 Knowledge Check Module 8 _ 2020 | NURS6501 Knowledge Check Module 8_A Grade

NURS 6501 Knowledge Check Module 8 2020 – Mercer County Community College Student Response This Knowledge Check reviews the topics in Module 8 and is formative in nature. It is worth 20 points where each question is worth 1 point. You are required to submit a sufficient response of at least 2-4 sentences in length for each question. Scenario 1: Acute Lymphoblastic Leukemia (ALL) A ten-year-old boy is brought to clinic by his mother who states that the boy has been listless and not eating. She 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. Child’s past medical history negative and he easily reached developmental milestones. Physical exam reveals a thin, very pale child who has bruises on his arms and legs in no particular pattern. The APRN orders complete blood count (CBC), and complete metabolic profile (CMP). The 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. The APRN recognizes that the patient appears to have acute leukemia and renal failure and immediately refers the patient to the Emergency Room2 where a pediatric hematologist has been consulted and is waiting for the boy and his mother. The diagnosis of acute lymphoblastic leukemia (ALL) was made after extensive testing. Question 1 of 2: What is ALL? 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. Question 2 of 2: How does renal failure occur in some patients with ALL?3 Renal failure occurs in some patients with ALL as a result of hyperuricemia. 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 in renal tubules or ureters and can lead to oliguria and acute renal failure. Scenario 2: Sickle Cell Disease (SCD) A 12-year-old female with known sickle cell disease (SCD) present to the Emergency Room in sickle cell crisis. The patient is crying with pain and states this is the third acute episode she has had in the last nine months. Both parents are present and appear very anxious and teary eyed. A diagnosis of acute sickle cell crisis was made. Appropriate therapeutic interventions were initiated by the APRN and the patient’s pain level decreased, and she was transferred to the pediatric intensive care unit (PICU) for observation and further management. Question 1 of 2: What is the pathophysiology of acute SCD crisis and why is pain the predominate feature of acute crises? The pathogenesis of sickling includes erythrocyte derangement, chronic hemolysis, microvascular occlusions, and tissue damage. Deoxygenation is probably the most important variable in determining the occurrence of sickling. Other significant variables that affect sickling include interaction of Hbs with other types of hemoglobin in the cell, mean cell hemoglobin concentration (MCHC), intracellular pH, and transit times of erythrocytes through the microcirculation. The intense pain of an acute crisis is due to- - - - - - - - - - - -- - - - - Scenario 13: Pituitary Dwarfism The parents of a 3-year-old boy bring the child to the pediatrician with concerns that their child seems “small for his age”. The parents state that the boy has always been small but did not worry until the child went to day care and they noticed other children of the same age were much bigger. They also note that his teeth were very late in coming in. Normal prenatal, perinatal and postnatal history and no medical history on either side of family regarding issues with growth and development. Physical exam is normal except for short limbs and small teeth. The pediatrician suspects the child has pituitary dwarfism. A complete laboratory and radiographic work up confirmed the diagnosis. Question: What is the pathophysiology of pituitary dwarfism? Growth hormone deficiency (GHD), also known as dwarfism or pituitary dwarfism, is a condition caused by insufficient amounts of growth hormone in the body. Children with GHD have abnormally short stature with normal body proportions. GHD can be present at birth (congenital) or develop later (acquired). The condition occurs if the pituitary20 gland makes too little growth hormone. It can be also the result of genetic defects, severe brain injury or being born without a pituitary gland. In some cases, there is no clear cause identified. Sometimes, GHD can be associated with lower levels of other hormones, such as vasopressin (which controls water production in the body), gonadotropins (which controls the production of male and female sex hormones), thyrotropins (which control the production of thyroid hormones) or adrenocorticotrophic hormone (which controls the adrenal gland and related hormones). Scenario 14: Osteogenesis Imperfecta (OI) A 4-year-old boy was brought to the Emergency Room by his parents with a suspected femur fracture. The parents state the child was playing on the couch when he rolled off and cried out in pain. There were no other injuries noted. Review of the child’s chart revealed this was the 4th Emergency Room visit in the last 15 months for fractures after low impact injury. The parents were suspected of child abuse and Child and Protective Services were consulted. The APRN assessing the child noted that the child had unusually thin and translucent skin, poor dentition, and blue sclera. The APRN suspects the child may have osteogenesis imperfecta (OI). Laboratory results revealed an elevated serum alkaline phosphatase and the diagnosis OI was made based on the clinical picture and elevated alkaline phosphatase. Question: What is the pathophysiology of OI?21 The major errors in OI lies in the synthesis of collagen, a triple helix with two matching alpha chains and one beta chain. Collagen is presented in the bone, cartilage, eye tissue, skin and vascular system. The severity of OI phenotype and the related anomalies of the eye, dentition, or vascular system are all dependent on the severity of the genetic anomaly and the part of the triple helix that is affected.