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Case Study 1 Made-to-Order Baby Keeli Oda Ray Yamada Erica Lee December 12, 2003 Worley Ethics Case Study Keeli Oda, Erica Lee, and Ray Yamada BF Step 1: a) What is the ethical problem? Should Jack and Lisa Nash conceive another child in hopes of saving Molly? b) Who will decide? Lisa and Jack Nash will make the decision. Other families dealing with FA, and John Wagner, M.D., would help make their decision. Step 2: a) List the information you already know form the opening scene of the case study or from your own previous knowledge of the topic? 1. Molly was born 35 weeks into Lisa’s pregnancy 2. Molly weighed five pounds 3. Molly was missing both thumbs and her right arm was 30% shorter than her left arm. 4. Both her hip sockets were undeveloped 5. She was diagnosed with Fanconi Anemia (FA) 6. Children with FA are highly vulnerable to a breakdown in bone marrow, leaving them at a risk of infection and leukemia 7. Most people die by the age of twenty 8. Lisa and Jack Nash both carried a mutation in the same gene 9. Their kids have a one-in –four chance of inheriting the defective genes form both parents and thus developing FA 10. Molly was isolated from other kids to minimize exposure to viruses and bacteria 11. The only cure available to Molly was a transplant of bone marrow with a fresh supply of stem cells 12. The odds of the transplant for Molly were less than one-in-five 13. Transplant involves wiping out defective marrow with chemotherapy and radiation, then replacing with donor cells 14. If the procedure fail, further attempts with donated cells would be unlikely to keep her alive 15. Stem cells from a healthy sibling carried an 85% chance of success. 16. Steps a. Couples with FA-affected children would conceive embryos through in vitro fertilization b. Embryo would be tested for FA and to make sure the new sibling’s cells would likely be accepted by the affected child’s body c. Healthy embryos would be implanted in the mother’s uterus 17. The umbilical-cord blood would provide stem cells to rebuild the defective bone marrow in the newborn’s brother or sister. b) List the factual questions you need to research 1. What is Fanconi Anemia? 2. How common is Fanconi Anemia? 3. What are the symptoms of Fanconi Anemia? 4. How can Fanconi Anemia be cured or prevented? 5. What are the causes of Fanconi Anemia? 6. What is bone marrow? 7. What is a bone marrow transplant? 8. How much does a bone marrow transplant cost? 9. Does insurance cover bone marrow transplant? 10. What are the chances of surviving Fanconi Anemia? 11. What are the treatments of Fanconi Anemia? 12. What are stem cells/ location / function? 13. What is umbilical cord blood? 14. What is in vitro fertilization? 15. What is chemotherapy and radiation and how does it treat leukemia? 16. What are chances of finding unrelated bone marrow donor? 17. What are the risks for bone marrow donor? 18. How are unborn baby and sibling affected? 19. What is embryo genetic testing? 20. What is leukemia? 21. What is the Catholic Church’s teaching of conceiving children in marriage? 22. What are the precedents in which a couple has conceived a child to save another? c) Answer the research questions that you listed above. 1. What is Fanconi Anemia? Fanconi Anemia is an inherited anemia that leads to bone marrow malfunction. If both parents carry a defect in the same Fanconi Anemia (FA) gene then their children have a 1 out of 4 chance of developing FA. Even though it is considered a blood disease, it can affect all parts of the body. FA occurs equally in both males and females and all ethnic groups. Fanconi Anemia is usually visible either at birth or before a person reaches the age of 12, but most FA affected people do not live to adulthood and die around the age of 20. Lynn and Dave, Frohnmayer. “What is Fanconi Anemia and How is it Diagnosed?” Fanconi Anemia Research Fund, Inc. 04 December 2003 2. How common is Fanconi Anemia? Scientists discovered that child have 25% chance of getting Fanconi Anemia if both parents have defected FA gene. FA genes include; A, C, D2, E, F, G and BRCA2. Mutation of these genes will cause Fanconi Anemia. In the United States the possibility of a child being born with Fanconi Anemia is 1 out of every 360,000 babies. Lynn and Dave, Frohnmayer. ・U>What is Fanconi Anemia and How is it Diagnosed?・/U> Fanconi Anemia Research Fund, Inc. 09 December 2003 3. What are the symptoms of Fanconi Anemia? People diagnosed with Fanconi Anemia suffer a variety of defects. One defect is a short stature or being short, a small head or eyes and a low body weight. They also may have missing arms or bones (skeletal problems). Parts of their kidneys may also be missing. Other defects include skin discoloration, mental retardation, and problems with their heart. Besides physical symptoms of Fanconi Anemia also have internal effects. Some such as abnormal secondary sex organs. In males, sex organs are undeveloped and in females, their menstrual cycle tends to show up late and menopause will occur early. More minor symptoms of Fanconi Anemia are tiredness, infections, nosebleeds and easy bruising. Baskind, Julie and Gonzalez, David. "Fanconi Amemia." 05 December 2003 4. How can Fanconi Anemia be cured or prevented? Fanconi Anemia can be prevented or delayed through various treatments even though it is considered a life-threatening disease. Some short term treatments include blood transfusions and antibiotics. Other long term treatments include Androgens, Growth factors, Bone marrow transplants, and gene therapy. If caught early, Bone marrow transplants with a fresh supply of stem cells can cure Fanconi Anemia but is not always successful. "About FA." B Positive B Positive Inc.. 09 December 2003 5. What are the causes of Fanconi Anemia? Fanconi Anemia is caused by a mutation in genes. It is inherited in autosomal recessive fashion or through the genes. When a copy of a defective gene is passed on by both parents with the gene is the result of Fanconi Anemia. FA is also caused by a genetic defect that prevents cells from fixing damaged DNA or removing toxic, which are oxygen-free and damage cells. Some genetic diseases that may cause FA are cystinosis, galactosemia, glycogen storage disease, hereditary fructose intolerance. Others may include the Lowe syndrome, Wilson disease, tyrosinemia, medullary cystic disease, vitamin D dependency, and familial idiopathic Fanconi’s syndrome. Cystinosis is lysomsomal storage disorders of unkown molecular defect, it is characterized by a deposition of cystine crystals in reticuloendothelial cells.Galactosemia is a metabolic disorder that is inherited. It is characterized by the deficiency in and enzyme that is vital for the metabolism of galactose. The results of galactosemia are elevated levels in galactose, which can cause mental retardation and other physical abnomalties. Glycogen storage disease is a metabolic error in which the body stores excess amounts of glycogen in the kidneys and liver. The results of the excess storage are clogged arteries and heart attacks. Hereditary fructose intolerance is an error in metabolism due to lack of hepatic fructose. One effect of hereditary fructose intolerance is vomiting. "Hereditary Fructose Intolerance." Medical Search Engine . 5 December 2003 "Dictionary.com." Lexico Publishing Group 08 December 2003 "Dictionary.com." Lexico Publishing Group 08 December 2003 Matsui, William. "Medline Plus Health Information." URAC A.D.A.M.. 05 Dec. 2003 6. What is bone marrow? Bone marrow is the soft, fatty, vessel carrying tissue that fills most bone cavities and is the source of red blood cells and many white blood cells. It is located in the center of all large bones. Another name for the bone marrow is “the factory” because it is where all blood cells are made. The bone marrow produces white blood cells, needed to fight infections or the red blood cells used to carry oxygen and remove waste products from the organs and tissue.
Approximate Word count = 5308
Approximate Pages = 21.2
(250 words per page double spaced)
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