Adverse drug response drugs predicted to be less

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adverse drug response. Drugs predicted to be less effective or likely to cause an adverse event could be avoided. For example, a person predicted to be at high risk for diabetes might be tested for hyperglycemia more frequently, placed on a medical diet earlier, and treated more aggressively for glucose intolerance. 2. Persons with the same type of cancer might respond differently to therapy because the genetic abnormalities in their tumors are different or because of differences, for example, in the way that chemotherapeutic drugs are metabolized. 3. Examples of polymorphisms that influence drug metabolism include variants of CYP2C9 and VKORC1 that influence the metabolism of warfarin, an anticoagulant drug; CYP2D6 variants that affect the biotransformation of β-adrenergic receptor antagonists, neuroleptics, and tricyclic antidepressants; NAT2 variants that affect the inactivation of isoniazid, a drug commonly used to treat tuberculosis; and G6PD that influences sensitivity to the antimalarial drug, primaquine. Response to antihypertensive β-blockers has been associated with variants in genes that encode subunits of the β-adrenergic receptor. 4. Potential obstacles to the use of genetic information in personalized medicine include an inability to identify genetic and environmental risk factors (and their interactions) that enable accurate prediction of clinically significant risk; lack of evidence demonstrating that individual risk assessment improves diagnostic accuracy and treatment outcome; lack of technologies for cost-efficient assessment of an individual’s genome; building an infrastructure for clinicians to access risk data, interpret risk information, and explain risk estimates to patients; and the need for guidelines and policies for how risk assessment information should be used in clinical and research applications. 5. The use of individual genetic variants to predict risk of disease and/or response to pharmacologic agents can be considered the practice of genetic medicine , whereas the assessment of the action of many genes simultaneously to predict disease risk or drug response distinguishes genomic medicine . 6. Potential uses of whole-genome data from an individual include screening for inborn errors, metabolism in newborns (i.e., newborn screening), testing for carriers of genetic disorders (e.g., sickle cell disease, cystic fibrosis), assessing risk for common diseases, predicting drugs that might influence risk for a serious adverse drug, and forensic identification. 7. The answer is B.
8. The answer is C. 9. G 10. g
Comprehensive Final Exam Review 1. The answer is B. The genome includes DNA outside of the nucleus, such as in the mitochondria. It is the DNA content, not the protein content, of a cell that is its genome. The correlation of genomic size and the amount of information encoded has a poor correlation especially in more complex organisms. 2. The answer is D. The current best estimate for humans is 22,000 functioning genes. The information from the genome project has been made widely available to the public. 3. The answer is D. 4. The answer is C. 5. The answer is A. 6. The answer is C. 7. The answer is B. By definition, pseudogenes do not code for any known functional protein.

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