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Am Rev Respir Dis 136(4): 1011–16 does not improve hemodynamics in critically ill patients 40 generic 500mg cefuroxime with mastercard medications rheumatoid arthritis. Cusi K cheap cefuroxime 250mg with mastercard symptoms concussion, Consoli A (1994) Alcoholic ketoacidosis and lactic How is acid–base balance maintained in patients with renal acidosis discount cefuroxime 500 mg without a prescription treatment plant. Philadelphia: Saunders buy cefuroxime 250mg online medications you cannot crush, xii, 899 p naemia in critically ill children: incidence, prognosis, and 44. Arch Dis Child 88(5):419–22 of pH on metabolic and cardiorespiratory responses during 23. J Appl Physiol 57(5):1558–63 in protein synthesis and degradation induced by extracel- 45. The effect of sustained hyperventilation on C277–C282 renal regulation of acid–base equilibrium. Anesth Analg 51(1):92–7 nel mediates hypotension in endotoxemia and hypoxic lac- 25. J Lab Clin Med 117(6):453–67 diet and stool composition on the net external acid balance 27. Garella S (1988) Extracorporeal techniques in the treatment 27(3):538–43 of exogenous intoxications. Philadelphia: Lippincott for cerebral edema in children with diabetic ketoacidosis. Williams & Wilkins, xl, 2072 p The Pediatric Emergency Medicine Collaborative Research 54. New J Med 344(4):264–9 York: McGraw-Hill, xiii, 1268 p Chapter 2 Disorders of the Acid–Base Status 33 55. Philadelphia: Wolters Kluwer Health/Lippincott samples for blood gas determinations. N Engl J Med 275(3):117–22 during development and correction of metabolic acidosis. Ventilation with lower tidal volumes as compared with an example of the emperor’s new clothes? Anesthesiology traditional tidal volumes for acute lung injury and the 56(1):41–4 acute respiratory distress syndrome. Am J Med ratory Distress Syndrome Network (2000) N Engl J Med 17(4):435–7 342(18):1301–8 Dyskalemias 3 E. Therefore a high intracellular K+ concentration (100– 150 meqL−1) and a steep transcellular gradient must 3. The homeostatic mechanisms responsible to maintain these gradients are Mean age-related values and standard deviations for influenced by a variety of physiologic factors that are plasma potassium concentration decline with children’s age, from 5. It is not surprising, then, that moderate deviation of plasma K+ outside the normal range is commonly seen These values are dependent upon the maintenance of external and internal K+ balance. Unlike adults, whose external balance must equal zero, in children this balance is adjusted for accretion commensurate with their growth rate [129]. Gastrointestinal losses may increase up to three- The K+ concentrations in the intracellular and extra- fold following adaptation to chronic hyperkalemia, as cellular space are regulated by conceptually separate may be seen in patients with renal failure [13, 18]. A high cytosolic K+ concen- kidneys are primarily responsible for K+ excretion, tration is required for growth, metabolism, cell divi- but this is delayed after an oral load, with only about sion, protein synthesis, and many other normal cellular one-half excreted during the first 4–6h [41, 42, 109]. This enzyme, and hence intracellular K+ have a significant influence on plasma K+ concen- K+ homeostasis, is physiologically regulated by insu- tration. Secretion well as excessive membrane depolarization in muscle, of these hormones is influenced by a variety of other as may be seen with depolarizing paralytic agents or stimuli, including dietary intake, plasma volume, and following strenuous exercise [116]. Hormonal dysregulation may result from of Henle, and the remaining distal nephron segments pathologic conditions present in critically ill children, have variable reabsorptive capacity linked to hydrogen such as the systemic inflammatory response syndrome. Here, principal cells secrete K+ and Chapter 3 Dyskalemias 37 absorb sodium ions (Na+) [55, 70]. Acute metabolic and respiratory alkalosis + when there is marked leukocytosis and procedural de- promote renal K excretion, whereas acute metabolic lay in refrigerating or separating the plasma. Chronic meta- cases, the pseudohypokalemia is not associated with bolic acidosis and organic acidemia both stimulate net + clinical features of hypokalemia [53, 95, 111, 116]. Aldosterone, glucocorticoids, and antidiuretic hormone stimulate net renal K+ excretion and Na+ absorption [12, 48, 49, 117], 3. Adaptive responses may result in very high rates of K+ excretion, even exceeding the fil- Hypokalemia hyperpolarizes cell membranes by incr- tered load, as may be seen in patients with renal insuf- easing the magnitude of the membrane potential. Its effects vary depending on the speed with which hypokalemia develops and the concentration of other electrolytes including calcium, magnesium, sodium, 3. Whereas a rapid fall in plasma K+ concentration typically results in marked symptoms, a Hypokalemia is defined as a serum K+ concentration stable and chronic K+ loss to the same concentration is below 3. At lower K+ concentra- by the associated intracellular acidosis and stimulated tions, near 2. This may also further flattening of the T waves, with prominent U account for the greater severity of hepatic encepha- waves are seen. Supraventricular longed hypokalemia, which may lead to a chronic and ventricular dysrhythmias are prone to develop, nephropathy associated with microscopic structural especially in patients who take digitalis, have conges- abnormalities as well [2, 53, 95, 116]. The most com- tive heart failure, or experience cardiac ischemia [4, mon functional disorder that develops is a urinary 51]. In individuals with extrarenal causes of hypoka- ventricular repolarization [141]. In the presence of acidosis within renal tubular cells due to chronic K+ a high salt diet, low K+ intake has also been implicated depletion also leads to H+ secretion and ammonia in causing hypertension [2]. The combined effect of Neuromuscular dysfunction typically manifests as these processes that result from chronic K+ depletion skeletal muscle weakness, usually in an ascending is fluid expansion with aldosterone suppression, and fashion, with worsening hypokalemia. Lower extremity mild metabolic alkalosis with acid urine, polyuria, and muscles are initially affected, followed by the quadri- polydipsia [53, 116]. Interestingly, K+ conservation is ceps, the trunk, upper extremity muscles, and later those not affected [106, 116, 145]. Reduced skeletal The microscopic structural abnormalities reported muscle blood flow may also result [2, 116]. Under such to result from chronic K+ depletion include interstitial conditions, exercise may lead to ischemia and result in fibrosis, tubular dilation and atrophy, and medullary cramps, tetany, and rhabdomyolysis [53, 75, 95, 116]. This is associated with Smooth muscle dysfunction related to hypokalemia reduced renal flow and glomerular filtration. A revers- typically includes nausea, vomiting, constipation, pos- ible lesion of the proximal tubular cells, characterized tural hypotension, and bladder dysfunction associated by the presence of intracytoplasmic vacuoles, is also with urinary retention [53, 95, 116]. Renal mineral handling is abnormal in several inher- Endocrine and metabolic perturbations associated ited syndromes associated with severe hypokalemia with hypokalemia include glucose intolerance, and K+ wasting, although not as a direct consequence growth restriction, and protein catabolism [53, 95, of hypokalemia. Marked hypercalciuria and nephrocalcinosis may dependent on K+ influx through specific channels, be seen in certain children with Bartter’s syndrome and this process is dampened by K+ depletion [2, 33]. Severe hypomagnesemia is often Hypokalemia- related impairment in glucose metabo- associated with exacerbations of Gitelman’s syndrome. However, this effect may be significant in those dren with Dent’s disease and proximal tubular disor- with subclinical diabetes, and marked in those with ders, collectively referred to as the Fanconi syndrome. Hence, unless patients are placed on K+-free intravenous fluids for prolonged periods along with The causes of hypokalemia are numerous and can dietary K+ restriction, insufficient intake is unlikely to be categorized mechanistically as due to the follow- be a primary cause of hypokalemia. Insufficient intake of K+ or Cl− as an isolated volume contraction may exacerbate hypokalemia due phenomenon is an exceedingly rare cause of hypoka- to secondary hyperaldosteronism [53, 116].

Wolcott Rallison syndrome

The Pima Indians living traditionally in Mexico still cultivate corn purchase 250 mg cefuroxime with amex symptoms 0f colon cancer, beans buy generic cefuroxime 250 mg online treatment centers near me, and potatoes as their main staples buy cheap cefuroxime 250 mg on-line symptoms 8 days after ovulation, plus a limited amount of seasonal vegetables and fruits such as zucchini buy cefuroxime 250mg lowest price harrison internal medicine, tomatoes, garlic, green peppers, peaches, and apples. The Pimas of Mexico also make heavy use of wild and medicinal plants in their diet. They work hard, have no electricity or running water in their homes, and walk long distances to bring in drinking water or to wash their clothes. They use no modern household devices; consequently, food preparation and household chores require extra effort by the women. In contrast, the Pima Indians of Arizona are largely sedentary and follow the dietary practices of typical Americans. Although roughly 16% of Native Americans in general in the United States have type 2, 50% of Arizona Pimas have type 2, and 95% of those diabetics are overweight or obese. By contrast, type 2 is a rarity among Mexican Pimas and only about 10% could be classified as obese. The average difference in body weight between the Arizona and Mexican Pima men and women is more than 60 lb. When patients are placed on a more traditional diet along with physical exercise, blood glucose levels improve dramatically and weight loss occurs. The focus right now by various medical organizations such as the National Institutes of Health is to educate children on the importance of exercise and dietary choices to reduce diabetes risk. Other Genetic and Racial Factors Racial and ethnic groups besides Pima Indians that have a higher tendency for type 2 include other Native Americans, African-Americans, Hispanic-Americans, Asian-Americans, Australian Aborigines, and Pacific Islanders. In all of these higher-risk groups, again, it is important to point out that when they follow traditional dietary and lifestyle practices, the rate of diabetes is extremely low. It appears that these groups are simply sensitive to the Western diet and lifestyle. Of individuals with type 2, 69% did not exercise at all or did not engage in regular exercise; 62% ate fewer than five servings of fruits and vegetables per day; 65% obtained more than 30% of their daily calories from fat, with more than 10% of total calories from saturated fat; and 82% were either overweight or obese. By comparison, the 300 million typical Americans living alongside them have, over the past 250 years, willingly adopted advances of modern technology, making life less physically demanding. Although the typical Amish person’s diet is not very different from the average American’s and the rates of obesity are very similar as well, the rate of diabetes is about 50% lower. Although the percentage of Amish with impaired glucose tolerance (prediabetes) is about the same as the rate among other white populations in America, apparently not as many Amish go on to develop diabetes. This trend suggests that physical activity has a protective effect against type 2, independent of obesity. Lifestyle changes alone are associated with a 58% reduced risk of developing diabetes in people at high risk (those with impaired glucose tolerance), according to results from the Diabetes Prevention Program, a large intervention trial of more than 1,000 subjects. The two major goals of the program were achieving and maintaining a minimum of 7% weight loss and a minimum of 150 minutes per week of physical activity similar in intensity to brisk walking. In an effort to qualify carbohydrate sources as acceptable or not, two tools have been developed: the glycemic index and glycemic load. The glycemic index is a numerical value that expresses the rise of blood glucose after a particular food is eaten. The standard value of 100 is based on the rise seen with the ingestion of glucose. The glycemic index of foods ranges from about 20 for fructose and whole barley to about 98 for a baked potato. The insulin response to carbohydrate-containing foods is similar to the rise in blood sugar. The glycemic index is often used as a guideline for dietary recommendations for people with either diabetes or hypoglycemia. In addition, eating foods with a lower glycemic index is associated with a reduced risk for obesity and diabetes. Obviously, quantity matters too, but the measurement of a food’s glycemic index is not related to portion size. The glycemic load takes the glycemic index into account but provides much more accurate information than the glycemic index alone. The glycemic load is calculated by multiplying the amount of carbohydrate in a serving of food by that food’s glycemic index, then dividing it by 100. In Appendix B, we provide the glycemic index and glycemic load for many common foods. Research studies are just starting to use glycemic load as a more sensitive marker for the role of diet in chronic diseases such as diabetes and heart disease. Preliminary results are showing that the glycemic load of a person’s food intake is a stronger predictor of diabetes than glycemic index. The Importance of Dietary Fiber in Reducing the Risk of Diabetes Population studies, as well as clinical and experimental data, show diabetes to be one of the diseases most clearly related to inadequate dietary fiber intake. The type of fiber that exerts the most beneficial effects on blood sugar control is the soluble form. Included in this class are hemicelluloses, mucilages, gums, and pectin substances. These are capable of slowing down the digestion and absorption of carbohydrates, thereby preventing rapid rises in blood sugar. They are also associated with increasing the sensitivity of tissues to insulin and improving the uptake of glucose by the muscles, liver, and other tissues, thereby preventing a sustained elevation of blood sugar. Although even the simple change from white-flour products to whole-grain versions is associated with a reduced risk for type 2,56,57 our recommendation is to consume at least 35 g fiber a day from various food sources, especially vegetables. Fiber supplements can also be taken to help lower the glycemic load of a food or meal. The Wrong Types of Fats Dietary fat plays a central role in the likelihood of developing type 2. Large controlled trials have shown that a reduction of fat intake as part of a healthful lifestyle, combined with weight reduction and exercise, reduces the risk of type 2. One of the key factors behind this linkage is the fact that dietary fat determines cell membrane composition. High consumption of saturated and trans fats leads to reduced membrane fluidity, which in turn decreases the binding of insulin to receptors on cellular membranes, decreases insulin action, or both. Trans-fatty acids, found in margarine, shortening, and other foods that are made with partially hydrogenated vegetable oils, are particularly problematic, as they interfere with the body’s ability to use important essential fatty acids. One study estimated that substituting polyunsaturated vegetable oils for margarine would reduce the likelihood of developing type 2 by 40%. Studies have shown that consumption of nuts is inversely associated with risk of type 2, independent of known risk factors for type 2 such as age, obesity, family history of diabetes, physical activity, smoking, and other dietary factors. Higher intakes of fiber, magnesium, and foods with a low glycemic index have been associated with reduced risk of type 2 in several population-based studies. Low Intake of Antioxidant Nutrients Cumulative free radical damage leads to cellular aging and is a major factor contributing to type 2, as well as many other chronic degenerative diseases. Several large population-based studies have shown that the higher the intake of fruit and vegetables, the better blood glucose levels are controlled and the lower the risk for type 2.

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Associate Professor Department of Pathology Quillen College of Medicine Johnson City cheap 250 mg cefuroxime visa medications during breastfeeding, Tennessee Student Reviewers Sara M generic cefuroxime 500mg on line treatment 5th finger fracture. Nesler University of Iowa College of Medicine Iowa City generic cefuroxime 500mg otc medicine mart, Iowa Class of 2002 Misha F cefuroxime 500mg line medicine 3605. Haque Baylor College of Medicine Houston, Texas Class of 2001 Joseph Cummings University of Iowa College of Medicine Iowa City, Iowa Class of 2002 Harvey Castro University of Texas—Galveston School of Medicine Galveston, Texas Class of 2002 McGraw-Hill Medical Publishing Division New York Chicago San Francisco Lisbon London Madrid Mexico City Milan New Delhi San Juan Seoul Singapore Sydney Toronto McGraw-Hill Copyright © 2002 by The McGraw-Hill Companies. 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McGraw-Hill has no responsibility for the content of any information accessed through the work. Under no circumstances shall McGraw-Hill and/or its licensors be liable for any indirect, incidental, special, punitive, consequential or similar damages that result from the use of or inability to use the work, even if any of them has been advised of the possi- bility of such damages. This limitation of liability shall apply to any claim or cause whatsoever whether such claim or cause arises in contract, tort or otherwise. The tenth edition of Pathology: PreTest® Self-Assessment and Review includes such new subject areas as pre- dictive values in the interpretation of laboratory data, the importance of cytokines, the molecular basis of genetic and other disease processes, and molecular biology techniques as these apply to lymphoproliferative disor- ders and other tumors. The medical student must feel submerged at times in the flood of in- formation—occasionally instructors may have similar feelings. This edition is not intended to cover all new knowledge in addition to including older anatomic and clinical pathology. It is, rather, a serious attempt to present important facts about many disease processes in hopes that the student will read much further in major textbooks and journals and will receive some assistance in passing medical school, licensure, or board examinations. Introduction Each PreTest® Self-Assessment and Review allows medical students to com- prehensively and conveniently assess and review their knowledge of a par- ticular basic science, in this instance pathology. Each question is accompanied by an answer, a paragraph explanation, and a specific page reference to an appropriate textbook or journal article. A bibliography listing sources can be found following the last chapter of this text. An effective way to use this PreTest® is to allow yourself one minute to answer each question in a given chapter. By following this suggestion, you approxi- mate the time limits imposed by the Step 1 exam. After you finish going through the questions in the section, spend as much time as you need verifying your answers and carefully reading the explanations provided. Pay special attention to the explanations for the questions you answered incorrectly—but read every explanation. The author of this material has designed the explanations to reinforce and sup- plement the information tested by the questions. If you feel you need fur- ther information about the material covered, consult and study the references indicated. The High-Yield Facts added for this edition are provided to facilitate rapid review of pathology topics. It is anticipated that the reader will use the High-Yield Facts as a “memory jog” before proceeding through the questions. Increased delivery of free fatty acids to liver • starvation • corticosteroids • diabetes mellitus 2. Decreased formation of apoproteins • carbon tetrachloride • protein malnutrition (kwashiorkor) 3. Physiologic • involution of thymus • cell death within germinal centers of lymph nodes • fragmentation of endometrium during menses • lactating breast during weaning 2. Composition • increased protein • increased cells • specific gravity greater than 1. Composition • no increased protein • no increased cells • specific gravity less than 1. Duchenne muscular dystrophy • defective dystrophin gene (muscle breakdown) • pseudohypertrophy of calf muscles • Gower maneuver (using hands to rise from floor) 2. Becker muscular dystrophy Metabolic Diseases • diabetes insipidus • Lesch-Nyhan syndrome Other Diseases • red-green color blindness • fragile X syndrome 24. Maternal deletion → Angelman’s syndrome • stiff, ataxic gait with jerky movements • inappropriate laughter (“happy puppets”) • may be due to two copies of paternal 15 chromosome (paternal uni- parental disomy) 14 Pathology 2. Paternal deletion → Prader-Willi syndrome • mental retardation • short stature and obesity • small hands and feet • hypogonadism • may be due to two copies of maternal 15 chromosome (paternal uni- parental disomy) 27. Due to cystic medial necrosis of aorta • hypertension • Marfan’s syndrome → due to defect in fibrillin gene 2. Transposition of the great vessels • need shunt to be present in order to survive (e. Diabetes mellitus Nephritic Syndrome • hematuria (red blood cells and red blood cell casts in urine) • variable proteinuria and oliguria • retention of salt and water (hypertension and edema) High-Yield Facts 29 Examples (proliferative glomerular disease): 1. Psammoma body: • papillary carcinoma of the thyroid • papillary tumors of the ovary • meningioma 2. Immunoglobulin • Russell body → cytoplasmic or extracellular • Dutcher body → nucleus (Waldenstrom’s) 3. Increased lipolysis of fat stores, which can result from starvation, dia- betes mellitus, or corticosteroid use, is most likely to cause steatosis (fatty liver) through which one of the listed mechanisms? Decreased free fatty acid excretion from the liver leads to free fatty acid accu- mulation in hepatocytes b. Increased free fatty acid delivery to the liver leads to triglyceride accumulation in hepatocytes d.

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Should David’s physicians have worked very hard to dissuade David from taking this gamble with his life? That is discount 250 mg cefuroxime otc symptoms 39 weeks pregnant, were his physicians derelict in their duties as physicians to protect David’s best medical interests? And those answers imply harsh moral criticism of both David’s parents and his physicians purchase 500mg cefuroxime visa medications depression. There are morally relevant con- siderations on the other side of the moral equation cheap 500mg cefuroxime mastercard medications quetiapine fumarate. To begin with quality 500mg cefuroxime the treatment 2014 online, one of the car- dinal principles of health care ethics today is the principle of respect for patient autonomy. In brief, that principle states that competent patients have a strong moral right to decide for themselves what is in their best medical interests. If such deci- sions are made freely by patients, if such decisions are a product of careful delib- eration (a careful weighing of risks and benefits), if such decisions emerge from a stable set of values and a certain stable understanding of what counts as a life worth living for that patient, then such patient choices ought to be respected. That is, such patients would have a presumptive right to see their choices carried out, and their physicians would be under a presumed moral obligation not to ignore, or worse, overturn those decisions. Among other things, this line of reasoning has led to the conclusion that there are a number of circumstances in which patients have the moral right to refuse life-sustaining care. The case of Dax, a 26-year-old Texas burn victim from 1973, is usually taken as a paradigmatic of just such a right. He saw himself as having been seriously morally wronged because he was forced to undergo 14 painful months of burn therapy in order to save his life. Dax wanted to be allowed to die, something that most physicians at the time were very strongly inclined to resist. But he wants to live in the same large world that he sees his friends and family enjoying, not the very constrained world of a plastic bubble in which he was forever denied, literally, ordinary human touch. If that in fact is what David very strongly desires, then who would have the moral right to deny him the medical interventions that might make that possible? This latter way of framing the issue does yield a very different moral perspective. The principle of respect for patient autonomy does not permit each and every patient to practice medicine as they wish, or to use physicians as mere instruments to achieve whatever health states they see as desirable in the context of their life goals. Physi- cians have their own moral integrity as physicians, and patients have no moral right to simply violate that integrity as they wish. He may feel the need to “bulk up” some, and he may see steroids as the key to accomplishing that goal quickly. He is beginning to rebel against the physical constraints on his life as well as the constraints imposed by his parents and physicians. What he wants is certainly reasonable in a general sense, but it is not reasonable for him now. Bone marrow transplantation does offer hope of release from his confined environment, but it is a very risky hope. If David is patient, then those unknowns and those risks may be substantially reduced over a period of years through expected medical progress. He should be counseled to let others assume the risks of medical pioneers, others who do not have as much to lose as he does. David is not seeking to misuse a medical therapy, as our hypothetical high school athlete is. But it might be argued that his choice is not autonomous enough that his physicians would be ethically obligated to accept that choice. That is, his choice may be short-sighted, a product of less than adequate deliberation and a less than stable balancing of competing personal values. Someone might argue, for example, that David’s decision is in the same moral category as that of any other adolescent who chooses to drive in excess of 100mph on a dark country road in a race against another adolescent. Someone might care to see David as a medical hero in a battle against diseases that afflict mankind. After all, the argument goes, adolescents who are only a few years older than David are permitted to fight in wars and risk their lives for what they believe to be noble causes. We are all mindful of the fact that young men can be seduced into participating in wars. Generals cannot prove their military skills by devising clever battle plans in libraries; they need to fight actual wars, and they need to recruit young men as soldiers. Similarly, medical researchers cannot prove their medical ingenuity merely be designing clever lab experiments; they need to recruit patients as participants in these experimental battles against disease. To continue the mili- tary analogy, victory does not go to the timid but to the courageous. Rarely do history books record the names of the soldiers who do the courageous things that win battles. There are enormous social and professional rewards attached to early medical breakthroughs. This can motivate sometimes inappropriate risk taking by medical researchers, or, to be more precise, an inappropriate imposition of risk on those who may be persuaded to participate in medical experiments. Should the researchers have delayed this experiment until they were more confident that a positive outcome was likely? In ordinary medicine the practice of informed consent is supposed to protect patients from the risks that are always part of medical practice. The role of a physician is to present honestly, and in a way that is intel- ligible to a particular patient, the risks and benefits associated with a proposed ther- apeutic intervention, along with other reasonable alternatives to that intervention. The physician may make a recommendation for a particular option, but ultimately the patient is supposed to be offered the opportunity to make that choice in the light of their own goals and values as they pertain to this medical encounter. Depending upon the seriousness of their medical problems, patients may be more or less anxious, more or less capable of making a rational assessment of their medical options. Good doctors are ethically obligated to be sensitive to the vulnerabilities of patients in these circumstances, and to assist patients to make decisions that in a meaningful sense are both their own and congruent with their own best interests. Most certainly, what good doctors are ethically forbidden from doing is advancing their own self-interest, that is, concern about their own economic well being, at the expense of the interests of their patients. Patients trust their doctors, and that trust is violated when doctors use patients and their medical problems to advance their own interests. In practice, ethically speaking, our understanding of informed consent needs to be modified when proposed interven- tions are very experimental. There are very standard, routine, simplified ways of appropriately eliciting informed consent in routine medical care. The core element of informed consent is information, reli- able, scientifically and clinically grounded information. If that were the case, then there would be no ethical justification at all for proceeding with the intervention. On the contrary, enough is known that clinical researchers are morally and medically warranted in believing that this intervention is as likely to yield a net therapeutic benefit as it is likely to yield a net harm. But there are also a lot of unknowns, which represent the potential for serious, perhaps fatal, harm to the patient. In the case of David, for example, we have no reason to believe that the researchers were negligent at that time in failing to detect the Epstein–Barr virus (suppressed) in the bone marrow of his sister.

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