Teaching professionalism - Why, What and How.

Due to changes in the delivery of health care and in society, medicine became aware of serious threats to its professionalism. Beginning in the mid-1990s it was agreed that if professionalism was to survive, an important step would be to teach it explicitly to students, residents, and practicing physicians. This has become a requirement for medical schools and training programs in many countries. There are several challenges in teaching professionalism. The first challenge is to agree on the definition to be used in imparting knowledge of the subjects to students and faculty. The second is to develop means of encouraging students to consistently demonstrate the behaviors characteristic of a professional - essentially to develop a professional identity. Teaching of professionalism must be both explicit and implicit. The cognitive base consisting of definitions and -attributes and medicine's social contract with society must be taught and evaluated explicitly. Of even more -importance, there must be an emphasis on experiential learning and reflection on personal experience. The general principles, which can be helpful to an institution or program of teaching professionalism, are presented, along with the experience of McGill University, an institution which has established a comprehensive program on the teaching of professionalism.

Renewing professionalism: an opportunity for medicine.

In recent decades, both the concept and the performance of professionals have been widely questioned. Professionalism and the idea of service have been placed under intense pressure, but they have survived. Medicine may now have an opportunity to reestablish itself as a respected, influential, and useful profession in Western society. The authors believe this could occur (1) because of the strength of the democratic process and the place of organized medicine within it; (2) because medicine's role as a source of relatively impartial expertise is being reestablished (because medicine no longer controls the health care system); and (3), most important, because of the importance of the individual physician as healer in both society's view of medicine and medicine's view of itself. To take advantage of this opportunity, the authors offer several recommendations, including (1) that medicine must continue current efforts to place first the doctor-patient relationship (the role of the healer) and the idea of service in redefining and fulfilling its obligations to society; (2) that there be a comprehensive education campaign to help physicians understand professionalism and its obligations (which the authors define); and (3) that physicians should assume responsibility for their local and national associations. If the individual medical professional and all the institutions connected with the practice and teaching of medicine truly understand and seek to fulfill their contracts with society and the obligations derived from these, the morality inherent in medical professionalism can be a dominant force, and better health care will result.

Teaching medicine as a profession in the service of healing.

As society, including the medical profession, moves into a new century, the rate of change in the relationship between professions and society is unprecedented. All societies need healers, and in the English-speaking world the services of the physician-healer have been organized around the concept of the professional. The great increase in both state control and corporate involvement has seriously intruded into the traditional autonomy enjoyed by both the medical profession and individual physicians, and further changes can be expected. More physicians are becoming either employees or managers in the state or corporate sector, while others are being forced to compete in a marketplace that rewards entrepreneurial behavior. It is the responsible behavior of the professional that will protect the role of the healer. Medicine has been rightly criticized for placing undue emphasis on both income and power and for protecting incompetent or unethical colleagues; and it has failed to accept responsibility for injustices or inequities in health care systems and has moved slowly to address new diseases or issues. Nonetheless, all evidence indicates that society still values the healer-professional and does not wish to abandon professionalism as a concept--it appears to prefer an independent and knowledgeable professional to deal with its problem rather than the state or a corporation. For this reason, medicine's professional associations and academic institutions must ensure that all physicians understand professionalism and accept its obligations. In doing so, the objective should be to encourage the moral and intellectual growth of physicians by setting standards based on higher aspirations than can or should be enforced. In facing the complex world of our future, such action will both serve society and maintain the integrity of the profession.

Principles and results of corrective lower limb osteotomies for patients with vitamin D-resistant hypophosphatemic rickets.

Forty-four lower limb osteotomies were performed in ten patients with vitamin D-resistant hypophosphatemic rickets. The average follow-up period was 51 months. Osteotomies were combined with shortening and compression plating. This allowed corrections of angular deformities in the sagittal plane as large as 70 degrees and in the coronal plane as large as 78 degrees. There was one complication, a compartment syndrome that resolved completely following prompt fasciotomy. Recurrence of deformity occurred in 27% of the cases. While osteotomies were safe and provided dramatic improvement to limb deformity, postoperative control of vitamin D metabolism was the one constant factor for maintenance of correction.

Gestational changes of thyroid hormone action in the developing fetal bovine epiphysis.

Thyroid hormones are essential for cartilage growth and maturation. In order to assess their actions during different periods of skeletal development, [125I]-triiodothyronine (T3) binding capacity in epiphyseal cartilage and triiodothyronine concentrations in serum were quantitated in bovine fetuses of the second and third trimesters of gestation (equivalent to fetal sizes of 10-90 cm crown-rump (CR) length), and related to the alkaline phosphatase activities in the same cartilaginous tissues. Nuclear T3 binding levels, which were initially low during 10-30 cm CR, rose to a peak value (1.7 pmol/mg DNA) at the end of the second trimester (40-50 cm CR). Then, following a sharp decline at 50-60 cm CR, T3 binding rose to a moderate level in the later gestational period (60-90 cm CR). Serum total triiodothyronine rose transiently in fetuses of 30-50 cm CR to a peak level (34 ng/100 ml), and subsequently increased continuously in the later period (60-90 cm CR). Alkaline phosphatase activities measured in epiphyseal chondrocytes rose significantly in fetuses of 60-90 cm CR. The coincident rise of cartilage triiodothyronine binding capacity and serum circulating triiodothyronine levels in the late second trimester suggests that this thyroid hormone induces its own binding sites in bovine epiphyseal cartilage; the dramatic increase in the level of serum triiodothyronine during the third trimester of gestation is temporally related to the increase in alkaline phosphatase activity of chondrocytes, as well as other recognized developmental changes in the fetal bovine skeletal tissues.

Temporal relationship between fetal bovine skeletal growth and circulating hormonal levels.

Skeletal growth and serum hormonal levels in bovine fetuses were studied cross-sectionally from late first trimester to late third trimester of gestation (corresponding approximately to 75-275 days of age, and a crown-rump (CR) 5-105 cm/in size). Measurements of tibial and femoral lengths showed that bone growth proceeds at a 30% faster rate in fetuses of 50-105 cm CR, coincident with the appearance and exponential growth (y = 0.000207 e 0.12522 x; y, dried weights of ossification in grams and x, CR in cm) of a secondary center of ossification in the epiphysis. During this period there is an increase in the proportion of [3H]-thymidine-labeled nuclei (measured by autoradiography) in the proliferative zone of the epiphyseal growth plate and a progressive hypertrophy of chondrocytes in the epiphysis; in serum there is a rise in alkaline phosphatase activity, a rise in the calcium, and a decrease in the phosphorus concentrations. Cellularity (nuclei/area) and the proportion of [3H]-thymidine labeled nuclei in epiphyseal cartilage decline during the period of 15-105 cm CR, except at 25-45 cm CR when both parameters of chondrocyte growth have transiently stabilized. [35S]-Sulfate and [3H]-proline incorporation (cpm/100 micrograms DNA) in epiphyseal cartilage also decline initially during 10-25 cm CR, then attain a stable level during 25-50 cm CR; subsequently, [35S]-sulfate incorporation gradually increases and [3H]-proline incorporation remains at a constant level. The proportion of [3H]-thymidine-labeled nuclei in the epiphyseal growth plate also declines in early gestation, then becomes stabilized at 20-50 cm CR. The whole growth plate thickness varies during gestation and is maximal during 20-50 cm CR. The proliferative zone attains maximal thickness at 20-50 cm CR while the hypertrophied and degenerative zone has maximal thickness at 40-80 cm CR. Gestational changes of hormone levels were quantitated in fetal serum. Glucocorticoids and thyroxine were measured by radioimmunoassay; somatomedinlike bioactivity was measured as the capacity of a serum sample to stimulate [3H]-thymidine incorporation in chondrocytes compared to that of a control serum. Temporally related to the changes occurring in the skeletal tissues, there is a high serum level of glucocorticoids at 10-20 cm CR when the cartilaginous activities are declining, a peak level of serum somatomedinlike bioactivity at 20-50 cm CR when cartilage growth and metabolism become stabilized, and a rise of thyroxine level after 45 cm CR during which time there is an increasing rate of bone formation.(ABSTRACT TRUNCATED AT 400 WORDS)

Gestational changes in the level of glucocorticoid-binding sites in fetal bovine cartilaginous tissues.

In order to assess glucocorticoid actions on fetal cartilage development, [3H]dexamethasone binding site levels in fetal bovine cartilaginous tissues from long bones were measured, using a whole cell assay at 37 degrees C. Displaceable [3H]dexamethasone binding in epiphysial growth cartilage was maximal (16.2 fmol/10(6) cells) in fetuses of 10-15 cm crown-rump length (CR), and declined to 22% of the maximum in fetuses of 20-30 cm CR. Subsequently, [3H]dexamethasone binding rose to a plateau (13.0 fmol/10(6) cells) in fetuses of 30-80 cm CR and declined in those of 80-100 cm CR. When measured in growth plate cartilage, [3H]dexamethasone binding was significantly higher in fetuses of 40-80 cm CR (39 fmol/10(6) cells) than in those of 80-100 cm CR. There was no significant change of [3H]dexamethasone binding affinities in epiphysial chondrocytes of 5-100 cm CR fetuses or in growth plate chondrocytes of 40-100 cm CR fetuses. These results demonstrate that fetal cartilaginous tissues during development possess varying cellular levels of glucocorticoid binding and may thus have temporal changes in sensitivity to glucocorticoid hormones.

Osteonecrosis of bone. Current concepts as to etiology and pathogenesis.

Experimental and some clinical evidence suggest that one or more mechanisms, alone or in combination, induce bone necrosis. These include marrow cell hypertrophy, microembolic phenomena, and lipid-induced osteocyte necrosis. Such events may result in local inflammatory exudates and/or vascular impedence. Either may effect an increase in the hydrostatic pressures in bone with the potential to limit blood flow and magnify the initial insult. Further experimental investigations are necessary to gain knowledge of etiologic mechanisms and a rational means of prophylaxis or treatment.

Corticosteroid-induced osteonecrosis of the humeral head.

Cortisone-induced osteonecrosis of the shoulder occurs in a fashion that is roughly similar to that seen in the hip. It appears that the cortisone itself is responsible for the lesion, and patients who develop the condition can have a minimal lesion that heals well, a moderate deformity that is well tolerated, or severe joint disease requiring surgical correction. A knowledge of the natural history of the condition allows for rational and generally successful therapy.