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Biomedical subjects

M S Wheby

Publications and source records attributed to M S Wheby.

At least 19 recordsLinked to original sources
PubMed1993

Evaluating faculty clinical excellence in the academic health sciences center.

Although excellence in the clinical care of patients is the cornerstone of medicine, academic health sciences centers have increasingly given more weight to research and correspondingly less emphasis to patient care. To better recognize and reward clinical excellence, it is first necessary to effectively evaluate physicians' performances in patient care. In addition to addressing the value of faculty clinical excellence in the academic setting, the authors discuss different approaches to clinical assessment, theoretical and practical problems in assessing the performances of clinical faculty, and a system of evaluation being initiated at the University of Virginia School of Medicine. This system of evaluation combines--in annual individual reviews--a limited amount of objective assessment data with subjective evaluations from several sources. The objective data include board certification and recertification, analysis of outcomes data, and documentation of scholarly activity. The subjective evaluations include letters of recognition and appreciation from faculty colleagues and written observations from department chairs, housestaff, students, and nurses. The system has been accepted by department chairs, members of the Promotion and Tenure Committee, and the general faculty. In implementing this new system, periodic review of the pace and direction of change will be crucial to track progress and provide feedback for further modification.

Academic Medical Centers↗
PubMed1992

Anemia in pregnancy.

In evaluating pregnant women with anemia, it is essential to do a complete history and physical examination, as well as a complete blood count with indices and a blood smear examination. Based on these findings, other tests such as ferritin and serum or red cell folate may be ordered. Because of the normal physiologic changes in pregnancy that affect the hematocrit, indices, and some other parameters, diagnosing true anemia, as well as the etiology of anemia, is challenging. Because of the increased nutritional requirements of the mother and fetus, the most common anemias are iron deficiency anemia and folate deficiency megaloblastic anemia. These anemias are more common in women who have inadequate diets and who are not receiving prenatal iron and folate supplements. Other less common causes of acquired anemia in pregnancy are aplastic anemia and hemolytic anemia associated with preeclampsia. In addition, congenital anemias such as sickle cell disease can impact on the health of the mother and fetus. Obviously, severe anemia has adverse effects on the mother and the fetus. There is also evidence that less severe anemia is associated with poor pregnancy outcome. The cause of this association has yet to be elucidated. It is important, however, to diagnose and treat anemia in pregnancy to provide for optimal health of the mother and infant.

Anemia↗
PubMed1992

Case report: sickle cell trait and recurrent deep venous thrombosis.

Thromboembolic events are unusual in patients with sickle cell trait, particularly in the absence of hypoxic stresses. A young black man with multiple episodes of lower extremity deep venous thrombosis, the first of which occurred when he was 18 years old, is reported. The only identifiable risk factor for recurrent venous thrombosis was the presence of sickle cell trait.

Adult↗
PubMed1990

Synovitis in angioimmunoblastic lymphadenopathy with dysproteinemia simulating rheumatoid arthritis.

We describe a patient with angioimmunoblastic lymphadenopathy with dysproteinemia who developed a symmetric, rheumatoid-like, peripheral polyarthritis. Radiographs of the involved joints revealed soft tissue swelling without erosions or cartilage loss. Rheumatoid factor and fluorescent antinuclear antibodies were negative, and C-reactive protein and erythrocyte sedimentation rate were normal. Synovial fluid analysis showed an inflammatory effusion (white blood cell count of 3,500/mm3, with 76% polymorphonuclear leukocytes). A closed synovial biopsy of the wrist revealed a mononuclear infiltrate consistent with angioimmunoblastic lymphadenopathy with dysproteinemia. Monthly parenteral chemotherapy treatment with high-dose methyl-prednisolone and cyclophosphamide resulted in remission of all manifestations of disease, including arthritis.

Arthritis, Rheumatoid↗
PubMed1990

Trisomy 19 in a patient with myelodysplastic syndrome and thrombocytosis.

A patient with refractory anemia with excess blasts, ringed sideroblasts, and thrombocytosis was found on cytogenetic analysis to have trisomy 19 as the sole abnormality. Although trisomy 19 in combination with other chromosomal anomalies has been encountered in association with a variety of hematologic malignancies, many solid tumors, and the myelodysplastic syndrome, its occurrence as the only cytogenetic aberration is rare and has not been reported in association with thrombocythemia.

Aged↗
PubMed1990

Fluoxetine and the bleeding time.

Fluoxetine (Prozac) is a nontricyclic serotonin (5-hydroxytryptamine) reuptake inhibitor commonly prescribed for the treatment of depression. Fluoxetine also blocks 5-hydroxytryptamine reuptake in platelets and could potentially lead to clinically significant platelet dysfunction. We describe a patient who developed petechiae and prolongation of the bleeding time while receiving fluoxetine therapy.

Adult↗
PubMed1986

Hemochromatosis heterozygotes may have significant iron overload when they also have hereditary spherocytosis.

A family is described in which four of six siblings have both hereditary spherocytosis and evidence of abnormal iron metabolism. Three of the four have significant iron overload. HLA typing, which permits the detection of the gene for hemochromatosis, indicates that all family members with hereditary spherocytosis who have abnormal iron metabolism or significant iron overload are heterozygous for the hemochromatosis gene. Family members having hereditary spherocytosis but not the gene for hemochromatosis have normal iron studies as does a family member heterozygous for hemochromatosis but no hereditary spherocytosis. Based on the findings in this kindred, it appears that the combination of chronic hemolysis and the gene for hemochromatosis results in increased iron absorption that may lead to significant iron overload.

Adult↗
PubMed1984

Hairy cell leukemia: a case of cryptococcosis appearing as hairy cell meningitis.

Hairy cell leukemia has rarely been shown to involve the central nervous system. We have reported a case of hairy cell leukemia with apparent hairy cell meningitis, later found to be cryptococcal meningitis. Spinal fluid abnormalities, including the hairy cell pleocytosis, resolved with treatment of the cryptococcal infection.

Cerebrospinal Fluid↗
PubMed1984

Liver damage in disorders of iron overload. A hypothesis.

The pathogenesis of liver damage in patients with iron loading disorders is not explained. Evidence concerning the following hypothesis is reviewed: Iron, absorbed from the intestinal tract when transferrin saturation is complete or almost so, remains unbound and is lost into the liver on first passage through the portal circulation. By still-to-be-determined molecular events, unbound iron is toxic to liver cells and produces progressive damage when this process occurs repeatedly.

Alcoholism↗
PubMed1981

Hemoglobin iron absorption kinetics in the iron-deficient dog.

In the absorption of Hb iron (HbFe), heme is separated from globin in the intestinal lumen and enters mucosal cells where Fe is split off and transported to blood. Previous studies indicated that this final step is the limiting one in absorption of HbFe in normal and Fe loaded animals but not in Fe-deficient animals. The present studies were designed to determine the limiting step in absorption of HbFe in Fe-deficient dogs. Varying Amounts of 59Fe labeled Hb were injected into closed duodenal loops in anesthetized dogs. Each step in the absorptive process was measured: intralumenal separation of the heme from Hb; mucosal uptake of heme; intramucosal splitting of Fe from heme; transport of Fe to blood. This process was characterized using a five compartment kinetic model. The resulting seven rate constants were determined to best describe the observed absorption data. Results show: 1) with increasing dose of 59HbFe, mucosal uptake of heme, Fe split from heme in mucosa, and Fe transported to blood all increase linearly. 2) Mucosal 59Fe-heme accumulates over the 3-hour period while 59Fe does not, indicating rapid transport of 59Fe split from heme. These results suggest that the rate limiting step in absorption of HbFe in Fe-deficient dogs is the splitting of Fe from heme in the mucosa.

Animals↗
PubMed1981

Disseminated intravascular coagulation in pregnancy. The role of heparin therapy.

Treatment of the underlying cause and supportive care constitute the basic principles of management of disseminated intravascular coagulation. The role of anticoagulation with heparin is controversial in the absence of any controlled studies. This case report describes two patients with acute obstetric disseminated intravascular coagulation in whom the use of heparin resulted in marked clinical improvement. Treatment with heparin may be of help in situations where there is a delay in elimination of the underlying cause.

Abortion, Therapeutic↗
PubMed1980

Effect of iron therapy on serum ferritin levels in iron-deficiency anemia.

The level of serum ferritin is a reliable indicator of body iron stores. Exceptions include liver disease, malignant diseases, and treatment of iron-deficiency anemia. The latter was noted in iron-deficient infants who showed a rise of serum ferritin to normal levels in the first week of treatment. To evaluate this in adults, 14 patients with iron-deficiency anemia were studied prior to and after beginning treatment with oral ferrous sulfate in standard dose, 300 mg t.i.d., or double dose, 600 mg t.i.d. Serum ferritin was assayed by radioimmunoassay. No rise occurred in the first 3 wk in 5 patients treated with standard dose, although hematologic response occurred. With double dose, 7 of 9 showed a ferritin rise in 2 days with return to subnormal levels within 6 days of discontinuing iron. This study indicates that standard treatment of iron deficiency anemia in adults does not cause a rise in serum ferritin until hemoglobin levels are normal. The early rise seen with double dose is most likely due to absorption of iron in excess of utilization for erythropoiesis resulting in temporary storage. When iron is discontinued, stores are rapidly depleted as reflected by the prompt decrease in serum ferritin.

Adult↗
PubMed1979

High-fiber diet: its role in the treatment of diabetes mellitus reviewed.

Dietary manipulation has long been a mainstay of treatment of adult-onset diabetes. Weight loss and a diet low in refined carbohydrate have often allowed either reduction or discontinuation of oral hypoglycemic agents or insulin. The evidence presented in this review suggests that complex carbohydrates and high-fiber compounds can play a significant role in this dietary manipulation and merit further study. The mechanism by which hyperglycemia is ameliorated may be the increased viscosity of intestinal contents with slower small bowel transit time resulting in slow, but sustained absorption of glucose.

Blood Glucose↗
PubMed1978

Medicinal iron-induced hepatic cirrhosis: reversal by phlebotomy: studies on pathogenesis.

A patient with no underlying hematologic or iron metabolic disorder developed iron induced hepatic cirrhosis as a consequence of long term medicinal iron ingestion. Marked improvement in liver histology followed removal of 28 grams of iron by phlebotomy. Radioautographic studies in rats showed a periportal hepatocyte concentration of radioiron absorbed from the intestine while plasma transferrin was saturated. Based on these and other observations an hypothesis is proposed to explain liver damage in disorders of iron overload.

Aged↗