Biomedical subjects
Publications and source records attributed to E L Coodley.
Pleural effusion represents an unusual but significant manifestation of actinomycosis, as illustrated in this case presentation. The diagnosis was made after bronchoscopy and examination of bronchoalveolar fluid and culture. No parenchymal abnormality was noted on the chest film.
Clearly, management of heart disease is quite different in the elderly than in younger patients, and it represents a significant problem in light of the increasing numbers of elderly patients. For physicians, the challenges are to recognize the many cardiac entities, to avoid the problems that can result from prescribing drugs in dosages similar to those given to younger patients, and to acquire a better understanding of cardiac anatomy and physiology associated with the aging process.
Comparison of studies on the elderly is difficult. This study is one of the largest done on healthy, ambulatory persons aged 65 and up. Findings indicate that most laboratory values in elderly persons fall in the normal range. A significantly abnormal test result should raise the suspicion of underlying disease. A small percentage of patients show an abnormality on specific tests (ie, for glucose, calcium, serum lipids). Changes in a few test values are to be expected with aging: These include an increase in alkaline phosphatase, a decrease in serum phosphorus, a decrease in creatinine clearance without a concomitant rise in serum creatinine, and an increase in postprandial glucose level. Vitamin deficiencies and decrease in serum albumin are usually the result of chronic malnutrition rather than aging.
Coronary heart disease is a major cause of morbidity and mortality in the older population. The recognition of such disease in the elderly varies in a number of parameters from that noted in younger patients. There are a number of physiologic changes in cardiac function as a result of aging, and they have an important bearing on the recognition of cardiac disease in the elderly. This review stresses the particular features of coronary disease in the aged and contrasts them with features more readily recognized in younger patients. Changes in the development of angina pectoris, heart failure, and the diagnosis of myocardial infarction vary significantly in the elderly population. The role of diagnostic modalities varies considerably in sensitivity and specificity when comparing younger and older patients. Potential areas for further research are stressed.
Cardiac arrhythmias result from conduction block, abnormal impulse formation, or a combination of both. The decision to treat arrhythmias depends on symptoms, hemodynamic problems, the presence or absence of organic heart disease, and the presence of malignant arrhythmias. Holter monitoring, treadmill exercise testing, and electrophysiologic stimulation can facilitate identification. Control involves correction of precipitating or contributing factors and selection of an appropriate antiarrhythmic drug or surgical technique.
Hypertension in the older population has a serious prognosis and this is true even for isolated systolic hypertension. There is a markedly increased risk of stroke, cardiovascular disease and central nervous system in such patients. The hemodynamics in hypertension of the elderly differs in a number of parameters from hypertension in the younger patient. In addition, drug metabolism is markedly altered by the aging process. This combination of factors requires a selective choice of agents for the management of hypertension in the elderly. The role of various drug modalities and their efficacy is reviewed in this presentation.
We treated a case of drug-induced cholestatic jaundice in which the causative agent was pizotyline (Pizotifen), a phenothiazine-related drug. The patient's symptoms were compatible with either hepatitis or biliary obstruction. Diagnostic laboratory studies were performed to exclude both of these entities. The history of drug ingestion plus the clinical and histologic features established pizotyline as the causative agent.
A double dilemma faces the clinician who suspects thyroid disease in the elderly--both lab tests and treatment protocol were developed using younger patients. Reviewing the literature and their own recent data, the authors suggest how to evaluate thyroid-related lab data, taking age into account.
Substantial hyperkalemia with ECG abnormalities developed in a patient. None of the common causes of hyperkalemia was found, eg, acidosis, hemolysis, rhabdomyolysis, renal failure, hypoadrenalism, leukocytosis, or thrombocytosis. The patient had been receiving indomethacin, a drug known to inhibit renin production, aldosterone excretion, and prostaglandin synthetase. The patient was rechallanged with indomethacin, and measurements of serum potassium and renin, urinary potassium, aldosterone, and creatinine levels were done. The study period clearly showed a hyporeninemic-hypoaldosterone states with diminished renal potassium excretion, leading to hyperkalemia associated with the indomethacin therapy. The development of hyperkalemia caused by indomethacin is probably unusual; however, we believe it is important to report this potentially serious pathophysiologic occurrence associated with a commonly used medication.
In a 74-year-old woman, excessive insensible water loss developed secondary to a period of hot, humid weather, associated with an underlying inability to obtain adequate water replacement. On admission to the hospital she was comatose, clinically dehydrated, and had laboratory values consistent with a water deficit of approximately 30% (9 L) of body water. Serum sodium concentration was 202 mEq/L. Serum osmolality was 430 mOsm/L. The patient remained comatose for seven days, during which time she was vigorously treated with fluids, and she gradually recovered. This case represents what we believe is a unique report in the literature of the severity of hypernatremia developing via this pathogenic mechanism and survival in an adult with this degree of disturbance of sodium and water homeostasis.
Serum glycoprotein levels were compared in two groups of age- and sex-matched patients, 15 with coronary artery disease and 14 normal controls. While total glycoprotein levels were increased in the coronary group, significantly higher levels were found in only five of 16 glycoproteins--C3c haptoglobin, GC-globulin, alpha1-acid glycoprotein, and C3 activator--with no change in 10 other glycoproteins and significant decrease in transferrin. This study demonstrates what appears to be a glycoprotein profile in coronary artery disease and reviews possible interactions of glycoproteins with known risk factors in atherogenesis.
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In view of known abnormalities of plasma proteins in diseases showing changes in platelet aggregation, the effect of one of the major serum proteins, alpha1-acid glycoprotein, on platelet aggregation was evaluated. This protein, when added to platelet-rich plasma, markedly inhibited platelet aggregation induced by both adenosine diphosphate (ADP) and epinephrine. Transferrin, similarly studied, had no effect. These results are consistent with the hypothesis that the relative concentration of alpha1-acid glycoprotein may influence platelet aggregation in diseases associated with abnormal concentrations of this protein.
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