Q: elevated serum creatine kinase (does/does not) equal myocardial infarction?
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Creatine Kinase↗
Biomedical subjects
F A Neelon
Publications and source records attributed to F A Neelon.
Spurious hypertension in the obese patient. Effect of sphygmomanometer cuff size on prevalence of hypertension.
We used standard, large adult, and thigh-size cuffs in random order to take BPs in 470 patients. The prevalences of definite high BP [( HBP]), greater than or equal to 160/95 mm Hg) and borderline HBP [( BHBP ], greater than or equal to 140/90 less than 160/95 mm Hg) were the same with all three cuffs in patients with an arm circumference less than 35 cm, a body mass index less than 34, and a weight of less than 95 kg. The large adult and thigh cuffs did not underestimate the prevalence of HBP in these nonobese patients. The prevalences of HBP and BHBP were twofold greater with the standard cuff than with the large adult or thigh cuffs in obese patients (arm circumference greater than or equal to 35 cm or body mass index greater than or equal to 34 or weight greater than or equal to 95 kg). Routine use of the large adult cuff will provide accurate BP measurement and avoid unneeded evaluation and treatment.
Adolescent↗
BP control. Improvement in a university medical clinic by use of a physician's associate.
Many hypertensive patients, especially those in outpatient clinics at large teaching hospitals, do not achieve BP control. We incorporated a physician's associate into an existing house staff medical clinic and evaluated whether this improved BP control. In patients with moderate or severe hypertension, BP control was achieved in 56% of patients observed by both the physician's associate and the house staff and in 32% of patients observed solely by house staff. Possible contributing factors were more frequent follow-up, simplification of drug regimens, reduced waiting time, more time spent with the patients, and overall greater satisfaction with the physician's associate. We conclude that the addition of a physician's associate to an outpatient clinic is an effective method for enhancing BP control. This can be achieved without establishing a separate hypertension clinic or depriving house staff of experience in the management of hypertension.
Blood Pressure↗
Interrogation and interview: strategies for obtaining clinical data.
During assessment of 55 outpatients, we recorded the numbers and kind of health problems noted during an open-ended interview and during an ;interrogation' based on a structured questionnaire. The combined strategies (interviews and questionnaires) identified a total of 269 problems which were clinically important (i.e. needed medical attention). One hundred and ninety-eight of these problems (74 per cent) were identified by the open-ended interview. Thirtyeight (14 per cent) were identified only by the interview, 71 (26 per cent) only by the questionnaire. We observed that few of the problems detected only by questionnaire were acted upon and that they were therefore only marginally important; most of the problems noted only during interview did lead to further medical action and so were unequivocally of clinical importance. Our data suggest that an open-ended interview, undertaken with the intention of identifying all the patient's health problems, detects those problems well. The routine addition of a lengthy interrogation adds little and is therefore unnecessary.
Data Collection↗
Sounding Boards. The case of bedside rounds.
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Attitude↗
Disordered control of thirst in hypothalamic-pituitary sarcoidosis.
We evaluated water metabolism in 11 patients with hypothalamic-pituitary sarcoidosis. Seven patients had abnormal water metabolism: one had partial antidiuretic hormone (ADH) deficiency, one had severe ADH deficiency, one had severe ADH deficiency and deficient thirst, one had only deficient thirst, and three had excessive thirst. In four of the five with thirst disturbances, there was loss of congruence of osmotic thresholds for thirst and ADH release. Five of our patients presented with polyuria and polydipsia, but only two had true diabetes insipidus, whereas three had organic primary polydipsia with adequate endogenous ADH. That disordered thirst resulting in polydipsia was more common than true diabetes insipidus is at odds with previously held views on the prevalence of ADH deficiency in this condition.
Adolescent↗
The assessment of pituitary function.
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Adolescent↗
Acetaminophen and liver disease.
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Acetaminophen↗
Hypothalamic insufficiency: the cause of hypopituitarism in sarcoidosis.
Ten patients with generalized sarcoidosis and hypopituitarism were studied. Six of these 10 patients presented with sarcoid involvement of the optic nerves resulting in asymmetric visual field defects. All patients had deficiencies of two or more anterior pituitary hormones and seven had abnormalities of water metabolism. Despite hypopituitarism, nine patients had a pituitary responsive to the synthetic hypothalamic releasing factors, thyrotropin releasing hormone and gonadotropin releasing hormone, and the tenth patient had a partially responsive pituitary. The demonstration of pituitary responsiveness allows us to infer hypothalamic insufficiency as the major cause for hypopituitarism in these patients. The combination of visual field defects and hypopituitarism in sarcoidosis is a medically treatable condition that simulates the clinical presentation of a pituitary tumor.
Adolescent↗
Acetaminophen and hepatic dysfunction in infectious mononucleosis.
Two family members developed severe hepatitic dysfunction in association with infectious mononucleosis and acetaminophen administration. Since severe hepatitis is an extremely rare complication of infectious mononucleosis, we postulate that the hepatic dysfunction was induced by acetaminophen.
Acetaminophen↗
Relationship between phosphaluria and acute hypercapnia in the rat.
Standard clearance studies were performed in mechanically ventilated intact and acutely thyroparathyroidectomized (TPTX) rats to document and characterize the effect of hypercapnia (HC) on urinary phosphorus excretion (U(P)V). HC as compared to normocapnia (NC) was associated with an increase in U(P)V in intact (62.5 vs. 7.93 mug/min) and TPTX (30.5 vs. 0.59 mug/min) rats, an increase in filtered load of phosphorus in intact (218 vs. 191 mug/min) and TPTX (243 vs. 146 mug/min) rats, an increase in blood bicarbonate concentration in intact (27.8 vs. 26.0 meq/liter) and TPTX (24.5 vs. 22.3 meq/liter) animals, and a decrease in blood pH in intact (7.15 vs. 7.42) and TPTX (7.07 vs. 7.39) rats. Additional TPTX rats with NC and HC were studied during phosphorus infusion at a comparable filtered load of phosphorus (NC = 307 mug/min and HC = 328 mug/min). U(P)V was 18.5 mug/min in NC and 85.2 mug/min in HC animals. Intact NC animals infused with NaHCO(3) achieved a blood bicarbonate of 45.9 meq/liter compared to 26.0 meq/liter in intact NC NaCl-infused rats. U(P)V was 10.0 mug/min in the NaHCO(3) and 7.93 mug/min in NaCl-infused animals. In intact HC animals infused with NaHCO(3), blood pH was 7.36 compared to 7.42 in NC intact NaCl-infused animals. U(P)V was 83.2 mug/min in the HC bicarbonate-infused and 7.93 mug/min in the NC NaCl-infused rats. These experiments demonstrate that elevated blood carbon dioxide tension per se increases U(P)V. Increases in filtered load of phosphorus and blood bicarbonate which are associated with HC contribute to the phosphaturia as does parathyroid hormone. The phosphaturia is not dependent upon reduction of extracellular pH.
Acidosis↗
Hypoparathyroidism: a possible cause of osteomalacia .
A 17 year old man with longstanding hypocalcemia and hyperphosphatemia presented with incapacitating bone pain and progressive weakness nad bowing of the legs. The serum abnormalities were due to idiopathic hypoparathyroidism as evidenced by a decreased serum concentration of parathyroid hormone and an appropriate rise in urinary cyclic AMP and phosphate excretion, and serum calcium concentration, in response to exogenously administered parathyroid extract. The serum concentration of 1,25-dihydroxycholecalciferol was appropriately decreased. The bone findings were due to osteomalacia as documented by physical findings, bone roentgenograms, and bone biopsy. Normal renal tubular function, blood pH, and serum concentration of 25-hydroxycholecalciferol and elevated serum alkaline phosphatase excluded the common causes of osteomalacia. The data are consistent with the hypothsis that lack of parathyroid hormone causes both hypocalcemia and a decreased serum concentration of 1,25-dihydroxycholecalciferol which, in turn, limit the availability of calcium and cause defective synthesis of bone matrix resulting in abnormal mineralization.
Adolescent↗
Adrenal physiology and pharmacology.
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Adrenal Cortex↗
Stimulation of cartilage macromolecule synthesis by adenosine 3',5'-monophosphate.
The role of cyclic AMP in the regulation of cartilage macromolecule synthesis in vitro was studied in pelvic cartilage from 10-12 day chick embryos. Incubation of cartilages in medium containing 0.5 mM cyclic AMP resulted in a 30% inhibition of 35SO4-2, [3H]leucine and [3H]uridine incorporation into proteoglycan, total protein and RNA, respectively. Higher concentrations of cyclic AMP had no greater effects. In contrast, butyrylated cyclic AMP derivatives (0.5-5.0 mM) added to the incubation medium stimulated (50-100%) the incorporation of these radiolabeled precursors into cartilage macromolecules. Theophylline, in concentrations (0.1-0.5 mM) which raise intracellular cyclic AMP, also increases the incorporation of radiolabeled precursors into macromolecules. The data indicate that exogenous cyclic AMP and butyrylated cyclic AMP derivatives have paradoxical effects on cartilage macromolecule synthesis. Butyrylated cyclic AMP derivatives, not exogenous cyclic AMP, mimic the effects of intracellular cyclic AMP. Incubation of embryonic chicken cartilage with exogenous cyclic AMP results in the extracellular degradation of the cyclic AMP to adenosine. Adenosine (0.125 mM) inhibits precursor incorporation into cartilage macromolecules. The metabolism of exogenous cyclic AMP generates sufficient adenosine to account for the observed inhibitory effects of exogenous cyclic AMP on cartilage macromolecule synthesis. Butyrylated cyclic AMP derivatives are not degraded during incubation with cartilage. The data indicate that cartilage is a tissue in which the effect of cyclic AMP is to stimulate anabolic processes.
Animals↗
Renal cyclic adenosine monophosphate: an accurate index of parathyroid function.
Measurement of total urine cyclic 3':5'-adenosine monophosphate (cyclic AMP) only incompletely discriminates between normal, hyperparathyroid, and nonparathyroid hypercalcemic patients. Only a fraction of total urine cyclic AMP is contributed by parathyroid hormone (PTH) action on the proximal nephron (renal cyclic AMP); the remainder is derived from plasma by glomerular filtration. We dtermined total urine and plasma cyclic AMP and PTH (by carboxy-terminal specific radioimmunoassay) in control, hyperparathyroid, nonparathyroid hypercalcemic, and surgically hypoparathyroid patients. Renal cyclic AMP was calculated as total urine cyclic AMP minus the filtered component. Of these determinations, only renal cyclic AMP segregated normal from hyperparathyroid, and hyperparathyroid from nonparathyroid hypercalcemic patients with complete accuracy. These data suggest that measurement of renal cyclic AMP provides an accurate index of parathyroid activity and allows clinical discrimination and appropriate treatment of the sub-groups of patients with malignancy and nonparathyroid hypercalcemia from those with hyperparathyroidism.
Adult↗
1,25-Dihydroxycholecalciferol deficiency: the probable cause of hypocalcemia and metabolic bone disease in pseudohypoparathyroidism.
Pseudohypoparathyroidism (PsH) is a genetic disease characterized by hypocalcemia, hyperphosphatemia, and metabolic unresponsiveness to parathyroid hormone (PTH). The administration of PTH elicits neither a significant rise in serum calcium (calcemic response) nor a decrease in the renal tubule reabsorption of phosphorus (phosphaturic response). The diminished phosphaturic response is due to an inability of PTH to generate cyclic AMP in renal tubule cells. We investigated the question of whether hypocalcemia and deficient calcemic response to PTH are due to a similar cyclic AMP defect in bone or to an acquired vitamin D deficiency. Four patients were studied. The active form of vitamin D (1,25-dihydroxycholecalciferol) was measured in 3 and was low. Treatment with vitamin D2 restored the serum calcium and the calcemic response to PTH to normal without changing the impaired renal response. Bone biopsy was performed in 2 patients and showed morphologic evidence of increased osteoclastic activity and osteomalacia. The data indicate that the hypocalcemia and bone disease in PsH are due to active vitamin D deficiency, possibly resulting from the genetic renal lesion.
Adult↗