Search PubMed⌕ Search

Biomedical subjects

M Emmett

Publications and source records attributed to M Emmett.

48 records · Page 3Linked to original sources

Simple and mixed acid-base disorders: a practical approach.

Metabolic and respiratory acid-base disorders occur as single and mixed entities. When induced perturbations in PCO2, HCO3(-), pH, and serum electrolytes are interpreted in the light of sound physiologic principles, even the most complicated mixed disorders may be easily diagnosed. The pathophysiology underlying the simple disturbances is defined and used as a framework for discussion of the mixed metabolic, respiratory acid-base derangements. Formulae are presented which allow one to predict what the appropriate degree of metabolic compensation should be for any primary respiratory disorder, or what the PCO2 should be for any given degree of primary metabolic acidosis or alkalosis. The various clinical settings in which mixed acid-base disorders occur most commonly are discussed.

Acid-Base Equilibrium↗

The nature of arginine auxotrophy in cutaneous populations of staphylococci.

L-Arginine was required for growth by a high percentage of strains of Staphylococcus species that were niche-specific and/or host-specific, but was usually not required for growth by species showing a wide host range. Growth stimulation patterns with arginine intermediates indicated that most of the auxotrophic strains had blocks in an early step(s) in arginine biosynthesis. These strains were designated phenotypically as Arg(CHG) according to the Salmonella typhimurium classification scheme. Staphylococcus simulans strains appeared to be either ArgA or Arg I. The ArgI strains of S. simulans and S. capitis had moderate to high ornithine carbamoyltransferase (EC 2.1.3.3) activities and therefore could not be designated as argI mutants. ArgI strains in other species had no or very low ornithine carbamoyltransferase activities. All of the natural Staphylococcus auxotrophs tested grew in the presence of L-citrulline and had moderate to high argininosuccinase (EC 4.3.2.1) activities. Arginine auxotrophs of species with a wide host range were often capable of reverting to arginine-independent or complete prototrophic growth, whereas auxotrophs of species that tended to be niche-specific and/or host-specific were incapable of reversion to arginine-independence, even in the presence of various mutagens. A relationship between the nature of arginine auxotrophy and habitat is suggested.

Arginine↗

Renal tranplantation in type 1 glycogenosis. Failure to improve glucose metabolism.

In glycogenosis type 1 (GT1), glucose synthesis is deficient due to absence of glucose-6-phosphatase. Development of renal failure in such a patient provided the opportunity to test whether or not this metabolic defect could be reversed by a renal allograft, which contains the missing enzyme and has potential for glucose synthesis. Despite normalization of renal function and both glucocorticoid therapy and the infusion of amino-acid precursors of glucose, fasting hypoglycemia persisted unabated. We conclude that a funtioning renal allograft is incapable of meeting the metabolic demands of a patient with glucose-6-phosphatase deficiency.

Adult↗

Disturbances in acid-base balance during hypophosphatemia and phosphate depletion.

Phosphate depletion leads to bone resorption, resulting in the accession of alkali to the blood and urine. There may also be a release of lactic acid from liver, resulting from ATP depletion and intracellular alkalosis. In general, the net result of these tissue effects is an alkali load discharged into the extracellular fluid. In the kidneys, phosphate depletion causes impaired proximal tubular reabsorption of bicarbonate, and perhaps other substrates, owing in all likelihood to both intracellular alkalosis and depletion of ATP. This impaired proximal capacity to reclaim bicarbonate results in hyperchloremic acidosis. The distal nephron may contribute to acidosis by virtue of inability to produce titratable acid (phosphate-free urine) and perhaps impaired ammonia production. Severe phosphate depletion, therefore, tends to produce hyperchloremic acidosis as a result of a diminished capacity for bicarbonate reclamation in the proximal tubule and probably some impairment of bicarbonate regeneration in the distal nephron. These effects, when marked, ultimately outweigh the contribution of alkali coming from bone breakdown. In the liver, phosphate depletion may stimulate lactic acid production by reducing hepatic ATP stores (Pasteur effect) and producing intracellular alkalosis. ATP depletion may also limit hepatic uptake of lactate. Finally, in muscle cells ATP depletion, resulting from either profound hypophosphatemia or the metabolism of massive fructose loads, may eventuate in frank rhabdomyolysis.

Acid-Base Imbalance↗

The pathophysiology of acid-base changes in chronically phosphate-depleted rats: bone-kidney interactions.

Acid-base disturbances may develop secondary to the changes in renal tubular function and bone dynamics which attend phosphate depletion (PD). This work characterizes the acid-base status of rats fed a low phosphate diet. After 18 days, PD rats had marked calciuria (pair-fed controls: 0.3 +/- 0.2; PD 32.2 +/- 2.5 mueq/h; P less than 0.001), severe bicarbonaturia (controls: 0; PD 17.6 +/- 0.2 meq/h; P less than 0.001), and negative net acid excretion (controls: 44.5 +/- 2.9; PD: --6.6 +/- 2.5 meq/h; P less than 0.001), but plasma pH, HCO3, and PCO2 were equal in both groups. After 45 days, plasma HCO3 fell to 21.1 +/- 0.9 meq/liter in PD (controls: 23.6 +/- 0.5 meq/liter; P less than 0.05), while bicarbonaturia (controls: 0.4 +/- 0.2; PD: 3.8 +/- 1 mueq/h; P less than 0.02) and calciuria were present but diminished. These data suggested the coexistence of bone HCO3 mobilization and renal HCO3 wasting in PD. To test this thesis, bicarbonaturia was eliminated by nephrectomy. 24 h later plasma HCO3 was higher in PD rats (controls: 19.3 +/- 0.02; PD: 22.6 +/- 0.8 meq/liter; P less than 0.05), consistend with the presence of extrarenal HCO3 production. After inhibition of bone resorption with colchicine (1 mg/kg), plasma HCO3 decreased to 16.8 +/- 0.6 meq/liter in PD rats (controls): 26.4 +/- 1 meq/liter; P less than 0.001) while bicarbonaturia persisted. These data indicate that the plasma HCO3 in PD is the net result of renal HCO3 wasting and bone HCO3 mobilization. These combined effects maintain normal blood HCO3 initially (18 days) but with time (45 days), bone resorption diminishes and the acidifying renal tubular defect predominates.

Acid-Base Imbalance↗

Clinical use of the anion gap.

The concepts underlying the clinical use of the anion gap (AG) and those disorders associated with its alteration are reviewed. A substantial increase in the AG usually indicates the presence of a metabolic acidosis, unless large doses of certain antibiotics or sodium salts of organic acids are being used. The etiology, pathogenesis and diagnosis of high AG metabolic acidoses are discussed. Stress is placed upon the utility of the AG in defining the cause of the acidosis, and as a guide to therapy in certain organic acidoses. A decrease in the normal AG occurs in dilutional states, hypoalbuminemia, hypercalcemia, hypermagnesemia, hypernatremia, diseases associated with hyperviscosity, bromide intoxication, and in certain paraproteinemias. The important clue provided by a low or negative AG in the diagnosis of certain of these life-threatening disorders is emphasized.

Acid-Base Imbalance↗

Amino acid requirements of staphylococci isolated from human skin.

Amino acid requirements and auxotrophic reversion properties were determined for 823 Staphylococcus strains isolated from natural populations on human skin. Ten species of Staphylococcus exhibited distinct amino acid requirement patterns. Proline, arginine, and valine were the most frequently required amino acids for the genus Staphylococcus.

Amino Acids↗

Studies on the secretion of serum proteins from rat hepatoma cells.

We have used crossed immunoelectrophoresis to identify and establish the relative amounts of serum proteins secreted by a differentiated cell line (Fao) derived from a Reuber H35 rat hepatoma. Our results show that these cells secrete at least 15 plasma proteins. Ten of these: albumin, alpha 1-antitrypsin, alpha 1-lipoprotein, alpha 1-macroglobulin, alpha 1-antichymotrypsin, GC-globulin (transcalciferin), fibronectin, hemopexin, transferrin and the C3 component of complement have been identified. To examine the feasibility of using the Fao cell line as a model for studies on the regulation of hepatic protein secretion, we measured the relative amounts of 10 serum proteins secreted into the growth medium after exposure of these cells to dibutyryl cyclic AMP, hydrocortisone and a combination of both compounds. We also examined the effects of growth temperature (33.5 degrees, 37 degrees and 39 degrees C) and the removal of fetal calf serum from the growth medium on the relative amounts of these proteins secreted. We found that the rates of secretion of most of the serum proteins were altered by one or more of the treatments used in these experiments. In addition, detectable levels of secretion of three serum proteins, fibronectin and two unidentified, occurred only under certain of the experimental conditions. These results demonstrate that the pattern of proteins secreted from Fao cells can be experimentally altered and indicate that this cell line may be a useful model for studies on the control of hepatic protein secretion.

Animals↗

Non-dialytic treatment of acute hyperkalemia in the dialysis patient.

Acute hyperkalemia occurs commonly amongst patients with chronic renal failure and is especially common in noncompliant individuals. These patients often present to the emergency room with weakness. This editorial addresses the issue of non-dialytic treatment of hyperkalemia. Is emergency dialysis indicated in every case? In my opinion, acute dialysis can often be delayed until the hospital's dialysis unit opens for "regular working hours."

Acute Disease↗

Competencies and concerns in end-of-life care for medical students and residents.

A palliative medicine comfort-confidence survey developed by Weisman et al was utilized to assess self-reported competence and comfort with four end-of-life dimensions and determine future educational preferences. The survey was completed by 3rd and 4th year medical students (M3 and 4) and residents PGY 1-5. Self-reported competence increased with level of training. All trainees indicated the least comfort with 1) discussing home-hospice referrals; 2) conducting a family conference; 3) discussing the change from curative to comfort care; and 4) discontinuing i.v. hydration in a dying patient not taking oral nourishment. When withdrawing parenteral antibiotics from a non-decisional dementia patient with sepsis at the request of his legal guardian, M3 and 4 expressed a greater concern for violating medical practice standards while PGY4 and 5 showed a greater concern for the violation of personal religious or ethical beliefs. Pain management, pain assessment, hospice care and end-of-life communication where the most requested topics for future education.

Adult↗