Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Metabolic alkalosis is a primary pathophysiologic event characterized by the gain of bicarbonate or the loss of nonvolatile acid from extracellular fluid. The kidney preserves normal acid-base balance by two mechanisms: bicarbonate reclamation, mainly in the proximal tubule, and bicarbonate generation, predominantly in the distal nephron. Bicarbonate reclamation is mediated mainly by a Na(+)-H(+) antiporter and to a smaller extent by the H(+)-ATPase (adenosine triphosphate-ase). The principal factors affecting HCO3(-) reabsorption include effective arterial blood volume, glomerular filtration rate, chloride, and potassium. Bicarbonate regeneration is primarily affected by distal Na(+) delivery and reabsorption, aldosterone, arterial pH, and arterial partial pressure of carbon dioxide. To generate metabolic alkalosis, either a gain of base or a loss of acid must occur. The loss of acid may be via the gastrointestinal tract or via the kidney. Excess base may be gained by oral or parenteral HCO3(-) administration or by lactate, acetate, or citrate administration. Factors that help maintain metabolic alkalosis include decreased glomerular filtration rate, volume contraction, hypokalemia, hypochloremia, and aldosterone excess. Clinical states associated with metabolic alkalosis are vomiting, mineralocorticoid excess, the adrenogenital syndrome, licorice ingestion, diuretic administration, and Bartter's and Gitelman's syndromes. The effects of metabolic alkalosis on the body are variable and include effects on the central nervous system, myocardium, skeletal muscle, and liver. Treatment of this disorder is simple, once the pathophysiology of the cause is delineated. Therapy consists of reversing the contributory factors that are promoting the alkalosis and, in severe cases, administration of carbonic anhydrase inhibitors, acid infusion, and low bicarbonate dialysis.
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PMID:Metabolic alkalosis. 1126 55

The carbonic acid/bicarbonate system, as defined by the Henderson-Hasselbach (H-H) equation, has traditionally formed the centrepiece of the presentation of acid/base physiology in nursing education. However, an alternative approach to describe acid/base physiology was proposed by Peter Stewart in 1983. Stewart determined, using the physiochemical principles of dissociation equilibrium, electroneutrality and conservation of mass, that hydrogen ion concentration [H+] was dependent upon the difference between the concentrations of strong cations and strong anions in a solution (the strong ion difference or SID), concentration of weak acid anions, and the partial pressure of carbon dioxide in plasma. Therefore, a change in pH (the [H+] expressed as its negative log) indicates that there must be a change in one of these independent variables, and not simply explained by movement of hydrogen ions or bicarbonate into or out of the body fluids. An analysis of the complex acid/base derangements commonly seen in the critically ill can be achieved using this approach. The acid/base consequences of vomiting, gastric aspiration, diarrhoea, diuretic therapy, the infusion of large volumes of normal saline, the contribution of lactate, and the effects of methanol and ethylene glycol poisoning can all be more readily understood considering Stewart's explanation of acid/base balance. This paper outlines this alternative approach and provides some examples for the intensive care setting.
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PMID:Introduction to an alternate view of acid/base balance: the strong ion difference or Stewart approach. 1224 Jun 97

Perioperative pain is still a major problem, and new pharmacological means should be explored to mitigate such pain. Adenosine is an ubiquitous endogenous substance; when exogenously administered, it provides a number of salutary effects including neuromodulation, antinociception, and cytoprotective actions. The aim of this study was to characterize the perioperative antinociceptive-analgesic effects of intraoperative adenosine infusion and determine the duration of actions in the postoperative period, and compare them to those of remifentanil in patients undergoing major surgical procedures in a double-blind study.Sixty-two patients were randomly assigned to one of the two treatments. After standard induction of anesthesia, the lungs were mechanically ventilated. Anesthesia was maintained with a constant alveolar concentration of inhaled anesthetics (3% desflurane and 65% nitrous oxide in oxygen). A variable-rate of intravenous infusion of adenosine (50-500 microg kg(-1) x min(-1)) or remifentanil (0.05-0.5 microg kg(-1) x min(-1)) was initiated 5 min before the skin incision and was titrated to maintain systolic blood pressure and heart rate within 20% of baseline values during surgery. Postoperative evaluations included the level of sedation, degree of pain severity, opioid analgesic (fentanyl, morphine) consumption, and cardiorespiratory variables for 48 h. Intraoperative inhibition of the cardiovascular responses to surgical stimulation could be equally achieved by adenosine or remifentanil, and both could maintain excellent hemodynamic stability. Postoperatively, however, there were striking differences: (1). initial pain score was reduced by 60% (P<0.001) in the adenosine group compared to the remifentanil group and it remained lower throughout the 48 h recovery period; (2). postoperative morphine requirements during the first 0.25, 2 and 48 h were consistently lower in the adenosine group as compared to the remifentanil group (78, 71 and 42%, P<0.001, respectively); (3). adenosine patients remained significantly less sedated at all evaluations; (4) the end-tidal and arterial carbon dioxide values in the remifentanil group were significantly higher when patients were admitted to the postanesthesia care unit. No adverse effect of adenosine was observed at any time. Intraoperative adenosine infusion provided a salutary recovery from anesthesia associated with a pronounced and sustained postoperative pain relief. Compared to remifentanil, adenosine significantly reduced the opioid requirements and minimized the side effects including protracted sedation, cardiorespiratory instability, nausea, and vomiting in the postoperative recovery period.
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PMID:Characterization of the analgesic actions of adenosine: comparison of adenosine and remifentanil infusions in patients undergoing major surgical procedures. 1250 7

Carbon monoxide (CO) is a colorless, tasteless, odorless, and non-irritating gas formed when carbon in fuel is not burned completely. It enters the bloodstream through the lungs and attaches to hemoglobin (Hb), the body's oxygen carrier, forming carboxyhemoglobin (COHb) and thereby reducing oxygen (O(2)) delivery to the body's organs and tissues. High COHb concentrations are poisonous. Central nervous system (CNS) effects in individuals suffering acute CO poisoning cover a wide range, depending on severity of exposure: headache, dizziness, weakness, nausea, vomiting, disorientation, confusion, collapse, and coma. At lower concentrations, CNS effects include reduction in visual perception, manual dexterity, learning, driving performance, and attention level. Earlier work is frequently cited to justify the statement that CO exposure sufficient to produce COHb levels of ca. 5% would be sufficient to produce visual sensitivity reduction and various neurobehavioral performance deficits. In a recent literature re-evaluation, however, the best estimate was that [COHb] would have to rise to 15-20% before a 10% reduction in any behavioral or visual measurement could be observed. This conclusion was based on (1) critical review of the literature on behavioral and sensory effects, (2) review and interpretation of the physiological effects of COHb on the CNS, (3) extrapolation from the effects of hypoxic hypoxia to the effects of CO hypoxia, and (4) extrapolation from rat behavioral effects of CO to humans. Also covered in this review article are effects of chronic CO exposure, the discovery of neuroglobin, a summary of the relatively new role for endogenous CO in neurotransmission and vascular homeostasis, groups which might be especially sensitive to CO, and recommendations on further research. The interested reader is directed to other published reviews of the literature on CO and historically seminal references that form our understanding of this ubiquitous gas.
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PMID:Carbon monoxide and the nervous system. 1266 97

Laparoscopy using carbon dioxide insufflation induces adverse effects in both the cardiovascular and the respiratory function. The use of low pressure pneumoperitoneum has been shown to reduce adverse hemodynamic effects. However, its effect on tissue trauma and postoperative pain and recovery remains controversial. The aim of this study was to compare tissue trauma, postoperative pain, and recovery in two groups of patients undergoing laparoscopic cholecystectomy, one at insufflation pressure of 8 (LC8) and the other at 15 mm Hg (LC15). Forty patients were randomized, 20 in each group. The characteristics of the patients were similar in the two groups. The procedure was completed in all patients in the LC15 group, but in 2 patients in the LC8 group the pressure was increased to 15 mm Hg to complete the operation. There were no significant differences in postoperative pain scores, analgesic consumption, and the incidence of nausea, vomiting, and shoulder pain between the two groups. C-reactive protein concentrations and white blood cell count rose significantly after surgery, but the increase was similar in the two groups. The median duration of surgery was similar, 23 minutes (range 15-65) in the LC8 group and 25 minutes (range 15-80) in the LC15 group. Using our technique of laparoscopic cholecystectomy, there were no advantages to tissue damage, postoperative pain, and recovery when a low pressure pneumoperitoneum was used.
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PMID:Randomized comparison between different insufflation pressures for laparoscopic cholecystectomy. 1296 Jul 86

Bartter's syndrome is characterized by hypochloremia, hypokalemia, metabolic alkalosis associated with renal potassium leakage, and normal blood pressure despite increased plasma renin activity. Although association of empty sella with Gitelman syndrome has been reported, no association has been reported with Bartter's syndrome. Here we report a patient with Bartter's syndrome and empty sella. A 12 month-old male patient presented with a history of nausea, vomiting, abdominal distension, constipation, and edema in the lower extremities that had begun in the early postnatal period. The patient was born at 32 weeks gestation by operative delivery for polyhydramnios. Blood pressure was normal. Serum sodium, potassium, calcium, phosphate, chloride, albumin and alkaline phosphatase levels were 129 mEq/l, 2.5 mEq/l, 9 mg/dl, 3.8 mg/dl, 72 mg/dl, 4.2 g/dl and 1285 IU/l, respectively. Serum magnesium level was normal. Arterial blood gas levels revealed pH 7.55 (normal, 7.35-7.45), PCO2 33.6 mm/Hg (36-46), base excess +7.1 (+/- 2.3), and total CO2 33.6 mmol/l (23-27). Renin and aldosterone levels were elevated. Urine had pH 8.0 and specific gravity 1.010. Urinary calcium excretion was 22.8 kg/day (urine calcium/creatinine ratio 0.46). Urinary potassium and chloride levels were elevated. MRI of the brain was normal except for partially empty sella. We present the first pediatric patient with the association of Bartter's syndrome and empty sella.
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PMID:Association of Bartter's syndrome and empty sella. 1451 87

Since 1993, the New York State Department of Health, funded by the Agency for Toxic Substances and Disease Registry, has collected data about non-petroleum hazardous substances releases through the Hazardous Substances Emergency Events Surveillance (NYHSEES) project. This study investigates risk factors for hazardous substances releases that may result in public health consequences such as injury or reported health effects. The 6428 qualifying events that occurred during the 10-year-period of 1993-2002 involved 8838 hazardous substances, 842 evacuations, more than 75,419 people evacuated, and more than 3120 people decontaminated. These events occurred both at fixed facilities (79%) and during transport (21%). The causative factors most frequently contributing to reported events were equipment failure (39%) and human error (33%). Five of the 10 chemicals most frequently associated with injuries were also among the 10 chemicals most frequently involved in reported events: sulfuric acid, hydrochloric acid, ammonia, sodium hypochlorite, and carbon monoxide. The chemical categories most frequently associated with events, and with events with adverse health effects were volatile organic compounds (VOCs) and solvents, and acids. Events with releases of hazardous substances were associated with injuries to 3089 people including employees (37%), responders (12%), the general public (29%) and students (22%). The most frequently reported adverse health effects were respiratory irritation, headache, and nausea or vomiting. Most of the injured were transported to the hospital, treated, and released (55%) or treated at the scene (29%). These data have been used for emergency response training, planning, and prevention activities to reduce morbidity and mortality from future events.
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PMID:New York hazardous substances emergency events surveillance: learning from hazardous substances releases to improve safety. 1551 63

Mitochondrial beta-ketothiolase and 2-methyl-3-hydroxybutyryl-CoA dehydrogenase (MHBD) deficiencies are inherited neurometabolic disorders affecting isoleucine catabolism. Biochemically, beta-ketothiolase deficiency is characterized by intermittent ketoacidosis and urinary excretion of 2-methyl-acetoacetate (MAA), 2-methyl-3-hydroxybutyrate (MHB) and tiglylglycine (TG), whereas in MHBD deficiency only MHB and tiglylglycine accumulate. Lactic acid accumulation and excretion are also observed in these patients, being more pronounced in MHBD-deficient individuals, particularly during acute episodes of decompensation. Patients affected by MHBD deficiency usually manifest severe mental retardation and convulsions, whereas beta-ketothiolase-deficient patients present encephalopathic crises characterized by metabolic acidosis, vomiting and coma. Considering that the pathophysiological mechanisms responsible for the neurological alterations of these disorders are unknown and that lactic acidosis suggests an impairment of energy production, the objective of the present work was to investigate the in vitro effect of MAA and MHB, at concentrations varying from 0.01 to 1.0 mmol/L, on several parameters of energy metabolism in cerebral cortex from young rats. We observed that MAA markedly inhibited CO2 production from glucose, acetate and citrate at concentrations as low as 0.01 mmol/L. In addition, the activities of the respiratory chain complex II and succinate dehydrogenase were mildly inhibited by MAA. MHB, at 0.01 mmol/L and higher concentrations, strongly inhibited CO2 production from all tested substrates, as well as the respiratory chain complex IV activity. The other activities of the respiratory chain were not affected by these metabolites. The data indicate a marked blockage in the Krebs cycle and a mild inhibition of the respiratory chain caused by MAA and MHB. Furthermore, MHB inhibited total and mitochondrial creatine kinase activities, which was prevented by the use of the nitric-oxide synthase inhibitor L-NAME and glutathione (GSH). These data indicate that the effect of MHB on creatine kinase was probably mediated by oxidation or other modification of essential thiol groups of the enzyme by nitric oxide and other by-products derived from this organic acid. In contrast, MAA did not affect creatine kinase activity. Taken together, these observations indicate that aerobic energy metabolism is inhibited by MAA and to a greater extent by MHB, a fact that may be related to lactic acidaemia occurring in patients affected by MHBD and beta-ketothiolase deficiencies. If the in vitro effects detected in the present study also occur in vivo, it is tempting to speculate that they may contribute, at least in part, to the neurological dysfunction found in these disorders.
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PMID:Inhibition of energy metabolism by 2-methylacetoacetate and 2-methyl-3-hydroxybutyrate in cerebral cortex of developing rats. 1590 53

Carbon monoxide is an insidious poison that accounts for thousands of deaths each year in North America. Clinical effects maybe diverse and include headache, dizziness, nausea, vomiting,syn-cope, seizures, coma, dysrhythmias, and cardiac ischemia. Children, pregnant women, and patients who have underlying cardiovascular disease are particularly at risk for adverse out-comes. Treatment consists of oxygen therapy, supportive care, and, in selected cases, hyperbaric oxygen therapy.
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PMID:Toxicity associated with carbon monoxide. 1656 27

Pain after craniotomy remains a significant problem. The effect of morphine and tramadol patient-controlled analgesia (PCA) on arterial carbon dioxide tension is unknown in patients having such surgery. Sixty craniotomy patients were randomly allocated to receive morphine PCA, tramadol PCA or codeine phosphate 60 mg intramuscularly. Baseline values of pain score (0-10), sedation and arterial carbon dioxide tension were recorded at the time of first analgesic administration and at 30 min, 1, 4, 8, 12, 18 and 24 h. Patient satisfaction was assessed at 24 h. There were no differences in arterial carbon dioxide tension or sedation between groups at any time, but in all three groups some patients had rises greater than 1 kPa. Morphine produced significantly better analgesia than tramadol at all time points (p < 0.005) and better analgesia than codeine at 4, 12 and 18 h. Patients were more satisfied with morphine than with codeine or tramadol (p < 0.001). Vomiting and retching occurred in 50% of patients with tramadol, compared with 20% with morphine and 29% with codeine.
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PMID:Comparison of the analgesic efficacy and respiratory effects of morphine, tramadol and codeine after craniotomy. 1799 Dec 73


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