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Possible thermalbreakdown products include oxides of nitrogen and hydrogen cyanide symptoms quit drinking purchase cheap phenytoin on line. Toxicity similar to xanax medications for anxiety 100mg phenytoin visa that of phosgene (see p 305) 5 medications for hypertension phenytoin 100mg generic, of which it is the nonchlorinated analog, in both magnitude and time course. Symptoms and signs include abdominal pain, anemia, mood or personality changes, and peripheral neuropathy. Symptoms include abdominal pain, headache, vomiting, diarrhea, nausea, itching, and lethargy. Lead chromate is a suspect human carcinogen owing to the carcinogenicity of hexavalent chromium and inorganic lead compounds. Vapors irritating to the eyes and mucous membranes and produce severe headaches and nausea. Major industrial sources include smelting, battery manufacture, radiator repair, and glass and ceramic processing. Still available (1% lotion or shampoo) as a scabicide, although safer alternatives exist. Dusts extremely irritating to eyes and respiratory tract; pulmonary edema may develop. Symptoms of systemic toxicity include nausea, tremors, confusion, blurring of vision, and coma. Very water-reactive, yielding highly flammable hydrogen gas and caustic lithium hydroxide. Exposure occurs in mining and milling of the metal, in ferromanganese steel production, and through electric arc welding. Mercury salts but not metallic mercury are primarily toxic to the kidneys by acute ingestion. Some inorganic mercury compounds have adverse effects on fetal development in test animals. Mercury, alkyl compounds (dimethylmercury, diethyl mercury, ethylmercuric chloride, phenylmercuric acetate): Well absorbed by all routes. Sources of exposure include small-scale gold refining operations by hobbyists and mercurycontaining instruments. Limited evidence for adverse effects on male reproduction and fetal development in test animals at high doses. Based on animal studies, may cause kidney damage, leukopenia, testicular atrophy, and birth defects. Hydrolyzed to methanol in the body with possible consequent toxicity similar to that of methanol (see p 260). Animal studies suggest a potential to injure heart, liver, kidneys, and lungs at very high air levels. In animal tests, acute inhalation at high levels caused death without signs of irritation, probably by a mechanism similar to that of acrylonitrile. Signs and symptoms include headache, nausea, abdominal pain, dizziness, shortness of breath, metabolic acidosis, and coma. Vapors highly irritating to eyes, skin, and respiratory tract; severe burns and pulmonary edema may result. Methyl bromide is a widely used fumigant in agriculture and in structural pesticide control. Causes peripheral neuorpathy by a mechanism thought to be the same as that of n-hexane. Evidence for adverse effects on both the testes and fetal development in test animals at high doses. A strong and fast-acting glue that can fasten body parts to each other or surfaces. Direct contact with the eye may result in mechanical injury if the immediate bonding of the eyelids is followed by forced separation. Based on animal studies, some liver and kidney injury may occur at chronic high doses. Based on analogy to other isocyanates, vapors are likely to be potent respiratory tract irritants and sensitizers. Possible thermal-breakdown products include oxides of nitrogen and hydrogen cyanide.
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See also antineoplastic agents treatment lead poisoning order phenytoin 100mg on line, 100107 acetylcysteine for poisoning caused by medications versed order phenytoin 100mg, 405407 extravasation of medicine river cheap phenytoin 100mg line, 106 toxicity of, 101t, 106 Doxycyline, for biological warfare agents, 372 Doxylamine. See caustic and corrosive agents, 157159 sodium hydroxide, 613t Drano Liquid Drain Opener. See caustic and corrosive agents, 157159 hypochlorite, 162164 sodium hydroxide, 613t Drixoral. See antihistamines (dexbrompheniramine), 9698 decongestants, (d-isoephedrine sulfate), 320322 Dronabinol, 252. See also marijuana, 252254 pharmacokinetics of, 253, 387t toxicity of, 252, 253 660 Droperidol, 451453. See guaifenesin, 387t hydrocodone, 289t pseudoephedrine, 320322 Dursban (chlorpyrifos). See also organophosphates and carbamates, 291295 hazard summary for, 551t toxicity of, 292t "Dust" (slang). See phencyclidine, 300302 Dusts, particulate/respirable bronchospasm caused by, 9t occupational exposure to, 519 Dusty miller, 313t. See also organophosphates and carbamates, 291295 hazard summary for, 575t toxicity of, 292t Dymelor. See triamterene, 188t Dyskinesia, 2526, 26t drugs and toxins causing, 26t Dysrhythmias, 9. See also low-toxicity products, 286 accidental exposure to, 288t "Easy Lay" (slang). See gamma-butyrolactone, 210213, 211t E coli, food poisoning/systemic infection caused by, 203, 204t. See also food poisoning, bacterial, 203205 E coli 0157:H7, food poisoning/systemic infection caused by, 203, 204t, 205. See ethacrynic acid, 188t Edema, pulmonary, 8 hypoxia in, 7t, 8 treatment of, 8 morphine for, 468469 "Edema factor," in anthrax toxicity, 368 Edifenphos. See also antiviral and antiretroviral agents, 111115 pharmacokinetics of, 387t toxicity of, 113t, 114 Effexor. See also glycols, 194198 hazard summary for, 569t toxicity of, 196t Eggplant, 313t. See also plants, 309319 Elimination of drugs and toxins in emergency evaluation/treatment, 3f, 5457, 58t in neonates, 62 Elixophyllin. See anesthetics, local, 7477 lidocaine, 74, 75t, 76, 462463 prilocaine, 75, 75t, 76 Empirin. See also chlorinated hydrocarbons, 161162 hazard summary for, 567t toxicity of, 161, 161t Endotracheal intubation, 46, 5f nasotracheal route for, 5, 5f orotracheal route for, 56, 5f neuromuscular blockers for, 56, 472475 for ventilatory failure, 7 Endrin. See also chlorinated hydrocarbons, 161162 hazard summary for, 568t toxicity of, 161, 161t English ivy, 313t. See also gases, irritant, 213215 exposure limits for, 214t, 596t 661 hazard summary for, 596t toxicity of, 214t Enhanced elimination of drugs and toxins, in emergency evaluation/treatment, 3f, 5457, 58t Enliven. See also nonsteroidal anti-inflammatory drugs, 283286 coma and stupor caused by derivatives of, 19t toxicity of, 284t Enoxaparin, protamine for overdose of, 497498 Entactogens (hallucinogens), toxicity of, 247249, 248t Enteric-coated preparations, abdominal x-ray showing, 46t Enteroinvasive Escherichia coli, food poisoning caused by, 204t. See also food poisoning, bacterial, 203205 Enterotohemorrhagic Escherichia coli (E. See also food poisoning, bacterial, 203205 Enterotoxigenic Escherichia coli, food poisoning caused by, 204t. See also food poisoning, bacterial, 203205 Enterotoxin B, staphylococcal, as biological weapon, 370t. See also warfare agents, biological, 367372 Enteroviruses, food-borne gastroenteritis caused by, 203 Envenomation insect, 225226 anaphylactic reaction caused by, 28t, 226 jellyfish (cnidarian), 236237 lionfish (scorpaenidae), 242243 morphine for pain associated with, 468469 scorpion, 334335 snake, 343346, 343t antivenoms for, 345, 407409, 408t, 410411 hypotension caused by, 16t ventilatory failure caused by, 6t spider, 346348 rigidity caused by, 26t, 347 Environmental tobacco smoke, hazard summary for, 568t Environmental toxicology, 510531 emergency medical response to hazardous materials incidents and, 510518 exposure guidelines and, 528530, 532628t health hazard information and, 526528, 532628t patient evaluation in chemical exposure and, 518526 Enzyme-containing detergents. See also organophosphates and carbamates, 291295 toxicity of, 292t Ephedra/Ephedra spp, 217t, 218, 320. See also ephedrine, 320322; herbal and alternative products, 215218 Ephedra viridis, 315t. See also plants, 309319 Ephedrine, 320322, 321t hypertension caused by, 18t, 321 monoamine oxidase inhibitor interaction and, 270t, 320321 pharmacokinetics of, 320, 387t phentolamine for overdose of, 322, 487488 tachycardia caused by, 13t toxicity of, 217t, 218, 320322 Epichlorohydrin, hazard summary for, 568t Epifoam. See pramoxine, 75t Epinephrine, 442443 for allergic/anaphylactic/anaphylactoid reactions, 28, 442443 for beta-adrenergic blocker overdose, 133, 442443 for calcium antagonist overdose, 146, 442443 for chloroquine overdose, 167 hyperglycemia caused by, 35t, 442 hypertension caused by, 18t, 442 hypokalemia caused by, 38t, 442 with lidocaine.
These kinases appear to treatment xyy discount phenytoin 100 mg amex play an important role in the regulation of Cl- transport in numerous different tissues medicine 95a pill safe 100mg phenytoin. The acidosis in all of these sodium transport disorders is secondary to medicine 360 order 100mg phenytoin decreased H+ secretion caused by an unfavorable electrical gradient in the distal tubule as well as decreased ammoniagenesis caused by the hyperkalemia. Frank metabolic acidosis may become evident when patients are stressed by diarrhea or other conditions that require compensation by augmented renal proton secretion. Although involving the kidney, this cannot be viewed as being caused by an intrinsic kidney defect. Toluene is rapidly absorbed through the skin and mucous membranes and is metabolized to hippuric acid. Both of these disorders are usually easily discovered after an adequate history has been obtained. Bonny O, Rossier B: Disturbances of Na/K balance: pseudohypoaldosteronism revisited, J Am Soc Nephrol 13:2399-2414, 2002. Brent J, McMartin K, Phillips S, et al: Fomepizole for the treatment of methanol poisoning, N Engl J Med 344:424-429, 2001. Figge J, Jabor A, Kazda A: Anion gap and hypoalbuminemia, Crit Care Med 26:1807-1810, 1998. Igarashi T, Sekine T, Inatomi J, et al: Unraveling the molecular pathogenesis of isolated proximal renal tubular acidosis, J Am Soc Nephrol 13:2171-2177, 2002. Kirschbaum B, Sica D, Anderson F: Urine electrolytes and the urine anion and osmolar gaps, J Lab Clin Med 133:597-604, 1999. Levraut J, Grimaud D: Treatment of metabolic acidosis, Curr Opin Crit Care 9:260-265, 2003. In addition, total parenteral nutrition using hydrochloric acid salts of various amino acids can produce a metabolic acidosis if an insufficient quantity of base (usually acetate) is added to the infusion mixture. In assessing a patient with metabolic alkalosis, two questions should be considered: (1) What is the source of alkali gain (or acid loss) that generated the alkalosis? Determination of urine electrolytes (especially [Cl-]) and screening of the urine for diuretics may be helpful. If the urine is alkaline, with an elevated [Na+] and [K+] but a urine [Cl-] lower than 10 mEq/L, the diagnosis is usually either vomiting (overt or surreptitious) or alkali ingestion. If the urine is relatively acid and has low concentrations of Na+, K+, and Cl-, the most likely possibilities are previous vomiting, the posthypercapnic state, or previous diuretic ingestion. If, on the other hand, neither the urine [Na+], [K+], nor [Cl-] is depressed, magnesium deficiency, Bartter or Gitelman syndromes, or active diuretic use should be considered. Gitelman syndrome is distinguished from Bartter syndrome by the presence of hypocalciuria and, on occasion, hypomagnesemia in Gitelman syndrome. For example, the presence of chronic hypertension and chronic hypokalemia in an alkalotic patient suggests either mineralocorticoid excess or a hypertensive patient receiving diuretics. Low plasma renin activity and urine [Na+] and [Cl-] values greater than 20 mEq/L in a patient not taking diuretics are consistent with a primary mineralocorticoid excess syndrome. The combination of hypokalemia and alkalosis in a normotensive, nonedematous patient can pose a difficult problem. Other examples of acute metabolic alkalosis resulting from alkali ingestion include the association of a pica for baking soda in pregnancy. Patients with this disorder are prone to developing nephrocalcinosis, kidney function impairment, and metabolic alkalosis. Discontinuation of alkali ingestion is usually sufficient to correct the alkalosis, but the kidney disease may be irreversible if nephrocalcinosis is advanced. Hypokalemia also increases ammonium production independently of acid-base status, which, in the face of enhanced H+ secretion, results in increased ammonium production and excretion; this in turn adds new bicarbonate to the systemic circulation (increase in net acid excretion). Therefore, hypokalemia plays an important role in the seemingly maladaptive response of the kidney to maintain the alkalosis. This can be recognized clinically by a low urinary chloride concentration (see Table 14. The parallel Na+/H+ ion exchanger remains functional, allowing Na+ to be reabsorbed and H+ to be secreted. Recently, the use of proton pump inhibitors has been advanced as a means of reducing chloride secretion by the parietal cells and thus reducing the diarrhea. K+ depletion probably induces the alkalosis, because colonic secretion is alkaline.