Hepatic intoxication with

Acute intoxication with DHBs occurs mainly by the oral route symptoms are close to those induced by phenol poisoning including nausea, vomiting, diarrhea, tachypnea, pulmonary edema, and CNS excitation with possibiUty of seizures followed by CNS depression. Convulsions are more frequent with catechol as well as hypotension due to peripheral vasoconstriction. Hypotension and hepatitis seem more frequent with hydroquinone and resorcinol. Methemoglobinemia and hepatic injury may be noted within a few days after intoxication by DHBs. 

Reversibility of Noncarcinogenic Systemic Effects. Most case reports of humans intoxicated with carbon tetrachloride indicate that, if death can be averted, clinical signs of renal and hepatic dysfunction diminish within 1-2 weeks, and recovery often appears to be complete. This is primarily because both liver and kidney have excellent regenerative capacity and can repair injured cells or replace dead cells (Dragiani et al. 1986 Norwood et al. 1950). However, high doses or repeated exposure can lead to fibrosis or cirrhosis that may not be reversible. The depressant effects of carbon tetrachloride on the central nervous system do appear to be reversible, although any neural cell death that occurs (Cohen 1957) is presumably permanent. 

For many drugs, at least part of the toxic effect may be different from the therapeutic action. For example, intoxication with drugs that have atropine-like effects (eg, tricyclic antidepressants) reduces sweating, making it more difficult to dissipate heat. In tricyclic antidepressant intoxication, there may also be increased muscular activity or seizures the body s production of heat is thus enhanced, and lethal hyperpyrexia may result. Overdoses of drugs that depress the cardiovascular system, eg, 13 blockers or calcium channel blockers, can profoundly alter not only cardiac function but all functions that are dependent on blood flow. These include renal and hepatic elimination of the toxin and any other drugs that may be given. 

Pascale LR, Waldstein SS, Engbring G, et al. 1952. Chromium intoxication with special reference to hepatic injury. J Am Med Assoc 149 1385-1389. 

Veno-occlusive disease (VOD) describes the occlusion of small hepatic veins and is defined as a radicular form of the Budd-Chiari syndrome. A variety of endotheliotoxic noxae, particularly phytotoxins, are responsible for this clinical picture. In 1951 reports were simultaneously published for the first time both in South Africa (G. Selzer et al.) and Jamaica (K. R. Hill) dealing with this disease of the small venous branches, which results from chronic intoxication with pyrrolizidine alkaloids, (s. pp 548, 571) Similar morphological and clinical effects can also be caused by cytostatic agents (6-mercaptopurine, dacarbazine, thioguanine), azathioprine, contraceptives and exposure to X-rays. Since 1957, the term Stuart-Bras syndrome has also been used to describe the occlusion of the small hepatic veins, (s. p. 832)... 

Treatment for salicylate intoxication is directed toward (1) decreasing further absorption, (2) increasing elimination, and (3) correcting add-base and electrolyte disturbances. Activated charcoal binds aspirin and prevents its absorption. Elimination of salicylate may be enhanced by alkaline diuresis and in severe cases by hemodialysis." Sodium bicarbonate may be given to alleviate metabolic acidosis. Indications for hemodialysis include serum salicylate >1000 mg/L, severe CNS depression, intractable metabolic acidosis, hepatic failure with coagulopathy, and renal failure. ... 

Moody DE, James JL, Clawson GA, et al. 1981. Correlations among the changes in hepatic microsomal components after intoxication with alkyl halides and other hepatotoxins. Mol Pharmacol 20 685- 693. 

It must be emphasized that the combination of extra-pyramidal and cerebellar dysfunction is quite characteristic for hepatic encephalopathy, and cannot be found in any other kind of metabolic encephalopathy, except Wilson s disease. Asterixis, however, which is considered a classic sign of HE, is also seen in other metabohe or toxic encephalopathies, such as urania, CO retention, hypomagnesemia or intoxication with antiepileptic drugs, for example. 

Tramadol ER should not be administered to patients who have previously demonstrated hypersensitivity to tramadol, any other component of this product or opioids. Tramadol ER is contraindicated in any situation where opioids are contraindicated, including acute intoxication with any of the following alcohol, hypnotics, narcotics, centrally acting analgesics, opioids, or psychotropic drugs. Tramadol ER should not be used in patients with creatinine clearance less than 30 mL/min, or severe hepatic impairment (diild-Pugh Class C). 

The antibody response to streptococcic vaccine [134, 137], Salmonella typhi vaccine [140, 145], and Brucella melitensis [146] is deficient in rabbits intoxicated with Pb(C2H5)4. The impairment of immunity is evident even with small Pb(C2H5)4 doses [140]. Hepatic damage [139], body temperature [132], thermic response to bacterial suspensions [133], enzymic activity [152], and metabolism [244] have been studied in rabbits poisoned with... 

Intoxication by aflatoxkis is referred to as aflatoxicosis. Edema and necrosis of hepatic and renal tissues seem characteristic of aflatoxicosis, and hemorrhagic enteritis accompanied by nervous symptoms often appear ki experimental animals. The mode of action of aflatoxkis kivolve an kiteraction with DNA and inhibition of the polymerases responsible for DNA and RNA synthesis (96). 

In the ED setting, the diagnosis of ketamine intoxication is a clinical one. Ketamine is not routinely detected by urine toxicology tests, although it can be detected with high-performance liquid chromatography (Koesters et al. 2002). As with MDMA, the initial assessment for ketamine intoxication includes the use of routine laboratory tests to detect electrolyte abnormalities and to evaluate renal and hepatic functioning (Koesters et al. 2002). 

The ammonia produced by enteric bacteria and absorbed into portal venous blood and the ammonia produced by tissues are rapidly removed from circulation by the liver and converted to urea. Only traces (10—20 Ig/dL) thus normally are present in peripheral blood. This is essential, since ammonia is toxic to the central nervous system. Should portal blood bypass the liver, systemic blood ammonia levels may rise to toxic levels. This occurs in severely impaired hepatic function or the development of collateral links between the portal and systemic veins in cirrhosis. Symptoms of ammonia intoxication include tremor, slurred speech, blurred vision, coma, and ultimately death. Ammonia may be toxic to the brain in part because it reacts with a-ketoglutarate to form glutamate. The resulting depleted levels of a-ketoglutarate then impair function of the tricarboxylic acid (TCA) cycle in neurons. 

Methods of detection, metabolism, and pathophysiology of the brevetoxins, PbTx-2 and PbTx-3, are summarized. Infrared spectroscopy and innovative chromatographic techniques were examined as methods for detection and structural analysis. Toxicokinetic and metabolic studies for in vivo and in vitro systems demonstrated hepatic metabolism and biliary excretion. An in vivo model of brevetoxin intoxication was developed in conscious tethered rats. Intravenous administration of toxin resulted in a precipitous decrease in body temperature and respiratory rate, as well as signs suggesting central nervous system involvement. A polyclonal antiserum against the brevetoxin polyether backbone was prepared a radioimmunoassay was developed with a sub-nanogram detection limit. This antiserum, when administered prophylactically, protected rats against the toxic effects of brevetoxin. 

Hepatic metabolism of ethanol involves a nonlinear saturable pathway. Young children have a limited ability to metabolize and thereby detoxify ethanol. Ethanol intoxication has been recorded in children with blood levels as low as 25 mg/dL. Alcohol has a volume of distribution of approximately 0.65 L/kg. Ingestion of 20 mL of a 10% alcohol solution will produce a blood level of 25 mg/dL in a 30 pound child. The American Academy of Pediatrics (AAP) Committee on Drugs recommends that pharmaceutical formulations intended for use in children should not produce ethanol blood levels of >25 mg/dL after a single dose. 

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