Hepatic necrosis is caused by:
Ans. D. All of the above. (Ref. H-17th/pg. 1949; Table 299-1)Harrison's medicine 17th/pg. 1949 ........."Liver injury may follow the inhalation, ingestion, or parenteral administration of a number of pharmacologic and chemical agents. These include industrial toxins (e.g., carbon tetrachloride, trichloroethylene, and yellow phosphorus), the heat-stable toxic bicyclic octapeptides of certain species of Amanita and Galerina (hepatotoxic mushroom poisoning), and, more commonly, pharmacologic agents used in medical therapy."TOXIC AND DRUG-INDUCED HEPATIC INJURY Direct Toxic Effect Idiosyncratic Other Features(Carbon Tetrachloride)(Acetamino phen)(Halothane)(Isoniazid)(Chlorpro mazine)(Oral Contraceptive Agents)1Predictable and dose-related toxicity++000+2Latent periodShortShortVariableVariableVariableVariable3Arthralgia, fever, rash, eosinophilia00+0+04Liver morphologyNecrosis, fatty infiltrationCentrilobular necrosisSimilar to viral hepatitisSimilar to viral hepatitisCholestasis with portal inflammationCholestasis without portal inflammation, vascular lesionsAgents producing toxic hepatitis are generally systemic poisons or are converted in the liver to toxic metabolites. The direct hepatotoxins result in morphologic abnormalities that are reasonably characteristic and reproducible for each toxin. For example, AgentCharacteristic type of hepatic injury1Carbon tetrachloride and trichloroethyleneCentrilobular zonal necrosis,2Yellow phosphorus poisoningPeriportal injury.3Hepatotoxic octapeptides of Amanita phalloidesMassive hepatic necrosis; the lethal dose of the toxin is ~10 mg, the amount found in a single deathcap mushroom.4Tetracycline, when administered in IV doses >1.5 g dailyMicrovesicular fat deposits in the liver.
Carbon tetrachloride
Phosphorous
Amanita phalloides
All of the above
Adverse Drug Effect