<prompt> Hepatic necrosis is caused by:Carbon tetrachloridePhosphorousAmanita phalloidesAll of the above  <response>: Ans. D. All of the above. Ref. H-17thpg. 1949; Table 299-1Harrisons medicine 17thpg. 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 FeaturesCarbon TetrachlorideAcetamino phenHalothaneIsoniazidChlorpro mazineOral Contraceptive Agents1Predictable and dose-related toxicity0002Latent periodShortShortVariableVariableVariableVariable3Arthralgia, fever, rash, eosinophilia00004Liver 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. 