Document MoaZrp1xV5zmp020w01rGxgYk

y , , ( .y, / . * ^* Gleason, Marlon N., et al. Clinical Toxicology of Commercial Products 3rd ed., 1969 32 SECTION III. THERAPEUTICS INDEX - ; ? .--2 Richter, C. P. The physiology and cytology of pulmonary edema and pleural effusions pro duced in rats by alpha-naphthvlthiourea (ANTU). J. Thoracic Surg. 23: 66-91 (1952). Saunders, J. P. and R. C. Sraulding. Effects of aoma substituted thioureas on alpha-naphthyl- thiourea (ANTU), Proe. Soc. Eipti. Biol Med. 76: 84-85(1951). Wanntorr, H. a-Napthvlthiourea (ANTU) as a cause of poisoning in dogs and its chemical identification in meterial of animal origin. Acta Pharmacol. Toxicol. 9; 313-321 (1933). ARSENIC Arsenic is a common ingredient of rodenticides, insectiddis, herbicides, paints, and other products. Many organic arsenic compounds are employed as therapeutic agents in clinical and veterinary medi cine. Toxicology: Arsenic was formerly used exten sively as s "criminal poison" because it is odorless and nearly tasteless. Accidental poisoning is still common because arsenic compounds ere widely used and readily available. The mortality in acute poisoning is high (SO to 73 per cent); death usually occurs within 46 hours. The lethal dcaa varies with the compound, but 0.2 to 0.3 gm. of the trioxide ("white arsenic") is usually fatal in an adult (Sollmann, 1957). Finely subdivided arsenic trioxide is significantly more toxic than coarsely powdered material, since appreciable amounts of the latter may be elminattd in feces without dissolving (Schwartzs, 1923). Both, however, may show up as radio-opaque material in the gastrointestinal tract (Hfifer and Mandat. 1962). In moat cases tht presenting symptoms are those of a severe gastritis or gastroenteritis. Because the lesions are due not to loal corrosion but to vascular damage from absorbed arsenic (Hanna and McHugo, i960; SoDmann, 1957), the first symptoms may be delayed several minutes or even a few hours. Event ually, a violent hemorrhagic gastroenteritis leads to profound loasas of fluid and electrolytes, re sulting in coilapee, shock, end death. Occasionally the alimentary symptoms era mild or absent, in which case the presenting complaints are usually referable to the central nervous system: headache, vertigo, muscle spasm, stupor, delirium, and some times mania (Webster, 1990). - Subacute end chronic exposures may reveal themselves in these and many other ways.. Among the protean manifestations of chronic poisoning art anorexia, mild gastrointestinal disturbances, low grade fever, pallor, weekneos, and a catarrhal in flammation of nose, throat, conjunctivas, and larynx--simulating an infectious coryza. Stomatitis and salivation are common (Cannon, 1936; Greenberg, 1949; Sollmann. 1937). Skin afflictions are many and varied: erythema, eczema, pigmentation (arsenic melanosis), keratosis (especially of palms and sotas), scaling and desquamation, brittle nails, loss of hair and nails, and localised subcutaneous edema (espooally of the eyelids) (Ayres and Ander son, 1934; Carieton et a/., 1948; Holmquist, 1931). Signs of renal damage develop. Hepatomegaly with jaundice (and aometimes pruritus) may evolve into cirrhosis with ascites (Franklin et of., 1950; Wade and Frazer, 1953). Severe blood dyscrasias result from depression of any and all cellular elements in bone marrow (Eagle and Magnuson, 1946; Kyle and Pease, 1969. Throe effects may be related to inhibition of folic acid metabolism (Van Tongeren et of., 1965). In advanced poisoning, nervous symp toms are prominent; encephalopathies have been described (Eagle and Magnuson, 1946; Prickman ahd Millikan, 1933), but peripheral neuritis is morecommon (Heyman et of., 1946). Sensation is in volved first (psrasthroia. hypesthrois, pain), but eventually paralysis and muscular atrophy appear, usually in the legs. In all cases it is presumsbly the ion of arsenious acid, rather than the element itself, which is the toxic principle. Tht in ctco conversion to arsenite explains why all chemical forms of arsenic eventu ally produce the same toxic syndrome. One exeepK tion is gaseous AsH- or arsine, which is a potent hemolvtic atent, unlike other arsenic derivatives (Rentier et aL, 1946; McKinstiy and Hickes, 1957; Pinto el of., 1930; Neuwirtova et at., 1961). Survi vors of arsine exposure usually experience acute renal failure secondary to hemolysis and shock (Elkina and Fafay, 1967; Neuwirtova et al., 1961). Aa arsenite the element it an active enzyme inhibitor, presumably because of its attachment to sulfhydrylgroups of essential proteins (Stocken and Thomp son. 1949; Voegtlin et al., 1923, 1925). Trivalent or ganic anenicab such ss phtnylaisenoxide are more potent inhibitors of certain sulfhydryl enzymes than are inorganic anenites (Barron et of., 1947; Peters ttaL, 1946). . Absorbed arsenic it excreted largely by the kid neys, but ftew, skin and hair sometimes contain ap preciable emounts (Webstar, 1941). After a single dose, excretion is essentially complete within 2 weeks. About 43 per cent of arsenic inhaled in cigarette smoke is excreted in the urine and about 2.5 par cent in the feero (Holland et at., 1959). Uri nary excretion is markedly enhanced, without dam age to the excretory organs, by the administration of -BAL (dimeteaprol). If prompt, this treatment ucc 002706