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Neuropathy arsenic poisoning

After initial contradictory reports it is now established that arsenic can cross the blood-brain barrier and produces alternations in whole rat brain biogenic amines levels in animals chronically exposed to arsenite (Tripathi et al, 1997). The neurological effects are many and varied. Usually, peripheral neuropathy, sensory neuropathy (Hafeman et al, 2005), and encephalopathy are the initial complaints associated with acute arsenic poisoning. Acute exposure to arsenic in humans has been shown to result in problems of memory, difficulties in concentration, mental confusion, and anxiety (Hall, 2002 Rodriguez et al, 2003). Other neurological symptoms arising due to arsenic are primarily those of a peripheral sensory neuritis, predominantly numbness, severe paresthesia of the distal portion of the extremities, diminished sense of touch, pain, heat and cold, and symmetrically reduced muscle power (Menkes, 1997). [Pg.122]

Answer E. The profile of lead toxicity includes decreased heme synthesis, anemia, nephropathy, and peripheral neuropathy, the last leading to foot drop or wrist drop. Garlic breath and watery stools are associated with arsenic poisoning. Chronic gingivitis and loose teeth are features of mercury poisoning. [Pg.308]

Subacute arsenic poisoning may affect a variety of organ systems, mimicking other disease states. Facial edema is characteristic, occurring in 85% of people exposed for two to three weeks to 3 mg per day of calcium arsenate in soy sauce (Mizuta et al.l956, as reported in NAS 1977). Peripheral neuropathy, with paresthesia and numbness of extremities, decreased touch, pinprick and temperature sensation, and muscle weakness and pain, may develop and persist for years, regardless of the form of arsenic (Tilson 1987). [Pg.1347]

IV. Diagnosis is usually based on a history of exposure combined with a typical pattern of multisystemic signs and symptoms. Suspect acute arsenic poisoning in a patient with abrupt onset of abdominal pain, nausea, vomiting, watery diarrhea, and hypotension, partiouiariy when followed by an evolving pattern of delayed cardiao dysfunction, panoytopenia, and peripheral neuropathy. Metabolic acidosis and eievated CPK may occur eariy in the course of severe cases. Some arsenic compounds, partiouiariy those of iower solubility, are radiopaque and may be visible on a plain abdominal x-ray. [Pg.117]

Chnical features like skin lesions and neuropathy are crude and imprecise indicators of the severity of poisoning. The early clinical symptoms of arsenic toxicity are headache, dizziness, insomnia, weakness, nightmare, numbness in the extremities, anemia, palpitations, and fatigue. White striae in the fingernails are also a useful clue in the diagnosis of... [Pg.123]

Arsenic (wood j preservatives, j pesticides, ant i poisons) Acute GI distress, garlic breath, rice water stools, torsades, seizures Chronic pallor, skin pigmentation, alopecia, stocking-glove neuropathy, myelosuppression Activated charcoal, dimercaprol Penicillamine or succimer... [Pg.298]

C. Neuropathy. A variety of dmgs and poisons can cause sensory or motor neuropathy, usually after chronic repeated exposure (Table 1-20). Some agents (eg, arsenic and thallium) can cause neuropathy after a single large exposure. [Pg.30]

The therapeutic endpoints of chelation are poorly defined. For chelation instituted to treat symptomatic acute intoxication, one empiric approach would be to continue treatment (initially parenterally, then orally) until total urinary arsenic levels are less than 500 mcg/24 hours (or spot urine < 300 mcg/L), levels below those associated with overt symptoms in acutely poisoned adults. Alternatively, oral chelation could be continued until total urinary arsenic levels reach background levels (< 50 mcg/24 hours, or spot urine < 30 mcg/L). The value of chelation for treatment of an established neuropathy (or prevention of an incipient neuropathy) has not been proved. [Pg.118]

Arsenic (CAS 7440-38-2) irritating to eyes and skin hyperplgmenta-tion, hyperkeratoses, and skin cancers have been dexribed. A general cellular poison. May cause bone marrow suppression, peripheral neuropathy, and gastrointestinal, liver, and cardiac injury. Some arsenic compounds have adverse effects on fetal development in test animals. Exposure linked to skin, respiratory tract, and liver cancer in workers (IARC 1). See also p 115. 0.01 mg/m (as As) A1 OSHACA NIOSH CA 5 mg/m (as As) Elemental forms vary In appearance. Crystals are gray. Amorphous fomes may be yellow or black. Vapor pressure is very low—about 1 mm Hg at 372°C (701°F). [Pg.539]


See other pages where Neuropathy arsenic poisoning is mentioned: [Pg.58]    [Pg.1233]    [Pg.1233]    [Pg.254]    [Pg.240]    [Pg.702]    [Pg.470]    [Pg.117]    [Pg.118]    [Pg.602]    [Pg.245]    [Pg.309]    [Pg.182]    [Pg.1233]    [Pg.1385]    [Pg.219]    [Pg.1138]   
See also in sourсe #XX -- [ Pg.123 ]




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Arsenic poisoning

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