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Chronic toxicosis

It is used foror therapy of chronic toxicosis (8 mgAg orally four times daily), or following parenteral calcium EE)TA therapy. [Pg.198]

Subacute toxicosis. Treatment is similar to that for chronic toxicosis fsee VIII H 3). [Pg.205]

Subacute or chronic toxicosis is characterized by chronic dermatitis, dermal necrosis, and peeiing of the epidermis. Subacute or chronic exposure can cause liver and kidney damage. [Pg.209]

Calves given 80 ig/kg HCDD and 8000 ig/l% OCDD extracted from PCP develop chronic toxicosis. These dosages are equivalent to the dioxins in a dosage of 80 mg/kg PCP. [Pg.221]

Chronic toxicosis is seen most often in heibivares, especially dairy cattle. [Pg.222]

Chronic toxicosis in poultry and dogs. Bone marrow depression with granulocytopenia, anemia, and hypoprothrombinemia suggest sulfaquinoxaline toxicosis in poultry or dogs. Analysis of musde, kidney, or liver tissue teveais sulfonamide concentrations above 20 ppm. d. Treatment... [Pg.335]

Chronic toxicosis. Abortirjn occurs in cattle during the first two-thirds of gestation. Aborted calves are small and the dam usually has a retained placenta. [Pg.399]

Serum bile acids may be elevated early in aflatoxicosis. Hyperbilirubinemia develops in chronic toxicosis. [Pg.416]

Arsenic Toxicosis. Urine arsenic is the best indicator of current or recent exposure. Atomic absorption spectrophotometry is preferred as the detection method. Hair or fingernail sampling may also be helpful. Use of blood is useful if analyzed soon after exposure or in cases of continuous chronic exposure. After acute exposure, chelation therapy is instituted utilizing either (1) Dimercaprol BAL (British Anti-Lewisite) and analogues ... [Pg.408]

Coccidial infections resulting from infections by Eimeria acervulina (duodenal coccidiosis) have been shown to affect nutrient absorption (21,26,35,38). Turk et al. (26), using radiolabeled Mn, reported that experimental TT acervulina infection decreased Mn absorption during the acute phase of infection (6 days postinoculation), but that the infection increased Mn absorption during the recovery period. Southern and Baker (32) and Brown and Southern (21) reported that chronic E. acervulina infection increased Mn absorption. Bone and bile Mn concentrations were increased and signs of Mn toxicosis symptoms, as assessed hematologically, were exacerbated by the infection. [Pg.43]

Trichothecene toxicosis is manifested by a broad spectrum of clinical disorders, which vary according to the specific causative toxin or mixture of toxins. Species differences in response are generally related to severity of the response, and young animals are more susceptible than adults. Toxicosis can be acute or chronic, with clinical signs remaining fairly similar. A comprehensive review of the pathophysiology of spontaneous and experimentally induced trichothecene mycotoxicosis is available (Beasley, 1989). [Pg.357]

Fluoride toxicosis reported primarily in animals can be acute or chronic. Acute toxicosis is by exposure to insecti-cides/rodenticides and volcanic dust. Fluoride is metabolized via renal excretion and is preferentially deposited in... [Pg.568]

Price LA, Walker NI, Clague AE, Pullen ID, Smits SJ, Ong TH, Patrick M. Chronic copper toxicosis presenting as liver failure in an Australian child. Pathology 1996 28(4) 316-20. [Pg.905]

In conclusion, the risk of an acute toxicosis or long-term chronic health effects of a mycotoxin contamination through consumption of mycotoxin-contaminated fruits and fruit products is relatively low compared to other food groups such as cereals. The occurrence of an endemic poisoning by... [Pg.70]

Helie P, Sauvageau RA. 1998. Chronic selenium toxicosis in growing-finishing pigs in southwestern Quebec. Can Vet J 39 591-592. [Pg.349]

Chronic exposure to subacute doses of trichothecene mycotoxins is not thought to be an effect of biological warfare. This type of exposure, however, was responsible for ATA toxicosis in humans and mycotoxicosis in domestic animals. In addition, chronic toxicity has been iatrogenically induced when repeated subacute doses of a trichothecene mycotoxin were administrated intravenously to cancer patients as a chemotherapy for colon adenocarcinoma. Alimentary Toxic Aleukia Toxicosis... [Pg.667]

Unknown postulated to be a chronic cyanide toxicosis or a lathyrogenic effect from [Pg.87]

A functional parathyroid adenoma would produce excess parathyroid hormone (PTH). PTH stimulates osteodasiic activity and increases renal tubular calcium resorption, leading to hypercalcemia by increasing bone turnover. Vitamin D is metabolized to the active 1,25 dihydroxy form, which interacts with parathyroid hormone to prodiKe hypercalcemia. Impaired renal tubular function in chronic renal disease Oncluding cadmium toxicosis)... [Pg.161]


See other pages where Chronic toxicosis is mentioned: [Pg.205]    [Pg.205]    [Pg.264]    [Pg.371]    [Pg.205]    [Pg.205]    [Pg.264]    [Pg.371]    [Pg.588]    [Pg.127]    [Pg.203]    [Pg.286]    [Pg.108]    [Pg.41]    [Pg.127]    [Pg.203]    [Pg.286]    [Pg.100]    [Pg.51]    [Pg.568]    [Pg.568]    [Pg.569]    [Pg.1731]    [Pg.321]    [Pg.1388]    [Pg.261]    [Pg.61]    [Pg.171]    [Pg.161]    [Pg.191]    [Pg.384]    [Pg.388]    [Pg.373]    [Pg.413]    [Pg.606]    [Pg.187]   
See also in sourсe #XX -- [ Pg.93 , Pg.337 ]




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Toxicosis

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