Toxicity laboratory diagnosis

Sunderman, F.W. 1970. Nickel poisoning. Pages 387-396 in F.W. Sunderman and F.W. Sunderman, Jr. (eds.). Laboratory Diagnosis of Diseases Caused by Toxic Agents. Warren H. Green, Inc., St. Louis, MO. 

In all poisoning situations, it is important to establish adequate respiration. Bicarbonate may be needed to counteract metabolic acidosis. In patients with suspected methanol intoxication, ethanol (10% solution) is often given intravenously before laboratory diagnosis is confirmed to block the formation of toxic products of ADH-catalyzed metabolism of methanol. Blood levels of methanol in excess of 50 mg/dL are an absolute indication for hemodialysis. Activated charcoal does not bind alcohols. The answer is (B). 

Laboratory diagnosis. Toxic prittoiples in plarrts are often r t lietected by routinely available tests in diagnostic orch nical laboratories. R is necessary to know the availability of confirmatory chemical testing for important plants of interest in a specific veterinary practice. 

W. J. Hayes, Jr., and E. R. Laws, Jr., eds.. Handbook of Pesticide Toxicology, Academic Press, Inc., San Diego, Calif., 1990. Three volume set provides detailed toxicological profiles of more than 250 insecticides, herbicides, and fungicides each compound described by identity, properties, and uses toxicity to humans, laboratory animals, domestic animals, and wildlife includes comprehensive coverage of diagnosis, treatment, prevention of injury, effects on domestic animals, wildlife, and humans - ISjOOO references. 

Early breast cancer is resected completely with curative intent, and adjuvant chemotherapy and hormonal therapy are initiated to prevent recurrence. During adjuvant chemotherapy, laboratory values to monitor chemotherapy toxicity are obtained prior to each cycle of chemotherapy. After completion of adjuvant therapy, patients are monitored every 3 months for the first few years after diagnosis, with intervals between exams extended as time from diagnosis lengthens. 

The determination of cholesterol is important for the diagnosis and prevention of a number of clinical disorders such as hypertension, arteriosclerosis, cerebral thrombosis and coronary heart disease. As the majority of cholesterol in human blood is present in an esterified form, a separate saponification step is required to obtain a total cholesterol analysis early methods for this involved caustic and toxic reagents, long analysis times and a relatively large sample volume. Free cholesterol can be determined chromatographically, although this requires cumbersome and expensive laboratory-based equipment. Modern methods use the enzyme cholesterol esterase to release esterified cholesterol which is then oxidised by a second enzyme, cholesterol oxidase (ChOx, Fig. 23.3) [48]. 

The differential diagnoses of TSPK include viral, toxic, bacterial, chlamydial, exposure, and dry eye causes of punctate epithelial keratopathy. Most of these conditions resolve in shorter time periods and are found to have a more obvious conjunctival involvement. Considering the lack of laboratory confirmatory tests, the diagnosis of TSPK remains solely clinical. 

As mentioned above, Wilson s disease is a genetic disorder of copper metabohsm that causes an increase in copper to toxic levels. The problems of diagnosis and appropriate laboratory investigations have been reviewed. 

If one of these features is absent, one cannot make a conclusive diagnosis of metal toxicity. The laboratory plays a key role in this process, and appropriate specimen coEection coupled with accurate analysis can make a major difference in correct diagnosis. 

Laboratory assays indicating exposure to cyanide and anticholinesterase compounds, such as nerve toxic agents, are known and available at many clinical facilities. However, there is currently no clinical test for skin-blistering agents and, therefore, initial diagnosis and treatment of injured are likely to be guided by observation of vital signs and symptoms by health care professionals on the scene. 

Percy Veere s symptoms and laboratory abnormalities did not slowly subside over the next 6 weeks as they usually do in uncomplicated viral hepatitis A infections. Instead, his serum total bilirubin, ALT, AST, and alkaline phosphatase levels increased further. His vomiting became intractable, and his friend noted jerking motions of his arms (asterixis), facial grimacing, restlessness, slowed mentation, and slight disorientation. He was admitted to the hospital with a diagnosis of hepatic failure with incipient hepatic encephalopathy (brain dysfunction caused by accumulation of various toxins in the blood), a rare complication of acute type A viral hepatitis alone. The possibility of a superimposed acute hepatic toxicity caused by the use of acetaminophen was considered. 

First of all, in order to establish environmental exposure, existence of a toxic red tide, and then confirm the diagnosis in the laboratory (seafood testing), it has to be decided whether the signs and symptoms (gastroenteritis and no temperature) and their evolution (benign, with complete recovery in 3-5 days) correspond to DSP or AZA whether the incubation period is short (30 min to a few hours) and whether there are antecedents of shellfish consumption (appropriate seafood ingestion) in its origin. 

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