Toxic drugs

Sama of drug Toxicity COQVUl- sant Action General Lepres- 6iOQ Anal-ge sle Exciting Effect Emetic Action Respi- ratory Effect... 

Fhtients with kidney disease may exhibit drug toxicity and a longer duration of drug action. The dosage of drugp may be reduced to prevent the accumulation of toxic levels in the blood or further injury to the kidney. 

While die patient is receiving a cholinergic drug it is important for the nurse to monitor for drug toxicity or cholinergic crisis. 

When two antiarrhythmic dragp are administered concurrently the patient may experience additive effects and is at increased risk for drug toxicity. When quinidine and procainamide are administered with digitalis, tiie risk of digitalis toxicity is increased. Hiarmacologic effects of procainamide may be increased when procainamide is administered with quinidine When quinidine is administered with the barbiturates or cimetidine, quinidine serum levels may be increased. When quinidine is administered with verapamil, there is an increased risk of hypotensive effects. When quinidine is administered with disopyramide, there is an increased risk of increased disopyramide blood levels and/or decreased serum quinidine levels. 

A QSAR for which the standard error of each descriptor is given concerns the bradycardic effect of a series of tetraalkylbispidines [47]. The QSAR models the selectivity between the desired bradycardic effect and the adverse contractile effect. It is important, in assessing and modeling drug toxicity, that the toxic effect is assessed relative to the desired effect as described above. The QSAR developed for the selectivity of the tetraalkylbispidines was ... 

There do not appear to be any published studies to date of ANNs being used for the prediction of drug toxicity, although they have been used for the prediction of toxicity of chemicals such as pesticides [68, 69]. 

There are undoubtedly a large number of other end points, at the specific and mechanistic levels, that require both data and modeling in the future to make QSAR a truly useful science for the prediction of drug toxicity. It is to be hoped that such data will become available in the not-too-distant future, perhaps through data-sharing facilities such as VITIC [105]. 

A better mechanistic appreciation of drug toxicity is needed. 

The first issue lies in the whole realm of the human disease process itself. Many adverse drug events mimic diseases and vice versa. Is an adverse event really an adverse event, or is it merely a natural occurrence of a disease process that is entirely independent of drug exposure The science of drug safety is often complicated by the lack of objective markers of drug toxicity that can systematically separate a disease process from an adverse drug event process [2]. Clinical trials, often viewed as the gold standard to assess efficacy, are simply too limited in scope to answer safety questions in a systematic way. 

XenobioticX CAR RXR(DRS) Androstanes Phenobarbital Protection against certain drugs, toxic... 

Methamphetamine and Related Drugs Toxicity and Resuiting Behaviorai Changes in Response to Pharmacoiogicai Probes... 

Frequently monitor the patient for signs of drug toxicity and seizures until the patient s drug concentrations have stabilized. Drug interactions are likely when patients are on more than one AED therefore, closely evaluate the patient s entire medication profile, and change medications or doses to minimize the interaction, if possible. 

Blood urea nitrogen (BUN) and serum creatinine are needed to dose antibiotics appropriately and to minimize or prevent drug toxicity (especially in the elderly patient). 

Resistance to drug toxic effects has also been observed in children. The incidence of aminoglycoside toxicity has been reported to be much lower in infants and children than in adults [39,48]. Diminished tissue sensitivity has been suggested as an explanation. 

Antipsychotic, or neuroleptic drug Used in the treatment of schizophrenia. They are also used in the management of psychotic episodes associated with psychotropic drug toxicity and some neurodegenerative disorders. 

The individual risk for drag inefficacy or drug toxicity is a product of the interaction of genes and the environment. Environmental variables include nutritional factors, concommittantly administered drugs, disease and many other factors in-... 

---