Drugs specific types

In liver disease, for example, the ability to metabolize or detoxify a specific type of drug may be impaired. If the average or normal dose of the drug is given, the liver may be unable to metabolize the drug at a normal rate Consequently, the drug may be excreted from the body at a much slower rate than normal. The primary health care provider may then decide to prescribe a lower dose and lengthen the time between doses because liver function is abnormal. 

Supplementary requirements for specific types of drug products are contained in other Parts ofGhapters 9 and 21 of the Gode of Federal Regulations, as summarised in Table 11.1. IGH Q7 guideline provides globally harmonised principles ofGMP for APIs. 

Table 11.1 US current Good Manufacturing Practice (cCMP) regulations for specific types of drug products.

Type III drugs specifically prolong refractoriness in atrial and ventricular fibers and include very different drugs that share the common effect of delaying repolarization by blocking potassium channels. 

The treatment of choice depends on the type of epilepsy (Table 52-2) and on drug-specific adverse effects and patient preferences. Fig. 52-1 is a suggested algorithm for treatment of epilepsy. 

Various parts of the ophthalmological examination are shown in Table 20.14. The most important common ophthalmological test to evaluate patients for the occurrence of chronic drug-induced toxicity is slit-lamp examination. Specific types of drugs with known potential for ocular toxicity may require that special attention be directed to other evaluations shown in Table 20.14. Most drugs that are to be taken... 

Liposomal preparations can be therapeutically beneficial based on their ability to decrease non-specific toxicities associated with the drug, or by being more efficacious against a specific type of cancer, increasing the response frequency, and/or the average time to relapse or response duration. 

Drug-specific antibodies of the IgE type combine via their Fc moiety with receptors on the surface of mast cells. Binding of the drug provides the stimulus for the release of histamine and other mediators. In the most severe form, a life-threatening anaphylactic shock develops, accompanied by hypotension, bronchospasm (asthma attack), laryngeal edema, urticaria, stimulation of gut musculature, and spontaneous bowel movements (p. 326). 

Opioid binding at medullary sites is consistent with the respiratory depressant effects of the drugs. Binding in the nucleus accumbens and the resultant release of dopamine by the /x- and 8-opioids is linked to the development of physical dependence. However, the K-opioids, which also bind extensively in the nucleus accumbens, are linked to a decrease in dopamine release, possibly explaining their lower abuse liability. The localization of different receptor subtypes within different-size fiber pathways has been established. The x- and 8-receptors appear associated with the large-diameter fibers, while the K-receptors appear to be located in the small to medium-size fiber bundles of the dorsal root ganglia. Such differences may explain the modulation of specific types of nociceptive stimuli by the different opioid agonists and opioid peptides. 

Chapter /, Modem Psychopharmaceuticals, written by Dr Hossein Fatemi, and Chapter 5, Psychopharmaceuticals and the Treatment of Mental Disorders, provide succinct, up to date, and well-referenced information on how to use the major classes of psychotropic drugs. The latter chapter discusses in a frank and balanced manner the ambivalence towards the use of pharmacologic agents in mental disorders felt by some, and the limitations on the achievements of current drugs as ideal therapies for schizophrenia, bipolar disorder and major depression in particular. Clearly, much has been accomplished, but many needs, especially for prevention of relapse, removal of specific types of symptoms, and restoraton of work and social function, remain to be accomplished by drug and psychosocial therapies. 

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