Inflammation, drug therapies

Before giving a nonnarcotic analgesic to a patient, the nurse assesses the type, onset, and location of the pain. It is important to determine if this problem is different in any way from previous episodes of pain or discomfort. If the patient is receiving a nonnarcotic analgesic for an arthritic or musculoskeletal disorder or soft tissue inflammation, the nurse should examine the joints or areas involved. The appearance of the skin over the joint or affected area or any limitation of motion is documented. The nurse evaluates the patient s ability to carry out activities of daily living. This important information is used to develop a care plan, as well as to evaluate the response to drug therapy. 

Patients with acute gout should be monitored for symptomatic relief of joint pain as well as potential adverse effects and drug interactions related to drug therapy. The acute pain of an initial attack of gouty arthritis should begin to ease within about 8 hours of treatment initiation. Complete resolution of pain, erythema, and inflammation usually occurs within 48 to 72 hours. 

An individualized approach to treatment is necessary (Fig. 2-1). For mild or moderate pain, topical analgesics or acetaminophen can be used. If these measures fail or if there is inflammation, nonsteroidal antiinflammatory drugs (NSAIDs) may be useful. Appropriate nondrug therapies should be continued when drug therapy is initiated. 

Moderate to severe autoimmune inflammation requires immunosuppression to minimize or stop progression of early disease. There now is consensus that autoimmune inflammation should be totally suppressed at an early stage when there is maximum susceptibility to immune-suppression with single or combination drugs therapy. In early stages of the disease changes are reversible with no consequent disability and joint deformity. 

The most important prognostic factors in autoimmune inflammatory disease are, disease duration, the degree of disease activity-dependent radiological erosion, previous drug therapy and previous exposure to immunosuppressants (IMN), i.e. IMN naivety. Early autoimmune inflammation can be totally eradicated, irreversible disability and damages can be prevented when adequate treatment has been initiated. 

Single drug therapy is mostly adequate in lupus nephritis (LN) classified as renal biopsy WHO Class I and II. Single drug therapy in lupus nephritis Class III-V, and in particular Class VI is less or not effective. One immunosuppressant cannot suppress all aspects of autoimmune inflammation in the more serious forms of the disease. The SBC-5-IMNs is not required in Class I, IL and also not in Class VI. In Class VI nothing helps, except renal dialysis or renal transplantation. 

Seydel, U., Ulmer, A.J., Uhlig, S., Rietschel, E.Th. Lipopolysaccharide, a membrane-forming and inflammation-inducing bacterial macromolecule. In Zimmer, G. (ed), Membrane Structure in Disease and Drug Therapy. Marcel Dekker Inc, New York, NY (1999), pp. 217-252. 

Adequate levels of an antibiotic must reach the site of infection in order for the invading microorganism to be effectively eradicated. Natural barriers such as those described below may cause inadequate penetration of the drug into certain tissues such as the brain, prostate, and bone, although inflammation can influence the response to drug therapy in these tissues. 

Q4 Excessive bleeding during the menstrual period is called menorrhagia. The blood loss reduces levels of iron in the body and may result in iron-deficiency anaemia. The causes of excessive bleeding could be inflammation, fibroids, endometriosis, cervical polyps, adenomyosis, ovarian tumours, intrauterine devices (IUDs), inherited clotting disorders, endocrine dysfunction, such as thyroid dysfunction, or mental stress. In terms of drug therapy, oral ferrous... 

Susceptibility faaors increase the risk for kidney disease but do not directly cause kidney damage. SusceptibEity factors include advanced age, reduced kidney mass and low birth weight, racial or ethnic minority, family history, low income or education, systemic inflammation, and dyslipidemia. Initiation factors initiate kidney damage and can be modified by drug therapy. Initiation factors include diabetes meUitus, hypertension, autoimmune disease, polycystic kidney disease, and drug toxicity. 

Mulder Cl, van den Hazel SJ. Drug therapy dose-response relationship of oral mesalazine in inflammatory bowel disease. Mediators Inflamm 1998 7(3) 135-6. 

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