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Aspirin belongs to a group of drugs that all possess analgesic, anti-inflammatory and antipyretic properties to different degrees. Because of the anti-inflammatory effects they are known as non-steroidal anti-inflammatory drugs, or NSAIDs ( Figure NSAIDs exert their effects by inhibition of the enzyme cyclo-oxygenase. This results in reduced production of prostaglandins and thromboxanes because COX normally catalyses their formation from arachidonic acid. Prostaglandins play a role in pain by sensitising sensory nerve endings to the effects of other mediators such as bradykinin.
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Aspirin should not be used because it competes with uric acid for tubular secretion in the kidney. Long-term treatment with drugs that control uric acid levels prevents future episodes of gout and helps resolve tophi. However, these drugs do not relieve the pain and inflammation of an acute attack and may take many months to have an effect. Concurrent treatment with colchicine or a NSAID is necessary for the first three to six months.
Some imidazoles enhance the anticoagulant properties of warfarin. However, these interactions are unlikely with topical application. Systemic administration of imidazoles is often necessary for tinea of the nail. Systemic use of antifungal drugs is considered in Chapter Terbinafine displays a broad spectrum of antifungal activity at low concentrations.
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These are known as drugdrug interactions and there are many possible mechanisms.
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The basal nuclei contain many excitatory cholinergic neurons.
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Fortunately, neurons that carry the sensation of pain are of the smallest diameter unmyelinated and myelinated type and as such are affected by low doses of local anaesthetic, leaving larger motor neurons unaffected.
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In these cases symptoms may be produced through stimulation of irritant receptors and release of mediators from sensory neurones.
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As a tumour gets larger growth slows down, partly because it outgrows its blood supply and partly because not all cells in the tumour divide continuously.
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