Page 77 - BSAVA Guide to Pain Management in Small Animal Practice
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BSAVA Guide to Pain Management in Small Animal Practice



        VetBooks.ir  Serotonin toxicity continued  with its peroxidase site, whose activity is
                                                  necessary for the cyclooxygenase site to
                                                  produce prostaglandins. Paracetamol is
             reupta e inhi itors  e.g.  uo etine ,
             monoamine oxidase inhibitors (e.g.   generally more e ective in inhibiting C    ,
             selegiline) and tricyclic antidepressants   and is anti in ammatory only in mild to
             (e.g. amitriptyline). The syndrome   moderate in ammatory states, when the
             is characterized by clinical signs   C     pathway is activated in preference to
             of autonomic hyper-reactivity,       C   1   raham et al.,   1  . In severe
             neuromuscular signs and altered mental   in ammatory states, where peroxidase levels
             status (e.g. diarrhoea, tachycardia,   are particularly high, paracetamol is less
             hypertension, hyperthermia, tremor,   e cient in inhibiting C    . In this setting,
             rigidity and seizures). The severity    coxibs are more e ective, as their activity is
             can range from mild clinical signs to   peroxidase independent  Anderson,    8 .
             death. Treatment is mainly supportive    Paracetamol, like NSAIDs, works both
             and involves discontinuation of the    centrally and peripherally inhibiting
             inciting drug.                       prostaglandin synthesis, but its antinociceptive
                                                  e ects are also due to interference with the
                                                  serotoninergic, endogenous opioids, and
                                                  endocannabinoid systems. Interaction with the
           Tapentodol                             nociceptive e ects of substance P and
                                                  glutamate has also been hypothesized
           Tapentodol is a MOP agonist and noradrenaline     raham et al.,   1  .  he only licensed
           reuptake inhibitor, which has similarities to   preparation of paracetamol contains
           tramadol. It does not require metabolism to an   paracetamol and codeine and is licensed for
           active metabolite in humans, and it has minimal   use in the dog only  Pardale V, N A ,   16 .
           e ect on serotonin reuptake, which reduces the   Although the Pardale-V datasheet states not to
           risk of serotonin toxicity. It has been shown to   use it with NSAIDs, paracetamol and NSAIDs
           be antinociceptive in dogs in an experimental   are often used in combination in human
           study; in the same study tramadol showed no   analgesia, and generic paracetamol
           antinociceptive properties (Kogel et al.,   14 .   (intravenous or oral) is often combined with
           However, oral bioavailability is poor in dogs   NSAIDs in dogs.
             iorgi et al.,   1   and further research is
           needed before recommendations regarding
           clinical use can be made.              The main advantage of paracetamol compared
              One potential disadvantage of tapentodol is   with conventional NSAIDs is its better
           its legal category, which is a Schedule II   gastrointestinal tolerance, and lesser
           Controlled Drug in the UK. This means it must   nephrotoxicity. The main metabolite of
           be kept in a locked cupboard with detailed   paracetamol in dogs is its glucuronide
           records of its acquisition and use.    conjugate, which is excreted in the urine. The
           Paracetamol                            half life of paracetamol is only  .96 hours in
                                                  the dog   u anich,   1  , and experimental
           Pharmacology                           studies failed to identify toxicity after
           Paracetamol is a unique drug in that, while it   administration of 1   mg kg  Savides et al.,
           does share similarities with NSAIDs, is not a   1984 .  ue to impaired glucuronidation
           strong anti in ammatory. Chemically,   capabilities, cats rely on sulphate conjugation
           paracetamol is a phenol, its protein binding is   alone to eliminate paracetamol in the urine,
           negligible, and it easily crosses cell   resulting in an increased risk of toxicity.
           membranes. Paracetamol inhibits        Hepatic toxicity is mainly caused by a reactive
           prostaglandin synthetase activity by interfering   metabolite, which is conjugated with

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