Term
| what characterizes pain due to radiation therapy? |
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Definition
| neuronal and other types of tissue can be altered by radiation. acute/chronic pain can result due to radiation-induced alteration of tissues, such as: inflammation, fibrosis (compression of surrounding nerves, subsequent peripheral nerve dysfunction and pain), direct injury to large peripheral nerve plexus, induction of neurogenic tumors, soft tissue ischemia, and necrosis. |
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Term
| what are oral complications due to radiation therapy? |
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Definition
| mucositis (can absorb more LA than normal), xerostomia (dry mouth), trismus (radiated muscles of mastication/TMJ: cell destruction/fibrosis - more common if sx also: hard to open mouth), and *osteoradionecrosis (least reversible/most severe oral damage, loss of osteocytes, progressive obliterative endarteritis, hyalinization of blood vessels in tx field, increased bone infection, impaired healing, and pathologic fractures). methods to reduce osteoradionecrosis: daily topical fluoride, topical anesthetics, and pre-radiation NSAIDs. |
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Term
| what characterizes the polyneuropathy due to chemotherapy? tx? |
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Definition
| vincristine/cis-platinum: burning pain and allodynia. *vincristine: sensory/motor, dose-related, motor: weakness of fingers, wrist, leg, and denervation findings. *cis-platinum: primarily sensory, demyelination. tx: TCAs (amytriptyline, despiramine), anticonvulsants (carbamazepine), topical capsaicin, and clonidine. |
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Term
| what are oral complications due to chemotherapy? tx? |
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Definition
| occurs w/bleomycin, doxorubicin, dactinomycin, 5-fluoracil, danorubicin, methotrexate and more severe w/radiotherapy. inflammatory lesions (max w/2-3 wks) can progress and involve the esophagus and rectal mucosa. tx: LA rinse. |
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Term
| what painful ADRs are associated w/steroids in CA tx? |
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Definition
| bone pain secondary to pathologic fractures and aseptic necrosis of femoral/humeral joints. tx: reduction of steroid dose, NSAIDs and opioid. |
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Term
| what are factors which will influence the dosage conversion in switching pts from one opioid to another? |
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Definition
| current daily narcotic dosage, length of time the pt has been recieving opioid therapy, dosing schedule (prn/fixed 24 hr/continuous), pathological changes (hepatic or renal dysfunction), presence of other CNS depressants in daily regimen (antidepressants [may directly stimulate opioid receptors/reduce biotransformation/inhibit serotonin uptake], anxiolytics, and sed/hypnotics), concurrent NSAID/acetaminophen, psychological status of pt, and present degree of pain relief. |
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Term
| what are 4 considerations for narcotic conversion for chronic CA pain pts? |
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Definition
| incomplete tolerance at high doses, assessment of analgesia at steady-state conditions, informing the pt, and narcotic-induced sedation. |
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Term
| how does incomplete tolerance at high doses affect narcotic conversion in chronic CA pain pts? |
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Definition
| for pts who are currently taking large amounts of one narcotic (e.g., about 100 mg or more of morphine Q 4H) and are to be switched to another, it is best to calculate the approximate equivalent dose of the second narcotic and then decrease it for the initial doses. this is b/c tolerance is not complete among narcotics and an equivalent dose of a different narcotic may produce greater CNS depression than desired. it is more acceptable to adjust the narcotic dose upwards to achieve greater pain control than to have to reduce the dose because of the more frequent occurrence of adverse reactions such as nausea, vomiting and/or significant respiratory depression. |
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Term
| how do steady state levels narcotic conversion in chronic CA pain pts? |
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Definition
| narcotic induced analgesia is more reliable when performed at steady state conditions (steady state is not synonymous with therapeutic range, it is just an equal amount of drug going in as that which is leaving). for most narcotics, the effective T1/2 is approximately 4 to 6 hours. that means that generally within 16 to 30 hours, steady state conditions will have been achieved for these opioids - however, for narcotics with a long T1/2 (methadone; levorphanol), the time required for achievement of steady state is greater; for methadone, it could take 5 days to reach this level. this means it will take long to stabilize the pt and more time will be necessary to eliminate the narcotic. |
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Term
| how is informing the pt necessary w/narcotic conversion in chronic CA pain pts? |
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Definition
| to minimize problems and maximize patient compliance during the conversion process, patients should be informed that they may experience a slight but temporary increase in pain. pts who properly understand the benefit vs risk ratio will be easier to stabilize. |
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Term
| how does narcotic-induced sedation affect narcotic conversion in chronic CA pain pts? |
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Definition
| pts may actually experience more sedation with the narcotic to which they have just been switched; since tolerance does develop within a few days to narcotic induced sedation, this will usually not be a major problem for patients on chronic narcotic therapy. |
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Term
| what characterizes the benefits of adjuncts to opioid therapy? |
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Definition
| a) enhancement of opioid analgesia (reduction of biotransformation or a similar MOA to opioids). b) provision of analgesia through a non-opioid MOA. proper utilization will provide improved analgesia for the pt and in addition, it may be possible to reduce the narcotic dosage = another major benefit: attenuation of opioid-induced ADRs (n/v, pruritus, sedation and respiratory depression). |
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Term
| what needs to be considered when using NSAIDs as opioid adjunct tx? |
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Definition
| most opioids have up to 660 mg of acetaminophen. percodan and lortab have ASA. max daily dose of acetaminophen: 4 g. |
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Term
| what is the problem w/mixing alcohol and extended release drugs? |
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Definition
| alcohol is a solvent and can cause immediate release of the entire dose |
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Term
| can antidepressants be used as opioid adjuncts? |
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Definition
| yes, some TCAs stabilize nerve membranes (but not great in geriatrics) and since serotonin is a major NT of pain, suppression of its reuptake = increase in analgesia. |
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Term
| how can capsaicin be used as an opioid adjunct? |
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Definition
| capsaicin causes localized depletion of substance P from terminals of peripheral sensory neurons = reduced conduction in type C fibers. |
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Term
| how can Ca++ channel blockers be used as an opioid adjunct? |
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Definition
| Ca++ channel blockers (nifedipine, ziconotide [intrathecal]) decrease entry of Ca2+ which reduces release of substance P. |
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Term
| how can alpha 2 agonists (clonidine) be used as an opioid adjunct? |
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Definition
| unknown MOA, but theory involves direct suppression of sympathetic nerves in s. cord and indirect increase of cholinergic activity. clonidine will also potentiate narcotics as well as GA/LA. shown to be effective in pts tolerant to morphine. |
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Term
| how can anticonvulsants be used as an opioid adjunct? |
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Definition
| the anticonvulsants *carbamazepine and *phenytoin reduce Na+ channel function, leading to a reduction in neuronal hyperexcitability. *lamotrigine does the same and inhibits Ca++ channels while *topiramate blocks Na+ channels and potentiates GABA. recent data indicates a possible reduction of neuropathic pain by inhibition of glutamate release in the spinal cord dorsal horn (accomplished by GABA). *gabapentin and *pregabalin are both GABA analogs. |
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Term
| how can local anesthetics/antiarrhythmics be used as an opioid adjunct? |
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Definition
| lidocaine and mexiletine block Na+ channels = reduction of neuronal excitability |
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Term
| how can psychostimulants be used as an opioid adjunct? |
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Definition
| caffeine, dextroamphetamine, and methylphenidate (ritalin) all increase CNS activity, which counteracts narcotic-induced drowsiness, sedation and confusion. |
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Term
| how can corticosteroids be used as an opioid adjunct? |
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Definition
| *dexamethasone, *methylprednisolone, and *prednisone are anti-inflammatory (decreased prostaglandin synthesis), edema reducers (decreased capillary permeability), and neuronal excitability reducers (direct effect on cell membranes). corticosteroids may be used for back pain due to spinal cord compression (edema), bone pain, h/a from brain mets (edema), neuropathic pain, and metastatic prostatic CA (decreased circulating androgens). may also improve appetite/nausea. immediate ADRs: HTN, hyperglycemia, immunosuppression, psychiatric disorders (affective disorders, psychosis, cognitive impairment) and possible peptic ulceration. long term ADRs: cushing's, proximal myopathy, osteoporosis, and aseptic necrosis of the bone. |
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Term
| how can NMDA receptor antagonists be used as an opioid adjunct? |
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Definition
| dextromethorphan, ketamine and memantine block NMDA receptors which appear to be involved in central sensitization. |
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Term
| how can bone-resorption inhibitors/bisphosphonates be used as an opioid adjunct? |
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Definition
| alendronate (beware), pamidronate disodium, risedronate, and zoledronic acid inhibit bone resorption via 1) adsorption to calcium phosphate crystals in bone (may block dissolution) and inhibition of osteoclast activity. these are efficacious in reducing pain due to bone mets (common in mult. myeloma and breast CA). give adequate hydration to reduce possibility of nephrotoxicity. |
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Term
| how can antispastics be used as an opioid adjunct? |
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Definition
| baclofen activates GABA B sites and if used intrathecally, it can reduce central pain in pts w/spinal lesions |
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Term
| how can spasmolytics be used as an opioid adjunct? |
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Definition
| scopolamine is anticholinergic and can reduce pain due to distention of hollow organs (bladder spasm; biliary, bowel and renal colic). |
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Term
| how can hemorheologics be used as an opioid adjunct? |
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Definition
| *pentoxifylline increases blood flow and tissue oxygenation by decreasing blood viscosity, increasing erythrocyte flexibility, and possible antiplatelet activity. it will produce pain relief in pts w/severe atherosclerosis and purpuric toe lesions. |
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Term
| how can BZDs be used as an opioid adjunct? |
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Definition
| BZDs are not inherently analgetic - but are useful in relieving anxiety and acute muscle spasms occurring w/chronic unrelieved pain. alprazolam and clonazepam have been reported to reduce neuropathic pain. |
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Term
| how can antipsychotics be used as an opioid adjunct? |
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Definition
| *methotrimeprazine may also provide analgesia as well as decrease anxiety and pain-induced stress. haloperidol, chlorpromazine, pimozide, and promethazine are useful in reducing nausea, agitation and psychological stress, factors known to increase pain sensitivity. ADRs: drowiness, orthostatic hypotension, pain at injection site, extrapyramidal reactions, tardive dyskinesia, cardiac toxicity, and agranulocytosis. |
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