Articles: opioid.
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J Pain Symptom Manage · May 2018
Comparative Study Observational StudyCharacteristics of Unscheduled and Scheduled Outpatient Palliative Care Clinic Patients at a Comprehensive Cancer Center.
There is limited literature regarding outpatient palliative care and factors associated with unscheduled clinic visits. ⋯ Unscheduled new FU patients have higher levels of physical and psychosocial distress and higher opioid intake. Outpatient palliative care centers should consider providing opportunities for walk-in visits for timely management and close monitoring of such patients.
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Substance use disorders (SUDs) are known to cause or complicate treatment of many types of cancers. ⋯ Veterans with cancer and SUD showed a specific risk for liver disease and a higher use of opioids. Collaborative teams involving oncology, palliative care, and psychiatry may be best able to address the challenge of providing adequate and safe opiate pain control for this vulnerable population.
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Pain is one of the most common reasons patients present to the emergency department (ED). Emergency physicians should be aware of the numerous opioid and nonopioid alternatives available for the treatment of pain. ⋯ Analgesia in the ED should be provided in the most safe and judicious manner, with the goals of relieving acute pain while decreasing the risk of complications and opioid dependence.
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The opioid epidemic, driven in part by increased prescribing, is a public health emergency. This study examines dispensed prescription patterns and approvals of new opioid analgesic products to investigate whether the introduction of these new drugs increases prescribing. ⋯ An online visual overview is available for this article at http://links.lww.com/ALN/B705.
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Repeated stimulation of mu-opioid receptors (MORs), by an MOR-selective agonist DAMGO induces type II priming, a form of nociceptor neuroplasticity, which has 2 components: opioid-induced hyperalgesia (OIH) and prolongation of prostaglandin-E2 (PGE2)-induced hyperalgesia. We report that intrathecal antisense knockdown of the MOR in nociceptors, prevented the induction of both components of type II priming. Type II priming was also eliminated by SSP-saporin, which destroys the peptidergic class of nociceptors. ⋯ Inhibitors of Src and mitogen-activated protein kinase (MAPK) also only attenuated OIH. Inhibitors of matrix metalloproteinase, which cleaves EGF from membrane protein, markedly attenuated the expression, but did not prevent the induction, of prolongation of PGE2 hyperalgesia. Thus, although the induction of prolongation of PGE2-induced hyperalgesia at the peripheral terminal of peptidergic nociceptor is dependent on Src, FAK, EGFR, and MAPK signaling, Src, FAK, and MAPK signaling is only partially involved in the induction of OIH.