| Popis: |
Pancreatic cancer pain sensation is neuropathic in origin. The interlinked processes of neuroplastic changes, neural remodeling, neuro-cancer and neuro-immune interactions seem to play a key role in the generation of pancreatic cancer pain. Neural invasion and pancreatic neuritis in pancreatic cancer initiate neural damage which stimulates neuropathic alterations via many neurotrophic and chemotactic factors, many of which themselves have nociceptive properties. This further facilitates preferential expression of neuropeptides frequently present in nociceptive neurons. The pain is even more exaggerated by cancer cell invasion of the adjacent coeliac plexus. All in all, generate a neuropathic pain sensation in pancreatic cancer. Due to its complex mechanism and multiple causes, pain in pancreatic cancer is difficult to treat and requires multimodal management. The secondary reasons of pain should firstly be excluded. For analgesic treatment, pharmacotherapy for pain in pancreatic cancer is guided by the WHO analgesic ladder that represents a stepwise escalation of medications with increasing analgesic effect. The arsenal of drugs that can be administered includes non-opioid painkillers such as acetaminophen, non-steroidal anti-inflammatory drugs and metamizole; adjuvant analgesics including pregabalin; opioids, ketamine; anti-psychotics, clonidine; steroids and cannabinoids. In refractory pain, intrathecal drug delivery systems, epidural analgesic administration and neurolytic therapies are effective alternatives. |
