Pain and Inflammation Medications PDF

PPT 1: PAIN AND INFLAMMATION analgesics and anti-inflammatory medications analgesics opioids non-opioids anti-inflammatory nsaids glucocorticoids...

PPT 1: PAIN AND INFLAMMATION analgesics and anti-inflammatory medications analgesics opioids non-opioids anti-inflammatory nsaids glucocorticoids analgesics: opioids / narcotics what alter pain perception used in moderate-severe pain have been around for 3000 years ○ opium poppies indicated in acute pain ○ surgery ○ trauma chronic pain ○ cancer common opioids codeine (paveral) fentanyl (sublimaze, duragesic patch) hydrocodone (vicodin) meperidine (demerol, pethidine) oxycodone (oxycontin, roxicodone) propoxyphene (darvon) tramadol (ralivia, ultram) types of opioids strong agonists ○ morphine ○ meperidine ○ fentanyl moderate agonists ○ codeine ○ oxycodone antagonists ○ naloxone ○ naltrexone mixed agonists / antagonists ○ butorphanol ○ nalbuphine ○ pentazocine primary mechanism of action act primarily on ○ spinal cord dorsal gray matter ○ brain medial thalamus hypothalamus bind to specific receptors located on ○ presynaptic nerve terminals ○ postsynaptic neurons. decreased release of NT decreased excitability of postsynaptic neuron affects peripheral neurons ○ decreased sensitivity that initiates painful impulse inflammatory joint pain descending pain pathways ○ remove inhibition of central anti-pain circuits summary can control pain in 3 ways ○ decrease synaptic activity in ascending pain pathways ○ decrease sensitivity of sensory neurons that end painful impulses to cord ○ activate descending anti-pain pathways adverse effects relatively minor ○ sedation ○ mood changes ○ confusion ○ nausea / vomiting ○ constipation severe ○ orthostatic hypotension ○ respiratory depression ○ potential for abuse / addiction tolerance physical dependence opioid tolerance exact reasons unclear possible change in receptor sensitivity and signaling time course ○ begins after 1st dose ○ obvious after 2-3 weeks ○ lasts 1-2 weeks after opioid is d/c’d physical dependence withdrawal can begin 6-10 hours after last dose ○ peak within 2-3 days symptoms lasts 5 days note ○ may crave drug indefinitely opioid withdrawal: physical body aches symptoms gooseflesh fever, shivering nausea, vomiting, diarrhea, cramps irritability, insomnia uncontrollable yawning weakness / fatigue leg cramps / tremors sneezing, runny nose loss of appetite sweating tachycardia risk of opioid tolerance and risk seems minimal if dependence ○ pt doesn’t have history of substance abuse ○ pain is physiological dosage matches pt’s pain levels opioid-induced hyperalgesia opioids may be ineffective or increase pain in certain patients possible mechanisms ○ opioids turn on nociceptive pathways that use glutamate reasons unclear genetic factors rehabilitation concerns be alert for orthostatic hypotension monitor signs of respiratory depression ○ dyspnea ○ cyanosis ○ SpO2 monitor pain levels ○ watch for signs of opioid-induced hyperalgesia role of patient-controlled analgesia pt activates pump ○ self-administers small amount of opioid pump is programmed to prevent overdose  role of patient-controlled analgesia benefits better pain control with fewer side effects ○ less sedation ○ tolerance ○ dependence increased pt satisfaction requires pt awareness, cognitive ability analgesics: non-opioids nonsteroidal anti-inflammatory drugs acetaminophen primary effect analgesic anti-inflammatory antipyretic anticoagulant anti-cancer specific nsaids otc ○ aspirin ibuprofen ○ naproxen ○ ketoprofen prescription ○ etodolac ○ fenoprofen ○ ketorolac ○ meclofenamate ○ piroxicam mechanism of action inhibit synthesis of prostaglandins prostaglandins ○ lipid compounds produced in cell ○ various effects pain fever inflammation coagulation decrease prostaglandins by inhibiting cyclo oxygenase prostaglandin membrane phospholipid biosynthesis ○ arachidonic acid cyclooxygenase enzyme pgg2 ○ pgh2 cyclooxygenase cox-1 subtypes ○ normal constituent certain cells ○ synthesizes PGs to protect cells, maintain function ○ stomach, kidneys, platelets cox-2 ○ induced when cells is injured ○ synthesizes PGs that mediate pain, inflammation ○ RA cox-2 selective drugs inhibit synthesis of PGs in pain, inflammation spare production of beneficial PGs in stomach, kidneys, platelets may decrease pain & inflammation with less toxicity ○ less gastritis ex ○ celecoxib (celebrex) cox-2 inhibition: cv promotes infarction problems ○ causes heart attack, stroke drugs recalled ○ vioxx ○ bextra some nsaids also more selective for cox-2; increased risk of infarction cox-2 selective nsaids 5-50 times more selective for cox-2 ex ○ diclofenac ( voltaren) ○ etodolac (lodine) ○ meloxicam (mobic) acetaminophen analgesic and antipyretic effects no gastric irritation no anti-inflammatory or anticoagulant effects high doses ○ liver toxicity acetaminophen and tramadol + acetam opioid combinations ○ ultracet hydrocodone + acetam ○ lortab ○ lorcet ○ vicodin oxycodone + acetam ○ endocet ○ roxicet ○ primalev adverse effects and gastric irritation rehab concerns ○ nsaids hepatic, renal toxicity ○ if previous damage cv problems ○ nsaids increase bp ○ increase risk of infarction nsaids impair bone & cartilage healing overdose ○ aspirin intoxication hearing loss tinnitus confusion headache inform patients ○ nsaids not equals to acetaminophen anti-inflammatory agents glucocorticoids nsaids glucocorticoids steroids ○ powerful anti-inflammatory and immunosuppressive effects many uses / indications resolve inflammation ○ disease process may continue common glucocorticoids ○ betamethasone ○ cortisone ○ dexamethasone ○ hydrocortisone ○ paramethasone ○ prednisolone ○ prednisone nsaids inhibit PG biosynthesis anti-inflammatory dose often higher than analgesic dose should be used continuously until inflammation is resolved ○ do not stop/start dosing effects act on inflammatory cells ○ macrophased ○ leukocytes drug binds to glucocorticoid receptor in cytoplasm drug receptor travels to nucleus ○ decreased expression of inflammatory proteins  cytokines enzymes ○ increased expression of anti-inflammatory proteins steroid mechanism administration methods oral, systemic ○ regular, maintenance dose ○ dose packs injection ○ intra-articular ○ 3-4 per year other ○ inhalation ○ topical ○ nasal ○ ophthalmic ○ otic adverse effects and primary problem rehab concerns ○ catabolic effect on bone, muscle, ligament, tendon, skin other ○ salt/water retention ○ increased infection ○ gastric ulcers ○ glucose intolerance ○ glaucoma adrenal suppression glucocorticoids: vascular collapse adrenocortical shock ○ severe hypotension ○ organ damage can occur when GCs are suddenly discontinued