General drill-pain mgmt, analgesic, NSAID, acetaminophen
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| type of pain that respond well to anlagesics, anti-inflamm and opioids | noceceptive pain (somatic, visceral)
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| neuropathic pain responds poorly to, more predictable to | poorly to analgesics, anti-inflamm, opioids. predictable response to anticonvulsants, antidepressants, antidysrhythmics
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| WHO analgesic step 1 | NSAIDs, acetaminophen, non-opioid analgesics
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| WHO analgesic step 2 | Step 1 plus mild-moderate opioids
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| WHO analgesic step 3 | Step1, 2 plus moderate-severe opioids (adjuvants can be used on any step)
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| constitutive COX-1 normal housekeeping functions | protect GI mucosa, promote platelet activation, RBF
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| inducible COX-2 location, functions | in CNS or periphery. Mediate pain, mediate inflammation
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| MOA acetaminophen non-opioid analgesic | CNS COX inhibitor . . .no COX-1 inhib effects . . .antipyretic and analgesic
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| What are the COX-1 inhibited SEs | gastric mucosal irritation, impaired RBF/urine production, since thromboxane inhibitied-->de-activated platelets
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| Acetaminophen / ETOH ADR MOA | acetaminophen metab induced by ETOH @ P450-->toxic metabolite, whereby gluthione enzyme normally mebtabolizes to non-toxic metabolite. The gluthione enzyme action impaired, leaving toxic metabolites
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| NSAID - C0X-1,2 - irreversible | ASA, analgesic and antiinflamm,
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| ASA SEs | COX-1 SE (GI, renal impair, platelet deactivation x 7-8 days. Note is qualitative platelet defect, not quantitative as with thrombocytopenia
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| Unique uses for ASA | cardioprotection, ischemic prevention for stroke (primary, secondary, TIAs)
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| ASA and Reyes | interacts with viral infections (varicella, influenza)-->fatty degen of liver-->encephalopathy
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| salicylism | ASA overdose
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| ASA (NSAISs possibly)hypersensitivity syndrome | NON Ag/Ab anaphylactoid-type rxn starts as tinnitus, asthma sxs, hives, laryngeal edema, angioneurotic edema. PTS SHOULD AVOID ALL NSAIDs in the future. can take acetaminophen and non-acetyl-salicylates
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| true ASA allergy is rare, these pts can take | NSAIDs and non-salicylates
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| take home message non-acetyl salicylate SEs | less platelet de-activation, less GI intolerance, less renal impairment
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| take home message COX-2 specific inhibitors | may have increased thrombotic events (non-cox-1 mediated)as they are predisposed to increased clotting. renal effects same. decreased GI SEs, decreased COX-1 platelet activation. ZERO cardioprotection
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| adjuvant drug classes for neurpathy | analgesics, TCA, atypical antidepressant, anticonvulsants, local anesthetics, antidysrhythmics
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| break through pain | always cover for this possibility
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| consitpation | anticipate, treat prophylactically, avoid anticholinergics if possible
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| sedation | common during early phase of pain relief tx, avoid CNS depressants when possible
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| nausea/vomiting | codiene worst, worse during early phase tx
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| itching | opioids cause non-allergic release of histamine
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| urinary retention | caused by opioid MOA, anticipate in pts predisposed to BPH, avoid anticholinergics if possible
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| orthostatic hypoTN | monitor ambulatory pts
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