Question | Answer |
type of pain that respond well to anlagesics, anti-inflamm and opioids | noceceptive pain (somatic, visceral) |
neuropathic pain responds poorly to, more predictable to | poorly to analgesics, anti-inflamm, opioids. predictable response to anticonvulsants, antidepressants, antidysrhythmics |
WHO analgesic step 1 | NSAIDs, acetaminophen, non-opioid analgesics |
WHO analgesic step 2 | Step 1 plus mild-moderate opioids |
WHO analgesic step 3 | Step1, 2 plus moderate-severe opioids (adjuvants can be used on any step) |
constitutive COX-1 normal housekeeping functions | protect GI mucosa, promote platelet activation, RBF |
inducible COX-2 location, functions | in CNS or periphery. Mediate pain, mediate inflammation |
MOA acetaminophen non-opioid analgesic | CNS COX inhibitor . . .no COX-1 inhib effects . . .antipyretic and analgesic |
What are the COX-1 inhibited SEs | gastric mucosal irritation, impaired RBF/urine production, since thromboxane inhibitied-->de-activated platelets |
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 |
NSAID - C0X-1,2 - irreversible | ASA, analgesic and antiinflamm, |
ASA SEs | COX-1 SE (GI, renal impair, platelet deactivation x 7-8 days. Note is qualitative platelet defect, not quantitative as with thrombocytopenia |
Unique uses for ASA | cardioprotection, ischemic prevention for stroke (primary, secondary, TIAs) |
ASA and Reyes | interacts with viral infections (varicella, influenza)-->fatty degen of liver-->encephalopathy |
salicylism | ASA overdose |
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 |
true ASA allergy is rare, these pts can take | NSAIDs and non-salicylates |
take home message non-acetyl salicylate SEs | less platelet de-activation, less GI intolerance, less renal impairment |
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 |
adjuvant drug classes for neurpathy | analgesics, TCA, atypical antidepressant, anticonvulsants, local anesthetics, antidysrhythmics |
break through pain | always cover for this possibility |
consitpation | anticipate, treat prophylactically, avoid anticholinergics if possible |
sedation | common during early phase of pain relief tx, avoid CNS depressants when possible |
nausea/vomiting | codiene worst, worse during early phase tx |
itching | opioids cause non-allergic release of histamine |
urinary retention | caused by opioid MOA, anticipate in pts predisposed to BPH, avoid anticholinergics if possible |
orthostatic hypoTN | monitor ambulatory pts |