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NURS 572 29, c30

General drill-pain mgmt, analgesic, NSAID, acetaminophen

QuestionAnswer
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
Created by: lorrelaws