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40 Cards in this Set

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  • Back
How do opioids work?
relief of moderate-severe pain by inhibiting porduction of substance P and prostaglandins.
they induce the endogenous analgesia system.
administering opioids:
IM, PO, or Sub-Q
*Are sig. 1st. pass metabolism drugs...oral needs much higher doses*
What two opioids form active mtabolites?
morphine and meperidine(Demerol)
--drug accumulates in liver/kidney disease--
What are the major endogenous analgesia receptors?
MU (most oppioid effects)
KAPPA (analgesia, sedation, <GI motility)
DELTA (unknown if oppioids bind to these)
Acute pain
sharp, lancing or cutting
A-delta fibers using glutamate.
usually responds to treatment within a few days.
Chronic pain
lasts >3 mos
"slow pain"--begins after 1 sec., increases over time.
type C fibers using Substance P
Cancer pain
can be acute and chronic, constant or intermittent.
usually chronic = tumor spread;acute = due to procedures
Somatic pain
stimulation of nociceptors in structural tissues.
"sharp, burnig, aching, gnawing, throbbing, or cramping"
can be acute (sprains) or chronic (arthritis)
Visceral pain
simultaneous stimulation of many nociceptors in abdo/thoracic tissues.
"deep, dull, aching, cramping"
not well-localized: type C fibers
Neuropathic pain
injury to nervous structures
common cause of chronic pain: "severe, shooting, burning, stabbing"
due to cancer, herpes zoster, DM.
Diff. to treat
Contraindications to opioids:
Resp. depression, chronic lung disease, liver/kidney disease, BPH, >ICP, or hypersensitivity to opioids/related drugs
What are three methods of neurotransmitter removal?
reuptake, diffusion, enzymatic destruction
Morphine metabolism:
Sig. 1st pass, excreted as an active metabolite.
30% bound to plasma proteins.
Opioid Analgesic dosing
IV, epidural, and intrathecal = acute pain.
Oral = most common in chronic pain. (oral is preferred when effective)
Opioid Analgesic frequency
Acute pain= PRN
chronic pain= around the clock
no prolonged dosage except for malignancy..stop orders usually = 48-72 hrs.
Treatment of opiate withdrawal:
1) give tapering doses of opiate.
2) give a long-acting opiate (Methadone) and taper off.
3) give Clonidine (anit-HTN)--=<norepinephrine release, and less sx.
What are opioid agonists/antagonists?
Have potent analgesic effects w/out high abuse potential due to antagonistic activity.
*may= withdrawal in dependent ppl.*
use of opioid antagonists?
relieve CNS and Resp. depression from opioids ONLY--not other drugs.
Why is morphine often 1st drug used for pain?
it is a non-cceiling up. limit with tolerance.
Important teaching points on opioids:
*opioids are often combo-ed with acetaminophen drugs--watch for acet. OD.
*Stay in bed 30 min after op. injection.
Take w/6-8 oz H2O, avoid alcohol/depressant drugs, do not crush SR pills.
Opioids in clients w/renal disease:
Give in min. doses for shortest amt/ time.
Morphine = active metab. that can accumulate.
Meperidine= becomes CNS stimulant Normeperidine--seizures, psychosis--naloxone won't help.
Opioid therapeutic effects:
pain releif, sleeping, >ADLs, <episodes of non-productive cough, <BP, HR, RR, dyspnea; <diarrhea
Opioid adverse effects:
Resp. depression; Hypotension; excessive sedation; N/V, constipation
Drugs that increase opioid effects:
CNS depressants
Anticholinergics (>constipation)
Anti-HTNs; MAO inhibs. (<detox, >CNS depress.)
Protease inhibs, Cimetidine
Drugs that decrease opioid effects:
opioid antagonists
Butorphanol, nalbuphine (analgesics that weakly interact w/opioids)
Functions of COX-1 enzymes:
Makes prostaglandins that up GI mucus, lower gastric acid, regulate renal blood flow and function, control vascular tone, and platelet function.
Where is COX-1 found?
made continuously; found in all tissue types, esp. platelets, endothelial cells, GI, kidneys.
Where is COX-2 found?
Brain, bone, kidneys, GI, female repro. sys.
Thought to be made only in small amounts or only in response to inflammation/pain.
Contra's to aspirin:
GI disorders, renal disease, children,pregnant women, HX of hypersensitivity, chronic ETOH abuse.
Lower doses for low serum albumin.
Contr's to celecoxib (Celebrex):
hx/ peptic ulcers (celecoxib = selective COX-2 inhibitor)
allergies to sulfonamides.
metabolism of acetaminophen:
4% becomes a toxic metabolite. This must be conjugated w/glutathione and excreted in urine.
Alcohol abuse causes enzyme induction--drug is metabolized quicker than glutathione is made;=toxicity)
What are the two categories of migraine meds?
Those that prevent migraines and those that treat the pain.
What common drug increases most NSAIDs actions?
How do the migraine meds triptans work?
Selective Serotonin 5-HT1 receptor agonists--increase serotonin in brain, causing vasoconstriction.
What are maximum single and daily doses of APAP?
single dose= 1000 mg
daily max= 4000mg
alcoholic daily max= 2000mg
AEs of analgesic/anti-pyretic/anti-inflam./antigout meds:
GI probs, bleeding probs, bone marrow depression(colchicine), CNS effects, rashes, dermatitis, hypersens. reactions, tinnitus(classic sgn of aspirin OD),blurred vision, nephrotoxicity, CV effects, hepatotoxicity.
Drugs that increase aspirin/NSAIDs:
acidifying agents (>excretion); ETOH; anticoagulants; opioids; corticosteroids (>GI upset)
Drugs that decrease effects of aspirin/NSAIDs:
alkanizing agents (<excretion); Misoprostol (Cytotec)--a prostaglandin used to prevent gastric ulcers from these meds
Drugs that decrease the effect of antigout meds:
alkanizing agents (good--prevent stone formation as acid is excreted)
colchine, diuretics, salicylates
What drugs should never be taken w/triptans?
MAOIs-->serum triptan levels
Ergots--severe HTN/stroke can occur