Pain Flashcards by Britney N

APAP mechanism of action and is best for what type of pain?
Ex?
SE/interaction

inhibit prostaglandin synthesis in CNS and block pain impulses in periphery for mild-mod pain. Usually initial therapy in most instances

Ex: low back pain and osteoarthritis

SE: liver so reduced x50-75% in renal/liver disease or ETOH intake

interact= warfarin if > 2000mg/day APAP

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aspirin mechanism of action and is best for what type of pain?
Ex?
SE/interaction

inhibit COX-1/COX-2 preventing prostaglandin synthesis
mild-mod pain

SE- GI irritation/bleeding limits use.

Hypersensitivity (asthma, nasal polyps, chronic urticaria at increased risk)
cross-sensitivity of other NSAIDs

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NSAIDs mechanism of action and is best for what type of pain?
Ex of meds & conditions?
SE

inhibit COX-1/COX-2 preventing prostaglandin synthesis
mild-mod pain.
ibuprofen, ketorolac

Ex:
** Preferred for pain mediated by prostaglandins **
RA, menstrual cramps, post-surgical pain, bony metastasis. NOT used in neuropathic pain

SE: flat-dose response curve (higher doses no greater efficacy) but increase SE. GI (PUD, bleeding, hepatic, renal, platelet, Na retention, CNS dysfunction

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NSAID contraindication/pt at increased risk of SE

increased risk GI: elderly, PUD, coagulopathy, high dose steroids

nephrotoxicity in elderly & Cr clearance < 50mL/min or those on diuretics

CAUTION w/ reduced cardiac output d/t Na retention & pt on antihypertensives, warfarin, lithium

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COX-1 and COX-2 effects

COX-1: contributes to GI/renal toxicity
COX-2: anti-inflammatory

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Concern w/ NSAID and aspirin

NSAID reduce cardioprotective effect of aspirin d/t compete in inhibition of COX-1

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opioids for mod pain

codeine, hydrocodone, tramadol, partial agonists

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opioids for severe pain

morphine & hydromorphone

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ex pure opioid agonist and benefit

morphine
analgesia increases w/ doses and doesn’t provide ceiling effect

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partial opioid agonists benefit/faults & ex

less conformational change & receptor activation
when dose increases, analgesia will plateau so increases will not provide additional relief but will increase SE
ex: burprenorphine, butorphanol, tramodol

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opioids to avoid/decreased metabolism or clearance in hepatic disease

methadone, meperidine, pentazocine

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meperidine/Normeperidine SE and who should AVOID

normeperidine (metabolite) can= tremors, myoclonus, delirium, seizures
AVOID in elderly, renal impair, PCA device, or > 1-2 days intermittent dosing

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methadone mechanism of action, SE/concerns

several mechanisms: U agonist, NMDA agonist, inhibit reuptake serotonin & norepinephrine
long half life x30 hours = longer dosing intervals

concern w/ accumulation w/ repeated dose= challenging dose conversion, concern w/ respiratory depression
arrhythmia d/t prolonged QT

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tramadol mechanism of action & similar efficacy to what drug? Tx what type of pain?
contraindication?!

U agonist & inhibit serotonin & norepinephrine
similar to codeine/APAP

pain= neuropathic & chronic

INCREASE RISK OF SEIZURE; contraindicated in seizure disorder, increased risk, w/ drugs lower seizure threshold
AVOID w/ SSRI= serotonin syndrome

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nociplastic pain and ex

pain sensitivity d/t abnormal processing or functioning of CNS in response to NORMAL stimuli
ex: fibromyalgia and IBS

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what fibers produce first, fast, sharp pain after nociceptor activation

A8-fibers

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what fibers produce second pain described as dull, aching, burning, and diffuse after nociceptor activation

C-fibers

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theory behind counterirritants & tanscutaneous electrical nerve stimulation (TENS) in pain management

brain can only process limited number of signals at one time so other sensory stimuli can alter pain perception

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allodynia

pain from stimulus that normally doesn’t cause pain like light touch in neuropathic pain

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acute pain should be treated aggressively before dx established EXCEPT in what conditions?

head or abdominal injury where pain might assist in differential diagnosis

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mild, mod, severe on pain scale

1-3 mild
4-6 moderate
7-10 severe

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how much to reduce APAP dose in renal/hepatic dysfunction

50-75%

max APAP daily dose normal and elderly

normally= 4000mg/day
elderly= 3000mg/day

ketorolac

NSAID
oral & parenteral dosage forms
limit use to 5 days d/t risk of serious GI SE

What does flat-dose response curve mean with NSAIDs

higher doses produce no greater efficacy than moderate doses by result in increased adverse effects

what receptor does pure opioid agonist bind to

u receptors to produce analgesia that increases with dose without a ceiling effect

example of partial opioid agonists at u receptor

buprenorphine, butorphanol, tramadol

partial opioid agonists with high affinity for k receptors & most likely SE

pentazocine, nalbuphine, butorphanol more likely to cause psychomimetic effects (as hallucinations or paranoid delusions)

opioids to avoid in renal disease d/t decreased clearance

meperidine and morphine

serotonin syndrome

Agitation or restlessness Insomnia Confusion Rapid heart rate and high blood pressure Dilated pupils Loss of muscle coordination or twitching muscles High blood pressure Muscle rigidity Heavy sweating Diarrhea Headache Shivering Goose bumps Severe serotonin syndrome can be life-threatening. Signs include: High fever Tremor Seizures Irregular heartbeat Unconsciousness

how to calculate dose of of iv morphine and usual starting dose morphine IV in opioid naive pts

10mg/70kg of body weight 5-10mg IV morphine every 4 hours

how to dose rescue doses

10% to 20% of total daily opioid requirement and should be every 2-6 hours PRN

how to increase opioid dose and when to switch to sustained release

based off pain; 50-100% or 30-50 % increase; some base it off number of rescue doses needed in 24 hours switch to sustained release if tx needed for more than a few days in CANCER related pain

what to reduce dose by when converting to sustained release of SAME ROUTE (oral to oral for ex)

reduce by 25% to avoid over sedation reduce by 25-50% to account for incomplete cross tolerance

first line tx for chronic pain

nonpharmacological tx and nonopioids

onset of oral opioids

45 mins

common opioids given via PCA pump & when commonly used

morphine, fentanyl, hydromorphone commonly used for postop and sometimes refractory chronic pain

when is epidural analgesia usually used

lower extremity procedures and pain

common SE of epidural analgesia and tx for it other SE

pruritis treated with naloxone other SE: respiratory depression, hypotension, urinary retention

what to do if using epidural analgesics on narcotic-dependent patients

systemic analgesics must be used to prevent withdrawal bc the opioid is not absorbed and remains in epidural space

dosing of epidural analgesia vs IV and intrathecal

epidural dosing 10 times LESS than IV dosing intrathecal 10 times LESS than epidural dosing ex: 10mg IV morphine = 1mg epidural morphine = 0.1mg intrathecal

most common analgesia in moderate pain

opioid and nonopioid combo

opioid allergy & drug selection with it

RARE and not to be confused with pruritus associated with opioids. Cross sensitivity unlikely so if allergic to drug in one chemical class of opioids, can select another agent in another chemical class ***drug selection= mixed agonists/antagonists should be treated as morphine line agents***

how and when to taper off opioids

pain resolved, ssx SUD, lack of improvement of pain, > 50 MME/day, overdose, early sign of overdose reduce by 10% per week

Patients with CYP450 pharmacogenetic variations & what opioids are substrates of it

may respond differently to opioids ranging from unresponsiveness > toxicity codeine, hydrocodone, morphine, methadone, oxycodone are substrates of CYP450

what two meds affect metabolism of methadone d/t CYP3A4

increased by phenytoin decreased by cimetidine

first line tx for neuropathic pain

gabapentin or pregabalin, lidocaine TD, or TCAs

other options for neuropathic pain

SNRIs duloxetine & venlafaxine has been successful for diabetes peripherally neuropathy

tx for central neuropathic pain

baclofen or clonidine

what kind of pain C-fibers cause

transmission of chronic pain

What stimulates nociceptors

Nociceptors may be stimulated by mechanical, chemical, or thermal stimuli.

What do A-fibers transmit

A-fibers are responsible for the transmission of acute, sharp pain.

where does modulation of pain occur

Modulation of pain impulses may occur in the dorsal horn, the brain, and the descending (efferent) system.