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45 Cards in this Set

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  • Back
Are there any neurphysio or chem tests to measure pain?
NSAIDs act at what level of pain pathway?
Transduction at peripheral nociceptors
Antidepressants act at what level of pain pathway?
Act on descending pathway to MODULATE pain perception
Pain impulses travel from the spinal cord to brain via the ___. What part of the brain is pain transmitted to which results in the emotional response to pain?
1. STT
2. Limbic system
What are the 2 major types of pain?
Nociceptive pain (from tissue damage) and neuropathic pain (from nerve damage)
What is the main problem with leaving pain untxed? Is it better to tx chronic pain PRN or on a regular basis?
Is it realistic that chronic pain will resolve 100%?
Pain begets pain via central sensitization.
Better to tx pain on a regular basis, PRN not good management, also give prophylactic tx for SE
- chronic pain will not resolve 100%, should instead try to see functional improvement
- Difference between true addicts and pseudo addicts?
- pseudoaddicts will stop wanting opioids after they get functional improvement whereas true addicts dont ever stop wanting
1. What meds should pts w/ mild pain from 0-3 be given?
2. For moderate pain (4-6) what meds should be given, or if mild pain persists?
3. For severe pain (7-10) what dosing?
1. Start w/ non opioid (NSAID, ASA, or APAP), =/- adjuvant
2. Add opioid, for bone pain opioid w/ NSAID, for neuropathic pain-- antidepressant+opioid
3. increase opioid potency and continue non opioid potency. Dose regularly
What meds are included in the non-opioid analgesic class of pain meds and do these meds have ceiling effect?
Do opioids have ceiling effect for analgesia?
- yes all have ceiling effect for analgesic effectiveness
- no opioids do not have ceiling effect but SE (esp resp depression will limit use)
Most non opioid anlagesics inhibit the activity of what? Why?

Does tolerance develop to non steroid analgesics
PGs b/c PG sensitize pain receptors to both mechanical and chem stimuli and modulate inflammation.

No, tolerance does not develop to the analgesic effect, often combined w/ opioids for additive/synergistic effects
- blocks PG synthesis in CNS but does not work on peripheral PGs
- has great GI tolerability
- less effective for pain w/ inflammation--i.e. RA
Tox: very NTI, hepatic toxicity at high doses (>3250 mg/day)
Precautions in pts w/ reduced glutathione, malnutrition, alcohol drinks
What is the tx for OD of APAP?
Mucomyst- acetylcysteine which resores hepatic glutathione
A small amt of APAP is metabilized by CCYP450 to NAPQI which has what effect on liver? What enzyme is involved in this process?
1. hepatotoxic
2. glutathione binds napqi and allows excretion (when OD glutathione is depleted)
- mild to moderate pain, additive analgesic effect w/ opioids, recommended for OA
- esp for pts w/ ASA allergy, txed w/ warfarin/glucocorticoids, upper GI sensitivity to NSAIDs, bleeding disorder, and for children
- PGE2 sensitizes nocicceptors by facillitating influx of Na+ and K+ efflux. NSAIDs stop conversion of ARA to PGE2
- difference in various drugs of NSAIDs b/c diff cox enzymes and diff types of PGs
1. pain
2. inflammation
3. inhibits plt aggregation
NSAIDs- AE, Risk factors
AE: GI bleeding via NSAIDs by ALL rts not just oral, diarrhea, minor dyspepsia, reversible plt inhibition, renal SE, hypersensitivity rxns- in asthmatics especially
Risk factors: pts > 60 yo, long NSAID use, cig smoking, xs alcohol us, multiple NSAID use, concomitant use of corticosteroids or anticoagulants
If pt begins to have GI bleed from NSAID what is the tx?
- stop the NSAID, add PPI, and add misoprostol (PGE1 analog)
NSAIDs- Use, difference from ASA?
- RA, OA, other bone pain from tumor metastases, pain from inflammation, post op pain, dental pain, dysmenorrhea, acute gout, fever, migraine HA. Preferred to ASA b/c less GI irritation, better anti inflam, and less freq dosing
- PUD, renal failure (b.c inhibits PGE2 which will cause vasodilation and increase RBF), CHF, NSAID induced asthma-- b/c of LT-- bronchoconstriction
- highly protein bound drugs-- warfarin, sulfonyureas, and anticonvulsants, Li (causes dec renal clearance) and decreases efficacy of diuretics
Does minor dyspepsia w/ NSAID use correspond to GI bleed?
No, often serious bleeds occur w/o warning
Which classes of NSAIDs have high analgesic actions?
- propionic acids (ibuprofen, ketoprofen, and naproxen)
- acetic acids (etodolac, ketorolac)
Ibuprofen- potency compared to ASA or APAP, GI compared to ASA
- is ibuprofen a good anti inflam?
- more potent that ASA or APAP, sig less GI effects compared to ASA
- Ibuprofen is not a good anti inflam
Naproxen- anti inflam compared to Ibuprofen?
- onset?
- better anti inflam
- longer t 1/2
- more RAPID onset
Etodolac- Onset, potency, use, GI profile
- VERY rapid onset
- more potent analgesic than ibuprofen
- better GI SE profile than other NSAIDs
Ketorolac- PK, Tox, Use
PK: ONLY NSAID --injectable
Tox: nephrotoxicity, GI toxicity- BLACK box warning limits use to 5 days
Use: for moderate to severe pain- post op, useful if opioids are CI
Which NSAIDs are used for anti-inflam action?
- propionic acids (oxaprozin), oxicams (piroxicam), acetic acids (nabumetone, sulindac)
Oxaprozin- Class, PK, Use,
Piroxicam- Class, PK, Use
Use- BOTH should not be used for short term pain management, both good for RA
PK: BOTH have LONG half lives- so requires about 2 weeks to reach steady state
Class- Oxaprozin- propionic acid
- piroxicam- oxicam
Diclofenac Voltaren Gel and Flector patch- Use
- modestly effective for jt pain, and minor strains-- will have to use A LOT
What is the triad ass w/ NSAID induced GI damage?
Which are the high risk NSAIDs?
Which are the low risk NSAIDs?
- perforated ulcers, gastric outlet obstruction, and bleeding
- piroxicam, indomethicin, ketorolac
- Nabumetone, and etodolac
Which drugs are used to protect form NSAID induced GI damage?
- misoprostol- PGe1 analog BUT CI IN PREGNANCY (even in women of child bearing age)
- PPI-omeprazole-DOC
COX 2 inhibitors- MOA
- why was it formulated?
- selective inhibition of COX 2 so that PGE2 is not made but PGE1 is (which will maintain gastric mucosa)
What is the main problem w/ COX 2 inhibitors?
Cox 1 promotes plt aggregation while BOTH COX 1 and COX 2 inhibit plt aggregation. So w/ COX 2 inhibited there is net pro thrombotic effect-- which makes for CV problems
COX 2 inhibitors- Precautions
- hypersensitivity-- avoids in pts w/ sulfonamide allergy, for pts w/ hx of asthma or allergic rxns to ASA or NSAIDs
- renal SE-- may lead to renal failure as w/ the non sel NSAIDs
- avoid in pts w/ cardiac risk factors
COX- 2 inhibitor- USE
- no advantage in pts w/ low GI risk
- in pts w/ high GI risk -- can use trad NSAID w/ PPI
- use w/ ASA to reduce CV effects is useless b/c ASA will cause the GI SE that COX 2 was meant to stop
Tramadol- MOA
- dual mech of action
- weak centrally acting opioid agonist at mu receptor
- inhibits re-uptake of NE and serotonin- modulates pain reception in descending inhibitory neurons
Tramodol- AE, CI
- milder opioid type effects- resp depression, low potential for addiction, constipation
- risk of seizures
- possible serotonin syndrom
CI- if pt is taking other drugs that change serotonin availability-- antidepressant, if pt has prior hx of seizures
Tramadol- Use
- moderate to moderately severe pain (not as effective as potent opioids)
- alt for pt w/ hx of PUD, renal insufficiency
- effective for both neuropathic and non neuropathic pain
Neuropathic pain charachterized by tingling, numbing, burning pain to stimuli that are not usually painful can be txed w/ ____
1. antidepressants
What are imp chronic pain mediators in the inhibtory descending pathway?
What tx can be used for pts w/ neuropathic pain problems?
- NE and serotonin
- TCAs (amitriptyline, nortryptiline) which inhibit nociceptive signals via descending inhibitor signals
Amitryptiline- Class, Use, SE
Class; TCA
Use: fibromyalgia, neuropathic pain (postherpatic neuralfia, nerve injury or infiltration w/ cancer, and diabetic neuropathy), prevention of migraine
- Anti cholinergic SE
Amitryptilline, nortriptyline- Dose, Class
- start w/ low dose, the analgesic dose is MUCH lower than the anti depressant dose
Class: TCAs
Name some other adjuvant analgesics-
1. anticonvulsants- suppress ectopic neuronal firing and create memb stabilization- dec pain impulses
2. antihistamines- may add to opiate induced analgesia and reduce N & V
3. caffiene- enhances analgesic effects of APAP, ASA, or ibuprofen
4. corticosteroids- reduce inflammation around effected nerves
5. topical -- capsacin- which will use up the substance P available
- transdermal lidocaine- useful in neuropathic pain