Non Opioid Analgesics

Front 1

Are there any neurphysio or chem tests to measure pain?

Back 1

No

Front 2

NSAIDs act at what level of pain pathway?

Back 2

Transduction at peripheral nociceptors

Front 3

Antidepressants act at what level of pain pathway?

Back 3

Act on descending pathway to MODULATE pain perception

Front 4

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?

Back 4

1. STT
2. Limbic system

Front 5

What are the 2 major types of pain?

Back 5

Nociceptive pain (from tissue damage) and neuropathic pain (from nerve damage)

Front 6

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%?

Back 6

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

Front 7

- Difference between true addicts and pseudo addicts?

Back 7

- pseudoaddicts will stop wanting opioids after they get functional improvement whereas true addicts dont ever stop wanting

Front 8

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?

Back 8

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

Front 9

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?

Back 9

ASA, APAP, NSAIDs
- yes all have ceiling effect for analgesic effectiveness
- no opioids do not have ceiling effect but SE (esp resp depression will limit use)

Front 10

Most non opioid anlagesics inhibit the activity of what? Why?

Does tolerance develop to non steroid analgesics

Back 10

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

Front 11

APAP-MOA

Back 11

- 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

Front 12

APAP- Tox, SE

Back 12

Tox: very NTI, hepatic toxicity at high doses (>3250 mg/day)
Precautions in pts w/ reduced glutathione, malnutrition, alcohol drinks

Front 13

What is the tx for OD of APAP?

Back 13

Mucomyst- acetylcysteine which resores hepatic glutathione

Front 14

A small amt of APAP is metabilized by CCYP450 to NAPQI which has what effect on liver? What enzyme is involved in this process?

Back 14

1. hepatotoxic
2. glutathione binds napqi and allows excretion (when OD glutathione is depleted)

Front 15

APAP- Use

Back 15

- 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

Front 16

NSAIDs- MOA

Back 16

- 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

Front 17

PGE2-?
PGF2-?
PGI2-?

Back 17

1. pain
2. inflammation
3. inhibits plt aggregation

Front 18

NSAIDs- AE, Risk factors

Back 18

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

Front 19

If pt begins to have GI bleed from NSAID what is the tx?

Back 19

- stop the NSAID, add PPI, and add misoprostol (PGE1 analog)

Front 20

NSAIDs- Use, difference from ASA?

Back 20

- 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

Front 21

NSAIDs- CI

Back 21

- PUD, renal failure (b.c inhibits PGE2 which will cause vasodilation and increase RBF), CHF, NSAID induced asthma-- b/c of LT-- bronchoconstriction

Front 22

NSAIDs- DI

Back 22

- highly protein bound drugs-- warfarin, sulfonyureas, and anticonvulsants, Li (causes dec renal clearance) and decreases efficacy of diuretics

Front 23

Does minor dyspepsia w/ NSAID use correspond to GI bleed?

Back 23

No, often serious bleeds occur w/o warning

Front 24

Which classes of NSAIDs have high analgesic actions?

Back 24

- propionic acids (ibuprofen, ketoprofen, and naproxen)
- acetic acids (etodolac, ketorolac)

Front 25

Ibuprofen- potency compared to ASA or APAP, GI compared to ASA
- is ibuprofen a good anti inflam?

Back 25

- more potent that ASA or APAP, sig less GI effects compared to ASA
- Ibuprofen is not a good anti inflam

Front 26

Naproxen- anti inflam compared to Ibuprofen?
- onset?

Back 26

- better anti inflam
- longer t 1/2
- more RAPID onset

Front 27

Etodolac- Onset, potency, use, GI profile

Back 27

- VERY rapid onset
- more potent analgesic than ibuprofen
- better GI SE profile than other NSAIDs

Front 28

Ketorolac- PK, Tox, Use

Back 28

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

Front 29

Which NSAIDs are used for anti-inflam action?

Back 29

- propionic acids (oxaprozin), oxicams (piroxicam), acetic acids (nabumetone, sulindac)

Front 30

Oxaprozin- Class, PK, Use,
Piroxicam- Class, PK, Use

Back 30

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

Front 31

Diclofenac Voltaren Gel and Flector patch- Use

Back 31

- TOPICAL NSAIDs
- modestly effective for jt pain, and minor strains-- will have to use A LOT

Front 32

What is the triad ass w/ NSAID induced GI damage?
Which are the high risk NSAIDs?
Which are the low risk NSAIDs?

Back 32

- perforated ulcers, gastric outlet obstruction, and bleeding
- piroxicam, indomethicin, ketorolac
- Nabumetone, and etodolac

Front 33

Which drugs are used to protect form NSAID induced GI damage?

Back 33

- misoprostol- PGe1 analog BUT CI IN PREGNANCY (even in women of child bearing age)
- PPI-omeprazole-DOC

Front 34

COX 2 inhibitors- MOA
- why was it formulated?

Back 34

- selective inhibition of COX 2 so that PGE2 is not made but PGE1 is (which will maintain gastric mucosa)

Front 35

What is the main problem w/ COX 2 inhibitors?

Back 35

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

Front 36

COX 2 inhibitors- Precautions

Back 36

- 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

Front 37

COX- 2 inhibitor- USE

Back 37

- 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

Front 38

Tramadol- MOA

Back 38

- 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

Front 39

Tramodol- AE, CI

Back 39

- 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

Front 40

Tramadol- Use

Back 40

- 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

Front 41

Neuropathic pain charachterized by tingling, numbing, burning pain to stimuli that are not usually painful can be txed w/ ____

Back 41

1. antidepressants

Front 42

What are imp chronic pain mediators in the inhibtory descending pathway?
What tx can be used for pts w/ neuropathic pain problems?

Back 42

- NE and serotonin
- TCAs (amitriptyline, nortryptiline) which inhibit nociceptive signals via descending inhibitor signals

Front 43

Amitryptiline- Class, Use, SE

Back 43

Class; TCA
Use: fibromyalgia, neuropathic pain (postherpatic neuralfia, nerve injury or infiltration w/ cancer, and diabetic neuropathy), prevention of migraine
- Anti cholinergic SE

Front 44

Amitryptilline, nortriptyline- Dose, Class

Back 44

- start w/ low dose, the analgesic dose is MUCH lower than the anti depressant dose
Class: TCAs

Front 45

Name some other adjuvant analgesics-

Back 45

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