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Flashcards in Pain management Deck (93)
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1

How should you treat acute/temporary pain?

remove the cause, treat early, use least potent analgesic, properly titrate dose, and admin for adequate amt of time

2

What forms is acetaminophen available in?

oral, rectal

3

What is the MOA of acetaminophen?

weak COX-1/2 inhibitor, decreases pain but has no anti-inflammatory effects. is a anti-pyretic

4

What are the dosages of acetaminophen?

325-1000mg every 4-6 hours. max dose 4gm/day. onset 15-30 minutes

5

What are SE of acetaminophen?

large doses cause liver toxicity, lethality, dizziness, disorientation. Normal doses can cause renal damage

6

What is the MOA of aspirin (salicylic acid)?

irreversibly inhibits COX and inhibits platelet aggregration

7

What are the effects of aspirin on the body?

reduces mild/moderate pain thru its effects on inflammation. inhibits pain stimuli at subcortical site

8

What else besides pain is aspirin used for?

anti-pyretic, decrease thrombosis after CABG, long-term use reduces risk of colon cancer

9

What patient popn should not receive aspirin and why?

children under 12 yrs old to avoid the development of Reye's syndrome

10

What are the SE of aspirin?

GI upset/ulcers, hepatotoxicity, renal toxicity, asthma, rashes, salicylism, overdoses

11

Describe salicyclism

vomiting, tinnitus, decreased hearing and vertigo due to too high of aspirin dose. is reversible with reduced dose

12

What happens as a result of toxic levels of aspirin?

metabolic acidosis, respiratory depression, cardiotoxicity

13

What are indications of NSAIDS?

mild to moderate pain of somatic origin due to soft tissue injury, HA, arthritis. anti-pyretic (ibuprofen)

14

What is the MOA of NSAIDS?

inhibits cyclooxygenase, impairing the transformation of arachnidonic acid to prostaglandins, prostacyclins, and thromboxanes. nonselective inhibitors of COX-1/2

15

What are physiologic effects of prostaglandins?

activation of the inflammatory response, elicitation of pain/fever, contraction/relaxation of smooth muscle, inhibition of acid synthesis and increased secretion of stomach mucus, increased blood flow to kidneys

16

What are the GI SE of NSAIDS?

N/V, heartburn, ulcers/bleeding, diarrhea

17

What are the renal SE of NSAIDS?

Na and H2O retention, HTN, damaging if taken with other nephrotoxic drugs (ACE, diuretics)

18

What are the dosages for ibuprofen (advil/motrin)?

200/400 mg every 4 hrs. No more than 600mg every 6 hrs or 3200mg/day

19

What are the dosages for naproxen (aleve)?

250-500mg every 12 hrs. max daily dose 1000mg

20

What are the different chemical classes of prescription NSAIDS?

propionic acid derivatives, acetic acid derivatives, enolic acid derivatives, fenamic acid derivatives

21

What are some propionic acid derivatives?

ketoprofen (Orudis), naproxen

22

What are some acetic acid derivatives?

indomethacin, ketorolac (Toradol)

23

What are some enolic acid derivatives?

peroxicam (Feldine), meloxicam (Mobic)

24

What is a fenamic acid derivative?

mefanamic acid (Ponstel)

25

What are the benefits of NSAIDS that are selective COX-2 inhibitors?

as effective as other NSAIDS, less GI toxicity

26

What is the one COX-2 inhibitor and what is it used for?

Celecoxib (Celebrex), good for arthritis. onset is 3 hrs

27

Who is at risk for gastroduodenal toxicity with NSAID use?

age >65, use of anticoagulants, previous GI bleed, acute PUD, use of glucocorticoids

28

What are other considerations for NSAID use besides the risk of gastroduodenal activity?

take with food, give daily or BID instead of TID, know renal status and other meds

29

What are three indications for opioid use?

acute postop pain, severe pain, chronic pain

30

What is the MOA of opioids?

exert effects on Mu1/2, delta, kappa receptors that are widely distributed thruout the body