Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

*Pharm > Non-opioid analgesics > Flashcards

Non-opioid analgesics Flashcards

1
Q

non-opioids are used for

A

-first line to trx mild to mod pain

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

describe ceiling effect of non-opioids

A
  • ASA and APAP b/n 650-1300 mg
  • ceiling effect = inc toxicity w/ no inc benefit
  • can go higher w/ NSAIDs than ASA
  • no tolerance development
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

How does APAP work?

A
  • antipyretic
  • blocks NMDAR in CNS and Sub P mediation in spinal cord to reduce pain
  • no peripheral/inflammatory action
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is APAP good to trx?

A
  • PUD/GI bleed
  • Peds
  • pts w/ abnormal platelets
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the dosing for APAP?

A
  • po = 325-650 mg Q4hrs
  • IV = 1gm over 15 min Q6 hrs
  • max 4gm in 24 hours (even lower in ETOH abuse pts)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Describe differences in peak times for IV/PO APAP

A
  • IV peaks in 15 mins
  • po peak in 30-45 mins
  • *for IV tylenol give it at the end of the case when you are about to wake pt up.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

How does APAP overdose cause fatal hepatic injury?

A

-glutathione metabolizes hepatotoxic metabolite in liver but when it is outnumbered then injury occurs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What other medication inc risk of toxicity with APAP?

A

INH for TB

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the antidote for APAP toxicity?

A
  • acetylcysteine - precursor to glutathione

- effective if given w/in 8 hrs of OD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Describe rental toxicity w/ APAP

A

-renal accumulation of metabolites can cause necrosis but NSAIDs are more toxic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Describe arachidonic acid metabolism and NSAIDs/COX

A
  • w/ inflammation phospholipid membrane releases phospholipase A which releases AA which ism metabolized by 3 enzyme pathways:
    1. CYCLOXYGENASE (PGs, etc), 2. LIPOXYGENASE (leukotrienes), 3. EPOXYGENASE
  • NSAIDs inhibit COX pathway which dec PGs
  • all AA will then use LIPO pathway which results in inc leukotrienes
  • inc leukotrienes can be fatal for asthmatics so USE CAUTION - ask asthmatics if they tolerate NSAIDs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Describe how NSAIDs targeting COX pathways

A
  1. AA+COX1 = widespread PGs in GI, renal, platelets
  2. AA+COX2 = PGs respond to inflammation, pain fever
    NSAIDs used to block COX2 but also block COX1 resulting in dec pain/fever/inflam but also dec GI/renal/platelet protection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is ASA used for?

A
  • mild to mod pain, arthritis
  • antipyretic
  • MI/stroke prevention (anti-platelet)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

How is ASA diff from other NSAIDs?

A
  • IRREVERSIBLE inhibition of COX
  • 1 dose inhibits lifespan of a platelet (8-10 days); must be held 7 days pre-op
  • large doses can dec prothrombin
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

How does ASA affect kidneys?

A
  • ESRD have chronic anticoagulant tendencies so may want to avoid ASA d/t prolonged bleeding
  • ASA less issue for ESRD than other NSAIDs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

How does ASA affect liver?

A

-inc LFTs (reversible)

17
Q

What is the dosing for ASA for
analgesia/antipyretic
anti-inflammatory

A
  • 325-650 mg (same as APAP)

- 1000 mg (3-5g/day) - rarely used d/t GI bleeds, follow salicylate serum levels, inc gradually

18
Q

What does salicylate OD cause?

A
  • metabolic acidosis (salicylic acid)

- tinnitus

19
Q

How is ASA w/ children?

A

-DO NOT use w/ virus bc of reye’s syndrome

20
Q

What is NSAID MOA?

A

-COX inhibitor = block AA conversion to PGs = dec pain, inflammation, fever
(also ends up inhibiting protective COX1 functions)

21
Q

How do NSAIDs (except ASA) affect platelets?

A

REVERSIBLE inhibition of platelet aggregation (blocking COX1 = blocks platelets)

22
Q

What are the cautions w/ pregnancy and NSAIDs?

A
  • best avoided but category B if necessary

- avoid in 3rd trimester where it is category D d/t premature closure of ductus arteriosus

23
Q

What can NSAIDs do in peri-op period?

A

all d/t COX1 inhibition (kidney/gastric/platelets)

  • renal injury
  • gastric ulcer
  • bleeding
  • impaired bone healing
24
Q

What GI adverse effects for NSAIDs? Risk factors?

A
  • dyspepsia, GI bleed, PUD
  • inhibiting COX1 = inc acid, dec mucous, dec blood flow
  • risk factors = high dose, prolong use, previous GI bleed, excessive ETOH, elderly, CORTICOSTEROID USE
25
Q

Which NSAIDs are low GI risk?
Moderate GI risk?
High GI risk?

A
  • low = ibuprofen and naproxen at low doses, etodolac, sulindac, celecoxib
  • mod = ibuprofen and naproxen at mod-high doses, diclofenac, oxaprozin, meloxicam, nabumetone
  • high = [K.I.T.P.A.] tolmetin, piroxicam, ASA, indomethacin, ketorolac
26
Q

What renal adverse effects for NSAIDs? Risk factors?

A
  • dec PGE2 = dec flow, fluid/Na+ retention, ARF, HTN

- risk = old, CHF, HTN, DM, renal insuff, ascites, volume depletion, diuretic therapy

27
Q

Which NSAIDs are renal risk?

A
  • ALL NSAIDs can cause renal issues
  • highly potent COX inhibitors = ketorolac, indomethacin
  • renal sparing/low risk = sulindac, nabumetone, celecoxib
28
Q

NSAID drug interactions w/

  1. highly protein bound drugs
  2. diuretics/beta bockers/ace inhibitors
  3. lithium
  4. anti-coags
  5. probencid
  6. ketorolac
A
  1. inc levels of warfarin, phenytoin, sulfonylureas, sulfonamides, digoxin
  2. decrease effects d/t suppressed renal PGs
  3. inc levels
  4. inc GI bleed risk
  5. inc NSAID levels
  6. avoid w/
29
Q

What is the only IV NSAID?

What other drug is it comparable to?

A
  • ketorolac (toradol) -IM or IV

- morphine but w/o vent/CV depression

30
Q

What is ketorolac’s max length of use?
IV onset?
DOA?
e1/2t?

A
  • 5 days
  • 10 min
  • 6-8 hrs
  • 5 hrs (longer in elderly)
31
Q

What is the dose for ketorolac? max dose?

A

30 mg IV x1 or Q6H
max dose = 120 mg
w/ elderly cut dose in 1/2

32
Q

What is the only COX2 inhibitor?

How is pain relief compared to nonselective NSAIDs?

A
  • celecoxib (celebrex)

- same pain releif but w/o COX1 inhibition

33
Q

What are the renal effects of celebrex?

A

-same as nonselective NSAIDs bc COX2 inhibitor blocks vasodilation

34
Q

What is the black box warning for selective and non-se NSAIDs?

A

FATAL CV/GI risks

  • inc risk of MI/stroke
  • CABG surgeries need to be cleared for trx of peri op NSAID
  • inc risk of bleeding, ulcer, perf
35
Q

What can be used for adjuvant analgesics?

A

antidepressants
anticonvulsants
rx neurpathic pain syndromes

36
Q

Name some adjuvant antidepressants

A

-TCAs, venlafaxine, duloextine (cymbalta)

37
Q

Name some adjuvant anticonvulsants

A
  • gabapentin
  • pregabalin
  • carbamazepine (trigeminal neuralgia)
  • phenytoin (dilantin), sodium valproate (depakote), clonazepam (klonopin), topiramate (topomax)
  • lamitrogen (lamictal)
38
Q

Other adjuvabt analgesics

A

-hydroxyzine - low dose IV/IM analgesic effect w/ opioids to relieve cancer/post op pain w/ dec N/V
-corticosteroids
-topical analgesics:
5%lidocain/lidoderm
topical emla
capsaicin cream (neuropathic/osteroarthritic pain)
transdermal clonidine

*Pharm (6 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions