Non opiates 1 Flashcards

1
Q

name a type of nociceptive pain and how you would treat first line

A

osteoarthritis, burns - acetaminophen

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2
Q

name a type of inflammatory pain and how you would treat first line

A

osteoarthritis, RA - NSAIDs

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3
Q

name a type of neuropathic pain and how you would treat first line

A

diabetic neuropathy, postherpetic neuralgia - antidepressants

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4
Q

name a type of functinoal pain and how you would treat first line

A

fibromyalgia, tension headaches - non-opiates

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5
Q

what is backup therapy for any type of pain?

A

opiates

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6
Q

MOA fo acetaminophen

A

blocks NMDA binding to a glutamate receptor

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7
Q

do opiates generally have a ceiling dose?

A

no

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8
Q

what is acetaminophen used for?

A

treatment of mild to moderate pain and fever

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9
Q

which is better for inflammation: ASA or acetaminophen

A

ASA

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10
Q

If a pt is taking a lot of combos with acetaminophen, are you worried about toxicity?

A

yes

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11
Q

describe the kinetics of acetaminophen

A

excellent absorption, uniform distribution, near complete elimination via the kidney

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12
Q

does acetaminophen need renally adjusted

A

nope

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13
Q

how is acetaminophen excreted?

A

relys on glucuronidation in the liver

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14
Q

ADR of acetaminophen

A

rash is possible, no other problems really

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15
Q

how does acetaminophen cause an overdose?

A

NAPQ1 normally binds to glutathione and now goes to other cells and kills them

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16
Q

how long do you have after acetaminophen toxicity to administer acetylcysteine?

A

4 hours

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17
Q

Describe stage 1 acetaminophen toxicity

A

first 24 hours; anorexia, n/v, malaise, hypokalemia

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18
Q

describe stage 2 acetaminophen toxicity

A

days 2-3; better anorexia, n/v, get abdominal pain, hepatic tenderness, elevated transaminases, elevated bilirubin and prolonged PT

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19
Q

describe stage 3 acetaminophen toxicity

A

days 3-4; anorexia, n/v, encephalopathy, anuria, jaundice, hepatic failure, metabolic acidosis, coaguloathy, renal failure, pancreatitis

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20
Q

describe stage 4 acetaminophen toxicity

A

day 5; clinical improvement and recovert or MSOF and death

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21
Q

90% mortality rate with this much acetaminophen

A

300mcg/ml

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22
Q

max dose of acetaminophen

A

4g/day

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23
Q

what does acetylcysteine smell like

A

sulfur

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24
Q

why is IV preparation of acetylcysteine better than oral

A

oral needs 17 doses, lasts 72 hours (good), need to mix with a drink and drink with a straw

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25
Q

fatal dose of acetaminophen

A

20-25g

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26
Q

how many tabs is 10-15g of tylenol

A

20-30tabs

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27
Q

what are the NSAID categories

A

propionic acids, acetic acids, enolic acid, fenamic acid, naphthylakanones, diaryl heterocyclic compounds

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28
Q

name the propionic acids

A

ibuprofen, flurbiprofen, naproxen, ketoprofen

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29
Q

name the acetic acids

A

indomethacin, diclofenac, sulindac, ketorolac

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30
Q

name the enolic acids

A

piroxicam, meloxicam

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31
Q

name the fenamic acids

A

mefenamic acid, meclofenamic acid

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32
Q

name the naphthylakanone

A

nabumetone

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33
Q

came the diaryl heterocyclic compounds

A

celecoxib

34
Q

what is the only injectable NSAID

A

ketorolac

35
Q

uses for nabumetone

A

arthritis pain - not severe

36
Q

MOA of NSAIDs

A

block Cox1 (maintenance) and cox2 (antiinflammatory)

37
Q

ceiling dose of NSAIDs per day

A

2400mg/day

38
Q

are NSAIDs toxic to the GI system?

A

1-2% rate of upper gI complications

39
Q

uses for ibuprofen

A

relief of fever, OA, mild-moderate pain, rheumatoid disorders

40
Q

uses for naproxen

A

gout, mild-moderate pain, OA, rheumatologic disorders

41
Q

uses for ketorolac

A

short term (5 days or less) management of moderate to severe pain requiring analgesia at the opiate level

42
Q

what should be given to a pt if they require opiates but have an allergy?

A

ketorolac 10-15mg

43
Q

ADR of ketorolac

A

acute psychotic rxn with 30mg (can also happen with advil in large doses)

44
Q

time to peak effect of NSAIDs

A

2-3 hours after

45
Q

are NSAIDs strongly or weakly bound to proteins?

A

strongly - 99% are bound to albumin

46
Q

t1/2 of ibuprofen

A

1-4 hours

47
Q

t1/2 of peroxicam

A

50 hours

48
Q

describe the kinetics of NSAIDs

A

rapidly absorbed, widely distributed, hepatic biotransformatino and renal elimination

49
Q

ADR of NSAIDs

A

GI, platelets, renal, CV, CNS, uterus (prolongatino of pregnancy), hypersensitivity

50
Q

what are the effects of cox2 on cardiac dysfunctino

A

increases mortality

51
Q

benefits of using celebrex

A

lower GI toxicity

52
Q

indications for celebrex

A

pain management, OA pian, RA

53
Q

what is celebrex a derivativ of?

A

sulfa

54
Q

what was the first tolerable systemic analgesic

A

Aspirin

55
Q

what is the 8th NSAID category?

A

salicylates

56
Q

name the salicylates

A

aspirin, magnesium salicylate, choline magnesium trisalicylate, salsalate, diflunisal

57
Q

which salicylate derivative doesn’t metabolize to salicylic acid in vivo

A

diflunisal

58
Q

which analgesic is 3-4x more potent than aspirin

A

diflunisal

59
Q

what schedule are opiates?

A

schedule II

60
Q

what are the mu receptor agonists?

A

opiates

61
Q

why are mu receptor agonists at a lower risk of dependence than other opiates?

A

lower affinity of parent compound for mu opiate receptor site

62
Q

what are immediate release mu receptor agonists used for?

A

manangement of moderate to moderately severe pain in adults

63
Q

what are extended release mu receptor agonists used for?

A

management of moderate to moderately severe chronic pain in adults who require around the clock treatment of pain for an extended period of time

64
Q

when are mu receptor agonists dosed renally?

A

CrCl below 30ml/minm also required in hepatic impairment

65
Q

how iare mu receptor agonists metabolised?

A

3A4

66
Q

drug interactions with mu receptor agonists

A

CYP3A4 inhibitors or inducers (may alter tramadol levels), trmamadol may enhance effects of SSRIs causing serotonin syndrome

67
Q

who has a lower chance of ADR with mu receptor agonists?

A

older pts

68
Q

max dose of tramadol

A

400mg/day (>65 y/o then 300mg/day)

69
Q

what are the mixed agonists/antagonists?

A

buprenorphine, butorphanol, nalbuphine, pentazocine

70
Q

what drug is a strong antagonist of kappa receptors?

A

nalbuphine

71
Q

Is nalbuphine a mu receptor agonist or antagonist?

A

antagonist

72
Q

what is nalbuphine structurally related to?

A

oxymorphone and naloxone

73
Q

what are benefits of using nalbuphine?

A

less likely to cause dysphoria (like pentazocine), less likely to cause cardiac problems (like pentazocine and butorphanol), 1:1 ratio to morphine, not a controlled substance

74
Q

route of administration options for nalbuphine

A

SC, IM, IV

75
Q

what is buprenorphine a derivative of?

A

thebaine

76
Q

how much more potent is buprenorphine than morpphine?

A

25-50X, longer DOA, longer dissociation times from opioid receptors

77
Q

is buprenorphine a controlled substance?

A

yes, C-III

78
Q

if buprenorphine-related respiratory depression is in place, is naloxone useful?

A

no

79
Q

ROA for buprenorphine

A

injection, transdermal for moderate to severe pain relief

80
Q

ADR of mized agonists/antagonists

A

CNS (sedation, drowsiness, dizziness, n/v), respiratory depression

81
Q

with which drug is respiratory depression more noted: nalbuphine or buprenorphine

A

buprenorphine