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Spring 15 - Pharm Unit I > Pain Management - Acute > Flashcards

Pain Management - Acute Flashcards

1
Q

WHO Pain Ladder Tx for Step 1

A
  • mild pain 1-3/10

- non opioid +-/ adjuvants

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2
Q

WHO Pain Ladder Tx for Step 2

A
  • mod pain 4-6/10

- weak opioid and non-opioid +/- adjuvants

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3
Q

WHO Pain Ladder Tx for Step 3

A
  • severe pain 7-10/10

- strong opioid + non-opioid +/- adjuvants

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4
Q

Acetaminophen/Tylenol Indication

A

-tx of mild to moderate pain

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5
Q

Acetaminophen/Tylenol MOA

A
  • analgesic: inhibit prostaglandin synthesis in CNS

- antipyretic: inhibits hypothalamic heat regulating center

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6
Q

Acetaminophen/Tylenol Usual Dose

A

325-650 mg q 4-6hr

  • max daily dose 4000 mg/day
  • max geri daily dose 3000 mg/day
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7
Q

Acetaminophen/Tylenol AEs

A
  • usually well-tolerated

- may cause hepatotoxicity, analgesic nephropathy, anemia, blood dyscrasias, rare skin rxns

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8
Q

Acetaminophen/Tylenol Hepatotoxicity Mechanism

A
  • small amount of APAP metabolized via CYP450 to hepatotoxic metabolite (NAPQI)
  • usually glutathione binds NAPQI to allow excretion
  • misuse/overdose uses up all the glutathione so NAPQI is not removed from body
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9
Q

NSAIDs MOA

A
  • AAA: analgesic, antipyretic, anti-inflammatory
  • NNSAIDs inhibit COX 1 and 2
  • PNSAIDs inhibit COX 2 more than COX 1
  • COX 2 only inhibits COX 2
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10
Q

NSAID Efficacy

A
  • most NNSAIDs are more effective than ASA or APAP

- some have greater analgesic effect than oral opioid combinations

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11
Q

NSAID AEs (general list)

A
  • GI
  • renal, hematologic, CV, hepatic
  • CNS: high doses can cause sedation/decreased cognition in older adults
  • skin: rare serious reactions like SJS or TEN
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12
Q

GI NSAID Mucosal Damage

A

-due to direct or topical irritation of gastric epithelium or systemic inhibition of prostaglandin synthesis

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13
Q

High Risk GI Patients (list the risk factors)

A
  • age > 60
  • prior PUD or GI bleed
  • high dose or more toxic NSAIDs
  • concurrent corticosteroid, bisphosphonate, or SSRI use
  • anticoagulant use, antiplatelet use (ASA, clopidogrel)
  • chronic illness (eg CV dz)
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14
Q

What NSAID is the least GI toxic? Which is most?

A
  • least celecoxib then ibuprofen

- most is ketorolac

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15
Q

NSAID Nephrotoxicity

A
  • NSAIDs decrease renal blood flow
  • interstitial nephritis, hyperkalemia, hyponatremia also reported

(toxicity is related to NSAID effects on renal prostaglandins that help increase renal blood flow)

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16
Q

Risk Factors for NSAID Nephrotoxicity

A
  • older age, HF, renal insufficiency
  • ascites, volume depletion, diuretic therapy

(basically anything that also will decrease renal blood flow)

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17
Q

Hematologic NSAID Toxicity

A
  • may prolong bleeding times due to anti-platelet effects
  • ASA inhibits platelet aggregation for platelet lifetime (7-10 days)
  • other NNSAIDs affect platelet aggregation to a lesser degree and only when drug is active in body
  • do not affect INR
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18
Q

Cardiovascular NSAID Toxicity

A
  • may increase CV risk
  • risk increases w/ higher dose, longer duration, and degree of COX-2 selectivity
  • NSAIDs may increase BP
  • avoid NSAIDs after MI indefinitely
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19
Q

NSAID Hepatotoxicity

A
  • no clear link between chemical structure and risk
  • histologic type of injury varies within/between chemical classes
  • no consistent MOI of liver from NSAIDs
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20
Q

Aspirin Indication

A
  • mild to moderate pain

- prevention of MI, CVA

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21
Q

Aspirin MOA

A
  • analgesic: same as N-NSAIDs

- antipyretic: inhibition of hypothalamic heat regulating center

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22
Q

Aspirin Usual Dose

A

325-650 mg q4 hours (max dose 5400 mg/day)

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23
Q

Aspirin AEs

A
  • platelet inhibition for life of platelet
  • ASA sensitivity (asthma, bronchospasm, angioedema) related to COX1 inhibition
  • Reye’s syndrome (esp kids with influenza or varicella)
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24
Q

AEs Nonacetylated (Salsalate, trisalicylate)

A
  • likely less GI toxicity than N-NSAIDs
  • no anti-platelet effects
  • occasional cross reactivity in ASA sensitive pts
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25
Q

What Med Should a Low GI/Low CV Risk Pt Get

A

-ibuprofen or other low GI risk NSAID (celecoxib)

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26
Q

What Med Should a Moderate GI/Low CV Risk Pt Get

A
  1. celecoxib alone
  2. NSAID + PPI or misoprostol
  3. NSAID + double dose H2 blocker
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27
Q

What Med Should a High GI/Low CV Risk Pt Get

A
  1. avoid NSAIDs if possible

2. celecoxib + PPI or misoprostol

28
Q

What Med Should a High CV/Low GI Risk Pt Get

A

-naproxen

29
Q

What Med Should a High CV/Moderate GI Risk Pt Get

A
  1. naproxen + PPI or misoprostol

2. naproxen + double dose H2 blocker

30
Q

What Med Should a High CV/High GI Risk Pt Get

A

avoid NSAIDs

31
Q

Opioid MOA

A

-stimulate opioid receptors in the CNS (mu, kappa, delta)

32
Q

Major Adverse Effects of Opioid Analgesics

A
  • dysphoria, euphoria
  • lethargy, drowsiness, apathy, inability to concentrate
  • nausea, vomiting, constipation
  • decreased resp rate
  • biliary spasm, urinary retention
  • urticaria, pruritus, asthma exacerbation
  • tolerance, dependence
33
Q

Most Common AEs of Opioids

A
  • drowsiness

- N/V/C

34
Q

Opioid Withdrawal Sxs

A
  • mild: rhinorrhea, lacrimation, excessive yawning, mild irritability, mild N/V
  • moderate: increasing irritability, tremors, abdominal cramps, anxiety, persistent N/V, increased HR/BP/hot or cold flashes/fever
35
Q

Opioid Agonists

A

maximal biologic response through binding to the opioid mu receptor

36
Q

Opioid Partial Agonists

A

submaximal response at the receptor even at high doses

37
Q

Opioid Agonist/Antagonist

A

divergent activities at different receptors:

  • analgesia ceiling
  • ceiling effect on respiratory depression
  • lower abuse potential
  • can precipitate withdrawal in pts who are dependent on full agonists
38
Q

Opioid Antagonist

A

reverse or inhibit the effects of agonists by preventing receptor access

use in event of overdose!

39
Q

What is opioid selection based upon?

A
  • severity and type of pain
  • duration of expected tx
  • duration of action necessary
  • route of administration
  • pt adherence
  • allergies or intolerances
  • concomitant medications
  • cost
40
Q

What opioid agonists can be used for moderate pain?

A
  • codeine or codeine/APAP (Tylenol 3)
  • hydrocodone or hydrocodone/APAP (vicodin)
  • oxycodone or oxy/APAP (percocet)
  • meperidine (Demerol)
  • tramadol (Ultram)
  • tapentadol
41
Q

Dose for Codeine/APAP (Tylenol 3)

A

1-2 PO q 4-6hr PRN (30/300 mg)

42
Q

Dose for Hydrocodone/APAP (Vicodin)

A

1-2 PO q4-6hr PRN (5/325 mg)

43
Q

Dose for Oxycodone/APAP (Percocet)

A

1-2 PO q4-6hr PRN (5/325 mg)

44
Q

What is a common side effect of codeine?

A

gastritis

45
Q

What is codeine metabolized to?

A

morphine

46
Q

Which moderate pain opioid has a black box warning and why?

A
  • oxycodone/APAP (Percocet)
  • CYP3A4 substrate –> if pt is on 3A4 inhibitors (eg erythro/clarithromycin, ketoconazole, protease inhibitors), it can lead to toxicity
47
Q

Why is use of meperidine discouraged?

A
  • metabolite (normeperidine) is a direct CNS irritant that causes seizures
  • do not use w/ MAOI –> life threatening HTN crisis
48
Q

What are the risks of using tramadol?

A
  • similar efficacy to codeine/APAP
  • risk for dependence/addiction, seizures (esp w/ sz disorder, anti-depressant or anti-psych use), death due to OD or suicide
49
Q

What opioid agonists can be used for severe pain?

A
  • morphine
  • hydromorphone
  • levorphanol
  • oxymorphone
  • fentanyl
  • methadone
50
Q

What is the gold standard for potent opioids?

A

morphine

51
Q

What are common side effects of morphine?

A

gastritis and histamine release

52
Q

What is unique about the Embeda form of morphine?

A

contains a core of Naltrexone (an opioid antagonist) to prevent or help with opioid addiction

53
Q

Which severe pain opioid is useful for terminal pain syndromes?

A

hydromorphone

54
Q

What is important to remember for oxymorphone?

A
  • take on an empty stomach –> taking with food can lead to excess peak levels
  • EtOH can increase oxymorphone levels leading to potential for OD
55
Q

What is unique about fentanyl?

A
  • patch for chronic pain

- time to patch peak activity 24-72 hours

56
Q

What is methadone used for? What is unique about it?

A
  • commonly used in narcotic maintenance programs or weaning protocols
  • long half life (8-59 hours) so good for chronic use
57
Q

What is butorphanol?

A
  • nasal spray used for migraine tx

- mixed opioid agonist/antagonist

58
Q

What is nalbupine/Nubain?

A

-2nd line mixed opioid agonist/antagonist for moderate to severe pain

59
Q

What is buprenorphine (Buprenex, Subutex)?

A
  • 2nd line partial agonst for moderate to severe pain

- also used to treat opioid dependence

60
Q

What drugs are opioid mu antagonists?

A
  • naloxone (Narcan)

- naltrexone

61
Q

What is naloxone/Narcan used for?

A

-reversal of respiratory depression, OD

62
Q

Opioid Dose Conversion Steps

A
  1. calculate total daily dose of current opioid
  2. convert to new opioid using equianalgesic dose chart
  3. determine new opioid dose (can usually start with a reduced equianalgesic dose then titrate up, unless pain was not controlled)
63
Q

What are the options for a pt with an opioid pseudoallergy?

A
  • nonopioid (APAP, NSAID)
  • avoid opioids more commonly assoc. w/ pseudoallergy (codeine, morphine, meperidine)
  • use more potent opioids that are less likely to release histamine
  • if necessary, give with diphenhydramine
64
Q

What are the options for a pt with a true opioid allergy?

A
  • nonopioid (APAP, NSAID)

- opioid in a different chemical class w/ close monitoring

65
Q

What analgesics are considered adjuvant treatment options?

A
  • caffeine 65-200 mg; may enhance effect of APAP, ASA or ibup
  • hydroxyzine
  • corticosteroids
66
Q

What are the risks with pentazocine?

A
  • may precipitate withdrawal in opioid dependent patients

- CI in pts with CV dz, increases plasma catecholamines

Spring 15 - Pharm Unit I (6 decks)

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