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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
What Med Should a Low GI/Low CV Risk Pt Get
-ibuprofen or other low GI risk NSAID (celecoxib)
26
What Med Should a Moderate GI/Low CV Risk Pt Get
1. celecoxib alone 2. NSAID + PPI or misoprostol 3. NSAID + double dose H2 blocker
27
What Med Should a High GI/Low CV Risk Pt Get
1. avoid NSAIDs if possible | 2. celecoxib + PPI or misoprostol
28
What Med Should a High CV/Low GI Risk Pt Get
-naproxen
29
What Med Should a High CV/Moderate GI Risk Pt Get
1. naproxen + PPI or misoprostol | 2. naproxen + double dose H2 blocker
30
What Med Should a High CV/High GI Risk Pt Get
avoid NSAIDs
31
Opioid MOA
-stimulate opioid receptors in the CNS (mu, kappa, delta)
32
Major Adverse Effects of Opioid Analgesics
- 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
Most Common AEs of Opioids
- drowsiness | - N/V/C
34
Opioid Withdrawal Sxs
- 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
Opioid Agonists
maximal biologic response through binding to the opioid mu receptor
36
Opioid Partial Agonists
submaximal response at the receptor even at high doses
37
Opioid Agonist/Antagonist
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
Opioid Antagonist
reverse or inhibit the effects of agonists by preventing receptor access use in event of overdose!
39
What is opioid selection based upon?
- 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
What opioid agonists can be used for moderate pain?
- codeine or codeine/APAP (Tylenol 3) - hydrocodone or hydrocodone/APAP (vicodin) - oxycodone or oxy/APAP (percocet) - meperidine (Demerol) - tramadol (Ultram) - tapentadol
41
Dose for Codeine/APAP (Tylenol 3)
1-2 PO q 4-6hr PRN (30/300 mg)
42
Dose for Hydrocodone/APAP (Vicodin)
1-2 PO q4-6hr PRN (5/325 mg)
43
Dose for Oxycodone/APAP (Percocet)
1-2 PO q4-6hr PRN (5/325 mg)
44
What is a common side effect of codeine?
gastritis
45
What is codeine metabolized to?
morphine
46
Which moderate pain opioid has a black box warning and why?
- oxycodone/APAP (Percocet) - CYP3A4 substrate --> if pt is on 3A4 inhibitors (eg erythro/clarithromycin, ketoconazole, protease inhibitors), it can lead to toxicity
47
Why is use of meperidine discouraged?
- metabolite (normeperidine) is a direct CNS irritant that causes seizures - do not use w/ MAOI --> life threatening HTN crisis
48
What are the risks of using tramadol?
- 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
What opioid agonists can be used for severe pain?
- morphine - hydromorphone - levorphanol - oxymorphone - fentanyl - methadone
50
What is the gold standard for potent opioids?
morphine
51
What are common side effects of morphine?
gastritis and histamine release
52
What is unique about the Embeda form of morphine?
contains a core of Naltrexone (an opioid antagonist) to prevent or help with opioid addiction
53
Which severe pain opioid is useful for terminal pain syndromes?
hydromorphone
54
What is important to remember for oxymorphone?
- 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
What is unique about fentanyl?
- patch for chronic pain | - time to patch peak activity 24-72 hours
56
What is methadone used for? What is unique about it?
- commonly used in narcotic maintenance programs or weaning protocols - long half life (8-59 hours) so good for chronic use
57
What is butorphanol?
- nasal spray used for migraine tx | - mixed opioid agonist/antagonist
58
What is nalbupine/Nubain?
-2nd line mixed opioid agonist/antagonist for moderate to severe pain
59
What is buprenorphine (Buprenex, Subutex)?
- 2nd line partial agonst for moderate to severe pain | - also used to treat opioid dependence
60
What drugs are opioid mu antagonists?
- naloxone (Narcan) | - naltrexone
61
What is naloxone/Narcan used for?
-reversal of respiratory depression, OD
62
Opioid Dose Conversion Steps
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
What are the options for a pt with an opioid pseudoallergy?
- 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
What are the options for a pt with a true opioid allergy?
- nonopioid (APAP, NSAID) | - opioid in a different chemical class w/ close monitoring
65
What analgesics are considered adjuvant treatment options?
- caffeine 65-200 mg; may enhance effect of APAP, ASA or ibup - hydroxyzine - corticosteroids
66
What are the risks with pentazocine?
- 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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