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Junior - Pharm II - 1 > 2 - Non-Opioid Analgesics > Flashcards

2 - Non-Opioid Analgesics Flashcards

1
Q

What is nociceptive pain?

A

Pain caused by an injury to body tissues

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2
Q

What is neuropathic pain?

A

Damage to or dysfunction of the nerves, spinal cord, or brain

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3
Q

Name some non-pharmacologic options for pain management:

A 
Physical therapy
Acupuncture
Exercise
Stretching
Weight loss
Cognitive therapy 
Yoga
Chiropractic
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4
Q

Therapeutic effects of analgesics:

A 
Antipyretic 
Anti-inflammatory
Ceiling effect to the analgesia 
Do not cause tolerance
Do not cause dependence
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5
Q

What releases arachidonic acid from the cell membrane?

A

Phospholipase A2

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6
Q

Cox 1, 2, and 3 coverts _____ to _____.

A

Arachidonic acid to prostaglandins

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7
Q

Cox 1 is found mostly in:

A

Platelets, endothelium, stomach

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8
Q

Cox 2 is found mostly in:

A

Inflammatory cells, kidney

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9
Q

Cox 3 is found mostly in:

A

The CNS

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10
Q

What are the chemical mediators that trigger inflammation?

A

Histamine, prostaglandins, bradykinin

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11
Q

Acetaminophen (Tylenol) - MOA:

A

Not fully understood

Inhibits prostaglandins (via unknown binding site)

Does not have significant anti-inflammatory or anti-platelet effects

CENTRALLY ACTING as analgesic and antipyretic

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12
Q

Acetaminophen (Tylenol) - clinical use:

A

Self-limiting painful condition (e.g. HA, MSK pain), osteoarthritis, lower back pain

Mild to moderate non-inflammatory nociceptive pain

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13
Q

Acetaminophen especially useful in patients with:

A

Gastric problems, or where bleeding time is a concern

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14
Q

Acetaminophen metabolism (primary):

A

Primary - glucuronidation and sulfation, then renally excreted

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15
Q

Acetaminophen metabolism (secondary):

A

CYP3A4, CYP2E1: N-hydroxylation

Toxic metabolite “NAPQI”

If glutathione is depleted, hepatic damage occurs

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16
Q

Acetaminophen (Tylenol) - AE’s?

A

N/V, HA

OD -> Hepatotoxicity

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17
Q

What level of APAP is hepatotoxic?

A

10 to 15 grams

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18
Q

What level of APAP is potentially fatal?

A

20-25 grams

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19
Q

First 24hrs s/p APAP OD - clinical symptoms:

A

Mild - GI s/s (N/V)

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20
Q

24 - 72 hrs s/p APAP OD - clinical presentation?

A

ABD pain
Liver tenderness
Elevated transaminase levels
Possible jaundice

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21
Q

4 days to 2 week s/p APAP OD - clinical presentation:

A

Either resolution or progressive deterioration to death from hepatic failure

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22
Q

Antidote for APAP OD?

A

N-acetylcysteine [NAC] (Mucomyst, Acetadote)

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23
Q

How does Acetadote work?

A

Increases supply of glutathione

Combines with NAPQI to produce non-toxic metabolite

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24
Q

What is the Rumack-Matthew nomogram?

A

Used to determine course of treatment for a patient that has overdosed on Tylenol

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25
Q

Indications for using N-Acetylcysteine:

A
  1. Concentration above the treatment line on Rumack-Matthew 4hrs s/p ingestion
  2. Suspected ingestion > 150mg/kg
  3. Unknown ingestion time, concentration > 10mcg/mL
  4. Pt hx APAP ingestion and ANY evidence of liver injury
  5. Delayed presentation (>24hrs) w/ evidence of liver injury
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26
Q

Max adult daily dose APAP?

A

4 grams

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27
Q

Children’s dose for Tylenol?

A

10-15mg/kg/dose q4-6hrs

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28
Q

NSAID’s - MOAS?

A

Reversibly inhibits COX-1 and 2 enzymes, which results in decreased formation of prostaglandin precursors

Has antipyretic, analgesic, and anti-inflammatory properties

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29
Q

Undesirable NSAID effects from COX-1 inhibition:

A

Gastrotoxicity —> ulcers

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30
Q

Undesirable NSAID effects from COX-2 inhibition:

A

Increased BP

Increased salt retention

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31
Q

Clinical uses of NSAIDS (four main categories):

A
  1. Antipyretic
  2. Anti-platelet
  3. Analgesic
  4. Anti-inflammatory
32
Q

What medicine is contraindicated in peds with viral infections (influenza, chicken pox), and why?

A

ASA, d/t Reye’s Syndrome

33
Q

What impact does higher COX-2 selectivity have an platelet aggregation?

A

Higher COX-2 selectivity DECREASES the beneficial effects on platelet aggregation

34
Q

Which is better at decreasing platelet aggregation - COX-1 or COX-2?

A

COX-1

35
Q

NSAID’s that are more ___ selective carry a higher cardiovascular risk:

A

COX-2

36
Q

AHA recommendations for patients with CVD who need pain meds:

A
  1. APAP
  2. ASA
  3. Tramadol
  4. Opioids (short-term)
  5. Non-acetylated salicylates

IF ALL THAT FAILS…NSAIDS

37
Q

Characteristics of “high risk” for NSAID ulcers:

A
  1. Hx of previously complicated ulcer

2. Multiple (>2) other risk factors

38
Q

Criteria of “moderate risk” for NSAID ulcers:

A
  1. Age > 65 yrs
  2. High-dose NSAID therapy
  3. Previous hx uncomplicated ulcer
  4. Concurrent use of ASA, corticosteroids, or anticoagulants
39
Q

How to prevent NSAID dyspepsia?

A

Combine NSAID with PPI or H2 blocker

40
Q

How to avoid NSAID cardiovascular complications?

A

Naproxen preferred NSAID for CV patients

In general, CVD patients should avoid NSAIDS

41
Q

What NSAID should be used cautiously in asthma patients?

A

ASA - can exacerbate asthma

42
Q

How many days before surgery must ASA therapy be stopped?

A

7 to 10 days

43
Q

Avoid NSAIDS in pregnancy (especially close to term) due to:

A

Risk of premature closure of ductus arteriosus

44
Q

NSAIDS and renal disease:

A

Avoid in pt’s taking ACEI’s and ARB’s

45
Q

Signs of salicylate toxicity:

A

Tachypnea
Tachycardia
Febrile
Metabolic acidosis and respiratory alkalosis

46
Q

Common NSAID drug interactions:

A

ACEI/ARB

Antiplatelet

Corticosteroids

47
Q

ASA can displace:

A

Highly protein-bound drugs

48
Q

General dosing principles for NSAIDS:

A

Use lowest dose possible to get desired effect

Ceiling effect (higher doses do not equal better therapeutic effects)

Lower doses for analgesia

Higher doses for inflammation

49
Q

What is the most commonly used salicylate?

A

ASA

50
Q

Do salicylates cross the BBB and placenta?

A

Yes

51
Q

Non-acetylated salicylates may be preferred when ______ is undesirable

A

COX-1 inhibition

52
Q

Describe Salsalate (Disalcid):

A

Non-acetylated salicylate

Indicated for relief of rheumatic disorder

53
Q

What is Choline Magnesium Trisalicylate indicated for?

A

OA, acute flare-up of RA, acute shoulder pain

54
Q

Describe Diflunisal:

A

Non-acetylated salicylate

For OA/RA (mild-moderate)

Does not cross BBB or placenta

55
Q

Describe Bismuth Subsalicylate:

A

Pepto-Bismol

Antisecretory, antimicrobial, anti-inflammatory

Diarrhea, heartburn, upset stomach

ADE: dark/black tongue

56
Q

ASA MOA?

A

Irreversibly inhibits COX-1 and COX-2 enzymes

Decreased production of TXA2 form AA

Lasts the life of the platelet (7 to 10 days)

57
Q

Clinical use for Ketorolac (Toradol)?

A

Not for peds

Can decrease opioid requirement up to 50%

moderate to severe pain

58
Q

Ketorolac (Toradol) - black box warning:

A

Bleeding risk

Use short term (<5 days)

59
Q

Ketorolac (Toradol) - CI’s

A

Surgery coming up soon

Don’t use with other NSAIDS

Don’t use in labor and delivery

Don’t use in pt’s with ESRD

60
Q

Which NSAID has the lowest CV risk?

A

Naproxen (Aleve)

61
Q

What specific disease is Naproxen approved for?

A

Gout attacks

62
Q

What is an advantage of Naproxen over other NSAIDS in terms of convenience?

A

Longer half life, BID dosing

63
Q

Indomethacin - clinical use:

A

NSAID of choice for gout attacks

Ophth preparation for conjunctival inflammation

Accelerated closure of PDA

64
Q

What was the first NSAID to show accelerated closure of PDA?

A

Indomethacin (Indocin)

65
Q

What is the most commonly used NSAID in the US?

A

Ibuprofen

66
Q

Ibuprofen - GI and CVD risks:

A

Low GI risk

Higher CVD risk

67
Q

Ibuprofen - AE’s?

A

GI irritation (less than with ASA)

Tinnitus

68
Q

Ibuprofen - CI’s?

A

Agioedema

Bronchospasm (if ASA sensitive)

69
Q

Nabumetone (Relafen) - clinical use:

A

OA/RA

70
Q

Nabumetone (Relafen) - characteristics:

A

Long half-life = once daily dosing

More expensive

COX-2 selective (less GI SE’s)

71
Q

Diclofenac (Cataflam) - clinical use:

A

Chronic MSK pain (mild to moderate)

OA/RA

Ophthalmic - post-cataract surgery

Topical - OA, sprains, strains

72
Q

Diclofenac - AE’s:

A

High CVD risk

73
Q

Celecoxib (Celebrex) - MOA:

A

Reversibly inhibits COX-2 (with minor COX-1)

74
Q

Celecoxib (Celebrex) - clinical use:

A

OA
RA
AS
Primary dysmenorrhea

Minimal GI SE’s

High CVD risk

75
Q

Celecoxib (Celebrex) - CI’s

A

Contains a sulfa-group - don’t give to pt with sulfa allergy

76
Q

Flurbiprofen - use:

A

Inhibition of intraoperative miosis

Junior - Pharm II - 1 (6 decks)

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