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Pharm II MHM - FINAL > NSAIDs and Acetaminophen > Flashcards

NSAIDs and Acetaminophen Flashcards

1
Q

Types of pain

A
  • Nociceptive (somatic, visceral)
  • Neuropathic
  • Psychogenic
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2
Q

What is the mechanism of pain and what are its mediators?

A
  • Neural mechanism

- Chemical mediators

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3
Q

Describe the stages of the neural pain pathway

A
  • Stimulation
  • Transmission
  • Modulation
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4
Q

What occurs in the stimulation phase of the neural pain pathway?

A
  • Noxious stimuli activate receptors

- Release of bradykinins, H and K ions, PGs, histamine, ILs, TNF, serotonin and Sub P

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5
Q

What occurs in the transmission phase of the neural pain pathway?

A
  • A and C afferent nerve fibers stimulated
  • Synapse along spinal cord dorsal horn releases NTs
  • Impulses passed along ascending pathway to the brain
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6
Q

What occurs in the modulation phase of the neural pain pathway?

A
  • Pain becomes a conscious experience via limbic system
  • Endogenous opiate system in CNS modulates pain impulses
  • Descending system of nerves may inhibit synaptic pain transmission
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7
Q

Describe inflammation

A
  • Subset of nociceptive pain

- Natural shift from protection of damage to promotion of healing

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8
Q

Describe maladaptive inflammation

A
  • Action outlives function
  • Chemical properties of neurons change which effects transmission of pain
  • Often caused by disease
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9
Q

What is the beginning component of the COX pathway normally?

A 
Arachidonic acid
(released upon trigger of natural inflammatory cascade)
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10
Q

General function of COX?

A

Oxygenates arachidonic acid which forms PGs, prostacyclin, thromboxane

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11
Q

What is misoprostol and what does it do?

A
  • Synthetic PGE1
  • Induces uterine contractions
  • Protects GI mucosa
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12
Q

What is alprostadil and what does it do?

A
  • Synthetic PGE1

- Maintain patent ductus arteriosis

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13
Q

What is latanoprost and what does it do?

A
  • Synthetic PGF2a

- Treatment of open angle glaucoma

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14
Q

What is prostacyclin and what does it do?

A
  • Synthetic PGI2

- Treatment of pulmonary HTN

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15
Q

Describe selective NSAIDs

A

Selectively blocks COX-2 (over COX-1)

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16
Q

Describe COX-1

A

Physiological “housekeeping”

  • Vascular homeostasis
  • GI, renal blood flow
  • Platelet function
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17
Q

Describe COX-2

A

Activated only as needed

  • Inflammation, fever, pain
  • Ovulation
  • Placental function
  • Uterine contractions
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18
Q

Major difference between aspirin and all other NSAIDs

A

Aspirin irreversibly (!) binds to COX-1 and COX-2

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19
Q

MOA of Aspirin

A

Irreversibly binds to COX-1 and COX-2 (inhibiting PG synthesis and preventing formation of TXA2)

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20
Q

Aspirin uses

A
  • Anticoagulant (mainly)
  • Antipyretic
  • Analgesic (at high doses)
  • Anti-inflamm (at high doses)
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21
Q

Peak plasma levels of aspirin occurs when?

A

1-2 hours

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22
Q

Is aspirin more selective to COX-1 or COX-2?

A

COX-1 as long as it is under 100 mg dosage

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23
Q

Contraindications to aspirin

A
  • Pregnancy C/D (avoid esp in 3rd trimester)
  • Hemophiliacs
  • Children under 16 yo w/viral illness (risk of Reye’s syndrome)
  • Asthma, nasal polyps, recurrent sinusitis
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24
Q

How does aspirin (or any salicylates) toxicity present?

A

Tinnitus

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25
Q

What is the MC used non-selective NSAID?

A

Ibuprofen

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26
Q

Ibuprofen MOA and use

A
  • Reversibly blocks COX-1 and 2

- Used in mild to moderate pain

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27
Q

What is the new formulation of ibuprofen and what does it do?

A
  • Caldolor (IV)
  • For moderate pain and used to decrease opioid dose required
  • Very expensive
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28
Q

Pediatric use of ibuprofen?

A
  • Commonly for fever and pain

- 5 to 10 mg/kg/dose Q6-8h

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29
Q

Dosing of ibuprofen

A

It has both an OTC dose (200-400 mg Q6-8h) and a prescription dose (600-800 mg Q6-8h)

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30
Q

Toxicity of ibuprofen

A
  • Similar to all non-selective NSAIDs

- May be more prone to GI side effects due to increased use vs. other products

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31
Q

Until recently, what was the only NSAID available IV?

A

Ketorolac

still most widely used

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32
Q

Ketorolac use

A
  • Most widely used IV NSAID
  • Used for moderate to severe pain (a level that would require opioid therapy)
  • Never used pre-op!
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33
Q

Ketorolac toxicity

A

Believed to be more potent than other NSAIDs so higher risk for ADRs

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34
Q

Ketorolac contraindications

A
  • All NSAID warnings

- Any situation with increased bleeding risk

35
Q

Naproxen key features

A
  • Found in numerous OTC products in various strengths

- Always dosed BID

36
Q

Max dose of naproxen a day? With CVD risk?

A
  • 660 mg/day

- 440 mg/day w/CVD risk

37
Q

What is the novel agent of naproxen?

A
  • Vimovo = naproxen/esomeprazole

- For patients w/GI bleed risks

38
Q

Dosing of ketorolac

A

Total dose should NOT exceed 5 days or 20 doses

39
Q

Nabumetone key features

A
  • Nonselective NSAID
  • 24+ hours half life (QD dosing)
  • Monitor renal function!
  • Preferred for chronic arthritis
  • Increased photosensitivity
  • Expensive
40
Q

Piroxicam key features

A
  • Nonselective NSAID
  • 36-80 hrs half life (QD dosing)
  • Much higher risk of ADRs
  • Super high risk of GI ulceration
41
Q

Oxaprozin key features

A
  • Nonselective NSAID

- 50 to 60 hrs half life (QD dosing)

42
Q

Which nonselective NSAIDs can be dosed once a day? Why?

A
  • Nabumetone
  • Piroxicam
  • Oxaprozin
  • Long half life!
43
Q

What is indomethacin and what population is it primarily used in?

A
  • Nonselective NSAID

- Neonates to close PDA when it is open

44
Q

What are the increased risks of indomethacin?

A
  • Pancreatitis

- CNS (HA, dizzy, psychosis)

45
Q

What is Sulindac and how is it dosed? What are the potential adverse effects?

A
  • Nonselective NSAID
  • Dosed BID
  • Increased risk of SJS and liver damage
46
Q

Diclofenac MOA

A

Somewhat selective for COX-2 (providing potentially less GI toxicity)

47
Q

What is a novel agent of diclofenac?

A
  • Arthrotec (diclofenac/misoprostol)
  • Pregnancy X bc of misoprostol
  • Increased diarrhea, cramping
48
Q

Meloxicam MOA

A

More selective for COX-2 but not fully

49
Q

Meloxicam dosing and half life

A

Can be dosed QD because half life is 15-20 hours

50
Q

Celecoxib key features

A
  • Only fully selective COX-2 still available in US
  • Similar efficacy vs. non-selective NSAIDs
  • Proposed decrease in GI toxicity
51
Q

What is celecoxib MC used for?

A
  • Osteoarthritis and RA

- Decreases pain and swelling, increases function (no effect on disease itself)

52
Q

Contraindications of celecoxib

A
  • Same warnings as other NSAIDs
  • Increased risk of MI/stroke (dose related)
  • Sulfa allergy
  • Preg Cat C prior to 30 wks gestation
  • Preg Cat D 30 wks and beyond
53
Q

General NSAID ADRs

A
  • GI (dyspepsia, ulceration)
  • Renal (decreased BF, interstitial nephritis)
  • CV (MI/stroke)
  • Pregnancy concerns
  • Hematologic (d/t inhibition of TXA2)
54
Q

Black box warnings of NSAIDS

A
  1. CV (esp post MI and stroke)
  2. GI (including bleeding, ulcers)
  3. CABG (contraindicated for peri-op pain during CABG)
55
Q

Which population is at greater risk for serious GI events with NSAIDs?

A

Elderly

56
Q

What is the cause of GI toxicity with NSAIDs?

A
  • Block of systemic PGE2/PGI2 synthesis

- Loss of cytoprotection in gut

57
Q

Which agents are proven to prevent NSAID induced gastric AND duodenal ulcers?

A
  • Misoprostol (not used by itself often though)
  • H2 blockers (can be used interchangeably 1st line with PPI)
  • PPIs (MC used)
58
Q

What class is misoprostol, what is it used for, and what is important to know about it?

A
  • Synthetic PGE
  • Prevention of NSAID induced ulcers
  • Preg Cat X
59
Q

How do NSAIDs cause nephrotoxicity?

A
  • PGs acts as vasodilators
  • NSAIDs block PGs
  • Afferent arteriole vasoconstricts which lowers GFR
60
Q

Populations at risk for NSAID induced nephrotoxicity

A
  • Volume depleted
  • Kidney disease
  • CHF
  • 65 yo or older
  • HTN
  • DM
  • Pts on methicillin abx
61
Q

What are the CV concerns with NSAID use?

A

COX2 selective NSAIDs!

  • Block COX2 (blocking PG synthesis) resulting in vasoconstriction
  • Lack of COX1 blockage results in platelet aggregation
  • Vasoconstriction and platelet aggregation increases risk of cardiac events
62
Q

Patients at risk for CV events with NSAID use:

A

Have had or have risk factors for: CABG, UA, MI, ischemic events

63
Q

What is the only NSAID studied to date that has NOT shown a risk of CV complications?

A

Naproxen

64
Q

If you have to use a COX-inhibitor, avoid CV concerns by:

A
  • Choosing NON-selective first (Naproxen)
  • Use COX2 selective agents LAST
  • Use lowest dose possible and titrate while monitoring closely
  • Add ASA 81 mg daily or a PPI if pt has a known thrombotic risk
65
Q

If a patient has known thrombotic risk and is using NSAIDs, what should be added to avoid CV concerns?

A

ASA 81 mg daily
OR
PPI

66
Q

Pregnancy concerns of NSAID use?

A
  • May be a/w miscarriage (weak evidence)

- Closure of ductus arteriosus and development of pulm HTN (a/w 3rd trimester use)

67
Q

NSAID drug-drug interactions

A
  1. Warfarin and anticoag (increased bleeding risk)
  2. ACE-I (renal toxicity and may decrease effectiveness of anti-HTN)
  3. Aspirin w/other NSAIDs
68
Q

If aspirin is taken with other NSAIDs, how should they be taken?

A

Space ASA by 2 hours and give it first

69
Q

When is the only time you would recommend ASA with another NSAID in a patient?

A

Known thrombotic risk

70
Q

Which NSAIDs should be avoided in hepatic dysfunction?

A
  • Diclofenac

- Sulindac

71
Q

Which topical NSAIDs have shown effectiveness in reducing pain?

A
  • Diclofenac (FDA approved)
  • Ibuprofen
  • Ketoprofen
  • Piroxicam
  • Benefit is likely only 2-4 wks
72
Q

Describe topical diclofenac

A
  • Patch (Flector), solution (Pennsaid), gel (Voltaren)
  • Wash hands after use!
  • Systemic warnings apply to topical diclofenac
73
Q

What is topical diclofenac used for?

A
  • Mild localized OA or RA

- Penetration limits use on hip arthritis

74
Q

What is methyl salicylate? MOA? How long should it be used?

A
  • Salicylic acid (similar but different than aspirin)
  • Bengay/Icy Hot
  • Causes vasodilation of cutaneous vasculature
  • Decreases PG synthesis (not believed to be through COX inhibition)
  • No more than 1 week use!
75
Q

Methyl salicylate ADRs

A
  • Mostly topical irritation

- Systemic toxicity can occur (tinnitus, increased HR, DOE)

76
Q

Patient education on methyl salicylate

A 
Avoid using with:
-Tight bandaging
-Heating pads
-Excessive exercise
(More absorption)
77
Q

What is acetaminophen? MOA? Use?

A
  • Used for mild-mod pain (antipyretic, analgesic)
  • NOT an NSAID, NO effect on inflammation
  • Blocks PG synthesis in CNS, prohibits peripheral pain impulses
  • May act on COX-3
78
Q

Peak plasma levels of acetaminophen? Half life?

A
  • 30-60 mins peak levels

- 2-3 hrs half life

79
Q

Max dose of acetaminophen per day?

A

4 grams (4000 mg)

80
Q

How is acetaminophen metabolized?

A

Hepatic (glucuronidation) primarily

81
Q

Acetaminophen ADRs

A
  • Increased AST/ALT

- Liver failure in acute or chronic OD

82
Q

When should acetaminophen be avoided?

A

Patients w/cirrhosis, liver failure, heavy drinking

83
Q

How can acetaminophen overdose be treated?

A

N-acetylcysteine (NAC) available PO and IV

84
Q

What is the new formulation of acetaminophen? What can it be used for?

A
  • IV (Ofirmev)

- May be used for inpatients to decrease opioid doses

Pharm II MHM - FINAL (17 decks)

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