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Clinical 1 (Part B) > 10 - OTC Pain Management > Flashcards

10 - OTC Pain Management Flashcards

1
Q

What are the two kinds of pain?

A

Nociceptive

  • Somatic
  • Visceral

Neuropathic

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2
Q

_____ pain: due to the activation of pain pathways by ongoing tissue damage

A

Nociceptive

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3
Q

Define somatic pain

A
  • Pain arising in the tissues of the body
  • Sharp, sometimes burning, aching, relatively localized
  • Osteomyelitis, osteoarthritis, bone fractures

ex. ankle sprain, tooth being pulled out

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4
Q

Define visceral pain

A
  • Pain arising in the organs of a body cavity
  • Deep, aching, cramping, diffuse and poorly localized
  • Could have nausea, sweating, and CV changes involved (i.e. systemic symptoms)
  • Endometriosis (pelvic), Chron’s disease (abdomen), angina (thorax)
  • Not often managed with OTC agents (Referral)
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5
Q

Define neuropathic pain

A
  • Caused by direct nerve damage or may be due to abnormal “processing” of a pain signal in the CNS pain pathways due to sensitization of pain neurons
  • More commonly chronic, but can be acute
  • Can be paroxysmal or spontaneous
  • Generally described as burning, tingling, shock-like or shooting
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6
Q

Hyperalgesia

A

Altered perception such that stimuli which would normally induce a trivial discomfort cause significant pain

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7
Q

Allodynia

A

Pain due to a stimulus that does not normally evoke pain

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8
Q

Phantom pain

A

Pain in a limb that is no longer there

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9
Q

Acute Pain:

Cause

A

Tissue damage often associated with inflammation

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10
Q

Acute Pain:

Duration

A

Days to weeks (2-4 weeks)
Sub-acute = 4-12 weeks
May depend on the cause

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11
Q

Acute Pain:

Course or prognosis

A

Predictable

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12
Q

Acute Pain:

Emotional response

A

Anxiety or overt pain behaviours (grimacing, limping, etc)

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13
Q

Acute Pain:

Treatment

A

Primarily analgesic

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14
Q

Chronic Pain:

Cause

A

Neuronal or CNS abnormality (sensitization)

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15
Q

Chronic Pain:

Duration

A

> 12 weeks (3 months)
Associated with a pattern of recurrence over months or years
May be associated with chronic disease (Rheumatoid arthritis, back pain)

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16
Q

Chronic Pain:

Course or prognosis

A

Unpredictable

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17
Q

Chronic Pain:

Emotional response

A

Quiet, depressed
Flat affect
May also have anxiety issues

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18
Q

Chronic Pain:

Treatment?

A

Multimodal

-Have to try different options, different HCP’s, different therapies, etc.

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19
Q

What is break-through pain?

A
  • Temporary increase in pain to greater than moderate intensity that occurs on a baseline pain of moderate intensity or less
  • Causes increased level of psychological distress and significant decrease in function
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20
Q

What is incident pain?

A

A type of breakthrough pain that is made worse by movement

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21
Q

List some tools for assessing pain

A

1) Numerical Rating Scale (NRS)
- Patients rate their pain on a scale of 0-10

2) Visual Analogue Scales (VAS)
- 100mm horizontal line, with the left side marked no pain and the right side marked the worst pain

3) Wong-Baker FACES Pain Rating Scales
- Faces ranging from happy to sad based on how they are feeling
* Good for children or people who don’t speak english

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22
Q

What are the 4 main pieces that are essential to pain information gathering?

A
  • Severity of pain
  • Location of pain
  • Onset and how long the pain lasts
  • Quality of pain (description of pain - dull ache, sharp pain, tingling or burning)
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23
Q

What is the role of OTC Pain medication

A
  • Effective when treating mild-moderate somatic pain from skin, muscle and joints
  • Also effective in treatment of dysmenorrhea and headache
  • Less useful in treatment of visceral pain (refer)
  • Effectiveness in neuropathic pain often demonstrates variable response
  • Treatment of neuropathic pain may involve a wide range of therapy
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24
Q

List the types of non-prescription pain medications

A

1) NSAIDs
- ibuprofen
- ASA
- naproxen

2) Acetaminophen

3) Opioids
- Codeine (8mg)

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25
Q

MOA of Acetaminophen?

A

Produces analgesic effect through central inhibition of PG (fever and pain perception) & peripherally blocking the generation of pain impulses.

  • Effective analgesic and antipyretic
  • Does not possess anti-inflammatory activity
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26
Q

Oral onset of action for acetaminophen ?

A

30 minutes

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27
Q

PR onset of action for acetaminophen ?

A

slowly and incompletely absorbed

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28
Q

Duration of effect for acetaminophen ?

A

4-6 hours

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29
Q

Acetaminophen:

Adult dosing

A

325-650 (1000) mg every 4-6 hours

max 4g/day

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30
Q

Acetaminophen is _____-dependent

A

dose

*meaning that 1000mg produces greater analgesia than 650 or 500 mg dose.

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31
Q

Acetaminophen:

Ceiling effect at ?

A

1000 mg - no further pain management, just further liver damage

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32
Q

Acetaminophen:

Pediatric dosing

A

PO: 10-15 mg/kg/dose every 4-6 hours

PR: 15-20 mg/kd/dose every 4-6 hours

Max 65 mg/kg/day (max 5 doses/day)

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33
Q

T or F: Acetaminophen is safe for short term use in children, pregnancy and lactation

A

true

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34
Q

Describe Acetaminophen Overdose

A

-It forms a toxic metabolite which is normally detoxified by glutathione. This system can be overwhelmed in an overdose as glutathione becomes depleted (starts to use hepatocyte instead)

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35
Q

What is the minimum toxic single dose in a healthy adult and healthy child?

A

Adult: 7.5-10g over 8 hours

Child: 150mg/kg over 8 hours

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36
Q

What strategies can be used to prevent accidental or unintentional overdose?

A
  • limit pack size
  • change the scheduling
  • make font of acetaminophen very large
  • just have one strength available for children
  • increase patient awareness on the dangers of acetaminophen overdose
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37
Q

Describe the symptoms of Acetaminophen OD

A

Flu like symptoms

-nausea, vomiting, drowsiness, confusion, sweating (12-24 hours after ingestion)

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38
Q

What is the antidote for Acetaminophen OD and when will you see results from it?

A

acetylcysteine

-optimal result with antipodal therapy seen within 16-24 hours

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39
Q

Why would an alcoholic have a lower threshold for acetaminophen liver damage?

A
  • possible induction of enzymes
  • hepatic dysfunction
  • decreased stores of glutathione

*severe liver injury reported in alcoholics who claimed to have taken less than 4g/day

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40
Q

Chronic alcoholism may result in higher blood levels of _____

A

NAPQ

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41
Q

What is NAPQ?

A

Acetaminophen metabolite which is toxic to liver cells and reduced blood levels of acetaminophen due to increased metabolism of acetaminophen by CYP2E1

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42
Q

List some non-Rx NSAIDs

A

ASA
Ibuprofen
Naproxen

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43
Q

What are the pharmacological properties of non-Rx NSAIDs

A
  • Analgesic
  • Antiplatelet
  • Antipyretic
  • Anti-inflammatory
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44
Q

ASA acts primarily in the _____

A

periphery

45
Q

What benefit do NSAIDs have over acetaminophen?

A

anti-inflammatory properties

46
Q

Why is ASA not a first line analgesic?

A

Higher ADR’s - Gastric irritation, nausea

47
Q

Do we give ASA to kids?

A

No - Risk of Reye’s syndrome

48
Q

ASA:

Adult dosing

A

325-650 mg every 4-6 hours

Max = 4g/day

49
Q

What are the other types of dosing for ASA?

A

80 or 81mg every 2 days to 325 mg TID

*antiplatelet often seen OD

50
Q

ASA:

Onset of action

A

within 60 minutes

51
Q

ASA:

Duration of action

A

4-6 hours

52
Q

ASA:

Adverse effects

A

abdominal pain, cramps, dyspepsia, GI irritation

53
Q

Ibuprofen:

MOA

A

inhibit PG synthesis both centrally and peripherally

54
Q

Ibuprofen:

Duration of action

A

6-8 hours

55
Q

Ibuprofen:

Onset of action

A

30-60 minutes

56
Q

Ibuprofen:

When should you not take it?

A

if allergic to ASA or other NSAIDs

57
Q

Ibuprofen:

Adult dosing for pain, fever, dysmenorrhea

A

200-400 mg every 6-8 hours

Max 1.2 g/day

58
Q

Ibuprofen:

Adult dosing for inflammatory disease

A

400-800 mg every 6-8 hours

Max 3.2 g/day

59
Q

Ibuprofen:

Child dosing for pain/fever

A

PO: 5-10 mg/kg every 6-8 hours

Max = 40 mg/kg/day

60
Q

Ibuprofen:

Child dosing for anti-inflammatory effects

A

PO: 30-45 mg/kg/24 hours divided every 6-8 hours

61
Q

Naproxen:

MOA

A

inhibits PG synthesis both centrally and peripherally

62
Q 
Naproxen:
Adult dosing 
(we do not give this drug to kids)
A

For 12-65 year olds:
220 mg every 8-12 hours

Max 440 mg/day

For >65:
220 mg every 12 hours

Max 440 mg/day

63
Q

Naproxen:

Onset of action

A

30-60 minutes

64
Q

Naproxen:

When should you not take it?

A

If allergic to ASA or other NSAIDs

65
Q

Naproxen:

How should you take it?

A

Take with good and a full glass of water (to decrease GI irritation)

66
Q

Why should NSAIDs be taken with food?

A

Because you are inhibiting PGs which are mucosally protective.

67
Q

How are NSAIDs able to cause GI damage?

A

1) Local irritant effect resulting from the drug contacting the gastric mucosa
2) Systemic effect from PG inhibition

68
Q

Risk factors for upper GI bleeding?

A
  • over 60
  • alcohol abuse
  • concomitant use of other NSAIDs, anticoagulants, anti platelet agents, bisphosphonates, SSRIs or systemic corticosteroids
  • history of uncomplicated or bleeding peptic ulcer
  • infection with H. pylori
  • NSAID related dyspepsia
  • rheumatoid arthritis
69
Q

Do EC forms help reduce GI bleeding?

A

No - EC forms only reduce mucosal lesions and local irritation

70
Q

How do you prevent GI bleeding when considering pain control?

A

Consider prophylaxis with:

  • Misoprostol
  • PPI’s (Omeperazole)
  • Cox-2 Agent (Celebrex)
71
Q

How do NSAIDs affect the kidneys?

A
  • PGs are important for maintenance of renal blood flow and tubular transport of electrolytes
  • Increase in PG release occurs to compensate for the increased level of angiotensin 2 and NE
  • NSAIDs inhibit PGs therefore it can lead to:
    • renal and systemic vascular resistance
    • increase BP
    • worsening of pre-existing CHF
72
Q

What is an important drug interaction with NSAIDs?

A

Antihypertensive agents

-ACEi, diuretics, beta blockers

73
Q

ASA-induced Asthma:

MOA

A

decreased PGs result in decreased leukotrienes (important mediator in asthma and allergies)

74
Q

ASA-induced Asthma:

Characterized by ??

A

onset of asthma 30 mins - 3 hours post ingestion of ASA

75
Q

What drugs inhibit platelet aggregation?

A

ASA and ibuprofen

76
Q

Ibuprofen anti platelet properties are _______

A

reversible

77
Q

ASA anti platelet properties are _______

A

irreversible

78
Q

Average lifespan of a platelet ?

A

5-9 days

79
Q

How long before surgery should ASA be discontinued?

A

about 7-10 days

80
Q

See on Page 8 important drug-drug interactions

A

ok

81
Q

Limitations of ASA?

A

don’t use in people under 18, for influenza-like illnesses or for chicken pox

82
Q

Limitations of ASA and ibuprofen regarding pregnancy?

A

Both not recommended in 3rd trimester

83
Q

Patients with asthma should avoid ___

A

ASA

84
Q

When is acetaminophen considered 1st line therapy?

A
  • ASA-sensitive asthma
  • gastritis or PUD
  • increased risk of bleeding
  • patients with renal dysfunction
  • CV or hypertensive patients
  • multiple concurrent drug therapy
  • Pregnant or breast feeding (especially 3rd trimester)
85
Q

Is codeine 8mg recommended for pain management?

A

No - too low of a dose to produce any significant analgesic effect

86
Q

Codeine 8mg:

MOA

A

-changes to it’s active analgesic metabolite (morphine)

87
Q

Is caffeine effective for pain management?

A

Yes - dose of caffeine was around 64-65mg

*it enhances the analgesic effect of ASA and acetaminophen

88
Q

Are tylenol #1 good for pain?

A

not really at all

  • dose of caffeine is too low for it to be effective (soda or coffee has higher levels of caffeine)
  • dose of codeine is too low to be effective
89
Q

What age do you refer pain?

A

under 2

90
Q

For ages 2-18, what do you recommend?

A

acetaminophen or ibuprofen

91
Q

When should NSAIDs be cautioned?

A

in patients with renal, CV or GI disease states

92
Q

What is the best choice for pregnant/lactating women?

A

acetaminophen

**NSAIDS need to be avoided in the 3rd trimester

93
Q

Red flags for pain

A
  • Pain is escalating
  • Pain has not responded to appropriate therapy
  • Pain is severe
  • Patient with pain is pregnant (need to determine underlying cause)
  • Patient uses concurrent therapies or has other illnesses
94
Q

Pathophysiology of migraines

A

-Neurovascular disorder that consists of headache pain, autonomic nervous system dysfunction and potentially neurologic symptoms

It is thought that a trigger causes CNS dysfunction resulting in:

  • dilation of intracranial and extracerebral blood vessels
  • activation of trigeminal sensory nerves
  • leads to pain signals in the brain
95
Q

2 types of migraines

A

with aura

without aura

96
Q

Describe an aura

A
  • develops over 5-20 mins
  • usually lasts less than 1 hour
  • migraine occurs within 60 mins after the aura ends
97
Q

When do you refer migraines?

A

If there has been no initial diagnosis.

*Mild, diagnosed symptoms can be treated OTC

98
Q

Pathophysiology of Tension headaches

A
  • Most common type of headache
  • Occurs due to mental stress and tension, but exact pathophysiology unknown
  • More prevalent in women but declines with age for both males and females
99
Q

See the modified CTMA 2 Table 1 on page 11

A

okay jose

100
Q

Describe a MOH (medication overuse headache)

A
  • Defined as frequent use (>15 days/month) for several months
  • Often mimics tension-type headaches
  • Most common with combo products containing caffeine and/or opioids
101
Q

Treatment for MOH (medication overuse headache)

A
  • Discontinue implicated drugs
  • Relieve withdrawl symptoms
  • Treat recurrent headaches with appropriate Rx migraine therapies
102
Q

Prevention for MOH (medication overuse headache)

A

Educate patients to try and avoid regular or daily use of pain relievers for headache/pain.

Frequency should be less than 15 days/month

103
Q

Red flags for Headaches

A
  • Severe or abrupt onset
  • Age of onset > 40 yrs
  • Recent head trauma
  • Medication-induced headache
  • Progressive severity and/or increased frequency
  • Neurological signs or symptoms (stiff neck, fever, reduced consciousness)
  • Systemic signs (fever, nausea, vomiting)
  • Nocturnal occurence or upon early morning awakening
  • Onset with exercise or exertion
104
Q

Non-pharm treatment for headaches

A
  • Cryotherapy
  • Relaxation techniques (quiet, dark room, sleep)
  • Massage, acupuncture
  • Stress management, CBT
  • Exercise helps some patients
105
Q

How do you prevent headaches?

A
  • Avoid triggers (food, chemicals, hormones)
  • Lifestyle changes: regular sleeping and eating times, decrease stress, decrease caffeine
  • *See table 3 - migraine triggers
106
Q

Pharmacological treatment for a migraine?

A
  • OTC therapy often helps with mild-moderate migraines
  • Will require Rx therapy if OTC trial does not help or if treatment is being used >15 days per month
  • RX options include: Triptans (treatment) or preventative therapies (propranolol, amitriptyline)
  • OTC pain relievers can still be used to manage breakthrough migraine pain
107
Q

Pharmacological treatment for a tension headache?

A

Acetaminophen, ASA, Ibuprofen, Naproxen

108
Q

Pharmacological treatment for an MOH?

A

Refer

109
Q

Monitoring ?

A
  • Relief of headache within 2 hours after taking meds

- If additional symptoms present, relief of those symptoms should also occur in that time

Clinical 1 (Part B) (11 decks)

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