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CDM 2 > Exam 2: Pain > Flashcards

Exam 2: Pain Flashcards

1
Q

T/F: Pain affects more Americans than DM, heart disease, and cancer COMBINED

A

True

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2
Q

T/F: Over-treatment of pain is a problem defined in literature

A

FALSE - UNDERtreatment is a problem within community, hospital, or nursing homes

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3
Q

Pain is a ___ and ___ experience. It is also (objective/subjective)

A

Sensory and emotional experience

It is SUBJECTIVE

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4
Q

How do you know if someone is in pain?

A

They say so – it is SUBJECTIVE

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5
Q

T/F: Pain is always objective

A

FALSE – it is SUBJECTIVE
Patient’s report of pain is most reliable info available
Pt must be given benefit of doubt of the presence/absence of pain
Deception is counterproductive and polarizes patient-caregiver relationship

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6
Q

Consequences of pain

A

Unnecessary suffering
Respond less well to curative medical or surgical treatments
Higher complication rate
Musculoskeletal injuries – further tissue damage
Show more emotional disturbance
Disability and loss of funciton
In some circumstances, die sooner

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7
Q

Which pt pops are at higher risk of undertreatment?

A

Elderly and young – inability to communicate or rate their pain

Use changes in behavior and physiologic s/sx (HR) to suggest pain (fussy, inconsolable, changes in eating patterns, crying out, or agitation)

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8
Q

Acute pain situations may result in OBJECTIVE data changes associated:

A

HTN, tachycardia, diaphoresis, mydriasis, pallor (but NOT diagnostic)

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9
Q

Acute pain duration

A

<3 months

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10
Q

Chronic pain duration

A

> 3-6 months

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11
Q

Common causes of acute pain

A

Surgery, acute illness (pancreatitis, sickle cell flair), trauma, musculoskeletal injuries, labor, post-op pain, etc.

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12
Q

Acute or Chronic?: Follows body injury and generally appears when the body heals, has a well-defined temporal onset, usually nociceptive in nature

A

Acute

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13
Q

How does acute pain serve as a warning or protective purpose?

A

It permits us to live in an environment fraught with dangers
Learning comes from the experience
Adaptive

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14
Q

Acute pain: Painful, continuous stimulation can induce:

A

Suffering
Neuronal remodeling
May contribute to the development of chronic pain (becoming maladaptive)

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15
Q

Acute or Chronic?: Usually defined as pain which lasts beyond the ordinary duration of time that the body needs to heal itself, does not resolve spontaneously, pain persists 3-6month or longer

A

Chronic

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16
Q

Chronic pain: Maladaptive pain characteristics

A

May not have well-defined temporal onset
underlying cause may not be treatable
Serves no physiologic roles an dit itself not a symptom, but a disease state (maladaptive)
May last months to years

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17
Q

Maladaptive pain results from ____ or _____ of the peripheral nervous system (PNS) and/or central nervous system (CNS)

A

damaging or abnormal functioning

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18
Q

Maladaptive pain often mixes causes with which 3 mechanisms present at the same time?

A

Nociceptive
Neuropathic
Centralized

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19
Q

Acute or Chronic?: Pathophysiologic pain, disengaged from noxious stimuli or healing

A

Chronic

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20
Q

Acute or Chronic?: Pain that persists beyond the normal healing time for an acute injury – post herpetic neuralgia

A

Chronic

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21
Q

Acute or Chronic?: Pain related to chronic disease – osteoarthritis, lower back pain

A

Chronic

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22
Q

Acute or Chronic?: Pain without identifiable organic cause – fibromyalgia

A

Chronic

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23
Q

Acute or Chronic?: Pain associated with cancer

A

Chronic

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24
Q

Acute or Chronic: Often associated with s/sx of depression

A

Chronic

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25
Q

What can result from untreated chronic pain?

A

May have profound morbidity associated
Disrupting normal living and degrading functional capacities

Immobility
immune system dysfunction
disturbed sleep
Poor appetite and nutrition
Over-dependence on family and other caregivers 
Overuse and inappropriate use of healthcare providers
Poor job performance
Isolation from society and family
Anxiety and fear
Hopelessness
Helplessness
Bitterness, frustration, suicide
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26
Q

Acute or Chronic?: USUALLY obvious source: injury, disease, iatrogenic (surgery)

A

Acute

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27
Q

Acute or Chronic? Intensity generally variable and indicative of underlying condition or situation

A

Acute

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28
Q

Acute or Chronic?: Prolonged functional impairment (physical and psychological)

A

Chronic

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29
Q

Acute or Chronic: Rubbing, moaning, crying

A

Acute

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30
Q

Acute or Chronic?: May or may not be a/w insomnia, anorexia, irritability, depression

A

Chronic

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31
Q

Acute or Chronic?: Often more difficult to manage

A

Chronic

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32
Q

Treatment goal of ACUTE pain

A

Cure

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33
Q

Treatment goal of CHRONIC pain

A

Funcitonality

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34
Q

WHO Step Ladder: Step 1 pain level

A

1-3 out of 10

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35
Q

WHO step ladder: Step 2 pain level

A

4-6 out of 10

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36
Q

WHO Step Ladder: Step 3 pain level

A

7-10 out of 10

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37
Q

Nociceptive pain results from _____

A

Injury to or inflammation of somatic or visceral tissues

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38
Q

T/F: Nociceptive pain is unresponsive to typical analgesics

A

False - responsive to typical analgesics

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39
Q

Examples of nociceptive pain

A 
Paper cut
Burn
Arthritis (hands, knees, and hips)
Trauma
Muscle strains or sprains
Tendonitis
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40
Q

What adjuvants are not typically used for nociceptive pain?

A

Anti-epileptic-like gabapentinoids (gabapentin and pregabalin)

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41
Q

4 Steps of physiologic process of pain

A

Stimulation
Transmission
Perception
Modulation

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42
Q

Stimulation of ____ is the first step in pain sensation

A

Free nerve endings (nociceptors)

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43
Q

_____ can distinguish between safe or harmful stimuli

A

Nociceptors

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44
Q

Nociceptors are found in…

A

Cutaneous structures
Somatic structures
Visceral structures

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45
Q

Nociceptors are activated and sensitized by ____, ____, and _____ impulses

A

mechanical
Thermal
Chemical

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46
Q

Stimulation: Injury to tissue causes cell breakdown and release various mediators of inflammation and those that communicate pain. What are some examples of these mediators?

A

Bradykinins, potassium, prostaglandins, histamine, leukotrienes, serotonin, substance P

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47
Q

Stimulation: ____ and ___ can result at this stage

A

Vasodilation and edema (redness/swelling)

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48
Q

T/F: Many of the nerve endings are minimally sensitized and function at their resting state

A

True

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49
Q

Stimulation: Some substances (___ and ___) can cause INCREASED sensitization of the nociceptor resulting in a lower threshold for firing and cause them to generate nerve impulses

A

Bradykinin and serotonin

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50
Q

Stimulation: Receptor activation leads to action potentials that are transmitted to the ____

A

spinal cord

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51
Q

Transmission: Signals created by the nociceptors travel primarily along 2 afferent fiber types to the spinal cord and brain – ____ and ____

A

A and C afferent fibers

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52
Q

A alpha and beta nerve fibers

A

Large, fast, and myelinated fibers

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53
Q

A delta nerve fibers

A

Small-diameted myelinated fibeers

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54
Q

______ nerve fibers transmit sharp, well-localized pain

A

A fibers

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55
Q

C fibers

A

Small-diameter unmyelinated fibers

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56
Q

___ nerve fibers transmit dull, aching, poorly localized pain

A

C fibers

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57
Q

Transmission: 2 processes must occur from transmission to be complete (for pain to be felt)

A

From periphery to spinal cord

Spinal cord to the brain

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58
Q

Transmission to the spinal cord: Most neural signals travel to the ___ of the spinal cord

A

Dorsal horn (DH)

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59
Q

Transmission to the spinal cord: The afferent fibers synapse on neuroreceptors in varying layers of the dorsal horn, releasing neurotransmitters like ___

A

Glutamate, substance P, and calcitonin gene-related peptide

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60
Q

Transmission to the spinal cord: These interactions influence pain ___, ___, and ____ to the pain (Gate Control Theory)

A

Pain sensation, magnitude, and response to the pain

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61
Q

___ is when the pain becomes a conscious experience

A

Preception

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62
Q

Perception: Nociceptive info from the DH travels to the brain via the ___ to the ____ where the input is mapped to preserve certain information like location, intensity, and quality

A

Via thalamus to the contralateral somatosensory cortex

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63
Q

Perception: There are at least ___ known ascending spinal cord pathways, ___ tract being the most known

A

At least 5 are known – spinothalmic tract is most known

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64
Q

After pain info is processed, the response is sent out of the brain via descending pathways from brain to ___ to ___

A

brain to spinal cord to periphery

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65
Q

Modulation: ___ and ___ modulate pain through a number of intricate processes (gate control theory)

A

Brain and spinal cord

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66
Q

Pain transmission: may be facilitated by _____ to make signals stronger and pain more intense

A

Neurotransmitters like glutamate and substance P

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67
Q

Pain transmission can be attenuated/inhibited by descending pathways that consists of ___ __ __ or ___

A

Endogenous opioids, GABA, NE, or serotonin

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68
Q

Modulation: Cognitive and behavioral functions can modify pain: Examples

A

Relaxation, distraction, meditation, and guided mental imagery may strongly influence pain perception and decrease pain sensation

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69
Q

Modulation: ____ often worsens pain

A

Depression or anxiety

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70
Q

Modulation: Neurotransmitters involved

A 
Glutamate
Substance P
Endogenous opioids
Serotonin
NE
GABA
Neurotenisn
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71
Q

Modulation: Cognitive and behavioral functions that may modify pain perception

A 
Relaxation
Distraction
Meditation
Guided mental imagery 
Stress, anxiety
Depression
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72
Q

2 important concepts that are involved in nociceptive pain (occur at and adjacent to the site of injury)

A

Adaptive inflammation

Central sensitization

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73
Q

Adaptive inflammation def

A

In response to trauma (sprain, surgical wound, traumatic injury) the body will purposefully cause inflammation/swelling

Decreases contact with and minimal movement to injured area (prevents further injury, allows healing to begin)

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74
Q

Central sensitization

A

In response to tissue damage and inflammation in the CNS – neurotransmitters change composition, transduction, and transmission properties, resulting in enhance excitability/responsiveness and result in ENHANCED pain

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75
Q

Changes caused by central sensitization may result in

A

Hyperalgesia – an exaggerated pain response
Allodynia - painful response to a normally non-noxious stimuli (pt with gout, breeze can feel painful)
Persistent pain

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76
Q

Hyperalgesia def

A

An exaggerated pain response

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77
Q

Allodynia def

A

Painful response to a normally non-noxious stimuli

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78
Q

T/F: Maladaptive inflammation can play a role in chronic pain

A

True

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79
Q

T/F: Central sensitization also plays a role in neuropathic pain, chronic pain, and fibromyalgia

A

True

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80
Q

___ pain is due to damaged or dysfunctional nerves

A

Neuropathic

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81
Q

Neuropathic pain: Nerves that are cut off from input from the periphery (amputation) that may become __active

A

hyperactive

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82
Q

Nociceptive or neuropathic?: “Dully, sharp, cramp, aching”

A

Nociceptive

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83
Q

Nociceptive or neuropathic?: “Burning, radiating, shooting, shock-like, electric, tingling”

A

Neuropathic

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84
Q

Nociceptive or Neuropathic: Responsive to typical analgesics

A

Nociceptive

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85
Q

Nociceptive or neuropathic?: Poorly responsive to typical analgesics

A

Neuropathic

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86
Q

Nociceptive or neuropathic: Peripheral neuropathy (DM, HIV/AIDS, Cancer), post herpetic neuropathy, phantom limp pain

A

Neuropathic

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87
Q

Neuropathic pain syndromes

A 
Diabetic neuropathy
Post herpetic neuralgia (shingles)
HIV-associated pain
Phantom limb pain
Post stroke pain
Spinal cord injury
Lower back pain
Multiple sclerosis
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88
Q

T/F: APAP and NSAIDs are helpful for neuropathic pain

A

False

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89
Q

Which meds are not helpful for neuropathic pain?

A

NSAIDS/APAP
Steroid injections
Hyaluronic acid injections

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90
Q

Centralized pain is also known as

A

functional pain

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91
Q

T/F: Nerve injury and inflammation exists for centralized (functional) pain

A

FALSE – NO nerve injury or inflammation exists

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92
Q

Centralized (functional) pain: Disturbances in pain processing within the nervous system that leads to pain hypersensitivity and subsequently spontaneous pain

A

Fibromyalgia
Irritable bowel syndrome (IBS)
Temporomandibular joint disorder
Chronic tension headaches.

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93
Q

____ is a result of an abnormal operation of the nervous system

A

Centralized (functional) pain

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94
Q

Explain Centralized (functional) pain pathophysiology

A

Caused by abnormal signal processing in the peripheral or CNS – nerve injury causing lower level of activation energy for action potential firing
Enhancement of NE, serotonin inhibition resulting in overall excitement of DH which manifests as mechanical hypersensitivity and allodynia or spontaneous pain

Nerve damage or persistent stimulation may cause pain circuits to rewire themselves both anatomically and biochemically

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95
Q

Describe fibromyalgia

A

A disorder of chronic, widespread pain and tenderness
Considered a rheumatoid disease (syndrome)

Etiology is unknown, typically presents in young or middle aged women but can affect either sex at any age

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96
Q

T/F: In fibromyalgia, painful muscles are accompanied by inflammation and body damage/deformity

A

FALSE - Painful muscles are NOT accompanied by inflammation and despite potentially disabling body pain, pts do not develop body damage or deformity

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97
Q

Fibromyalgia: Studies suggest that the CNS may be somehow ___-sensitized

A

super sensitized

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98
Q

Which meds are not used for centralized(functional) pain?

A

Steroid injections
Hyaluronic acid injections

(non-opioids, weak opioids, opioids are not THAT effective but still can be used)

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99
Q

Non-opioid analgesics (APAP/NSAIDs) primary indication

A

Pain relief for pts who do not respond to non-pharmacologic interventions

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100
Q

APAP or NSAIDs: Anti-inflammatory mechanism of pain relief

A

NSAIDs only

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101
Q

APAP or NSAIDs?: Can be used monotherapy or in combo

A

BOTH

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102
Q

APAP or NSAIDs: Can be combined with opioids

A

BOTH

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103
Q

APAP or NSAIDs?: Fever reducing properties

A

BOTH

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104
Q

APAP or NSAIDs?: Central acting mechanism of pain relief

A

BOTH

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105
Q

APAP effective in what type of pain?

A

Mild
Mild-moderate

NOT effective for chronic low back pain

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106
Q

T/F: APAP is effective in chronic low back pain

A

FALSE - it is NOT effective in chronic low back pain

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107
Q

NSAID effective in what type of pain?

A

Mild
Moderate
Severe

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108
Q

APAP Rx or OTC?

A

OTC, dosing based on safety

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109
Q

NSAIDs Rx or OTC?

A

Rx and OTC

Max dosing based on if Rx or OTC

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110
Q

APAP or NSAIDs?: Considered 1st line oral agent due to safety profile (particularly if tx is long term or in high safety risk individuals)

A

APAP – safer than NSAIDs hence why it is 1st line but it may not be as effective

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111
Q

NSAIDs: Are oral or topical agents considered to be safer?

A

Topical – but more expensive (2nd line or alt therapy)

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112
Q

NSAIDs safety profile matters

A

GI risk (can be minimized with PPI use)
Renal
CV
Concomitant med use (HTN, warfarin)

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113
Q

When to use non-opioid analgesics (APAP/NSAIDs) prn examples

A 
Headache
Dysmenorrhea
Short lived muscle pain – strain or sprain
Short lived knee pain - injury
Fever
Tendonitis
Bursitis
Osteoarthritis
Rheumatoid arthritis
Post-op from surgery
Trauma
Cancer-related pain
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114
Q

When to use non-opioid analgesics (APAP/NSAIDs) Long term use

A 
Osteoarthritis
Rheumatoid arthritis
Severe sprain
Chronic back pain
Cancer-related pain
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114
Q

When to use non-opioid analgesics (APAP/NSAIDs) Long term use examples

A 
Osteoarthritis
Rheumatoid arthritis
Severe sprain
Chronic back pain
Cancer-related pain
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115
Q

APAP: Dosage forms

A

Tablet, capsule, liquid, rectal supp (rectal bioavailability 50-60% of that achieved by oral administration), IV

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116
Q

APAP onset of pain or fever relief

A

30 min

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117
Q

APAP duration

A

about 4 hrs

Increased to 6-8 hrs with ER formulations

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118
Q

APAP renal dosing

A

CrCl 10-50 give q6h

CrCl <10 give q8h

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119
Q

APAP Side effects

A

Well tolerated
If using other products that contain APAP - Be mindful of total daily APAP dose
Overdose
Liver toxicity *be careful of high doses!
Uncommon SE: GI (> 2 g/day) and nephrotoxicity (high dose, chronic use)

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120
Q

APAP DDI

A

Warfarin (increase INR)
Alcohol (hepatotoxicity, 3+ drinks/day)
CBZ, phenytoin, rifampin, (induces metabolism and increases toxic metabolite, hepatotoxicity – limit APAP to 2g/day)
Black cohosh (actaea racemosa, hepatotoxicity if used long term with high dose APAP)
Kava (piper methysticum, hepatotoxicity if used long term with high dose APAP)
Milk thistle (decreased APAP efficacy)

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121
Q

APAP Overdose

A 
Delayed sx (N, V, drowsiness, confusion, abdominal pain)
Manifestations of hepatotoxicity begins 2-4 days post ingestion (jaundice, increased LFTs, etc..)
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122
Q

When to use APAP

A

Mild - moderate pain syndromes
Fever reducer
Safer in long term pain control

Safer for:
Pregnancy / breastfeeding / elderly
Taking anticoagulants
Dz states: 
CV dz, HTN, renal dz, GI disorders

Commercially available opioid combo products
Tylenol #3 (codeine + APAP)
Vicodin (hydrocodone + APAP)
Percocet (oxycodone + APAP)

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123
Q

APAP is considered safer for…

A

pregnancy/breastfeeding/elderly
Taking anticoags
Disease states - CV, HTN, renal, GI

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124
Q

APAP Combo products

A

Tylenol #3 (codeine + APAP)
Vicodin (hydrocodone + APAP)
Percocet (oxycodone + APAP)

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125
Q

Tylenol #3 is combo with ___ and ___

A

codeine and APAP

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126
Q

Vicodin is combo product with __ and __

A

Hydrocodone and APAP

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127
Q

Percocet is combo product with __ and __

A

Oxycodone and APAP

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128
Q

When to NOT use APAP

A

Significant liver disease
Significant alc use (≥3 drinks/day)
Achieving pain relief only at high doses

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129
Q

APAP liver failure – chronic use of ___g/day can lead to increased LFTs after > ___ days (does not necessarily suggest progression to liver failure)

A

4g/day

after >4 days

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130
Q

APAP max dosing (Rx and OTC)

A

4000mg/day OTC (No Rx APAP – prescriptions written so it is covered by insurance but it is same as OTC)

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131
Q

Ibuprofen max dosing (Rx and OTC)

A

3200mg/day Rx

1200mg/day OTC

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132
Q

Naproxen max dosing (Rx and OTC)

A

1500mg/day Rx

600mg/day OTC

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133
Q

Naproxen sodium max dose (Rx and OTC)

A

1375-1650mg/day Rx

660mg/day OTC

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134
Q

Ketoprofen max dose (Rx and OTC)

A

300mg/day Rx

75mg/day OTC

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135
Q

APAP IV formulation name

A

Ofirmev

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136
Q

APAP IV (Ofirmev) approved for ages ___ and up

A

2yo and up

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137
Q

APAP IV (Ofirmev) approved for

A

mild-moderate pain and moderate-severe pain with opioids

Fever reduction

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138
Q

APAP IV (Ofirmev) dosing

A

Weight based

650mg IV q6h prn pain
15min infusion

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139
Q

APAP IV (Ofirmev) common ADRs

A

N/V
HA
Insomnia

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140
Q

APAP IV (Ofirmev) Cautions

A 
Hepatic impairment or active liver disease
Alcoholism (≥3 drinks/day)
Chronic malnutirition 
Severe hypovolemia
Severe renal impariment
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141
Q

NSAIDs MOA

A

Relieves pain through peripheral inhibition of COX and subsequent inhibition of prostaglandin synthesis

142
Q

Prostaglandin effects on the stomach

A

Inhibits gastric acid secretion

Stimulates synthesis of GI mucous

143
Q

Prostaglandin Effect on renal

A

Maintains renal blood flow

144
Q

Prostaglandin Effect on blood

A

Enhances platelet aggregation – increases clotting (vasoconstriction)

145
Q

Prostaglandins inflammatory effect

A

Inflammation – pain, fever, edema (vasodilation)

146
Q

COX 1 inhibition effects

A

GI – epigastric distress, ulceration, hemorrhage
Renal – Na, H2O retention, edema, interstitial nephritis
Anti-coagulant effects

147
Q

COX 2 inhibition effects

A

Anti-inflammatory
Analgesic
Anti-pyretic

148
Q

COX 1 effects which parts

A

GI, Renal, Platelets

149
Q

COX 2 effects which parts

A

Inflammation – pain, fever, edema (vasodilation)

150
Q

T/F: NSAIDs have a class effect – if one doesn’t work, all the NSAIDs options probably don’t work

A

FALSE – they do not have a class effect, if ibuprofen doesn’t work, try naproxen

Little literature substantiates that one agent is more effective than another
Patients who do not tolerate or is ineffective to one particular agent, may do well with another

151
Q

NSAIDs formulation types

A 
PO
Topical
Rectal
IM
IV
152
Q

NSAIDs onset of action

A

30min

153
Q

NSAIDs duration for Naproxen

A

12h

154
Q

NSAIDs duration of action for ibuprofen

A

6-8 hours

155
Q

Which NSAID is used in acute settings due to availability as injectable?

A

Ketorolac – available as IM/IV/PO (Limit to 5 days of use total to avoid ADEs)

156
Q

Ketorolac limit use to ___ days

A

5 days

157
Q

NSAIDs: Avoid oral diclofenac due to increased

A

CV events, causes more liver toxicity, more GI toxicity

Topical diclofenac is less risky due to low absorption

158
Q

Naproxen sodium (OTC) strength and directions

A

220mg q8-12hours

First dose you can take 2 caps within first hours
Do not exceed 2 caps in any 8 to 12 hour period
Do not exceed 3 caps in 24hr period

Do not take more than directed, use smallest effective dose

If taken with food, may take longer before it works

159
Q

Ibuprofen (OTC) strength and directions

A

200mg 1 tab q4-6 hours

Do not take more than directed, use smallest effective dose
If pain does not respond to 1 tab, then take 2 tabs

Max 6 tabs/24hr period

160
Q

Naproxen sodium (Rx) strength

A

IR - 275, 550mg

ER- 375, 500mg

161
Q

Ibuprofen (Rx) strength

A

400, 600, 800mg

162
Q

NSAIDs safety profile considerations: Kidney disease

A

Avoid if renal insufficiency – CrCl <30ml/min

163
Q

NSAIDs safety profile considerations: HTN

A

NSAIDs promote water retention can increase about 5 mmHg and make anti-HTN meds less effective

164
Q

NSAIDs safety profile considerations: CAD

A

Risk of MI, stroke based in PG inhibition

Contraindicated in the setting of CABG surgery

165
Q

NSAIDs safety profile considerations: HF

A

NSAIDs promote water retention, increased risk of HF exacerbation and CV event (MI or stroke)

166
Q

NSAIDs safety profile considerations: Severe liver disease

A

Bleeding risk due to anti-platelet effects and direct stomach irritation (people with severe liver disease have compromised clotting factor synthesis)

167
Q

NSAIDs safety profile considerations: GI disorder

A

Bleeding risk due to anti-platelet effects and direct stomach irritation

168
Q

NSAIDs safety profile considerations: Pregnancy

A

Category C, lactation: Possibly unsafe (naproxen)

Category B, lactation: safe (ibuprofen)

169
Q

NSAIDs safety profile considerations: Elderly

A

Greater risk for GI adverse effects and other side effects based on age or other comorbidities

170
Q

NSAIDs safety profile considerations: Pediatrics

A

Weight based dosing - look it up

Self-care: can use IBU for ≥6 months of age and naproxen >12yo

171
Q

NSAIDs safety profile considerations: Veterinary

A

Don’t give IBU or naproxen to cats or dogs ever?? apparently

172
Q

NSAIDs ADEs

A

GI - dyspepsia, ulcer, bleeding (dyspepsia due to direct irritation to stomach, not COX)
CV - thrombotic events
Renal - sodium and fluid retention, acute renal failure

173
Q

NSAIDs ADE: explain GI ADEs

A

Dyspepsia due to direct irritation to the stomach
Ulcers - COX inhibition decreases mucous production and causes ulcers
Bleeding - COX inhibition causes inhibition of platelet agg and increases risk of bleeding

174
Q

NSAIDs: Moderate risk factors for GI bleeding

A

60yo and up
Current high dose of NSAID
Uncomplicated peptic ulcer history
Concomitant use of ASA, anticoags, or corticosteroids

175
Q

NSAIDs: High risk factors for GI bleeding

A

Hx of previous complicated/bleeding ulcer

Multiple (>2) risk factors

176
Q

NSAIDs: Other risk factors for GI bleeding

A

H. pylori infection
cigarette smoking
alcohol use
Chronic debilitating disorders (esp. CV)

177
Q

NSAIDs: GI ADEs: How to protect from dyspepsia

A

Take with food
Antacids, H2 blockers, PPI
Enteric coated, buffered, SR, or PR dosage forms

178
Q

NSAIDs: GI ADEs: How to protect from Ulcer/bleeding

A

Choose COX2 selective NSAID

Enteric coating, buffering, sustained-release DO NOT protect from bleed risk!!!

179
Q

Selective NSAID example

A

Celecoxib

180
Q

Celecoxib Max dosing

A

200mg/day

181
Q

Which NSAID is safest for GI SE

A

Celecoxib

182
Q

If pt is at high risk of GI ADEs, add on ____

A

PPI, misoprostol, or high dose H2 blocker

183
Q

Out of non-selective NSAIDs, which is more likely to be safe for GI risk?

A

Ibuprogen

184
Q

When to stop celecoxib for procedure with risk of bleeding (colonoscopy)

A

1 day before (no antiplatelet effects)

185
Q

When to stop non-selective NSAIDs prior procedure with bleeding risk?

A

7 days prior (ASA has longer anti-platelet effects than other non-selective NSAIDs)

186
Q

NSAID issue for CV risks

A

Renal effect - sodium, water retention, edema, interstitial nephritis – affects BP, preload, etc. !!
Vasoconstriction/dilation balance

187
Q

Which non-selective NSAID increases cardiac risk (MI or stroke)?

A

ALL – naproxen is likely safer for CV risk

188
Q

Which COX 2 inhibitor increases CV risk (MI or stroke)?

A

Vioxx – risky at low doses, starts shortly after starting drug (taken off the market)
Celecoxib (Celebrex) – increased risk over 200mg/day

189
Q

High CV Risk considerations with NSAIDs

A

Hx of CV event, DM, HTN, HLD, obesity

190
Q

Administering NSAID ___ ASA may diminish the antiplatelet effect/cardiac benefit of ASA

A

BEFORE – do not take NSAID within 2hrs

191
Q

NSAIDs: concurrent drugs that increase bleeding risk

A

Anticoags, steroids, SSRIs

192
Q

NSAIDs: Drug interactions (renal)

A

Diuretics
ACEi/ARBs
All anti-HTN meds (reduces HTN med efficacy)
May increase the toxicity of lithium and methotrexate

193
Q

Which NSAID should you avoid use in G6PD deficiency

A

ASA

194
Q

How many weeks does it take to fully evaluate NSAID efficacy?

A

2-4 weeks

195
Q

When do you stop NSAID and call doctor

A

Sx of bleeding (black/tarry stool)
Pain worsens or lasts longer than 7-10 days
Fever worsens or lasts longer than 3 days
Any new sx appear

196
Q

Topical NSAIDs exampels

A

Diclofenac – Voltaren gel, Pennsaid solution, Flector patch

197
Q

Potential advantages of TOPICAL agents over systemic agents

A 
delivery at site
Lower rates of systemic absorption (lower risk of systemic ADEs but higher derm side effects)
Similar efficacy to oral NSAID
Pt preference
Recommended in older patients (>75yo)
198
Q

T/F: Systemic side effects are impossible with topical NSAIDs

A

FALSE – systemic conc can be achieved and systemic SE are possible, CV and GI warnings are in all topical package inserts

199
Q

T/F: You can combine NSAID topicals with oral agents

A

FALSE – do NOT combine

200
Q

Voltaren gel strength and approved uses

A

Voltaren gel 1% for OA

Voltaren gel 3% for Actinic keratosis

201
Q

Important counseling notes to know for voltaren gel

A

of joints matter! – dose limits for a single joint and total daily amount for all joints used (look it up when counseling)

Don’t use it on open skin wounds/infections/rash/burns

Do not cover treated skin or expose to heat (can increase absorption and cause harmful effects)

Wash hands after (don’t wear gloves until 10min after)

After applying, wait 10min before dressing and at least 1 hr before showering

Do not use oral NSAIDs in combo

202
Q

Flector Patch dosing

A

1 patch q12 hours

No advantage in efficacy or safety than topical gel – more expenisve

203
Q

Pennsaid important notes

A

It’s good for s/sx of OA of knees

40 drops per knee, 4 times/day

204
Q

Opioids work on which receptors?

A

Mu, kappa, delta

205
Q

Opioids that are STRONG agonists on mu, kappa, delta receptors

A 
Morphine
Hydromorphone
Methadone
Meperidine
Fentanyl
Oxycodone
206
Q

Opioids that are MILD to MODERATE agonists on mu, kappa, delta receptors

A

Codeine

Hydrocodone

207
Q

Opioids that are PARTIAL agonists on mu, kappa, delta receptors

A

Buprenorphine

208
Q

ANTAGONISTS of mu, kappa, delta receptors

A

Naloxone

209
Q

Recommendation for opioid in acute pain

A

3-7 day supply (try to use it less for acute pain)

210
Q

Avoid chronic pain dosing ≥ ____mg/day morphine equivalents (MME)

A

50mg/day MME

211
Q

50mg/day MME is about ___mg/day of hydrocodone

A

50mg/day

212
Q

50mg/day MME is about ___mg/day of oxycodone

A

30

213
Q

___ should be co-prescribed with chronic opioids

A

Naloxone

esp if hx of OD, substance use disorder, taking 50mg/day MME, concurrent benzodiazepine use

214
Q

Avoid opioid use with ___ or ___

A

benzodiazepines or muscle relaxants

215
Q

Opioids: Avoid or careful dosing considerations for:

A

Renal/hepatic dysfunction
Elderly ≥65yo
Pregnant
Other diseases (severe COPD, sleep apnea)
Other meds with CNS ADEs (benzo or msucle relaxants)

LOWER DOSES

216
Q

When to use IR opioids

A

Used PRN when pain is severe an duration of pain is expected to be short or infrequent

217
Q

Why should you NOT use IR opioids for scheduled basis for chronic pain

A

Shorter duration of effect – increasing pain at the end of dosing interval, needs multiple doses per day (creates pain cycles)
Pill burden
Higher risk of abuse

218
Q

When to use ER opioids

A

Usually starts with IR prn and then switch to appropriate ER dosing (oral or patch)

Prevents pain cycle

219
Q

When should you NOT use ER opioids

A

In opioid naive patients

on a prn basis

220
Q

Scheduled dosing for ER opioids - oral

A

every 12 hours (sometimes 8 hrs)

221
Q

Scheduled dosing for ER opioids - patch

A

Fentanyl patch every 72hrs (3 days)

222
Q

Most common IR opioid examples

A 
Morphine
Oxycodone
Oxycodone + APAP (percocet)
Hydrocodone + APAP (Vicodin)
Hydromorphone (dilaudid)
223
Q

Most common ER opioids use

A

Morphine (Contin, Roxanol, Kadian)
Oxycodone (OxyContin)
Fentanyl (Duragesic Patch)
Hydrocodone (Zohydro ER)

224
Q

Opioids: IR to ER calculations

A

Add up total daily dose of IR in 24 hour period

Divide by 2 (q12h dosing )

225
Q

ER opioids + prn IR opioids is reserved for ____

A

SEVERE pain situations, cancer pain, or end of life pain situations
NOT for typical chronic pain syndromes like OA, low back pain

226
Q

Breakthrough dose for severe chronic pain calculations

A

Add up total daily dose in 24hr period

10-15% of total every 4-6hours prn of IR formulation of same med of ER formulation

227
Q

NEW ER + IR breakthrough pain dose calculations

A

Add up total dose (ER + IR)
Divide by 2 for ER dosing q12h
10-15% of total daily dose q4-6 hours for IR dosing

228
Q

Switching from one opioid to another calculations

A

Add up total daily dose in 24hr period
Use conversion table
Reduce by 50% to help offset incomplete cross-tolerance
Divide daily dose based on duration of actions of drug/dosage form
Consider if a breakthrough regimen is needed and monitor

229
Q

Patient counseling for opioids

A

Do not increase dose w/o calling prescriber
Explain PRN meaning
Do not drive while using med
Do not use alcohol or sedatives unless approved by prescriber
When switching opioids, dosing must be titrated to response (different per person)
ADEs
Disposal of leftover pills

230
Q

Opioids ADEs

A

Constipation (need to treat)
Urinary retention (tolerance may develop)
N/V (may resolve after 48-72hrs)
Pruritis (histamine release, common with morphine, less with fentanyl, using antihistamine may be helpful)
Sedation, confusion, hallucinations, nightmares, dysphoria, euphoria, inability to concentrate
Accumulation - restlessness, agitation, tremor, myoclonus, seizure (meperidine, not with methadone)
Respiratory depression
DDI - additive CNS SE, serotonin syndrome with SSRI (tramadol, methadone)

231
Q

Opioids OD treatment

A

Naloxone – Injection (IV/IM/SC) or intranasal

232
Q

Opioid addiction treatment

A

Methadone
Buprenorphine +/- naloxone (Subutex or Suboxone)
Naltrexone (IM monthly injection, Vivitrol)

233
Q

Subutex generic

A

Buprenorphine

234
Q

Suboxone generic

A

Buprenorphine + naloxone

235
Q

Opioid true allergies: Morphine like agonist (Phananthrenes) examples

A 
Morphine
Hydromorphone
Hydrocodone
Codeine
Oxycodone
236
Q

Opioid true allergies: Meperidine like agonist (Phenylpiperidines) examples

A

Meperidine (Demeral)

Fentanyl (Duragesic)

237
Q

Methadone-like agonist (Diphenylheptanes)

A

Methadone

238
Q

Morphine Schedule

A

CII

239
Q

Morphine use

A

Excellent and cost effective first choice for severe acute and chronic pain management

Used in pain control associated with MI (decrease myocardial oxygen demand in ischemic cardiac pts)

240
Q

Oxycodone schedule

A

CII

241
Q

T/F: Oxycodone is superior than other opioids

A

FALSE - not more effective than other opioids

242
Q

Hydromorphone (Dilaudid) Schedule

A

CII

243
Q

Hydromorphone is ___ potent than morphine

A

MORE

244
Q

Which opioid is the gold standard

A

Morphine

245
Q

Hydrocodone schedule

A

CII

246
Q

Hydrocodone IR availability

A

Not available alone as IR but in combo with APAP (Vicodin)

247
Q

Hydrocodone ER options

A

Zohydro ER, Hysingla ER

Dosed q12hrs, alt to morphine and oxycodone use in chronic pain

248
Q

Vicodin schedule

A

CII

249
Q

Codeine schedule

A

Alone (CII)
with APAP or ASA (CIII)
Cough syrups (CIII or CV)

250
Q

Codeine is ___ potent than morphine

A

LESS

251
Q

T/F: Codeine is used for moderate pain

A

True

252
Q

Tylenol #2 has __mg codeine

A

15mg

253
Q

Tylenol #3 has ___ mg codeine

A

30mg

254
Q

Tylenol #4 has ___mg codeine

A

60mg

255
Q

Codeine: Many pts c/o ___

A

GI upset (not an allergy)

256
Q

Describe metabolism of codeine

A

Codeine is prodrug that is metabolized to morphine by CYP2D6
Ultra rapid metabolizers may develop toxic blood levels (converts faster and more completely)
Hydrocodone and oxycodone also metabolized to active metabolites by CYP2D6 (be careful)
Morphine not metabolized to active metabolites by CYP2D6

257
Q

Describe metabolism of codeine

A

Codeine is prodrug that is metabolized to morphine by CYP2D6
Ultra rapid metabolizers may develop toxic blood levels (converts faster and more completely)
Hydrocodone and oxycodone also metabolized to active metabolites by CYP2D6 (be careful)
Morphine not metabolized to active metabolites by CYP2D6

258
Q

Which opioids are metabolized into active metabolites?

A

Codeine, hydrocodone, and oxycodone metabolized to active metabolites by CYP2D6

Morphine NOT metabolized to active metabolites by CYP2D6

259
Q

Codeine Contraindications

A

All kids <12yo
Kids <18 after tonsilectomy or adenoidectomy

Do not use in kids 12-18 who are obese or have sleep apnea

Avoid in breastfeeding women – may be ultra rapid CYP2D6 metabolizer and cause toxicity to infant

260
Q

Methadone schedule

A

CII

261
Q

Methadone MOA

A

Opioid agonist, NMDA receptor antagonists, SNRI activity

262
Q

Methadone use

A

Used for opioid dependence and analgesic (chronic pain (nociceptive or cancer pain) and neuropathic pain (4th line, there’s better options)

263
Q

Methadone has ___ half-life and duration of action compared to other opioids and has ___ risk of accidental OD

A

LONGER half life

HIGHER risk

264
Q

Methadone DDI

A

Increases QT interval (antidepressants, antipsychotics, antiarrhythmic, macrolides, etc.)

Increase methadone levels (clarithromycine, erythromycin, azoles, fluoxetine, verapamil, etc.)

Decrease methadone levels (CBZ, phenytoin, rifampin, etc.)

Sedation (BDZ, Z-drugs, sedating antihistamines, ETOH)

HIV antivirals may increase or decrease levels (depends)

265
Q

Meperidine (Demeral) schedule

A

CII

266
Q

Meperidine is __ dosing only

A

Acute

Short acting – 3-4hrs

267
Q

Meperidine: When nor-metabolite accumulates what can occur?

A

Psychosis, tremos, muscle twitching, seizures

268
Q

Meperidine: Caution and avoid in

A

AVOID in renal insufficiency
Caution in elderly and hepatic impairment

No real adv to use with alt available

269
Q

Fentanyl schedule

A

CII

270
Q

Fentanyl formulations

A

IM, IV, transdermal patch, transmucosal

271
Q

Fentanyl may be used in pts with true allergy to ___

A

morphine

272
Q

___ may cause less pruritus and constipation than traditional opioids

A

Fentanyl

273
Q

Converting from other opioids to fentanyl patch

A

Calculate 24hr total daily dose (ER and IR)

Use table to get patch dose

274
Q

When can you use fentanyl patch

A

For chronic pain and for already opioid tolerant patients!!

275
Q

Can you cut/trim fentanyl patch

A

No

276
Q

Fentanyl patches are dependent on ____ and it will increase release of medication from patch

A

TEMPERATURE – high fever, heating pad, electric blanket, sauna/hot tub

277
Q

What to do when you DISCONTINUE fentanyl

A

Remove patch and titrate dose to a new analgesic based on pt report of pain

278
Q

___ hours or more are required for a 50% decrease in serum fentanyl conc

A

17

279
Q

How to dispose of fentanyl patches

A

Fold in half (adhesive folds to itself)

FLUSH down toilet (don’t put in trash– caution for children and pets)

280
Q

Fentanyl transdermal patch only indicated for pts

A

requiring continuous ATC opioid for an extended period of time

281
Q

Tramadol schedule

A

CIV

282
Q

Tramadol is effective for ___ nociceptive pain and neuropathic pain

A

Mild to moderate

Ultracet (tramadol + APAP) used for short term, mod acute pain

283
Q

Ultracet generic

A

Tramadol + APAP

284
Q

Tramadol brand name

A

Ultram, Ultram ER, Ryzolt

285
Q

Explain how tramadol is effective for neuropathic pain

A

Metabolite binds to mu receptor

Inhibits reuptake of serotonin and NE

286
Q

Tramadol ADEs

A

Nausea
Constipation
Drowsiness

(Less than other opioids)

287
Q

Tramadol efficacy is similar to ____

A

Tylenol #3

Less risk for respiratory depression
Risk for dependence
Limited to 5 refill on prescription

288
Q

tramadol refills are limited to only ___ refills

A

5

289
Q

Tramadol DDI

A

Serotonin syndrome risk with antidepressants that effect 5HT, triptans, lithium

Lowers seizure threshold (avoid in risk pts)

Others:

  • Hx of seizure, alc abuse, head trauma, taking bupropion, antidepressants (TCA), antipsychotics
  • increase levels of other drugs - warfarin dig
  • Other opioids - increase risk of adverse effects
  • CYP3A4 inducers: carbamazepine
290
Q

Tramadol metabolism

A

Prodrug

Converted to active metabolite by CYP2D6 (also 3A4)

291
Q

Tramadol contraindications

A

All kids <12yo
Kids <18yo after tonsilectomy and adenoidectomy
12-18 with sleep apnea
Breastfeeding women

292
Q

Tramadol place in thearpy

A

Acute, moderate pain (nociceptive or neuropathic)
Alt to stronger opioids in select pts for chronic pain (third alt after APAP or NSAIDs)
Fibromyalgia (3rd line behind anticonvulsants and antidepressants)

293
Q

First line agents for neuropathic pain

A

Anti-convulsants: Pregabalin, gapapentin
Antidepressants (SNRI): duloxetine, venlafaxine
Antidepressants (TCA): nortriptyline, desipramine (secondary amine for better SE profile)
Topicals: Lidocaine, capsaicin

294
Q

If there is no clinically meaningful effect after using first line agents for neuropathic pain what should yoou do next?

A

Try another one
Combo
Or add tramadol if trying another one or combining doesn’t work

295
Q

Pregabalin and gabapentin MOA

A

Selectively binds to voltage-gated CA channels – reduces calcium current and modulates excitatory neurotransmitters (glutamate, norepinephrine, substance P)

296
Q

Pregabalin brand name

A

Lyrica

297
Q

Pregabalin is FDA approved for

A

Diabetic peripheral neuropathy
Postherpetic neuralgia
Fibromyalgia

298
Q

Pregabalin can be used in combo with

A

Lidocaine, capsaicin, TCA, SNRI

299
Q

Pregabalin side effects

A

Dizziness, nausea, somnolence, peripheral edema, weight gain, confusion

CAUTION in elderly

300
Q

Pregabalin DDI

A

No clinically sig DDIs – additive CNS effects with other agents with CNS effects

301
Q

Pregabalin schedule

A

CV

302
Q

Pregabalin ___mg dose ratings of “good drug effect” “high” and “liking” similar to 30mg of diazepam

A

450mg

303
Q

Pregabalin dosing frequency/adjustments

A

BID or TID

Dose titration needed to tolerate ADEs

Renal adj

304
Q

Pregabalin onset usually within ___

A

a week

305
Q

Pregabalin caution in

A

elderly and pts with substance abuse hx

306
Q

Pregabalin must be tapered over ___ week when d/c

A

> 1 week

307
Q

Gabapentin IR brand

A

Neurontin

308
Q

Gabapentin enacarbil ER brand name

A

Horizant

309
Q

Gabapentin has enhanced efficacy when used in combo with ___

A

nortriptyline

310
Q

Gabapentin can be in combination with

A

lidocaine
capsaicin
TCA
SNRI

311
Q

Gabapentin FDA approved for

A

Post herpetic neuralgia

Gabapentin enacarbil ER (Horizant) for Restless Leg Syndrome (RLS)

312
Q

Gabapentin is effective in

A 
DM neuropathic pain
Post herpetic neuralgia
Trigeminal neuralgia
Restless leg syndrome (RLS)
Hot flashes
ETOH dependence
Fibromyalgia
313
Q

T/F: Only pregabalin (not gabapentin) has to be tapered with d/c

A

FALSE - both should be tapered when D/C

314
Q

T/F: Only gabapentin (not pregabalin) should be titrated to avoid ADEs

A

FALSE – both are titrated

315
Q

Gabapentin onset should be within __

A

a week

316
Q

Gabapentin for restless leg syndrome dosing frequency

A

Once daily

317
Q

Gabapentin dosing adjustments?

A

Renal insufficiency

318
Q

Gabapentin DDIs

A

Chelation with calcium, iron, antacids (2 hr separation)

Additive CNS effects with other agents with CNS effects

319
Q

Pregabalin or Gabapentin: which has higher risk of dependence?

A

Pregabalin

320
Q

Duloxetine (Cymbalta) can be used in combo with

A

Anticonvulsants or topicals

BUT NOT with other antidepressants

321
Q

Duloxetine ADEs

A

Nausea, dizziness, somnolence, fatigue

Take on full stomach

322
Q

Duloxetine FDA approved for

A

DM neuropathy
Fibromyalgia
LBP/OA

323
Q

Duloxetine onset within

A

a wekk

324
Q

Duloxetine brand name

A

Cymbalta

325
Q

Duloxetine dosing

A

60mg daily (start 30mg daily x1 week, then increase dose)

326
Q

Duloxetine DDIs

A 
CYP1A2 substrate
CYP2D6 substrate
CYP2D6 inhibitor, moderate
Antiplatelet effects
CNS depression
Hyponatremia
Lowers seizure threshold
Strong serotonergic effects – combining with other agents modulating serotonin can cause serotonin syndrome
327
Q

SNRI are likely effective for neuropathic pain because of modulation of ___ more than ___ modulation

A

NE (not serotonin)

328
Q

SNRI Examples for neuropathic pain

A

Duloxetine

Venlafaxine

329
Q

___ is as effective as imipramine for polyneuropathies

A

Venlafaxine

330
Q

Venlafaxine ADEs

A

Nausea, somnolence, HA, insomnia
HTN
cardiac rhythm change

331
Q

T/F: Venlafaxine low doses are just as effective as high

A

FALSE - low doses are inaffective

332
Q

Venlafaxine doses

A

150-225mg daily

333
Q

TCA has no FDA indication for pain but useful in pain stated for ___

A

those with or w/o depression

334
Q

Difference in efficacy between TCA

A

No diff – all are effective but amitriptyline most studied

335
Q

T/F: TCA lower doses are effective for pain

A

True - lower doses than antidepressant effects/doses

336
Q

Can use TCA in combo with

A

Anticonvulsants or topicals

337
Q

TCA sedation onset

A

1-3 hrs

338
Q

When to take TCA

A

10-12hrs before awake time (rather than “bedtime”

Start low dose to minimize ADEs

339
Q

Amitriptyline dosing

A

50-150 mg HS

340
Q

Nortriptyline dosing

A

50-150mg HS

341
Q

Imipramine dosing

A

100mg QD

342
Q

Despramine dosing

A

100mg QD

343
Q

TCA ADEs

A 
Sedation
Anticholinergic SE (dry mouth, constipation, urinary retention, blurred vision, tachycardia) -- caution elderly BPH
Interaction characteristics (CNS depression, CYP2D6 substrate, hyponatremia, lowers seizure threshold, serotonin effects, prolonged QT interval
344
Q

Avoid using TCA in

A

Second or third-degree heart block, arrhythmias, prolonged QT interval, severe liver disease, recent MI

345
Q

SSRI for neuropathic pain

A

Inferior to TCAs but better SE profile
Partially effective for DM neuropathy
Fluoxetine generally NOT effective

346
Q

Fibromyalgia non-drug approaches

A

Exercise
Reduce stress
Sleep hygiene
Cognitive behavioral therapy

347
Q

Fibromyalgia FDA approved agents

A

Duloxetine (Cymbalta)
Milnacipran (Savella)
Pregabalin (Lyrica)

348
Q

Fibromyalgia non-FDA approved agents

A

Gabapentin
Tramadol
TCA
Cyclobenzaprine

349
Q

Agents to avoid in Fibromyalgia bc lack of benefit

A

NSAIDs
Capsaicin
Opioids

350
Q

Cancer pain def

A

Pain syndromes associated with malignant pain or cancer pain

Can be pain caused by the disease itself, or by painful diagnostic procedures or treatments

351
Q

Why does cancer pain have its own classification?

A

Has both acute and chronic components
Often has multiple etiologies
Hard to classify based on duration/pathology
Although there is a distinct pain syndrome called Cancer Pain, many clinicians will diagnose a patient with cancer with either acute or chronic pain

352
Q

What is bone pain and how is it described?

A

Pain resulting from bone disruption bc of a malignant tumor is growing on the bone

“sore” “aching”

353
Q

Bone pain treatment options

A

NSAID, radiopharmaceuticals, opioids – tumors active nociceptors by pressure, ischemia, or secretion of locally acting algesic substance (prostaglandin E2)

Bisphosphonate therapy - imbalance between bone formation and resorption resulting in an imbalance and bone destruction

CDM 2 (8 decks)

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