Pain Basics-Chronic Pain Flashcards
No Opioids
1
Q
Pain is an unpleasant _______ and _________ experience associated with, or resembling that associated with, ______ or _________ tissue damage
A
sensory; emotional; actual; potential
2
Q
Men vs. women: Which is chronic pain more common in?
A
Women
3
Q
There is a disparity among race/ethnicity in terms of chronic pain. Which group in Canada has the highest prevalence?
A
Indigenous Peoples
4
Q
What are 4 occupations/activities commonly associated with chronic pain?
A
- Veterans
- Physical labor
- Repetitive strain injuries
- Desk work
5
Q
What is the biopsychosocial model of pain? (5)
A
Pain affects all aspects of one’s life:
- Reduced QoL and general health
- Mental and emotional health
- Problems with cognitive function
- Decreased social connections and support
6
Q
What are the 3 classifications of pain?
A
- Nociceptive
- Neuropathic
- Nociplastic
7
Q
Acute vs. Chronic Pain: Duration
A
Acute: < 3 months
Chronic: > 3-6 months
8
Q
Acute vs. Chronic Pain: Organic cause
A
Acute: Common
Chronic: Uncommon
9
Q
Acute vs. Chronic Pain: Relief of pain
A
Acute: Highly desirable
Chronic: Highly desirbale
10
Q
Acute vs. Chronic Pain: Treatment goal
A
Acute: Pain reduction (“cure”)
Chronic: Functionality
11
Q
Acute vs. Chronic Pain: Dependence and tolerance to medication
A
Acute: Unusual
Chronic: Common
12
Q
Acute vs. Chronic Pain: Psychological component
A
Acute: Usually not present
Chronic: Often a major concern
13
Q
Acute vs. Chronic Pain: Environmental/family issues
A
Acute: Small
Chronic: Significant
14
Q
Acute vs. Chronic Pain: Depression
A
Acute: Uncommon
Chronic: Common
15
Q
Acute vs. Chronic Pain: Insomnia
A
Acute: Unusual
Chronic: Common component
16
Q
What is nociceptive pain?
What is it usually described as?
A
- Arises from damage to body tissue; typically pain one experiences as a result of injury, disease, or inflammation
- Usually described as sharp, aching, or throbbing pain
17
Q
Burning your hand on a hot stovetop is an example of what kind of pain?
A
Nociceptive
18
Q
What is neuropathic pain?
What is it usually described as?
A
- Arises from direct damage to the nervous system itself, usually peripheral nerves but can also originate in CNS
- Usually described as burning or shooting/radiating, the skin might be numb, tingling, or extremely sensitive - even to light touch (allodynia)
19
Q
Post-herpetic neuralgia (i.e., shingles pain) is an example of what kind of pain?
A
Neuropathic
20
Q
What is nociplastic pain?
What is it usually described as?
A
- Arises from a change in the way sensory neurons function, rather than from direct damage to the nervous system; sensory neurons become more responsive (sensitization)
- Usually described similar in nature to neuropathic pain
21
Q
Fibromyalgia is an example of what kind of pain?
A
Nociplastic
22
Q
Within nociceptive pain, there are two types, somatic and visceral. What does each arise from?
A
Somatic: skin, bone, joint, muscle, or connective tissue
Visceral: internal organs (e.g., large intestine, pancreas)
23
Q
Within nociceptive pain, there are two types, somatic and viscreral. What are each described as?
A
Somatic: sharp, hot, stinging, throbbing
Visceral: dull, cramping, colicky, gnawing, aching, squeezing, pulsing
24
Q
Within nociceptive pain, there are two types, somatic and visceral.
Where is each localized?
A
Somatic: Generally localized with surrounding tenderness
Visceral: Poorly localized
25
Fracture, strain, laceration, burn, arthritis (osteo- and inflammatory) are what kind of nociceptive pain?
Somatic
26
Pancreatitis, appendicitis, peptic ulcer disease, menstrual cramping are what kind of nociceptive pain?
Visceral
27
What are the names of each step of nociceptive pain pathophysiology? (TCTPM)
1. Transduction
2. Conduction
3. Transmission
4. Perception
5. Modulation
28
What are the steps of transduction of nociceptive pain? (SNDAp)
1. Mechanical, thermal, and chemical impulses lead to release/activation of NTs that *stimulate* -->
2. *Nociceptors* that have to -->
3. *Distinguish between* -->
4. Either innocuous stimuli or noxious stimuli. If noxious -->
5. Activate the nociceptors to transmit *action potentials* along afferent nerve fibers to the spinal cord
29
What are the steps of conduction of nociceptive pain? (2 then branches)
1. Receptor activation involving voltage-gated sodium channels
2. Generation of action potentials conducted along afferent A-ẟ and C-nerve fibers to spinal cord
3a. A-ẟ stimulation = sharp, localized pain
3b. C-fiber stimulation = achy, poorly localized pain
30
What are the steps of transmission of nociceptive pain? (4)
1. A-δ and C-nerve fibers synapse in various layers (laminae) of the spinal cord’s dorsal horn
- Release excitatory neurotransmitters (e.g. glutamate, substance P)
2. N-type voltage-gated calcium channels regulate the release of these excitatory neurotransmitters
3. Pain signals reach brain through various ascending spinal cord pathways (including spinothalamic tract)
- Thalamus acts as relay station within brain
4. Pathways ascend and pass impulses to higher cortical structures for further pain processing
31
What is going on in the perception of nociceptive pain? (2)
1. Pain becomes a conscious experience
2. Occurs in higher cortical structures
32
In nociceptive pain modulation, the brain and spinal cord modulates pain via numerous ways. How does it strengthen/intensify it?
Strengthened/intensified by additional release of glutamate, substance P
33
In nociceptive pain modulation, the brain and spinal cord modulates pain via numerous ways. How does it attenuate/inhibit it?
Attenuated/inhibited by descending pathways with endogenous opioids (endorphins, enkephalins), GABA, NE, serotonin
34
What are 2 ways in which neuropathic pain differs from nociceptive pain?
1. No noxious stimuli
2. Result of damage or abnormal functioning of the PNS +/- CNS
35
Within neuropathic pain, there are two types, peripheral and central. What does each arise from?
Peripheral: Peripheral nerves
Central: Central Nervous System
36
Within neuropathic pain, there are two types, peripheral and central. What is each described as?
Both described the same:
- Sharp, shooting/radiating, tingling, burning, freezing, itching
37
Within neuropathic pain, there are two types, peripheral and central. Where is each localized?
Peripheral: Generally localized with shooting/radiation up the nerve fiber
Central: Poorly localized
38
Post-herpetic neuralgia, diabetic peripheral neuropathy, chemotherapy-induced neuropathy, are examples of which kind of pain + subcategory?
Neuropathic - peripheral
39
Post-ischemic stroke, multiple sclerosis are examples of which kind of pain + subcategory?
Neuropathic - central
40
Describe the steps of how nociplastic pain develops. e.g., X leads to Y, which leads to Z
Tissue or nerve damage leads to pain circuits rewiring themselves, which leads to chronic pain
41
Nociplastic pain is also known as?
The faulty smoke detector
42
Step 1 of nociplastic pain is tissue or nerve damage. What is happening here? (2)
1. Tissue damage or nerve damage may cause both peripheral and/or central changes in neurotransmission
2. PLUS predisposing risk factors: family history of pain, history of recurrent pain, mental health disorders,
abuse/trauma, and many others not yet fully understood
43
Step 2 of nociplastic pain is pain circuits rewiring themselves. What is happening here? (3)
1. Neuroplasticity (rewiring of anatomical/biochemical nerve systems)
2. Produces a mismatch between pain stimulation/inhibition
3. Increases discharge of dorsal horn neurons
44
Step 3 of nociplastic pain is chronic pain. What is happening here? (3)
1. Patient presents with episodic or continuous pain transmission, hyperalgesia, dysesthesias, and allodynia
2. Ongoing pain generator is not found
3. Pain is often widespread and/or migrating
45
What are some general clinical presentations of acute pain?
1. Obvious distress
2. Children/infants: change in feeding, fussiness
3. People with dementia: change in eating, ↑ agitation, facial grimacing, calling out
46
Mental/emotional factors can influence pain perception. How might pain threshold be increased?
Increased pain threshold by rest, mood elevation, sympathy
46
Mental/emotional factors can influence pain perception. How might pain threshold be decreased?
Decreased pain threshold by anxiety, depression, fatigue, anger, fear
47
What are some potential signs of acute pain? (6)
1. HTN
2. Tachycardia
3. Diaphoresis (sweating)
4. Mydriasis (dilation of the pupil)
5. Pallor (pale)
6. May have no obvious signs
48
True or False? There is a lab test that can be done to check for acute pain
False
49
Pain management is most effective when validated and accurate pain assessments are carried out. What are the 2 tools?
1. Self-rated pain intensity scales
- Adult: visual analogue or numerical rating scale
- Child: Faces scale (Bieri or Wong-Baker)
2. Observational tools
- If unable to communicate
- PAINAD (dementia), FLACC (> 2 months), CHEOPS (>1 year), PACSLAC (dementia)
50
What are the P's of PQRSTU assessment of pain? (2)
P:
- Provocative
- Palliative
51
What are the Q's of PQRSTU assessment of pain? (2)
Q:
- Quality
- Quantity
52
What are the R's of PQRSTU assessment of pain? (2)
R:
- Region
- Radiation
52
What is the S of PQRSTU assessment of pain?
S:
- Severity
52
What are the T's of PQRSTU assessment of pain? (2)
T:
- Timing
- Treatment
53
What is the U of PQRSTU assessment of pain?
U:
- Understanding
54
Go through the acute pain treatment approach. 5 steps.
1. Assess patient thoroughly, in collaboration with diagnostician(s)
2. Compare, contrast, and select treatment (therapeutic thought process)
* Select the most effective analgesic with fewest ADEs/risk
* Lowest dose for shortest duration, around the clock for first few days then prn
3. Identify non-pharm and interdisciplinary resources
4. Educate patient, including setting expectations
5. Communicate with others and document plans, including preparing for periods of transition (e.g., discharge from hospital, opioid exit strategy)
55
The primary goal of therapy for pain depends on type of pain present and should be tailored to individual pain and circumstance. What are 2 good goals for acute pain? What are 2 good goals for pain in general?
Acute:
1. Acute pain: achieve level of pain relief that allows patient to attain certain functional goals (usually = get back to normal function) → cure
2. Realistic pain reduction = may be possible to fully eliminate pain, unlike in chronic pain
General:
3. Prevent or minimize ADEs
4. Improve quality of life
56
What is THE overarching non-pharmacologic therapy for acute pain?
Education
57
List some non-pharmacologic therapies that could be used for acute pain? (10 - dont really need to get them all)
1. Distraction and relaxation
2. Cold (< 48 hours post-injury)
3. Positioning
4. Acupuncture
5. Exercise
6. MEAT
7. Heat (> 48 hours post-injury)
8. Immobilization
9. Massage
10. TENS
58
Although not fully understood, what is the MOA of acetaminophen?
Inhibit CNS prostaglandins, peripherally block pain impulse generations
59
What are 4 ADEs associated with acetaminophen?
1. Liver toxicity
2. Overdose
3. May increase systolic BP (~3-4mmgHg)
4. Rare neutropenia or thrombocytopenia
60
What places in therapy does acetaminophen have? (3)
1. Reduction of fever (1st line)
2. Mild-moderate acute pain
3. Pediatric moderate pain
61
What are 2 CI's of acetaminophen?
1. Acetaminophen-induced liver disease
2. Hypersensitivity to acetaminophen, or any component of the formulation
62
What is the max acetaminophen dose for adults per 24 hours?
4g (4000mg)
63
What is the dosing of immediate release regular strength acetaminophen in adults?
325-650mg q4-6h
64
What is the dosing of immediate release extra strength acetaminophen in adults?
500-1000mg q4-6h
65
What is the dosing of extended release acetaminophen (e.g., Tylenol Arthritis) in adults?
1300mg q8h
66
What is the max dosing of acetaminophen in children?
75 mg/kg/day or 4000mg/24 hours (whichever comes first)
67
What is the dosing of oral acetaminophen in children?
10-15 mg/kg/dose q4-6h (PRN)
68
What is the dosing of rectal acetaminophen in children?
Dosing can be 10-20 mg/kg/dose; same daily max as oral
69
What is the MOA of non-selective NSAIDs? (2)
1. Inhibit COX-1 and 2 enzymes, which results in decreased formation of prostaglandin precursors
2. Antipyretic, analgesic, and anti-inflammatory properties
70
What is the MOA of COX-2 inhibitors (Coxibs - NSAID type)? (3)
1. Inhibit prostaglandin synthesis by decreasing the activity of the enzyme, COX-2, which results in decreased formation of prostaglandin precursors
2. Antipyretic, analgesic, and anti-inflammatory properties
3. Do not inhibit COX-1 at therapeutic concentrations
71
What are the places in therapy for NSAIDs? (3)
1. Mild to moderate pain (osteoarthritis, acute & chronic low back pain)
2. Dysmenorrhea-induced pain
3. Fever (only ibuprofen and naproxen)
72
What are the CI's of NSAIDs? (8)
1. CKD (CrCl < 40mL/min)
2. Hyperkalemia
3. Cirrhosis/ Liver impairment
4. GI Ulcer (duodenal/ peptic) + IBD
5. Uncontrolled Heart Failure
6. MI
7. Thrombocytopenia
8. Transplant
73
What are the ADE's of NSAIDs and ASA? (8)
1. Dyspepsia
2. Edema
3. GI Bleed
4. N/V
5. Phototoxic Reaction
6. CNS : Dizziness, drowsiness, headache, tinnitus, confusion (especially in the elderly & with indomethacin). CNS effects may be dose related.
7. Minor or serious skin rashes, pruritus
8. COX-2 selective – similar efficacy & renal/CV toxicity to other NSAIDS, but less GI risk
74
What are 3 cautions to using NSAIDs?
1. Asthma
2. CVD, HTN
3. Risk of bleeding increases perioperatively, discontinue pre-surgery
75
What is the MOA of ASA? (2)
1. Irreversibly inhibits COX-1 and COX-2 enzymes via acetylation which decreases formation of prostaglandin precursors
2. Antipyretic, analgesic, and anti-inflammatory properties
76
What place in therapy (pain-wise) does ASA have? (2)
1. Mild-moderate pain (short term use)
2. Reduction of fever
77
What are 3 CI's of ASA?
1. Hypersensitivity to NSAIDs, anaphylaxis
2. CKD (CrCl < 40mL/min)
3. GI Ulcer
78
What are 3 cautions to using ASA?
1. Concurrent antiplatelet and/or anticoagulant therapy
2. Risk of Reye syndrome in children
3. Toxic in overdose (tinnitus, vertigo, hyperventilation, respiratory alkalosis, hyperthermia, coma, death)
79
ASA Dosing:
How much to reduce platelet aggregation?
< 300 mg/day
80
ASA Dosing:
How much to be antipyretic and analgesic?
300-2400 mg/day (325-650 mg po q4h prn)
81
ASA Dosing:
How much to be anti-inflammatory?
2400-4000 mg/day
82
What is the max amount of ASA per day?
4g
83
What is the most COX-2 selective NSAID?
Diclofenac
84
What is the most COX-1 selective NSAID?
Ketoprofen
85
What is the po dose of diclofenac IR and SR? What is the max dose/day?
IR: 50mg BID (prn)
SR: 75-100mg daily (prn)
Max = 100mg/day
86
What is the dosing of IR ibuprofen for adults?
OTC and Rx
Should know the max dose as well
OTC: 200-400mg q4-6h (prn) (max 1200 mg/day)
Rx: 600mg q6h (prn) (max 2400-3200mg/day)
87
The NSAID with the highest risk of GI toxicity is?
Ketorolac (Toradol)
88
What is the dosing of ketorolac?
What is the max?
10mg QID (prn)
Max: 40 mg/day, 5 days limit b/c of increase GI bleed risk
89
What is the dosing of naproxen sodium (OTC)?
What is the max?
125-500mg BID (prn)
Max: 1500mg/day
90
What is the dosing of naproxen base (Rx)?
What is the max?
250-500mg BID (prn)
Max: 1000mg/day
91
____________ __ produced by the COX-1 pathway on activated platelets is platelet ___________ and ________________
Thromboxane A2; aggregating; vasoconstricting
92
____________ produced by the COX-2 pathway in nearby smooth muscle cells is a platelet _________ and ____________
Prostacyclin; inhibitor; vasodilating
93
Why is ASA cardioprotective?
ASA, as a non-reversible COX inhibitor (COX-1>COX-2), inhibits platelet aggregation even at low doses and is cardioprotective
94
Selective COX-2 inhibitor NSAIDs "tip the balance" in favor of: (3)
1. Vasocontriction
2. Platelet aggregation
3. Thrombosis
95
There is a concern of cardiac risk with all NSAIDs/COXIBs. They appear to be dose related (higher dose higher risk). Which 2 (and what dose) are good to know for increasing CV risk?
1. Diclofenac (≥ 150 mg/day)
2. Celecoxib (> 200 mg/day)
96
What is the most neutral CV NSAID? What is the dose?
Naproxen (≤ 750 mg/day)
97
How do prostaglandins produced by the COX-1 pathway work on the GIT? (3)
Increases in:
1. GI mucosal blood flow
2. Mucous and bicarbonate production
3. Epithelial growth
98
NSAIDs inhibit COX-1 which leads to what GI issues? (3)
1. Decrease prostaglandins
2. Decrease gastroduodenal mucosal production
3. Increase GI ulcer risk
99
How might we manage GI risk associated with NSAIDs?
Consider misoprostol or PPI (add-on or combo product)
100
What are the criteria for high risk of NSAID GI toxicity? (2)
1. History of complicated ulcer, especially recent
2. Multiple (>2) risk factors (seen in the moderate chart)
101
Moderate risk of NSAID GI toxicity is having 1-2 risk factors. What are 5 potential risk factors?
1. Older age ≥60 years, ≥70 years
2. NSAID use: high dose or multiple agents
3. History of uncomplicated ulcer
4. Concurrent ASA (including low dose), corticosteroids, anticoagulants, or SSRIs
5. History of CVD
102
Recommendations for Prevention of NSAID complications:
Low GI risk + Low CV risk. What to give?
NSAID alone
103
Recommendations for Prevention of NSAID complications:
Moderate GI risk + Low CV risk. What to give?
NSAID + PPI/misoprostol
104
Recommendations for Prevention of NSAID complications:
High GI risk + Low CV risk. What to give?
Alternate therapy OR COX-2 inhibitor + PPI/Misoprostol
105
Recommendations for Prevention of NSAID complications:
Low GI risk + High CV risk. What to give?
Naproxen + PPI/Misoprostol
106
Recommendations for Prevention of NSAID complications:
Moderate GI risk + High CV risk. What to give?
Naproxen + PPI/Misoprostol
107
Recommendations for Prevention of NSAID complications:
High GI risk + High CV risk. What to give?
Avoid NSAIDs & COX-2 inhibitors. Use alternate therapy
108
What is the renal risk associated with NSAIDs/COXIBs? (2+2)
1. Prostaglandins (PGE2, PGI2) produced by the COX-1 and COX-2 pathways are vasodilating
2. NSAIDs inhibit COX-1 and COX-2 which leads to
- Vasoconstriction of afferent renal arteriole
- ↓ ability for kidneys to regulate blood flow
109
What are the 2 managment options for NSAID/COXIBs and renal risk?
1. Avoid in CKD (CrCl < 40 mL/min)
2. Monitor creatinine, urea within 3-7 days after initiating therapy
110
What are 7 risk factors for NSAIDs/COXIBs and renal risk?
1. Age ≥ 70 years
2. Pre-existing renal disease
3. Volume depletion (diuretics)
4. Combined use with ACEI or ARB (dilate efferent arteriole)
5. HF
6. Cirrhosis
7. Long-term history of NSAID use
111
What is the main advantage of Celecoxib?
It being a selective COX-2 inhibitor, which is primarily involved in pain and inflammation. Spares the inhibition of COX-1, which decreases the risk of GI complications and has minimal platelet effect
112
What are 2 cautions for Celecoxib?
1. Dose adjustments recommended for elderly and CYP2C9 metabolizers
2. Carries similar renal risk as non-selective NSAIDs
113
What is the dosing of celecoxib for acute pain? What is the max?
Celecoxib 400mg PO as a single dose on the first day, followed by 200mg PO once daily (up to 7 days);
Max dose = 400mg/day for up to 7 days
114
What is the dosing of celecoxib for other indications?
What is the max?
Dose ranges from 100-200mg PO once daily to twice daily (max dose = 200 or 400mg per day, depending on indication)
115
What are 5 DI's seen with NSAIDs/COXIBs?
1. ↓ anti-HTN effect: ACE-I, ARB, beta-blocker, thiazides
2. ↑ toxicity of: lithium, methotrexate, steroids, tenofovir, warfarin
3. ↑ risk of GI bleed: warfarin, heparin, corticosteroids, SSRI
4. ↑ nephrotoxicity: ACE-I, ARB, diuretics
5. ↓ efficacy of ASA antiplatelet effect if co-administered
116
NSAIDs/COXIBs in pregnancy. Yay or nay?
Nay
117
NSAIDs/COXIBs in lactation. Yay or nay?
May consider agents with shorter half-life
- Ibu, diclofenac
118
What is the MOA of the muscle relaxants? (Baclofen, Cyclobenzaprine, Methocarbamol)
- Centrally-acting drugs via heterogeneous mechanisms
- Little/no actual relaxant effect on tissues --> misnomer
- Effect linked to sedation and resultant central relaxation?
119
What is a CI for muscle relaxants?
Age > 65 years old
120
What are 4 cautions for using muscle relaxants?
1. Increased CNS adverse effects
2. Hepatic toxicity (esp with Tylenol)
3. Hypotension
4. Risk usually > benefit, esp in chronic treatment
121
What is the place in therapy for muscle relaxants? (3)
1. Might consider for spasms (ACUTE low back pain)
2. No evidence that they are more effective than acet/NSAIDs
3. Limit use to < 1-2 weeks
122
WHO recommends a 3-step ladder approach to using nonopioids as initial treatment and escalating to either “weak” or “strong” opioids based on mild, moderate, severe pain intensity ratings (Controversy regarding analgesic ladder use)
Go through the approach (btw, this is for cancer pain)
1. Nonopioid (acet, ASA, NSAIDs). If pain persists -->
2. Weak opioid (codeine). If pain persists or increases -->
3. Strong opioid and nonopioid (morphine, hydromorphone, fentanyl)
123
When to refer someone for pain?
Use of acet/NSAIDs for self-medication of pain should generally not exceed 10 days in adults or 5 days in children, unless directed by a prescriber
124
What is chronic secondary pain? (2)
1. Diagnosed when pain originally emerges as a symptom of another underlying health condition
2. May persist even after the underlying condition has been treated, in which case it is considered a disease in its own right
125
What is chronic primary pain? (3)
1. Persists or recurs for longer than 3 months, and
2. Is associated with significant emotional distress (e.g., anxiety, anger, frustration, depressed mood) and/or significant functional disability (interferes with activities of daily living (ADLs) and participation in social roles), and
3. The symptoms are not better accounted for by another diagnosis
126
What is the general presentation of neuropathic pain? (2)
1. Severity may be out of proportion to the degree or severity of the pathology or initial nerve injury
2. Ongoing nerve damage from persisting factors (e.g., poorly controlled diabetes) can worsen or spread pain over time
127
What are the symptoms of neuropathic pain? (4)
1. Constant or pulsating pain (shock-like, burning, buzzing, stinging, itching, shooting, radiating [AKA radiculopathy if shooting from lower back down leg(s])
2. Hypersensitivity to external (e.g., hot/cold, touch) or internal (e.g., anxiety) stimuli
3. Hyperalgesia: exaggerated pain by normally painful stimulus
4. Allodynia: pain caused by normally nonpainful stimulus
128
What are 3 signs (tests) of neuropathic pain?
1. ↓ pinprick sensitivity threshold measured with weighted needles
2. ↓ vibratory sense measured using tuning fork
3. Slowed peripheral nerve conduction on nerve conduction studies (can be very painful)
129
What is tuning fork neuropathy testing for neuropathic pain?
1. Tap the tuning for to create vibration
2. Apply base of the tuning fork to a bone on the tip of the great toe
3. Ask the patient to tell you where the vibration stops
4. Confirm
130
What is the general presentation of nociplastic pain? (2)
1. Can appear to have no noticeable suffering to complete writhing over pain for all waking hours
2. Note mental/emotional factors influence pain perception
- ↓ pain threshold by anxiety, depression, fatigue, anger, fear vs. ↑ pain threshold by rest, mood elevation, sympathy
131
What are symptoms of nociplastic pain? i.e., how are they described and how does it change throughout the day? (2)
1. Described in any possible way, often varying in location or “migrating”
2. Symptoms may change throughout the day or over time (often occur without a temporal association to an obvious noxious stimuli)
132
What are the signs of nociplastic pain? (3)
1. In most cases, no obvious signs
- Some conditions specific (e.g., CRPS - redness, swelling, hair or nail changes in one limb)
2. Comorbid conditions very commonly present (e.g. insomnia, depression, anxiety) - not always
3. Outcome of treatment often unpredictable
133
What is the Brief Pain Inventory (BPI) Intensity and Interference used for/what do they tell us? (2 - 1 for intensity, 1 for interference)
Intensity: Use responses to individual questions or the mean score from all four questions to track pain fluctuations and/or management over time
Interference: Use responses to individual questions or the mean score from all seven questions to track function of pain in ADLs over time
134
The best pain treatment uses a combination of the 4 P's. What are they?
1. Prevention
2. Psychological
3. Physical
4. Pharmaceutical
135
What is 1st line for chronic pain?
Non-pharmacological therapies
- Essential to long-term success in chronic pain
136
What are 5 barriers to non-pharmacological therapies for pain management?
1. Cost
2. Availability
3. Motivation
4. Practical limitations
5. Logistics
137
What are 5 enablers to non-pharmacological therapies for pain management?
1. Realized benefit on physical, mental, and social wellbeing
2. Adequate and regular identification of personal motivators
3. Education about hurt vs. harm
4. Generally less risk than meds
5. Low-cost or free services available
138
What are 5 possible red flag symptoms for when you'd refer for back pain?
1. Possible fracture
2. Possible cancer
3. Possible cauda equina syndrome
4. Possible infection
5. Possible inflammatory condition
139
What is cauda equina syndrome/what are the symptoms? (5)
1. Bladder dysfunction
2. Saddle anesthesia
3. Severe or progressive neurologic dysfunction in legs
4. Lax anal sphincter
5. Major motor weakness
140
Acetaminophen in chronic back pain. Yay or nay? (4)
1. Does not appear effective, is not recommended by guidelines
2. If patient finds benefit, use lowest effective dose (consider max 3200 mg/day)
3. PRN/adjunct use for acute or chronic pain
4. First choice for people with dementia due to effectiveness in this population and safety
141
NSAIDs for chronic back pain. Yay or nay? (4)
1. May be effective for some to manage chronic inflammation causing pain
2. Lowest effective dose, shortest duration (reassess as risks may > benefits over time)
3. Non-selective and COX-2 inhibitor comparable efficacy, must consider individualized risk vs. benefit
4. PRN/adjunctive use for acute or chronic pain
142
Muscle relaxants for chronic back pain. Yay or nay? (2)
1. No role in chronic pain unless concurrent spasicity
- Short term use only (< 2 weeks) for acute low back pain
2. May cause more of a sedative effect than actual relaxant effect
143
Evidence-wise, what are our top 3 interventions for chronic lower back pain?
1. Exercise
2. Oral NSAIDs
3. SNRIs (duloxetine)
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What are 2 other "non-pharms" that have evidence of benefit for chronic lower back pain?
1. Spinal manipulation
2. Psychotherapy (CBT)
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As of 2021 what 2 interventions fall into the 'very low' category grade of evidence for neuropathic pain?
1. Acupuncture
2. TCAs
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As of 2021, what 2 interventions fall into the 'moderate' category grade of evidence for neuropathic pain?
1. Anticonvulsant medications
- Gabapentin
- Pregabalin
- Oxcarbazepine
- Topiramate
2. SNRIs
- Duloxetine
- Venlafaxine or desvenlafaxine
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Thoughts on exercise for neuropathic pain treatment?
Not the foundation of the treatment plan as with back pain. But we should still encourage pts to move as much as possible, just not going to influence pain intensity as much
148
What are the limitations with chronic pain literature? (6)
1. Pain is entirely subjective and cannot be measured in a consistently reliable way
2. Primary outcomes are not always meaningful to patients and are heterogeneous across trials
3. Drug trials were historically funded by industry
4. Drug trials are relatively short in duration (< 12 weeks) ?long-term net benefit
5. Multimodal therapy introduces additional potentially confounding factors into drug trials
6. Recruitment of participants in active treatment trials/arms (e.g., exercise, CBT) may be subject to selection bias
149
For painful diabetic neuropathy:
What is the dosing of amitriptyline or nortriptyline?
25-100 mg/day HS
150
For painful diabetic neuropathy:
What is the dosing of duloxetine?
Venlafaxine?
Desvenlafaxine?
Dulox: 40-60 mg/day
Ven: 75-225 mg/day
Des: 200-400 mg/day
151
For painful diabetic neuropathy:
What is the dosing of pregabalin?
Gabapentin?
Pregab: 300-450 mg/day (divided BID-TID)
Gaba: 1800 mg/day (900-3600 mg, divided TID-QID)
152
For post-herpetic neuralgia:
What is the dosing of amitriptyline or nortriptyline?
75-150 mg/day
153
For post-herpetic neuralgia:
What is the dosing of duloxetine?
60 mg/day
154
For post-herpetic neuralgia:
What is the dosing of pregabalin?
Gabapentin?
Pregab: 300-600 mg/day (divded BID-TID)
Gaba: 1800 mg/day (1800-3600 mg, divided TID-QID)
155
For trigeminal neuralgia:
What is the dosing of carbamazepine?
200 mg QID
156
What is the MOA of gabapentinoids?
Block release of excitatory NTs by binding specific Ca channels in the CNS (structurally similar to GABA but NO effect on GABA NTs)
157
What are the ADEs of the gabapentinoids? (9)
1. Dizziness/drowsiness
2. H/A
3. N/V
4. Mood changes
5. Tremor
6. Nystagmus (rapid, uncontrollable eye movement)
7. Ataxia (loss of muscle control in arms and legs)
8. Peripheral edema
9. Weight gain
158
What are some DIs of gabapentinoids? (2)
1. CNS depressants and anticholinergics (pharmacodynamic interactions)
2. Serotonergic agents or potentiators (e.g., mirtazapine, opioids)
159
Where are gabapentinoids eliminated?
100% renally
160
True or False? Gabapentin F is proportional to dose?
False - gabapentin F is inversely proportional to dose due to saturable absorption, pregabalin has regular PK
161
What is the MOA of TCAs?
Inhibit the reuptake of serotonin and NE, block Na channels, block N-methyl-d-aspartate (NMDA) agonist-induced hyperalgesia
162
What are the ADEs of TCAs? (5)
1. Anticholinergic
2. Postural hypotension
3. Sedation
4. Confusion
5. QT prolongation
163
What are the CIs of TCAs? (2)
1. MAOI use in past 7 days
2. Severe liver impairment
164
TCA dose for pain is _____ than for depression
lower
165
When starting and/or ending gabapentinoids, TCAs, or SNRIs, doses should be ________ and _______
titrated; tapered
166
What is the MOA of SNRIs?
Inhibit the reuptake of serotonin and NE at neuronal junctions
(duloxetine also has weak inhibition of dopamine reuptake)
167
What are the ADEs of SNRIs? (6)
1. Drowsiness
2. Sedation
3. Constipation
4. Nausea
5. Hypotension OR increased HR/BP
6. Hyponatremia
168
What are the key characteristics of fibromyalgia? (4)
1. A condition that can wax and wane over time
2. Diffuse body pain
3. Present for at least 3 months
4. Symptoms of fatigue, sleep disturbance, cognitive changes, mood disorder, and other somatic symptoms
169
The best strategy for fibromyalgia pain is?
Non-pharmacological. Exercise specifically.
