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Pain 1 Flashcards

1
Q

What is pain?

A

an unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage
-a highly personal experience

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2
Q

What type of role does pain usually serve?

A

an adaptive role
-may have adverse effects on function, social, & psychosocial well-being

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3
Q

True or false: pain is the same as nociception

A

false

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4
Q

How prevalent is pain?

A

1/5 Canadians live with chronic pain
a 17.5% increase projected between 2019-2030
1/14 have “high impact chronic pain”
1/3 over the age of 65 live with chronic pain

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5
Q

True or false: pain is more common in women

A

true
-women > 65 have the highest prevalence of chronic pain

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6
Q

What is the biopsychosocial model of pain?

A

pain affects all aspects of ones life
-reduced QOL and general health
-mental and emotional health
-problems with cognitive function
-school/work absence and reduced productivity
-decreased social connections

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7
Q

Based on pathophysiology, what are the classifications of pain?

A

nociceptive
neuropathic
nociplastic

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8
Q

Differentiate acute and chronic pain.

A

duration:
-acute: < 3 months
-chronic: > 3-6 months
organic cause:
-acute: common
-chronic: may not be present
relief of pain:
-both: highly desirable
treatment goal:
-acute: pain reduction(“cure”)
-chronic: functionality
dependence and tolerance to medication:
-acute: unusual
-chronic: common
psychological component:
-acute: usually not present
-chronic: often a major concern
environmental/family issues:
-acute: small
-chronic pain: significant
depression:
-acute: uncommon
-chronic: common
insomnia:
-acute: unsual
-chronic: common

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9
Q

Provide the general definition for the three classifications of pain based on pathophysiology.

A

nociceptive:
-arises from damage to body tissue; typical pain one experiences as a result of injury, disease, or inflammation
neuropathic:
-arises from direct damage to the nervous system, usually peripheral nerves but can also originate in CNS
nociplastic:
-arises from a change in the way sensory neurons function, rather than from direct damage to the nervous system; sensory neurons becomes more responsive (sensitization)

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10
Q

What are the two types of nociceptive pain?

A

somatic
visceral

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11
Q

Describe somatic nociceptive pain.

A

arises from:
-skin, bone, joint, muscle, or connective tissue
described as:
-sharp, hot, stinging, throbbing
localization:
-generally localized with surrounding tenderness
examples:
-fracture, strain, laceration, burn, arthritis

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12
Q

Describe visceral nociceptive pain.

A

arises from:
-internal organs
described as:
-dull, cramping, colicky, gnawing, aching, squeezing, pulsing
localization:
-poorly localized
examples:
-pancreatitis, appendicitis, PUD, menstrual cramping

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13
Q

What are the steps involved in the pathophysiology of nociceptive pain?

A

transduction
conduction
transmission
perception
modulation

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14
Q

Describe transduction as the first step in nociceptive pain.

A

stimuli–>nociceptors which have to distinguish between:
-innocuous stimuli
-noxious stimuli: activate nociceptor to transmit action potentials along afferent nerve fibers to the spinal cord

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15
Q

Describe conduction as the second step in nociceptive pain.

A

receptor activation involving Na-gated channels
generation of action potentials conducted along afferent A-S and C-nerve fibers to spinal cord
-A-S stimulation=sharp, localized pain
-C-fiber stimulation=achy, poorly localized pain

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16
Q

Describe transmission as the third step in nociceptive pain.

A

A-S and C-nerve fibers synapse in various layers of the spinal cords dorsal horn
-release excitatory neurotransmitters
N-type voltage-gated Ca channels regulate release of these excitatory neurotransmitters
pain signals reach brain through various ascending spinal cord pathways
pathways ascend and pass impulses to higher cortical structures for further pain processing

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17
Q

Describe perception as the fourth step in nociceptive pain.

A

pain becomes a conscious experience
occurs in higher cortical structures
physiology of perception not well understood

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18
Q

Describe modulation as the final step in nociceptive pain.

A

brain and spinal cord modulate pain via numerous ways
strengthened/intensified by additional release of:
-glutamate, substance P
attenuated/inhibited by descending pathways with:
-endogenous opioids, GABA, NE, 5HT

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19
Q

What is the pathophysiology of neuropathic pain?

A

different from nociceptive pain:
-no noxious stimuli
-result of damage or abnormal functioning of the PNS +/- CNS

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20
Q

What are the two types of neuropathic pain?

A

peripheral nerve injury
central nerve system injury

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21
Q

Describe peripheral neuropathic pain.

A

arises from:
-peripheral nerves
described as:
-sharp, shooting/radiating, tingling, burning, freezing, itching
localization:
-generally localized with shooting/radiation up the nerve fibre
examples:
-PHN, diabetic neuropathy, chemo induced

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22
Q

Describe central neuropathic pain.

A

arises from:
-central nervous system
described as:
-sharp, shooting/radiating, tingling, burning, freezing, itching
localization:
-poorly localized
examples:
-post ischemic stroke, MS

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23
Q

Describe the pathophysiology of nociplastic pain.

A

tissue or nerve damage:
-may cause both peripheral and/or central changes in neurotransmission
-plus predisposing risk factors
pain circuits rewire themselves:
-neuroplasticity
-produces a mismatch between pain stimulation/inhibition
-increases discharge of dorsal horn neurons
chronic pain:
-patient presents with episodic or continuous pain transmission, hyperalgesia, dyesthesias, allodynia
-pain is often widespread and/or migrating

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24
Q

How long is acute pain?

A

typically < 3-6 months

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25
What is the cause of acute pain?
tissue damage signaling harm or potential for harm -serves a useful purpose -may outlive its biological usefulness and have -ve effects
26
True or false: acute pain typically does not have an identifiable cause
false
27
Typically, what kind of pain is acute pain?
usually nociceptive, sometimes neuropathic
28
What are the symptoms of acute pain?
sharp, dull, shock like, tingling, shooting, radiating, fluctuating in intensity, varying in location -occur in a timely response with an obvious noxious stimuli
29
What are the signs of acute pain?
may be no obvious signs -HTN, tachycardia, diaphoresis, mydriasis, pallor -comorbidities not usually present -outcome of treatment often predictable
30
What are the expected lab test of acute pain?
no specific lab test pain is always subjective -best diagnosed based on patient description/history
31
When is pain management most effective?
when validated and accurate pain assessments are carried out
32
What are examples of self-rated pain intensity scales?
adult: visual analogue or numeral rating scale child: faces scale (Bieri or Wong-Baker)
33
What is the PQRSTU assessment?
provocative/palliative -what makes it worse/better? quality/quantity -what does it feel like? how bad is it? region/radiation -where is the pain? does it move around? severity -how bad /10? timing/treatment -when did it start? constant or episodes? tried anything? understanding -what do you think is causing it?
34
What are the red flags for referral of back pain?
cauda equina syndrome: -bladder dysfunction -saddle anesthesia -dysfunction in legs -lax anal sphincter -motor weakness
35
What is the approach to treatment of acute pain?
1. assess patient thoroughly 2. compare, contrast, and select treatment -most effective analgesic with fewest AEs/risk -lowest dose for shortest duration, scheduled then prn 3. identify non-pharm and interdisciplinary resources 4. educate patient, including setting expectations 5. communicate with others and document plans
36
What are the goals of therapy for acute pain?
achieve level of pain relief that allows patient to attain certain functional goals --> cure -may be possible to fully eliminate pain, unlike in chronic pain prevent or minimizes AEs improve QOL
37
What are the non-pharmacological therapies for acute pain?
distraction and relaxation cold (< 48h post-injury) heat (> 48h post-injury) positioning immobilization acupuncture massage exercise TENS
38
What is the pharmacologic overview for acute pain?
acetaminophen NSAIDs opioids
39
What is the MOA of acetaminophen?
believed to inhibit PG in the CNS and work peripherally to block pain impulse generations -minimal effect on peripheral PG synthesis (no anti-inflammatory activity)
40
What is the place in therapy for acetaminophen?
reduction of fever (1st line) mild-moderate acute pain pediatric moderate pain
41
What are the adverse effects of acetaminophen?
liver toxicity overdose may increase SBP (~4mmHg) rare neutropenia and thrombocytopenia
42
What are the contraindications to acetaminophen?
acetaminophen-induced liver disease hypersensitivity to acetaminophen
43
What are some cautions of acetaminophen?
one of the most frequent causes of accidental poisoning in infants and toddlers hepatotoxicity has occurred in pts receiving high or excessive doses with therapeutic intent
44
What is the dosing of acetaminophen?
adults: -IR RS: 325-600mg q4-6h (max 4000mg/24h) -IR ES: 500-1000mg q4-6h (max 4000mg/24h) -ER: 1300mg q8h (max 4000mg/24h) children: -10-15mg/kg/dose q4-6h -max 75mg/kg/24h
45
What is the MOA of NSAIDs?
non-selective: -inhibit COX 1 and 2 which decreases formation of PG precursors -antipyretic, analgesic, anti-inflammatory COX-inhibitors (coxibs): -inhibit PG synthesis by decreasing activity of COX-2 -do not inhibit COX-1 at therapeutic doses -antipyretic, analgesic, anti-inflammatory
46
What is the place in therapy of NSAIDs?
mild-moderate pain dysmenorrhea-induced pain fever (only ibuprofen and naproxen)
47
What are the contraindications to NSAIDs?
CKD hyperkalemia cirrhosis/liver transplant GI ulcer + IBD HF MI thrombocytopenia transplant
48
What are the adverse effects of NSAIDs?
dyspepsia edema GI bleed NV phototoxic reaction CNS (dizzy, drowsy, HA, tinnitus, confusion) minor or serious skin rashes, pruritis COX-2 selective: similar efficacy & CV/renal risk but less GI risk
49
What some cautions for NSAIDs?
asthma CVD, HTN risk of bleeding periop.
50
What is the MOA of ASA?
irreversibly binds COX-1 and COX-2 to decrease formation of PG precursors analgesic, antipyretic, anti-inflammatory
51
What is the place in therapy of ASA?
mild-moderate pain reduction of fever
52
What is the difference in dosing for ASA?
< 300mg/d: reduce platelet aggregation 300-2400mg/d: antipyretic and analgesic 2400-4000mg/d: anti-inflammatory max: 4g/d
53
What are the contraindications to ASA?
hypersensitivity to NSAIDs CKD GI ulcer
54
What are the adverse effects of ASA?
same as NSAIDs
55
What are some cautions for ASA?
concurrent antiplatelet and/or anticoagulant therapy risk of Reye syndrome in children toxic in overdose
56
What is the role of COX-1?
mucosal protection (GI) renal blood flow hemostasis
57
What is the role of COX-2?
inflammation pain fever
58
What is the max dose of ketorolac?
40mg/d (5 day limit due to high GI bleed risk)
59
What is the dosing of ibuprofen?
OTC: 200-400mg q4-6h (max 1200mg/day) Rx: 600mg q6h (max 2400-3200mg/day) children up to 12: 5-10mg/kg/dose q6-8h (max 40mg/kg/d)
60
Which NSAIDs are we concerned about cardiac risk with?
all NSAIDs/COXIBs -dose related
61
Which NSAIDs are higher CV risk? Which are neutral?
higher CV risk: -indomethacin -diclofenac (>150mg/d) -meloxicam -celecoxib (>200mg/d) neutral: -naproxen (<750mg/d) -ibuprofen (<1200mg/d) -celecoxib (<200mg/d)
62
How do we manage the cardiac risk associated with NSAIDs?
select patients carefully; use the lowest effective dose
63
Differentiate prostacyclin and thromboxane A2.
thromboxane A2 -produced by COX-1 pathway on activated platelets -platelet aggregating and vasoconstricting prostacyclin -produced by COX-2 pathway -platelet inhibitor and vasodilating *selective COX-2 inhibitors tip the balance in favour of vasoconstriction, platelet aggregation, and thrombosis*
64
How do NSAIDs increase blood pressure and exacerbate heart failure?
sodium and water retention
65
What is the normal effect of COX-1 on the GI tract?
increase GI mucosal blood flow mucous and bicarbonate production epithelial growth
66
What are the impacts of NSAIDs which inhibit COX-1 on the GI tract?
decreased PGs decreased gastroduodenal mucosal protection increased GI ulcer risk
67
What are the risk factors which increase the risk of GI outcomes from NSAIDs?
age > 65 comorbidities history of GI bleed or presence of H. pylori multiple NSAIDs high dose NSAIDs concomitant anticoagulant, antiplatelet, SSRI, corticosteroid history of heart disease
68
What is the management of the GI risk from NSAIDs?
consider misoprostol or PPI -Arthrotec (diclofenac + misoprostol) -Vimovo (naproxen + esomeprazole)
69
Describe the general overview for prevention of NSAID complications.
low CV risk: -low GI risk: NSAID alone -moderate GI risk: NSAID + PPI/misoprostol -high GI risk: alternate therapy or COX-2 +PPI/misoprostol high CV risk (ASA required): -low GI risk: naproxen + PPI/misoprostol -moderate GI risk: naproxen + PPI/misoprostol -high GI risk: avoid NSAIDs & coxibs, use alternate therapy
70
Differentiate between low, moderate, and high risk for NSAID GI toxicity.
low risk: no risk factors moderate risk: 1-2 risk factors -older age -NSAID use (high dose or multiple agents) -history of uncomplicated ulcer -concurrent ASA, corticosteroid, anticoagulant, SSRI -history of CV disease high risk: -history of complicated ulcer OR > 2 risk factors
71
What are the normal effects of COX-1 and COX-2 on the kidneys?
vasodilating
72
What happens to the kidneys when NSAIDs inhibit COX-1 and COX-2?
vasoconstriction of afferent arteriole decreased ability for kidneys to regulate blood flow
73
What are the risk factors for renal risk from NSAIDs?
age > 70 pre-exisiting renal disease volume depletion (diuretics) combined use with ACEI or ARB HF cirrhosis long-term history of NSAID use
74
What is the management of the renal risk from NSAIDs?
avoid in CKD monitor SCr, urea within 3-7 days after initiating therapy
75
What is the attractive feature of celecoxib?
selective COX-2 inhibition -COX-1 primarily involved in homeostatic bodily functions -->maintains normal lining of GIT -->maintains blood patency COX-2 primarily involved with pain and inflammation -reduced risk of GI complications, minimal platelet effect
76
Which patients require dose adjustments for celecoxib?
elderly and CYP 2C9 metabolizers
77
True or false: celecoxib has a lower renal risk than non-selective NSAIDs
false
78
What is the dosing of celecoxib?
acute pain: -400mg po single dose x 1d, then 200mg po OD up to 7d -max dose=400mg/d for up to 7d
79
What is the risk of higher doses of celecoxib?
200mg BID (400mg/d) or more increases risk of serious CV events
80
What are the drug interactions of NSAIDs/COXIBs?
decrease anti-HTN effect: ACEI, ARB, BB, thiazides increased toxicity of: lithium, MTX, steroids, tenofovir, warfarin increased risk of GI bleed: warfarin, heparin, steroids, SSRI increased nephrotoxicity: ACEI, ARB, diuretics decreased efficacy of ASA antiplatelet effect if co-administered
81
What are the recommendations regarding NSAIDs/COXIBs in pregnancy and lactation?
pregnancy: do not recommend in general low dose ASA has some pregnancy-related indications lactation: may consider agents with short t1/2 -ibuprofen, diclofenac, naproxen
82
What is the role of topical NSAIDs, capsaicin, anesthetics, and compounded creams in acute pain?
limited role -topical NSAIDs have evidence for use in non-LBP MSK injury -some evidence in specific disease states mostly limited to pre/intrasurgical or medical procedures
83
What is the MOA of muscle relaxants?
centrally-acting drugs via heterogenous mechanisms: -methocarbamol: sedative-->skeletal muscle relaxation -baclofen: centrally acting in spinal cord-->relief of spasticity -cyclobenzaprine: similar to TCA in structure and AE little to no actual relaxant effect on tissues -effect linked to sedation and resultant central relaxation
84
What is the place in therapy of muscle relaxants?
might consider for spasms (ACUTE low back pain) no evidence they are more effective than acetaminophen/NSAIDs limit use to < 1-2 weeks
85
What are contraindications to muscle relaxants?
age > 65 (although commonly seen)
86
What are some cautions of muscle relaxants?
++CNS adverse effects hepatic toxicity hypotension risk usually > benefit
87
What is the WHO Ladder?
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
88
What are the downfalls of the WHO Ladder?
aimed at treatment of chronic cancer related pain may put excess faith in opioids ignores non-pharm management
89
When should we refer for acute pain?
use of acetaminophen/NSAIDs for self-medication should not exceed 10 days in adults or 5 days in children (unless directed by a prescriber)

PHAR255 (24 decks)

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