Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PHAR255 > Pain 1 > Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What type of role does pain usually serve?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

True or false: pain is the same as nociception

A

false

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

True or false: pain is more common in women

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Based on pathophysiology, what are the classifications of pain?

A

nociceptive
neuropathic
nociplastic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the two types of nociceptive pain?

A

somatic
visceral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

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

A

transduction
conduction
transmission
perception
modulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What are the two types of neuropathic pain?

A

peripheral nerve injury
central nerve system injury

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

How long is acute pain?

A

typically < 3-6 months

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What is the cause of acute pain?

A

tissue damage signaling harm or potential for harm
-serves a useful purpose
-may outlive its biological usefulness and have -ve effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

True or false: acute pain typically does not have an identifiable cause

A

false

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Typically, what kind of pain is acute pain?

A

usually nociceptive, sometimes neuropathic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are the symptoms of acute pain?

A

sharp, dull, shock like, tingling, shooting, radiating, fluctuating in intensity, varying in location
-occur in a timely response with an obvious noxious stimuli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are the signs of acute pain?

A

may be no obvious signs
-HTN, tachycardia, diaphoresis, mydriasis, pallor
-comorbidities not usually present
-outcome of treatment often predictable

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What are the expected lab test of acute pain?

A

no specific lab test
pain is always subjective
-best diagnosed based on patient description/history

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

When is pain management most effective?

A

when validated and accurate pain assessments are carried out

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

What are examples of self-rated pain intensity scales?

A

adult: visual analogue or numeral rating scale
child: faces scale (Bieri or Wong-Baker)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

What is the PQRSTU assessment?

A

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?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What are the red flags for referral of back pain?

A

cauda equina syndrome:
-bladder dysfunction
-saddle anesthesia
-dysfunction in legs
-lax anal sphincter
-motor weakness

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What is the approach to treatment of acute pain?

A
  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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What are the goals of therapy for acute pain?

A

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
Q

What are the non-pharmacological therapies for acute pain?

A

distraction and relaxation
cold (< 48h post-injury)
heat (> 48h post-injury)
positioning
immobilization
acupuncture
massage
exercise
TENS

38
Q

What is the pharmacologic overview for acute pain?

A

acetaminophen
NSAIDs
opioids

39
Q

What is the MOA of acetaminophen?

A

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
Q

What is the place in therapy for acetaminophen?

A

reduction of fever (1st line)
mild-moderate acute pain
pediatric moderate pain

41
Q

What are the adverse effects of acetaminophen?

A

liver toxicity
overdose
may increase SBP (~4mmHg)
rare neutropenia and thrombocytopenia

42
Q

What are the contraindications to acetaminophen?

A

acetaminophen-induced liver disease
hypersensitivity to acetaminophen

43
Q

What are some cautions of acetaminophen?

A

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
Q

What is the dosing of acetaminophen?

A

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
Q

What is the MOA of NSAIDs?

A

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
Q

What is the place in therapy of NSAIDs?

A

mild-moderate pain
dysmenorrhea-induced pain
fever (only ibuprofen and naproxen)

47
Q

What are the contraindications to NSAIDs?

A

CKD
hyperkalemia
cirrhosis/liver transplant
GI ulcer + IBD
HF
MI
thrombocytopenia
transplant

48
Q

What are the adverse effects of NSAIDs?

A

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
Q

What some cautions for NSAIDs?

A

asthma
CVD, HTN
risk of bleeding periop.

50
Q

What is the MOA of ASA?

A

irreversibly binds COX-1 and COX-2 to decrease formation of PG precursors
analgesic, antipyretic, anti-inflammatory

51
Q

What is the place in therapy of ASA?

A

mild-moderate pain
reduction of fever

52
Q

What is the difference in dosing for ASA?

A

< 300mg/d: reduce platelet aggregation
300-2400mg/d: antipyretic and analgesic
2400-4000mg/d: anti-inflammatory
max: 4g/d

53
Q

What are the contraindications to ASA?

A

hypersensitivity to NSAIDs
CKD
GI ulcer

54
Q

What are the adverse effects of ASA?

A

same as NSAIDs

55
Q

What are some cautions for ASA?

A

concurrent antiplatelet and/or anticoagulant therapy
risk of Reye syndrome in children
toxic in overdose

56
Q

What is the role of COX-1?

A

mucosal protection (GI)
renal blood flow
hemostasis

57
Q

What is the role of COX-2?

A

inflammation
pain
fever

58
Q

What is the max dose of ketorolac?

A

40mg/d (5 day limit due to high GI bleed risk)

59
Q

What is the dosing of ibuprofen?

A

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
Q

Which NSAIDs are we concerned about cardiac risk with?

A

all NSAIDs/COXIBs
-dose related

61
Q

Which NSAIDs are higher CV risk? Which are neutral?

A

higher CV risk:
-indomethacin
-diclofenac (>150mg/d)
-meloxicam
-celecoxib (>200mg/d)
neutral:
-naproxen (<750mg/d)
-ibuprofen (<1200mg/d)
-celecoxib (<200mg/d)

62
Q

How do we manage the cardiac risk associated with NSAIDs?

A

select patients carefully; use the lowest effective dose

63
Q

Differentiate prostacyclin and thromboxane A2.

A

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
Q

How do NSAIDs increase blood pressure and exacerbate heart failure?

A

sodium and water retention

65
Q

What is the normal effect of COX-1 on the GI tract?

A

increase GI mucosal blood flow
mucous and bicarbonate production
epithelial growth

66
Q

What are the impacts of NSAIDs which inhibit COX-1 on the GI tract?

A

decreased PGs
decreased gastroduodenal mucosal protection
increased GI ulcer risk

67
Q

What are the risk factors which increase the risk of GI outcomes from NSAIDs?

A

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
Q

What is the management of the GI risk from NSAIDs?

A

consider misoprostol or PPI
-Arthrotec (diclofenac + misoprostol)
-Vimovo (naproxen + esomeprazole)

69
Q

Describe the general overview for prevention of NSAID complications.

A

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
Q

Differentiate between low, moderate, and high risk for NSAID GI toxicity.

A

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
Q

What are the normal effects of COX-1 and COX-2 on the kidneys?

A

vasodilating

72
Q

What happens to the kidneys when NSAIDs inhibit COX-1 and COX-2?

A

vasoconstriction of afferent arteriole
decreased ability for kidneys to regulate blood flow

73
Q

What are the risk factors for renal risk from NSAIDs?

A

age > 70
pre-exisiting renal disease
volume depletion (diuretics)
combined use with ACEI or ARB
HF
cirrhosis
long-term history of NSAID use

74
Q

What is the management of the renal risk from NSAIDs?

A

avoid in CKD
monitor SCr, urea within 3-7 days after initiating therapy

75
Q

What is the attractive feature of celecoxib?

A

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
Q

Which patients require dose adjustments for celecoxib?

A

elderly and CYP 2C9 metabolizers

77
Q

True or false: celecoxib has a lower renal risk than non-selective NSAIDs

A

false

78
Q

What is the dosing of celecoxib?

A

acute pain:
-400mg po single dose x 1d, then 200mg po OD up to 7d
-max dose=400mg/d for up to 7d

79
Q

What is the risk of higher doses of celecoxib?

A

200mg BID (400mg/d) or more increases risk of serious CV events

80
Q

What are the drug interactions of NSAIDs/COXIBs?

A

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
Q

What are the recommendations regarding NSAIDs/COXIBs in pregnancy and lactation?

A

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
Q

What is the role of topical NSAIDs, capsaicin, anesthetics, and compounded creams in acute pain?

A

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
Q

What is the MOA of muscle relaxants?

A

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
Q

What is the place in therapy of muscle relaxants?

A

might consider for spasms (ACUTE low back pain)
no evidence they are more effective than acetaminophen/NSAIDs
limit use to < 1-2 weeks

85
Q

What are contraindications to muscle relaxants?

A

age > 65 (although commonly seen)

86
Q

What are some cautions of muscle relaxants?

A

++CNS adverse effects
hepatic toxicity
hypotension
risk usually > benefit

87
Q

What is the WHO Ladder?

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

88
Q

What are the downfalls of the WHO Ladder?

A

aimed at treatment of chronic cancer related pain
may put excess faith in opioids
ignores non-pharm management

89
Q

When should we refer for acute pain?

A

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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions