Midterm 1 Flashcards

1
Q

What is stress-induced analgesia?

A

When stress inhibits pain
Study:
- Similar wounds between soldiers and civilians
- The soldiers were much more likely to say there was a little pain vs the civilians who described more pain
- Civilians wanted narcotics more
- Only difference: context

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2
Q

What were the confounds in the study of pain and narcotics between soldiers and civilians?

A

Confounds: soldiers are young and civilians are middle-aged, levels of stress differ

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3
Q

Explain the osteoarthritis example

A

MAIN POINT: Injury is not the thing that causes the pain in everyone, only some people
Every participant had knee OA that a rheumatologist diagnosed
- Most didn’t have pain in their knee, even though they all had the injury
- You can have OA but not knee pain and you can have knee pain but not OA
- OA sort of causes this pain

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4
Q

Pain is the #1 _____

A
  • reason to seek healthcare
  • concern of patients with chronic disease
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5
Q

What are the top 10 presenting complaints at doctor visits?

A

Cough*
Back pain*
Abdominal pain*
Sore throat
Dermatitis
Fever*
Headache*
Leg pain
Respiratory
Fatigue

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6
Q

What are the most common and least common pain events?

A

Most common:
- scratched skin (95.2%)
- paper cut (95.2%)
- pinched skin (94.6%)

Least common
- heart attack (0%)
- advanced cancer (1.1%)
- childbirth (1.1%)

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7
Q

Pain (in some form) is experienced by ___ of the population

A

100%

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8
Q

Around ___% of the population have had chronic pain in their lifetime

A

50%

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9
Q

Around __% have chronic pain right now

A

20%

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10
Q

Explain prevalence vs incidence

A

prevalence = current cases
incidence = new cases

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11
Q

explain out-patients vs in-patients

A
  • Out-patients: given a prescription that you take home
  • In-patients: people being treated in the hospital
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12
Q

Explain the back pain and NHS pyramid

A

surgery: 24,000
in-patients: 100,000
out-patients: 1.6 mil
consulting GP: 3 mil-7 mil
population prevalence: 16.5 mil

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13
Q

Explain prevalence of pain - headache in children study

A
  • Type of population: schools, general practice, community, girl schools
  • Studies had very different sample sizes (1,000-10,000)
  • Age ranges are different
  • Migraines range from 3%-10.6%
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14
Q

Explain self-reported prevalence of specific CHRONIC CONDITIONS by sex, household, and population aged 15 years and older, Canada 2007-2008 (most and least common)

A

Most common:
- back pain
- high blood pressure
- arthritis

Least common:
- alzheimer’s/dementia
- stroke
- cancer

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15
Q

Prevalence of pain by body part

A

Head = 15%
Neck = 8%
Upper back = 5%
Hip = 8%
Lower back = 18%
Shoulder = 9%
Leg = 14%
Hand = 6%
Knee = 16%

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16
Q

Describe the burden of pain

A
  • functional activities (sleep, work, household, leisure, energy)
  • social consequences (martial, family, intimacy, social isolation)
  • Socioeconomic (healthcare costs, disability, productivity)
  • emotional (irritable, angry, anxious, depressed)
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17
Q

Explain types of pain vs difficulty with basic/complex actions (%)

A
  • severe headache or migraine: 31/33.5
  • lower back: 51.6/55
  • neck pain: 30.2/34.4
  • knee pain: 37.7/38.6
  • shoulder pain: 17.7/21.4
  • finger pain: 14.3/16.3
  • hip pain: 15/18.4
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18
Q

What are the most and least common social dislocations among chronic pain patients?

A

Most common:
- postponed housecleaning (81%)
- postponed household duties/laundry (79%)

Least common
- stayed in bed (18%)
- decline in sexual relations (24%)

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19
Q

What is comorbidity?

A

the likelihood that one disease is linked with another

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20
Q

Which kind of patients experience significant comorbid symptoms?

A

Patients with peripheral neuropathic pain

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21
Q

Why does chronic pain costs more than heart disease, cancer, and diabetes?

A
  • Because of scans, x-rays, CTs, etc.
  • Biggest economic burden: employment costs (amount lost to the economy because they couldn’t go to work and someone had to leave work to take care of them)
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22
Q

Explain pain in Abrahamic religions

A
  • Pain as punishment for sin (Eve ate the apple)
  • Pain as redemption (Jesus)
  • Pain as personal atonement/redemption (Muslim)
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23
Q

Aristotle view of pain

A

pain is an emotion, in the heart

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24
Q

Galen view of pain

A

pain is a sensation, in the brain

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25
Q

Avicenna view of pain

A

pain is an independent sensation from touch/temperature

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26
Q

Descartes view of pain

A

there exists a “pain pathway” from the body to the brain

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27
Q

What is the order of philosophers regarding pain?

A

Aristotle
Galen
Avicenna
Descartes

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28
Q

What is theodicy?

A

an attempt to justify or defend God in the face of evil

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29
Q

What is dualism?

A

Mind and body are separate

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30
Q

What is monism?

A

Mind and body are together

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31
Q

People should have the right to:

A
  • Access to pain management without discrimination
  • An acknowledgement of their pain and to be informed about how it might be assessed
  • To have access to appropriate assessment and treatment by trained healthcare professionals
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32
Q

Pain in art - what was the name of the work?

A

“The Broken Column” by Frida Kahlo

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33
Q

Name the top 3 and bottom 3 countries for opioid consumption

A

Top:
- Canada
- Switzerland
- Germany
Bottom:
- Egypt
- Venezuela
- West Africa

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34
Q

Until _____ there was no generally accepted definition of pain

A

1979

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35
Q

What does the IASP stand for?

A

IASP: international association for the study of pain

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36
Q

What is masochism?

A

non-unpleasant pain

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37
Q

What is a drive state?

A

Something that compels action

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38
Q

What are adequate stimuli for the other 4 senses?

A
  • For vision: photon
  • Audition: air pressure changes on eardrum
  • Olfaction: any odor in environment that you have an olfactory receptors
  • Taste: 5 tastes, rest are combos of them
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39
Q

What is the adequate stimulus for pain?

A
  • Mechanical pressure
  • Inflammation
  • Noxious cold/heat
  • Any number of natural compounds/chemicals in the environment
  • Skin damage
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40
Q

Why does surgery hurt after patient wakes up?

A
  • Inflammation
  • Actual tissue damage
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41
Q

What causes pain for the colon?

A

Distention, NOT heat

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42
Q

Why can brain surgery can be done through local anesthetic ?

A

after the meninges, there’s no pain felt

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43
Q

What is neuropathic pain?

A

pain due to damage of the nervous system itself, usually the peripheral NS

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44
Q

The old definition of pain

A

An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.

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45
Q

The new definition of pain

A

An unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage.

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46
Q

Difference between anesthesia and analgesia

A
  • Anesthesia (local): no pain, no touch, no heat, nothing. (no sensory transmission at all)
  • Analgesia: no pain
    (All analgesics are not anesthetics)
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47
Q

What is nociception?

A

Not pain – the workings of the nervous system that eventually lead to the perception of pain
- The neurons and their firing
- The biological happenings that eventually lead to pain

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48
Q

What things maybe have pain?

A

Worms, primary cortex, or any part of the cortex

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49
Q

Explain the thermal grill illusion

A
  • If you touch an individual tube you won’t feel anything
    • If you took multiple, you feel pain
    • There’s no noxious stimulus
  • Example of how pain can be constructed
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50
Q

Describe Fordyce’s Behavioural Model of Pain

A

nociception –> pain –> suffering –> pain behaviour

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51
Q

Why do we have acute pain? (seconds to minutes)

A
  • It enables us to avoid or minimize tissue damage
  • It’s a teaching signal (one-try learning)
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52
Q

Why do we have tonic pain? (hours to weeks)

A
  • To motivate you to rest and recover
  • Wounds heal better if you don’t move (especially broken bones)
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53
Q

Why do we have chronic pain? (weeks to years)

A
  • There’s no reason, it’s a pathology (which means that something’s gone wrong and that it has no function at all)
  • It’s like a broken smoke alarm that’s stuck on even though there’s no smoke
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54
Q

What is anhidrosis?

A

inability to sweat
- usually associated with congenital insensitivity to pain

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55
Q

Average lifespan of people with Congenital sensitivity to pain

A

38 years

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56
Q

How do most people with congenital insensitivity to pain die?

A

Most die from repeated hip fractures, which leads to infection (sepsis)

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57
Q

Explain the lumping and splitting problem

A

One thing to study (lump) vs multiple things to study (split)

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58
Q

Pain becomes chronic when it has lasted for ___

A

3+ months

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59
Q

What is etiology?

A

the underlying reason for something

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60
Q

What is nociceptive pain?

A
  • pain where there is no NS lesion but also no inflammation
  • evoked by high intensity stimuli
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61
Q

What is inflammatory pain?

A

Inflammatory: pain with inflammation
- more noxious stimulus –> more pain (stimulus dependent)

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62
Q

What is dysfunctional pain?

A

no known NS lesion and no inflammation
- sensory amplification
- present with lack of stimulus
- AKA noci-plastic pain

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63
Q

What is neuropathic pain?

A

NS lesion or disease of NS
- Pretty much the same as inflammatory
- Pain with no stimulus

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64
Q

What are the types of chronic pain (on the graph)?

A

Nociceptive (inflammatory), neuropathic, visceral, mixed

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65
Q

What is superficial pain?

A

Skin pain

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66
Q

What is deep pain?

A

In the muscles, joints, bones

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67
Q

What is visceral pain?

A

Pain in the viscera (internal organs)
- Often feels like it’s somewhere else, like the surface

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68
Q

Where do you feel neuropathic pain?

A

You feel it in the skin territory that the nerve serves (this can be a very different place)

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69
Q

What is phantom limb pain?

A

the pain is located in space (ex: where their hand should be but isn’t)

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70
Q

What is spontaneous pain?

A
  • Pain coming from the inside by itself (you don’t need to do anything for it to hurt)
  • Nothing needs to touch it to hurt
  • Could be continuous or paroxysmal (happens sometimes but goes away)
  • Most common type of pain but we know the least about it
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71
Q

What is evoked pain?

A

pain hypersensitivity to various types of touching

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72
Q

What is allodynia?

A

People with allodynia are extremely sensitive to touch
- Things that don’t usually cause pain can be very painful

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73
Q

What is hyperalgesia?

A

An increased sensitivity to feeling pain and an extreme response to pain

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74
Q

Difference between static and dynamic stimulus

A

Static: unmoving stimulus / Dynamic: moving stimulus
- dynamic more common (activity evoked)

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75
Q

What is numbness?

A

anesthetic in a body part (no feeling)

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76
Q

What is paresthesia?

A

a funny feeling that’s not pain but not normal (non-unpleasant tingling)

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77
Q

What is dysesthesia?

A

Paresthesia that you find unpleasant
Ex: your arm falls asleep
- Both are symptoms of chronic pain disorders

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78
Q

What is a paradoxical thermal sensation?

A

when a cold/hot sensation feels hot/cold

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79
Q

What is an aftersensation?

A

a sensation that lasts longer than it should

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80
Q

What is mechanical allodynia?

A

When a normally non-noxious stimulus is now noxious
- someone touching your back when you have a sunburn

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81
Q

What is mechanical hyperalgesia?

A

Noxious to more noxious
Ex: having a shower that’s too hot (noxious) –> with a sunburn (more noxious)

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82
Q

Explain the difference of hyperalgesia vs allodynia

A

Allodynia = pain due to a stimulus that does not normally elicit pain
Hyperalgesia = increased pain from a stimulus that normally provokes pain

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83
Q

Explain the difference between a sign and a symptom

A

Sign: something that the clinician observes themselves
- Requires examination
Symptom: something that a patient complains of
- Requires interview

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84
Q

Explain most and least common in Relative Frequency of Signs & Symptoms

A

Most:
- deep pain
- ongoing pain
- evoked pain

Least
- Touch-evoked pain
- Moving stimuli pain
- Warmth-evoked pain

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85
Q

Summarize Crook et al study

A
  • Put squid in a tank and let in a bass (who eat squid)
  • In 30 min, the bass picked off 4 out of 20 squid
  • Mere presence of anesthetic = no effect
  • Injured squid: 11 out of 40 eaten
  • Injured + anesthetic = even more got eaten
    - Inhibiting pain made it worse
    - Chronic pain causes hypervigilance to remind
    you you’re injured so you’re more careful
  • Injured were more careful
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86
Q

What is trephination?

A
  • Idea is that pain was caused by evil spirits in the brain
  • The only way to let them out was to drill a hole in people’s skulls
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87
Q

What is theriac?

A

reduces pain because of the active ingredient opium

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88
Q

In 1500 AD, pain was treated with ____

A

Pain was treated with willow bark (generally boiled into a tea) or opium poppy (which could be drunk straight from a plant)

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89
Q

What was the first pharmaceutical company called?

A

Merck
- founded in 1668 in Darmstadt, Germany
- Came up with a process to make standardized doses of morphine

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90
Q

Explain the significance of “Ether Dome” (1846)

A

Was a surgical operating ampitheatre in the Bulfinch Building at Massachusetts General Hospital
- Before this, people had surgeries without anesthetic
- The event occurred when William Morton, a local dentist, used ether to anesthetize Edward Abbott
- John Warren, the first dean of Harvard Medical School, then painlessly removed part of a tumor from Abbott’s neck

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91
Q

What is opioid?

A

Things that are like opium

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92
Q

What is equianalgesic?

A

that dose at which two opioids (at steady-state) provide approximately the same pain relief

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93
Q

What is half-life?

A

time it takes for ½ the drug to still be in your system

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94
Q

What is the half-life of methadone?

A

4-8 hours

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95
Q

What is subcutaneous?

A

into the skin

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96
Q

What is intravenous?

A

into but not through the vein

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97
Q

What is transdermal (topical)?

A

patch put on the skin (adv: less side effects)

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98
Q

What is implantation?

A

pump shooting right into the dermis

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99
Q

What is intrasynovial?

A

into joint

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100
Q

What is intracardiac?

A

into the heart

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101
Q

What is intrathecal?

A

into spinal cord

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102
Q

Why are there so many roots of drug administration?

A

It’s a matter of time and where it needs to go

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103
Q

What is the difference between pharmacokinetics and pharmacodynamics?

A

Pharmacokinetics: what the body does to the drug (ADME)
Pharmacodynamics: what the drug does to the body

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104
Q

What does ADME stand for?

A

Absorption
Distribution
Metabolism
Elimination

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105
Q

What is Patient-controlled analgesia (PCA)?

A

IV unit that releases drug into IV drip
- People use a lot less when they can control it

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106
Q

What are the most and least common side effects for opiates?

A

MOST:
- Constipation (biggest problem – 80%): can produce pain that may rival the pain you started with
- Nausea or vomiting
- Sedation

LEAST:
Dry mouth
Urine retention
Pruritis: itch

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107
Q

Why would OTC analgesics not be approved today?

A

they can cause serious liver damage

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108
Q

Why are OTC analgesics available?

A

they were introduced a long time ago when we weren’t as concerned with side effects

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109
Q

What does dextromethorphan treat?

A

Cough
- Doesn’t do it very well
- No evidence it really works at all, but doesn’t really cause any problems

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110
Q

What does metastatic mean?

A

Goes into your bloodstream

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111
Q

Explain the WHO analgesic ladder for cancer pain

A

Level 1: pain
- non-opioid, +/– adjuvant
Level 2: pain persisting or increasing
- weak opioid, +/– adjuvant, +/- non-opioid
Level 3: pain persisting or increasing
- strong opioid, +/– adjuvant, +/- non-opioid
—> freedom from cancer pain

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112
Q

What can steroids help treat?

A

inflammation

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113
Q

What can antidepressants help treat?

A

Effective for treatment of chronic pain
- The dose is different for pain vs depression

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114
Q

The treatment of chronic pain is often the drug that:

A

was developed for something else

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115
Q

Explain otomies and ectomies

A

when you cut something (doesn’t work very well for pain because you can’t cut everything and there are a lot of roots)

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116
Q

Explain the Anesthesiological method of blocks

A

Taking a local anesthetic and injecting it somewhere where it’s going to prevent the pain signal from being transmitted
- Extremely effective, at least at first
- Question of how long they’ll last

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117
Q

What is the western default medicine?

A

allopathic medecine
(opposite of complementary/alternative)

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118
Q

Why are data for complementary pain medicine hard to find?

A

they aren’t drugs, so they’re hard to prove
- Once it’s proven, its no longer complementary medicine (turns into allopathic medicine)

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119
Q

Summarize Stephens et al

A

if people were put in pain and told to swear vs not swearing, those that were allowed to swear reported lower pain

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120
Q

Summarize Guetin et al

A

if people were allowed to listen to music while being put in pain, they reported lower pain levels than those in the control group

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121
Q

Name some self-management behaviours for coping with pain

A
  • exercise
  • pacing
  • relaxation
  • assertiveness
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122
Q

Explain the story of Jeffrey Lawson (1985)

A

In 1985, that baby had open heart surgery without anesthesia, but it was given a muscle paralyzer
- This was because doctors didn’t believe that babies felt pain
- The baby died

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123
Q

What is the only way to get blood from babies?

A

heel lance

124
Q

What does analgesic mean?

A

to relieve pain

125
Q

What methods are analgesic in babies?

A

Sucrose, breastfeeding, and kangaroo care – holding the baby against bare skin

126
Q

Who is John Bonica?

A
  • Used to be a wrestler (he was 4’11)
  • Wrote the first-ever textbook of pain called “The Management of Pain”
  • Came up with the 1st multidisciplinary pain clinic
127
Q

Explain difference between curative and palliative intent

A
  • curative: treatment to cure
  • palliative: treatment to lessen symptoms and pain (patient will probably end up dying)
128
Q

What is a vital sign?

A

something that a nurse is required to write down every time the nurse visits the patient in the hospital
- pain was introduced as the 5th vital sign

129
Q

Explain the pyramid of evidence-based medicine

A

TOP
systematic reviews and meta-analyses
randomized controlled double-blind studies
cohort studies
case control studies
case series
case reports
expert opinion
personal opinion
BOTTOM

130
Q

Why are Case reports better than expert opinions ?

A

because someone has written it down (and published)

131
Q

What is a case series?

A

More than one case report and you write a paper about what you’ve done

132
Q

Why are Randomized control double-blind study (RTCs) not at the top of the pyramid?

A

not at top since sometimes they disagree with each other

133
Q

What are meta-analyses?

A

a bunch of RCTs (has to be a bunch of good ones)

134
Q

The gold standard of meta-analyses are done through the _______

A

Cochrane collaboration

135
Q

Explain the steps of RCTs

A
  • Enrolment (assessed for eligibility + randomized)
  • Allocation (receive intervention)
  • Follow-up
  • Analysis
136
Q

What are the inclusion criteria for RCTs?

A

you have to have pain levels above a certain number

137
Q

What are the exclusion criteria for RCTs?

A

already received treatment, haven’t had pain for long enough, comorbidities, etc.

138
Q

Explain the 3 arm experimental design

A
  • 1 group placebo, 1 group active control, 1 group experimental treatment
  • Parallel design: groups are being run in parallel
  • Double-blind procedure
139
Q

Explain the crossover experimental design

A
  • Two groups and two phases
  • All participants get both drugs
  • Advantage: more powerful statistically (you can compare everyone to themselves), you can use less people because of this
  • Disadvantage: it may matter what order the drugs are given in
140
Q

Difference between crossover and parallel

A

parallel: cleaner / crossover: more powerful

141
Q

Explain the enriched experimental design

A
  • Enroll people into your study, and everyone gets the real drug
  • You raise the dose until everyone responds (as long as there are no intolerable side effects)
  • Only at that point are they randomized where half takes placebo and half take the drug
  • May not be predictive of drug working in the real world
142
Q

Summarize Lidoderm study

A
  • 3 groups in study
  • Placebo had just as much pain relief after two hours, but Lidoderm appears to beat placebo
143
Q

What was the patient preference for Lidoderm vs placebo?

A

Lidoderm: 78%
Placebo: 9%

144
Q

How long did patients use the lidoderm vs placebo patches?

A

Lidoderm: used 14 days
Placebo: used for 6 days
- Does longer or shorter use indicate how well it worked for pain?

145
Q

Explain odds ratios (relative risk)

A

Big question: the proportion of who gets cancer and who doesn’t
no link to cancer (denominator) / link to cancer (numerator)
result: (?)x more likely to get cancer than people in population B

146
Q

What is the odds ratio (rlative risk) equivalent for analgesic pain?

A

drug and placebo

147
Q

What does relative risk of 1 mean?

A

nothing

148
Q

Explain the forest plot of relative risk to wheezing

A
  • Relative risk shown by squares
  • Size of squares show how big the study was
  • Two lines: 95% CI
  • One study had no bars overlapping
  • The others didn’t which means that these studies didn’t necessarily work
  • Conclusion: this intervention does not affect parent-reported wheezing
149
Q

What happens when every study is above diagonal in the l’abbe plot?

A

higher percentage were more responsive to drug than placebo
Can conclude that drug works

150
Q

What drug seems to work on the l’abbe plot on the right?

A

Amitriptyline

151
Q

What is a l’abbe plot?

A

A type of meta-analysis

152
Q

What is number needed to treat (NNT)?

A

You need to treat (x) patients to get one to respond that wouldn’t respond to a placebo
- How much extra advantage does the drug give over a placebo
ex: NNT of 4 –> 1 in 4 patients

153
Q

What is the NNT formula?

A

1/(proportion benefitting from experimental intervention - proportion benefitting from a control intervention)
OR
1/(patients responded to treatment/total patients receiving treatment) - (patients responded to control treatment/total patients receiving control)

154
Q

What is paracetamol?

A

what they call acetaminophen in Europe

155
Q

Explain Finnerup et al graph

A
  • Pfizer funded really big trials to show that gabapentin/pregabalin worked (NNT ~5)
  • Challenges the notion of what it means for the drug to work
156
Q

What is the NNT of peptic ulcer?

A

1.1
curing ulcers a year later: 1.8

157
Q

NNT of antidepressants

A

4

158
Q

NNT of Painful diabetic neuropathy

A

2.9

159
Q

NNT of low dose aspirin

A

40 (you need to treat 40 people to prevent 1 death)
- Why use it?
- It’s for trying to reduce the number of heart attacks in SOCIETY, not just you
- Through a societal perspective, NNT of 40 is fine

160
Q

Where on a graph would the perfect analgesic lie?

A

Top left corner –> want NNH to be low but NNT to be high

161
Q

How to calculate NNH

A

1/(proportion reacting from experimental intervention - proportion reacting from a control intervention)

162
Q

What is an equivalent measure of NNT?

A

effect size

163
Q

Explain first line, second line, ect. drugs

A

If patients don’t respond to first-line drugs, then move to the second, then so on

164
Q

Why are there so many anesthesiologists in the IASP?

A

The neurologists and rheumatologists have their own associations

165
Q

What two journals does IASP publish?

A

PAIN and pain reports

166
Q

Why are there more neuropathic (6%) than arthritis (3%) studies?

A

neuropathic more attractive to neuroscientists

167
Q

What is the dorsal root ganglion?

A

collection of cells that is just outside of the spinal cord

168
Q

Why is dorsal important for pain?

A

Sensory info goes up dorsally and motor info comes down ventrally

169
Q

What are ascending pathways (the “pain matrix”)?

A
  • thalamus
  • somatosensory cortex
  • limbic cortex
  • prefrontal cortex
170
Q

What are pain-relevant loci (for pain below the neck)?

A
  • skin/muscle/joint/viscera (“periphery”)
  • dorsal root ganglion (DRG)
  • dorsal horn of the spinal cord
  • brain
171
Q

What are descending pathways (not motor)?

A
  • hypothalamus
  • midbrain
  • brainstem
  • spinal cord
172
Q

Why have descending pathways?

A
  • The brain wants to have some control over its input
  • It sends info back down to the spinal cord
173
Q

What is glabrous skin?

A

skin only on palms of your hand and soles of your feet

174
Q

What initiates pain sensations?

A

Specialized Schwann cells
(as well as free nerve endings)

175
Q

What is a bipolar neuron?

A

cell body in middle, one side axon terminal and other side dendrite

176
Q

What is a multipolar neuron?

A

Many dendrites and one axon

177
Q

What is a unipolar neuron?

A

There’s one line that goes from dendrites to axons on other end, cell body on the side

178
Q

Where do the longest primary afferent neurons go?

A

up your toe to your spinal cord

179
Q

what are primary afferent neurons?

A

first neuron going up (sensory info)

180
Q

Why do some pain syndromes show a “glove and stocking” distribution (starts at the feet and goes up)?

A
  • The longest nociceptors in the body are the ones coming from the feet
  • The longer the neuron = the more fragile
181
Q

afferent vs efferent

A

afferent: from the periphery up to the CNS
Efferent: going down from higher levels of CNS out to the periphery (how the NS controls the muscles)

182
Q

What do the A afferent fibers have?

A

Myelin (c does not)

183
Q

a-alpha

A

Speed: 100m/s
For proprioception (feeling where your body is)

184
Q

a-beta

A

for touch/vibration

185
Q

a-delta

A

Speed: 25 m/s
For thermal and pain

186
Q

c fibers

A

Speed: 1 m/s
For pain and sweating

187
Q

what is first and second pain mediated by

A
  • First pain: mediated by A-deltas (instant)
  • Second pain: Cs (dull but lasts longer, because they’re slower)
    • The route is much longer
188
Q

what keeps axon bundles alive?

A

blood capillaries

189
Q

rostral

A

towards the head

190
Q

caudal

A

towards tail

191
Q

dorsal

A

towards back

192
Q

ventral

A

towards stomach

193
Q

anterior

A

front

194
Q

posterior

A

back

195
Q

medial

A

towards midline

196
Q

lateral

A

to the side

197
Q

ipsilateral

A

on the same side of

198
Q

contralateral

A

on the opposite side to

199
Q

cervical

A

closest to brain

200
Q

thoracic

A

upper back

201
Q

lumbar

A

lower back

202
Q

sacral

A

hips, genitals

203
Q

what does t1 to t2 divide

A

divides chest from belly button

204
Q

primary afferent fibers going in at t2 are:

A

carrying sensory info from that part of the skin

205
Q

efferent fibers coming out of t2 are going to:

A

control muscles

206
Q

what is shingles?

A

very restricted and painful rash

207
Q

why does the vertebra have to be broken up?

A

because the spinal nerves need a place to get out

208
Q

ventral root and dorsal root converge into:

A

a mixed spinal nerve

209
Q

ventral root is where:

A

motor neurons are going out to the muscles

210
Q

dorsal root is where?

A

sensory info is coming in from the periphery to the spinal cord up

211
Q

what kind of nerve is the spinal nerve?

A

mixed nerve (afferent and efferent)

212
Q

spinal ganglion is the same thing as:

A

dorsal root ganglion

213
Q

what is a ganglion?

A

a collection of neuron cell bodies that’s outside of the CNS

214
Q

The spinal ganglion is a bulge –why?

A

Cell bodies are bigger than axons, hence the bump

215
Q

spinal cord is covered with:

A

meninges

216
Q

what is the hole in the middle of dorsal root ganglion?

A

cerebral spinal fluid

217
Q

what is the central canal

A

where cerebral spinal fluid goes

218
Q

function of dorsolateral fasciculus

A

where primary afferent are coming in

219
Q

what is the substantia gelatinosa?

A

laminae 1 and 2 looped together

220
Q

Explain the journey of sensory info

A

dendrites in skin –> primary afferent neuron –> DRG –> SC + dorsolateral fasciculus –> 2nd order neuron –> CNS

221
Q

function of 2nd order neurons

A

fire, cross, ascend
- either in laminae 1 and 2 OR 5 and 6

222
Q

what is between primary and 2nd order neuron?

A

interneuron

223
Q

what are the 2 classes on c fibers?

A

CGRP+
IB4+

224
Q

what is NeuN?

A

makes all neurons fluorescent

225
Q

what lights up in CGRP?

A

dorsolateral fasciculus in laminae 1

226
Q

what lights up in IB4?

A

dorsolateral fasciculus in laminae 2 (more restrictive stain)

227
Q

what does Nav1.7 light up?

A

all nociceptors

228
Q

where do a-betas terminate?

A

mostly in lamina 3 and 4 and maybe a bit in 5

229
Q

where do a-deltas terminate?

A

some going to 1 and some going to 5

230
Q

where do Pepditergic c fibers terminate?

A

in 1

231
Q

where do non-Pepditergic c fibers terminate?

A

in 2

232
Q

what was the modern molecular definition of sensory neurons defined by?

A

defined by single-cell RNA-sequencing (i.e., gene expression) of DRG cells (followed by principal components analysis (i.e., clustering)
- 622 neurons

233
Q

How many neurons does the category of TH have?

A

233

234
Q

what does NF mean

A

neurofilamentary heavy chain

235
Q

what does NP mean

A

non-peptidergic

236
Q

what does PEP mean

A

peptidergic (2 categories)

237
Q

what does TH mean

A

tyrosine hydrolase-expressing (1 category)

238
Q

what is the efferent function of nociceptors?

A

Produces neurogenic inflammation
- When a nociceptor being stimulated by noxious stimuli, AP is going up and going towards CNS
- They also have collateral branches, where things can be released at the end (efferent function)
- Released: CGRP and substance p (SP)
- Both are good at making arterioles dilate, leading to plasma extravasation (fluids that were inside the arteriole now get released out into the tissue)

239
Q

what is the purpose of plasma extravasation?

A

to release white blood cells to cause an immune response to deal with the wound causing the noxious stimulation

240
Q

reflexes bypass the brain by:

A

spinal reflex

241
Q

how does spinal reflex work?

A

Sensory neuron goes into dorsal horn –> interneuron –> motor neurons –> muscles –> withdrawal of limb

242
Q

why don’t we study spinal reflexes?

A

We don’t study them because we don’t want to modify them (we want to preserve them)

243
Q

The higher you go, the more:

A

white matter

244
Q

in terms of columns, sensory info goes up:

A

in dorsal column or anterolateral column (where fibers of 2nd order neurons are)

245
Q

what is a tract?

A

in the CNS whenever fibers go from one place to another long distance

246
Q

spinothalamic tract

A

SC to thalamus
- Sensory info (in general)

247
Q

spinoreticular tract

A

SC to reticular formation (midbrain, pons, medulla) – most deadly area to have trauma
- function: God knows

248
Q

spinoparabrachial tract

A

SC to a particular nucleus in the pons called parabrachial nucleus
- Emotional pain info (general)

249
Q

what is somatotopy?

A

the principle by which the location of the neural info corresponds to the part of the body it came from or is going to

250
Q

explain the trigeminal system

A
  • Parallel system, just above the neck
  • In cranial nerve 5 (hence the V)
    V1, v2, v3
  • Trigeminal ganglion
  • A-detas and cs project to the brainstem
  • Lower part of brainstem is equivalent to spinal cord
251
Q

what is the NTS (nucleus tractus solitarius) important for?

A

important for visceral sensation

252
Q

what is the most complicated pathway? why?

A

visceral
- because sometimes they go to their own ganglia (that’s nowhere near the SC) to ganglia near the SC

253
Q

explain somatic vs visceral fiber termination

A

Somatic: they terminate very specifically
- Easy to identify where pain is
Visceral: fibers terminate in a more diffuse pattern
- Why its hard to precisely localize visceral pain
- Has the ability to affect a lot of second-order neurons

254
Q

visceral pain is:

A

referral

255
Q

what is ischemia?

A

lack of blood supply

256
Q

what is distention?

A

pain when plugged up or blocked

257
Q

Somatic and visceral info terminate on:

A

the same 2nd order neurons

258
Q

where can muscle pain also be referred to?

A

to the skin

259
Q

describe the first referral on a conscious patient

A
  • Doctor was able to touch the part of the body 12 inches away from where it was hurting
  • If you inject saline that’s too hypo/hypertonic it’s painful
260
Q

what is pain far away from injection?

A

referred pain

261
Q

what is the first and oldest brain mapping technique

A

lesions
- induced: lesion on purpose
- TMS: reversible lesion of the brain

262
Q

what is stimulation?

A

measuring electrical signals
- EEG, MEG (indirect)
- electrodes, optical imaging (direct)

263
Q

what is the most popular brain mapping technique

A

hemodynamic (blood and oxygen)
- PET, SPECT, FMRI (so popular because you can do things over a big range of space and time)

264
Q

which brain mapping techniques cause no damage?

A

fMRI and ERP

265
Q

how was the pain matrix discovered?

A

using fMRI
- Problem: these parts aren’t just for pain
- Nonetheless, these parts light up when people are in pain

266
Q

what does the difference in brain activation between normal subjects and clinical pain subjects suggest?

A

Suggests pain matrix is just for experimental pain and the PFC is more suggestive of clinical pain

267
Q

name the percentages of pain in normal pain subjects

A

ACC 87%
Som 1: 75%
Som 2: 75%
Insula: 94%
Thalamus:80%
Pre-frontal: 55%

268
Q

name the percentages of pain in clinical subjects

A

ACC: 45%
S1: 28%
S2: 20%
IC:58%
Th: 59%
PFC: 81%

269
Q

explain the results of the motivational-affective aspects of pain study

A
  • After suggestion for intensity: som 1 went up and down
  • After hypnotic suggestion for unpleasantness: anterior cingulate cortex went up and down
270
Q

why does pain pathway split in two?

A

because they can be independently manipulated

271
Q

what are the S-D aspects and the M-A aspects of the hypnosis study?

A

S-D:
- localization of pain
- quality of pain
- intensity of pain

M-A:
- unpleasantness
- meaning of pain

272
Q

explain the modern view parts of the pain matrix

A

Sensory discriminative
Motivational
Affective
Cognitive
Descending modulation
Inferential

273
Q

what are the two descending systems (pain modulatory pathways)?

A

1: PAG, RVM, dorsal horn of spinal cord
2: midbrain, pons (locus cerulea), dorsal horn of spinal cord

274
Q

what is the specificity theory?

A

there exists primary afferent neurons that don’t respond to anything but noxious stimuli
- The more noxious, the more they fire until it fires the fastest it can fire

275
Q

what is the intensity theory?

A

the same neurons will fire weakly, but when the stimulus is noxious, they’ll fire much more
- The amount of firing is coding the strength of the stimulus
- There are nocicpetors that are specific more different modalities to pain (heat, cold, mechanical)

276
Q

what is the pattern theory?

A

there are just primary afferents, its at higher levels of the NS that different firing of the neurons is decoded
- Its only then we’ll figure out what kind of stimulus it is
- The patterns tell us if it’s pain and what type
- Info is not in any particular afferent neuron

277
Q

what paper did wall and melzack publish?

A

“Pain mechanisms in new theory”

278
Q

explain the gate control theory

A

More activity in small –> gate open (pain info)
More activity in large –> gate closes (no pain info)
SG: interneuron in gelatinosa
- Large: excites it –> T inhibition –> no pain
- Small: inhibits it –> T excitement –> pain

279
Q

what are large/small fibers in gate control theory?

A

Large fibers: a betas – touch info
Small: Cs and a deltas

280
Q

what is an SG neuron in gate control theory

A

neuron in substantia gelatinosa in spinal cord

281
Q

gate control theory: what happens when both small and large fire?

A
  • It matters which wins the battle of large vs small, but if there’s enough large input you’re going to inhibit the T neuron
282
Q

How does this explain why people rub where it hurts?

A

Rubbing (touching) increases L input, thus inhibiting s input, which inhibits T (pain sensation)

283
Q

what is electrophysiology?

A

looking at neurons and how they fire

284
Q

what is Microneurography?

A

Electrophysiological Recording of Primary Afferent Fibers (in humans)
- You can record form c fibers in humans right from the periphery
- Why can’t you record any higher in humans?
- It’s unethical, no one wants to do it obviously

285
Q

Explain the graphs in the electrophysiological recording of dorsal horn cells

A

Left: dorsal horn firing more and longer the hotter the stimulus is
Right: sin-1 firing
- Brush stimuli: doesn’t fire much
- Press: fires little more
- Pinching: little more than that
- Fired to heat

286
Q

what are the 3 different types of dorsal horn projection neurons?

A

Wide dynamic range: being excited by a-betas, a-deltas, and cs
- Basically the equivalent of intensity theory concept
- They will respond to a wide range of input

Nociceptive specific: only input from a-deltas and cs

Low threshold mechanosensitive: a-betas only
- touch is low threshold
- After injury (inflammation or nerve damage), it causes a change in the cells such that it turns them into nociceptors
- Instead of providing touch info to the brain, you feel pain
- Why they’re called silent nociceptors, because they have the ability to change into them
- Possible explanation for sensitization/allodynia

287
Q

explain the Electrophysiological Recording of Anterior Cingulate Cells (with the rat)

A
  • Squeezed the rat in 8 locations
  • Wherever it was squeezed, that neuron fired
    OR that cell has a receptive field of the entire body, because it doesn’t really matter where you put the noxious stimulus
  • The cingulate doesn’t care where the pain is, it only cares that there’s pain
288
Q

What is CPM?

A

conditioned pain modulation
- pain inhibits pain (counter-irritation)

289
Q

what is Transcutaneous Electrical Nerve Stimulation (TENS)?

A

a unit with pads placed on skin
- Doesn’t work super well, but works at least a little (maybe placebo)
- Electricity penetrates the skin
- A-beta fibers have their nerve endings a lot closer to epidermis than a-deltas and cs

290
Q

How does gate control theory explain TENS?

A

TENS current increase L input, but don’t affect S input (bc the current can’t penetrate far enough)
- Works the same way that rubbing works

291
Q

what is the sciatic nerve?

A

Mixed nerve
Serves the foot and back part of the leg

292
Q

what is sensitization

A

the longer pain goes on, the worse it gets

293
Q

what is skin-nerve preparation?

A

Recording and stimulating skin directly with a noxious stimulus

294
Q

who was the first person to do central sensitization?

A

clifford woolf

295
Q

difference between peripheral and central sensitization

A

Primary afferent: peripheral sensitization
- If primary fires more, dorsal horn in CNS will fire more (only because its getting more input)
2nd order: central sensitization (injury only in CNS)
- dorsal horn neuron will fire more but no change in primary afferent (not sensitized in periphery)

296
Q

explain the Woolf sensitization study

A

Ipsilateral: after injury dorsal horn neurons fire more and for longer
Contralateral: DORSAL HORN Neurons also fire after injury, but basically not at all before (caused an increased sensitivity to the right leg)
- Due to changes within central nervous system

297
Q

what is wind-up?

A

the more stimuli you give, the more the neurons fire (sensitization basically)

298
Q

what is temporal summation?

A

noxious stimuli summating in time as long as stimuli are close enough together

299
Q

what is spatial summation?

A

More probes that are simultaneously going off, more pain reported

300
Q

primary vs secondary hyperalgesia

A

primary: site of injury (peripheral sensitization)
secondary: site around injury (central sensitization)

301
Q

what is the flare?

A

redness around injury

302
Q

two types of secondary hyperalgesia

A
  • Inside zone: stroking hyperalgesia (but not punctate) – if you take a paint brush in the area and people say that hurts
  • Outside zone: punctate (take a q-tip and poke straight down)
    - Area of punctate is wider than stroking (you can get it in stroking too)
303
Q

You can show mechanical secondary hyperalgesia but not heat secondary hyperalgesia - Why?

A

LTM neurons (low mechanical threshold)

304
Q

what is mirror pain

A

central sensitization

305
Q

structural vs functional plasticity after injury

A

functional: possible changes of function
structural: possible changes to dendrites or terminals

306
Q

explain the difference in positive/negative scores in regards to CPM

A

Negative score: CPM working (normal)
- Didn’t respond to drug
- You already have as much internal pain inhibition
- CPM is reflective of your natural pain inhibition systems
Positive score: CPM not working
- Instead of becoming analgesic, they became hyperanalgesic (CPM wasn’t working)
- Duloxetine (drug) worked

307
Q

explain chronic pain and CPM

A
  • People with chronic pain syndrome show less CPM than normal
  • Fibromyalgics had impaired CPM