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BRB Final > Pain > Flashcards

Pain Flashcards

1
Q

Types of nociceptors

A
  1. Thermal: respond to low and high extremes (45degC). Adelta fibres.
  2. Mechanical: respond to P, nociceptive mechanical, pinch, pin prick. High threshold. Adelta fibres.
  3. Polymodal: respond to mechanical, chemical or thermal. C fibres - diffuse aching burning pain
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2
Q

nociceptive vs neuropathic pain

A

2 pain mechanisms:
Nociceptive: normal pain pathway. Nociceptors activated&raquo_space;
response to tissue damage, inflammatory pain
(muscles, bones, organs, skin…)

Neuropathic: pain system malfunctioning.

  • no activation of nociceptors. damage in PNS/CNS nerves> abnormal signalling > pain perception
    ex: post-herpetic neuralgia, central pain, phatom limb pain, diabetic neuropathy, peripheral nerve damage, cord injury, stroke
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3
Q

what is axon reflex

A

aka neurogenic inflammation:

  • lesion > signals goes to C fibres > spinal cord
    1. pass the DRG on way to spinal cord to activate withdrawal reflex
    2. branches in peripheral nerve terminals > release PEPTIDES: CGRP and Substance P >
    a. blood vessels: vasodilate (red), increase permeability (swelling), release BRADYKININ
    b. mast cells: release HISTAMINE > effects on blood vessels
    c. platelets: relese SEROTONIN
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4
Q

what causes inflammation?

A

axon reflex and tissue damage

-red, warm, swelling

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5
Q

inflammation after tissue damage

what activitates and sensitize nociceptors

A

Nociceptors are activated by:

  1. mast cells via histamine
  2. platelets via serotonin
  3. plasma via bradykinin

Nociceptors are sensitized by:

  1. damaged cells via K+, prostaglndins, leukotrienes
  2. axons via Substance P
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6
Q

nsaid mechanism

A

decrese pain due to tissue damage

  • analgesic, antipyretic, anti-inflamm
  • block COX> decrease production of prostaglandins > decrese sensitization

ex: aspirin, ibuprofen, naproxen, indomethacin

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7
Q

PAG matter purpose in pain

A

Periaqueductal grey in midbrain

  • descending input to dorsal horns > release ENKEPHALINS (like morphine) from dorsal horn interneurons > act on opioid receptors to inhibit pain transmission via:
    1. inhibit NT release from 1ry neuron
    2. hyperpolarize 2ary neuron
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8
Q

referred pain

A

convergent afferent fibres from viscer nd body surfce @ 2ry neuron so cn’t localize
(ex: diaphragm > shoulder. appendicitis > umbilicus)

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9
Q

gate-control theory

A

inhibition of touch afferents > pain signal doesn’t go.
ex: TENS, rubbing helps relieve pain

-activate Abeta (touch fibres) > activates inhibitory neuron on 2ry pain neuron on its way to STT > no pain transmission
Closes the gate which is activated by 1ry pain fibres (Adelta, C)

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10
Q

what is algesia

A

sensitivity to pain

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11
Q

what is analgesia

A

no sensitivity to pain

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12
Q

what is hyperalgesia/hypoalgesia

A

increased/decreased sensivitity to pain

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13
Q

what is allodynia

A

pain from usually non-painful stimulus

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14
Q

what is dysesthesia

A

abnormal unpleasant feeling

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15
Q

what is noxious

A

stimulus causing tissue damage

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16
Q

Types of cutaneous fibres: Abeta, Adelta, C

A

Abeta: touch via DCML.
Adelta: fast pain. well localized.
C: slow pain: distressing, emotional, achy

17
Q

what is pain sensitization?

ex mech

A

decrease threshold for activation
> hyperalgesia
ex: prostglandins enhance response to bradykinin > activate nociceptors to fire

18
Q

Pain pathway

explain dull, achy pain

A

C and Adelta fibres > spinal cord > decussate > ascend via STT > Spinal Lemniscus > thalamus > 1ry somatosensory cortex

1ry: C fibres
2ry: in SL
3ry: branch off in thalamus to reticular nuclei > CINGULATE GYRUS of LIMBIC SYSTEM

19
Q

Tension Headaches describe

A
  • most common
  • bilateral, non-throbbing
  • featureless
  • not disabling > dont’ seek help
20
Q

Migraines describe

A
  • throbbing
  • starts on 1 side
  • photo/phonophobia
  • nausea
  • aura/non aura
  • disabling, need help

-episodic headache, 4-72hrs with
any 2: unilateral, throbbing, worse iwth activity, moderate/severe
and any 1: nausea/vomitting, photophobia and phonophonia

21
Q

Epi of migraines

A
  • common, higher than other common diseases (>10% prev globally, most burden brain issue)
  • more in women, peak in reprod yrs
  • higher in boys
  • genetic link
  • develop with other associated disorders: depression, anxiety, sleep
  • risk factors: female, young, low SES, trauma, concussion, obesity, medications, stress, bad SLEEP, depression/anxiety, allodynia
22
Q

what is aura

A
  • most ppl do not have aura
  • at least 2 ttacks
  • visual, sensory, speech, motor (positive or negative)
  • 5min-60min
23
Q

Course of a migraine

A

Prodrome: 12-24hr before. mood changes, yawning, crave carbs, maybe aura, DOPAMINE
Headache: sensory hyper-excitability
Resolution: like being drunk
postdrome

24
Q

Triggers of migraines

A
  • wheather change
  • poor sleep
  • weekends/holidays
  • menstruation
  • stress
  • strong smells
  • skipping meals
  • foods: dyes, msg, wine, caffeine
25
Q

Cause of migraines: trigeminovascular system

A

Increased vulnerability to triggers (genetic)
>hyper excitable/ brainstem dysfunction:
> activate migraine generator centre in brainstem
> Cortical spreading depression
> reduce blood flow across cortex
> cells not as active (aura)
> activate trigeminal nucleus > PAIN

26
Q

Sinus headache

A

2ry headache

  • face pain not forehead
  • worse lying down
  • other nasal symptoms: discharge, fever
27
Q

Tx for migraines

A

Education
Lifestyle
Vit/Herbal
Meds: initial therapy, back-up, or rescue:

28
Q

What are triptans

A

drugs for migraines - 1st line

  • agonist on serotonin receptors
  • early in attack use else trigeminovascular neurosn are sensitized and allodynia already kicked in
  • don’t use with vscular risk fctors or complicated aura

Adverse effects mild
-rare = serotonin syndrome

29
Q

Other drugs for migraines

A 
Triptans
Dihydroergotamine
NSAIDS
corticosteroids
antiemetics
30
Q

acute vs chronic pain syndrome

A

Acute:

  • source. autonomic and reflex signs
  • distress gone when source eliminated

Chronic:

  • lasting beyond 6 mo / regular healing time of injury
  • reflex signs decrease but psychological response increase
  • affect fnc: sadness, hopelessness, failed tx…
31
Q

factors that modify pain exp

A

affet perception and expression of pain

  • culture
  • envt
  • age
  • sex
  • presence of hyperalgesia, allodynia
32
Q

altered states of mind?

A
  • change brain waves > change pain perception
  • higher theta waves (slow, sleep, creative thinking, detach from reality)

Meditation: equl pain intensity, but less unpleasantness, enhanced activity in insula, cingulate

CBT: increase gray matter volume. decrease pain catastrophizing

Yoga: change sensory inputs, emotional rxn, insula involved

33
Q

placebo effect

A
  • may be due to symbolic significance
  • ineffective tx believed to be effective
  • mediated by endorphins
34
Q

pain and gray matter changes

A

Anterior Cingulate Cortex (ACC): attention, emotion
Anterior ACC and posterior insula: subjective pain perception

Chronic pain imaging: thinning of: cingulate, insula
-maybe thinning: thalamus, 1deg SS, prefrontal cortex

35
Q

risk factor for chronic pain

A
  • abuse
  • marital discord
  • family issues
  • trauma
  • family hx
  • stress
36
Q

Red flags for Chronic Pain Disorder

A
  • pain beyond expected healing time
  • spreading or new pain after initial
  • failure to respond to tx
  • PTSD, anxiety after injury
  • pessismistic beliefs
  • difficulties at work/unmodified work
37
Q

How does hypnosis work

A

supress pain but

  • plitting consciousness
  • activating spinal cord descending pathwayst hat block pain transmission (BUT not the endogenous opioid system)
  • alter meaning of pain
38
Q

Tx for recurrent migraines

A
  • TCAs
  • B blockers
  • botox

BRB Final (8 decks)

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