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physio exam 3 > Pain and headache > Flashcards

Pain and headache Flashcards

1
Q

What is pain?

A
  • A protective mechanism: conscious awareness about or impending tissue damage, unpleasant sensory and emotional experience
  • cause of major discomfort, major health concern
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2
Q

What is perception of pain?

A
  • Stimulation of pain receptors (nociceptors) or direct injury to nerves (neuropathic)
  • almost always accompanied by motivated behavioral responses and emotional reactions (child, painful stimuli - cry)
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3
Q

How is perception of pain affected?

A

by motivational and emotional responses

  • (pain at dentist at a previous appointment makes you dread dentist because you know pain accompanies it)
  • bravery when in severe pain i.e. soldiers and marines, motivation can dull sensation of pain
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4
Q

What are nociceptors?

Define: mechanical and thermal, chemical/silent. polymodal

A

Pain receptors

  • mechanical and thermal: Aδ fibers - faster, felt first
  • chemical/ silent and polymodal: C fibers = felt second
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5
Q

What is the process of receptor stimulation when you get a paper cut?

A

You feel a sharp pain right away from the Aδ fibers, followed by a dull aching pain from C fibers

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6
Q

Mechanical receptors

A

pressure sensation

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7
Q

thermal receptors

A

heat/cold

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8
Q

chemical/silent receptors

A

receptive to chemicals

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9
Q

polymodal receptors

A

responsive to mechanical, thermal, and chemical/silent nociceptors

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10
Q

How are pain receptors sensitized?

A

by chemicals released by tissue damage:
damage leads to release of prostaglandins and bradykinin which stimulate substance P which results in the release of histamine from mast cells (positive feed back loop )

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11
Q

Do pain receptors adapt to sustained or repetitive stimuli?

A

no

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12
Q

What is CGRP?*

A

calcitonin gene related peptide - a neruomodulator (because it is a peptide)

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13
Q

How are substance P and CGRP similar?

A

they are neuromodulators

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14
Q

What is the difference between neruotransmitters and neuromodulators?

A

a neurotransmitter is a messenger released from a neuron at an anatomically specialised junction, which diffuses across a narrow cleft to affect one or sometimes two postsynaptic neurons, a muscle cell, or another effector cell. A neuromodulator is a messenger released from a neuron in the central nervous system, or in the periphery, that affects groups of neurons, or effector cells that have the appropriate receptors

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15
Q

Pain receptors would be classified as?

a. tonic receptors
b. phasic receptors

A

a because they respond slowly

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16
Q

What are first order neruons?

A

they are close to nociceptors

  • detect stimuli that threaten the integrity of innervated tissues
  • direct tissue injury ( cause inflammation of mediators i.e. substance P, prostaglandins,etc)
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17
Q

What are second order neurons?

A

They process nociceptive information ( may form a part of reflex arc) and send the info to the brain

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18
Q

What are third order neurons?

A

They project pain information to the brain (thalamus -> somatosensory cortex - sensory homunculus where pain sensation ultimately ends up - why certain parts of the body are more sensitive to pain than others)

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19
Q

Are Aδ fibers myelinated or unmyelinated?

A

myelinated

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20
Q

What part of pain are Aδ fibers responsible for?

A

the first generation of pain (quick, sharp)

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21
Q

Are C fibers myelinated or unmyelinated?

A

unmyelinated

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22
Q

What part of pain are C fibers responsible for?

A

second pain, continued, dull

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23
Q

How is the response of Aδ fibers to increased amount of stimuli?

A

The number of stimuli/peaks don’t change - same response every time

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24
Q

How do the number of stimuli affect the response of the c fiber?

A

The more stimuli, the longer the response/ sensation and duration of pain

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25
Q

What do fast fibers (Aδ) release?

A

neurotransmitters (glutamate) which can act on two different glutamate receptors

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26
Q

What are the two glutamate receptors?

A

AMPA & NMDA (Aδ works on these)

- both are ligand gated ion channels

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27
Q

What happens when NMDA receptors are activated?

A

release calcium into cell which can bring about increased sensitivity to pain, etc

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28
Q

What happens when AMPA receptors are activated?

A

sodium comes into cell, responsible for generating action potentials

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29
Q

What happens in C fiber stimulation?

A

glutamate acts on AMPA receptors to generate action potentials, NMDA receptors bring about release of calcium
- substance P acts on certain receptors neruokinin (NK1) receptors which can also release calcium,

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30
Q

What is the difference between Aδ fiber stimulation and C fiber stimulation?

A

In Aδ stimulation the calcium influx is very small which explains why the amount of stimuli does not change the response

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31
Q

Describe generation and transmission of pain:

what do the first oder neurons do/release? what happens to the second order neurons?

A

First order neurons release:

  • Glutamate
  • Substance P

Second order neurons (ascending pathways) activated, followed by 3rd, 4th, order neurons, etc

32
Q

During transmission of pain what do the ascending pathways provide input to?

Think of the brain and what each part of brain is responsible for when processing pain

A
  • somatosensory cortex
  • thalamus
  • reticular formation
  • Reticular activating system and thalamus (increases alertness to pain - stimulates arousal center) provides input to hypothalamus & limbic system
33
Q

How is pain modulated?

A

A built in analgesic system: PAG and RAS (loss of sensation of pain)
- electrical stimulation of PAG and RAS produces profound analgesia, certain endogenous opiates (endorphins, enkephalins and dynorphins) are also released: bind to opiate receptors (act as morphine/ same as morphine receptors) on afferent pain fiber terminal and inhibit release of substance P and glutamate thus blocking transmission of pain

unclear how activated

34
Q

what are some current theories about how pain modulation is activated?

A
  • exercise (runners high) - feel lessened sensation of pain
  • stress can have neg impact on modulation
  • Acupuncture - relieve pain, release endogenous opiods releasing analgesic sensation
35
Q

What is the pain threshold?

A

The point at which a stimulus is perceived painful, fairly uniform between individuals - everyone feels the same pain

36
Q

What is pain tolerance?

A

The maximum intensity or duration of pain that an individual is willing to endure berfore wanting to do something about it, differs from one individual to another (one person wants med for pain, the other doesn’t)

37
Q

What are some things that affect pain tolerance?

A

culture and gender (i.e. boys shouldn’t feel/ complain about pain)

why we shouldn’t judge people about pain

38
Q

Why is assessment of pain important?

A

for:

- diagnosing, managing and relieving pain

39
Q

How is pain usually assessed?

A

By self report: pain onset, description, localization, radiation, intensity, quality, pattern, relieving or exacerbatory factors, personal reaction to pain

40
Q

What is the numeric pain intensity?

A

rating pain on scale of 0-10

41
Q

What is the visual pain analog?

A

a straight line, no pain to most intense

42
Q

What is a verbal descriptor of pain?

A 
none = 0
severe = 4
43
Q

McGill pain questionnaire, Memorial Pain Assessment card

A

self assessment questionnaire

44
Q

Types of pain/ classifying pain based on source or location

A

Somatic: cutaneous (paper cut, sharp burning), or deep (diffuse and throbbing - harder to localize)
Visceral: (difficult to localize, poorly defined -> ischemia of visceral organs)

45
Q

Types/ classification of pain based on site of referral

A

referred pain: pain radiates at one site but is perceived at a different site (i.e. heart attack, left arm, shoulder and hand pain) - occurs because pain terminals are synapsing in the same place where the other cells (1st and 2nd order neurons) start

46
Q

Types/ classification of pain based on duration

A

acute: less than six months
chronic: more than six months

47
Q

As long as the time period for being in pain is normal for a particular procedure it is known as:

a. acute pain
b. chronic pain

A

a

48
Q

What type of pain is a major problem?

A

chronic pain

49
Q

What may headaches be due to?

A

Primary or secondary disorders

50
Q

If a headache is due to primary disorder, what type of headache can an individual have?

A
  • migraine headache
  • tension type headache
  • cluster headache
  • chronic daily headache
51
Q

What types of secondary disorders can cause a headache/

A

Meningitis, tumor, etc

52
Q

What does diagnosis/ classification of a headache require?

A

It is difficult to diagnose, they require history and physical exams to exclude secondary causes first

53
Q

What is the prevalence of migraines?

A

affect 20 million people in US, 18% women, 6% men (most common in women)

  • in children gender doesn’t matter
  • runs in families: genetic influence - autosomal dominant (not limited to sex chromosome)
54
Q

What are the two types of migraines?

A

Migraines with aura and migraines without aura

55
Q

What are characteristics of a migraine without aura?

A
  • they are common ~ 85% of migraines
  • pulsatile, throbbing unilateral (one side of head) headache lasting 1-2 days
  • aggravated by routine physical activity
  • accompanied by nausea, vomiting, sensitivity to light (photophobia) and sound (sonophobia)
  • visual hallucinations: stars, sparks, flashes of light
56
Q

What are characteristics of a migraine with aura?

A

they are initially a classical migraine, but are much more likely inhibited
~15% of migraines
- visual/neuorlogic symptoms (blurred, cloudy vision, see a spark across visual system, mood or energy change) before the headache
- an aura develops over 5-20 minutes, lasts less than an hour
- all characteristics seen in migraine without aura present as well

57
Q

What are some predictions of migraine etiology?

A
  • trigeminal nerve activation: releases CGRP (calcitonin gene related peptide) leading to vasodilation and inflammation -> sensation of pain
  • (best explanation) trigger: cortical spreading depression -> decrease blood level to brain - move from one part of brain to the other
  • dysfunction of ion channels e.g. VG calcium channels (need neurotransmitter exocytosis) - hypersensitive, often stimulated by small stimulus
  • hormonal variations: coincide with menstrual period on women (estrogen levels) - not an explanation for men
58
Q

Which type of migraine is easier to treat?

A

Migraine with aura because there is a warning about it so medicine needs to be taken immediately

59
Q

What are nonpharmacologic ways to treat migraines?

A
  • having a set routine: regular eating/ sleeping schedule
  • avoid triggers: food e.g. MSG, cheese, wine, chocolate, stress
  • triggers can be different for different people so be sure to avoid your trigger
60
Q

What are some pharmacologic methods to treat migraines?

A
  • abortive treatment: aspirin, aspirin + acetaminophen, ceffeine + NSAIDs, serotonin receptor agonists, ergotamine derivatives, antiemetics
  • Preventative (med must be taken all the time if severe migraines 3+ times a month): beta adrenergic blockers, antidepressants, antiseizure medications
61
Q

What dosage form would you use for an outpatient migraine patient who may be suffering severe vomiting?

a. tablets
b. IV
c. aerosol (nasal)

A

C. because tablets would not have time to absorb, and at home most people cannot/won’t administer their own IV

62
Q

What gender are cluster headaches more prevalent in?

A

Men

63
Q

What are cluster headaches?

A

They are relatively uncommon

  • occur in clusters over weeks/ months followed by long headache free periods
  • severe, unrelenting, unilateral pain rapid in onset, peaks in 10-15 minutes, lasts 15- 180 minutes
  • feels stab in eye, eyelid swolle, conjunctival redness, associated with restlessness/agitation
  • often mistaken for sinus/dental problems
  • heredity plays a role
64
Q

Why are oral drugs not used for abortive drugs to treat cluster headache?

A

oral dosage form won’t be efficacious ( need to treat right away - only 15-180 mins long, oral drug may take that long to kick in)

65
Q

What are the abortive and preventative treatments for cluster headaches?

A

abortive: oxygen, sc sumatriptan, nasal lidocaine
preventative: ergotamine, verapamil, lithium carbonate, corticosteroids

66
Q

What are characteristics of a tension type headache?

A
  • not a migraine
  • no nausea or vomiting
  • not worsened by activity
  • dull, aching, diffuse, nondescript headaches, occurring in hatband distribution
  • can be infrequent episodic or chronic
67
Q

What are ways to treat tension type headaches?

A

More responsive to non-pharmacologic treatments

- pharmacologic: aspirin, acetaminophen, NSAIDs

68
Q

What are chronic daily headaches?

A
  • occur 15 or more days per month
69
Q

What are causes of chronic daily headaches?

A

transformed migraine headaches

  • evolved tension - type headaches
  • new daily persistent headache
  • post-traumatic headache
70
Q

What are ways to treat chronic daily headaches?

A
  • more responsive to non-pharmacologic treatments

- pharmacologic: aspirin, acetaminophen, Nsaids

71
Q

What does the glutamate do that is released by first order neurons?

A
  • Glutamate: activates AMPA & NMDA receptors to generate action potentials
72
Q

What does substance P released by first order neurons do?

A
  • Substance P: prolongs Ca2+ second messenger systems via NMDA receptors, leading to hyperexcitability (tissue damage has already occurred, even a light sensation may cause a response)
73
Q

What part of pain is the somatosensory cortex responsible for?

A

localization of pain (sensory homunculus)

74
Q

What part of pain is the thalamus responsible for?

A

perception of pain

75
Q

What part of pain is the reticular formation responsible for?

A

increasing levels of alertness

76
Q

What do RAS and the thalamus do during pain?

A

provide input to the hypothalamus and limbic system

77
Q

What it the role of the hypothalamus and the limbic system in pain?

A

emotional and behavioral responses

physio exam 3 (6 decks)

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