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552 Pathophysiology > Pain > Flashcards

Pain Flashcards

1
Q

According to WHO, pain is an unpleasant ________ & ________ experience associated with actual or potential ____________

A

sensory
emotional
tissue damage

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2
Q

Dysesthesia

A

any abnormal sensation described as unpleasant by patient; may not be pain

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3
Q

Hyperalgesia

A

exaggerated pain response from a normally painful stimulus

usually includes aspects of summation w/ repeated stimulus of constant intensity and aftersensation

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4
Q

Hyperpathia

A

abnormally painful and exaggerated reaction to a painful stimulus; related to hyperalgesia

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5
Q

Hyperesthesia (hypesthesia)

A

exaggerated perception of touch stimulus

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6
Q

Allodynia

A

abnormal perception of pain from a normally non-painful mechanical or THERMAL stimulus; usually has elements of delay in perception and of aftersensation

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7
Q

Hypoalgesia (hypalgesia)

A

decreased sensitivity and raised threshold to painful stimuli

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8
Q

Anesthesia

A

reduced perception of all sensation; mainly touch

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9
Q

Pallanesthesia

A

Loss of perception of vibration

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10
Q

Analgesia

A

reduced perception of pain stimulus

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11
Q

Paresthesia

A

mainly spontaneous abnormal sensation that is not unpleasant; “pins and needles”

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12
Q

Causalgia

A

BURNING PAIN in the distribution of one or more peripheral nerves

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13
Q

Protopathic sensation

A

noxious

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14
Q

Epicritic sensation

A

non noxious; i.e. pressure, light touch; temperature discrimination

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15
Q

Fast pain

A

thinly myelinated type AD fibers

  • felt ~ 0.1 sec after stimulus
  • felt on surface of body: sharp, pricking, electric pain
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16
Q

Slow pain

A

unmyelinated type C pain fibers

  • felt @ 1 sec after stimulus
  • felt in deeper tissue and surface tissue: slow burning, aching, throbbing, chronic
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17
Q

What type of painful stimuli goes on both fast and slow pathwathways?

A

mechanical and thermal

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18
Q

what kind of painful stimuli goes with slow pain pathways only?

A

chemical

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19
Q

What are 5 chemicals that act as painful stimuli?

A
  1. bradykinin
  2. ACh
  3. prostaglandins
  4. substance P
  5. proteolytic enzymes ( increase permeability to ions ie K)
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20
Q

What are the 4 physiologic processes to nociceptive stimuli?

A
  1. Transduction
  2. Transmission
  3. Modulation
  4. Perception
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21
Q

Transduction

A

Noxious stimuli causes cell damange w/ release of sensitizing chemicals ( ie substance p, bradykinin). These substances activate nociceptors and lead to generation of AP.
noxious stimuli converted to electric activity at the sensory nerve ending

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22
Q

Transmission

A

Action potential continues from site of injury to spinal cord; spinal cord; spinal cord to brainstem and thalamus; thalamus to cortex for processing:
propagation of impulses through the sensory nervous system

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23
Q

Modulation

A

Neurons originating in the brainstem descend to spinal cord and release substances (endogenous opiods) that inhibit nociceptive impulses:
process of transmission modified by neural influences

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24
Q

Perception

A

Conscious experience of pain:

Transduction, transmission, modulation interact w/ the psychology of the patient to create what is perceived as pain

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25
Q

primary afferent neurons

A

first order neurons
send axons into SC via the dorsal (sensory) root
May synapse w/ inter-neurons, sympathetic neurons and ventral horn (motor) neurons

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26
Q

Second order neurons

A

in gray matter of ipsilateral dorsal horn

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27
Q

Spinothalamic tract

A

STT
Spine to thalamus
axons of most 2nd order neurons cross midline and form the spinothalamic tract.
Major pain pathway to the thalamus, RF, nucleus raphe magnus & periaqueductal gray
LIes anterolaterally in white matter of spinal cord

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28
Q

3rd order neurons

A

located in thalamus and send fibers to somatosensory areas I & II in the parietal cortex, and superior wall of the sylvian fissure
Responsible for perception and localization of pain

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29
Q

alternate pain pathway that causes insomnia due to pain

A

spinorecticular tract

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30
Q

pathway that activates anti-nociiceptive descending pathways

A

spinomesencephalic tract

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31
Q

these 2 tracts activate the hypothalamus and evoke emotional behavior

A

spinohypothalamic and spinotelecephalic tracts

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32
Q

Neospinothalamic tract

A

fast pain pathway

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33
Q

first order neurons in neospinothalamic tract

A

travel via AD fibers and terminate on lamina I (lamina marginalis) of dorsal horn of SC

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34
Q

2nd order neurons on fast pain pathway

A

give rise to long fibers which CROSS midline through anterior white commisure and pass upwards in anterolateral columns (STT)

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35
Q

A few of the 2nd order neurons in the fast pain pathway terminate on the ________ causing insomnia

A

reticular formation

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36
Q

Where do most of the 2nd order neurons from fast pain pathway travel to

A

ventrobasal complex (VBC) of thalamus

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37
Q

3rd order neurons fast pain pathway

A

communicate w/ somatosensory cortex

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38
Q

Paleospinothalamic pathway

A

slow pain pathway

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39
Q

slow pain pathway: 1st order neurons

A

go via type C to laminae II and III of dorsal horns (together known as substantia gelatinosa)

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40
Q

2nd order neurons: slow pain pathway

A

take off and terminate in lamina V (also in dorsal horn)

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41
Q

3rd order neurons: slow pain pathway

A

join fibers from fast pathway and cross opp side via anterior white commissure and travel upwards through the anterolateral pathway

42
Q

2nd order neurons in slow pathway can be _________ or ___________ and can travel up to the brain via __________ or ____________

A

short or long

can travel up DC (dorsal column) or STT (mostly uses STT)

43
Q

Where do 3rd order neurons for the slow pathway terminate?

A

mostly in BRAINSTEM
1/10 in thalamus
rest in medulla, pons, tectum of midbrain mesencephalon periqueductal grey

44
Q

Fast pain can be localized easily if ____________ are stimulated together with ____________

A

AD fibers

tactile receptors

45
Q

Slow pain is poorly _____________

A

localized

46
Q

What 3 major components in the brain mediate the analgesia system?

A
  1. periaquaductal grey matter (midbrain)
  2. nucleus raphe magnus (medulla)
  3. nociception (pain) inhibitory neurons w/in the dorsal horns of SC– act to inhibit pain-transmitting neurons also located in spinal dorsal horn
47
Q

Epicenter of analgesia in the brain

A

periaquaductal grey matter

48
Q

This is afferently stimulated from axons in the SC and cerebellum

A

nucleus raphe magnus

49
Q

This area in the brain plays a role in the descending modulation of pain and in defensive behavior

A

periquaductal grey mater

50
Q

The main function of the _________ is mostly PAIN MEDIATION; it sends projections directly to the ____________ of the SC

A

nucleus raphe magnus

dorsal horn

51
Q

Substance P

A

released slower; building over a few minutes: slow chronic pain

52
Q

Glutamate

A

acts instantly, only lasts a few milliseconds: fast pain

53
Q

CGRP

A

calcitonin gene-related peptide

chronic pain: migraines

54
Q

Where do modulators occur? Do they suppress or aggravate pain?

A

peripherally at nociceptors
in spinal cord
or supraspinal structures
can suppress or aggravate pain

55
Q

example of a modulator

A

NMDA receptor role

56
Q

Neuroendocrine response

A 
increase secretion of catabolic hormones
stress response
decrease anabolic metabolism: insulin, testosterone
ACTH release
hyperglycemia
57
Q

Cardiac responses to pain

A

increased HR, BP, SVR, CO
MI, CHF, dysrrhythmias
decrease myocardial oxygenation secondary pulmonary dysfunction: atelectasis
Coronary artery constriction: high catecholamines
increase plasma viscosity: plt induced occlusion

58
Q

Release of serotonin may induce ______________-

A

coronary vasospasm

59
Q

pulmonary responses to pain

A

increased total body O2 consumption, CO2 production, minute ventilation

60
Q

What capacities decrease w/ pain?

A

TV, VC, FRC

61
Q

what is the most detrimental alteration in post surgical lung volume

A

FRC: as it decreases, resting lung volume approaches closing volume
as this continues atelectasis results, VQ mismatch and hypoxemia ensue

62
Q

Pulmonary function __________ w/ abdominal thoracic incision (splinting)

A

decreases

63
Q

What happens to the vascular system from stress

A

platelet adhesion and hyper-coagulability: DVT, pulmonary edema

64
Q

Where is visceral pain referred to?

A

somatic sites

65
Q

What are some other responses to pain your body has?

A

increased sphincter tone, decreased gastric mobility: ileus; n/v
stress ulcers
urinary retention

66
Q

Periosteal and somatic irritation initiate reflex motor response leading to ___________

A

muscle spasm

67
Q

Chronic pain is pain that persists ______________.

A

one month longer than expected

68
Q

T/F: Chronic pain is protective

A

False

69
Q

What are the main types of chronic pain?

A

low back pain, h/a, recurrent facial pain, cancer pain, arthritis

70
Q

Chronic pain caused by peripheral mechanisms respond to what?

A

NSAIDs; often from chronic inflammation in periphery

71
Q

What is the reflex role in chronic pain?

A

excessive muscle tension and tendon stretch

SNS hyperactivity can create local ischemia and persistent disruption of the microcirculation

72
Q

Peripheral-Central Mechanism

A

lesions of peripheral nerves, dorsal roots, or dorsal ganglion cells

Found in: causalgias, other reflex sympathetic dystrophy, phantom pain

73
Q

Circle Mechanism

A

intense stimulation of nerve fibers in spinal cord activated internuncial neurons creating an abnormal reverberatory activity in a closed loop
Difficult to treat: don’t know what is stimulating the nerve

74
Q

Chronic nerve compression

A

i.e. spinal stenosis; these patients often come in for surgery

75
Q

Central Pain Mechanism

A

found in lesions to the thalamus and SC injury such as paraplegia
see often in TBIs

76
Q

Psychophysiologic Mechanism

A

severe stress: usually seen in chronic tension h/a & chronic pain from muscle spasms in shoulder, back, chest

77
Q

Learned Mechanisms

A

secondary gain
These patients frequently develop reactive depression and hypochondriasis
-psychogenic component; difficult to treat

78
Q

When a person has chronic pain, how do they handle minor injuries? Why?

A

handle them poorly: serotonin and endorphins are depleted

79
Q

How does chronic pain affect a person’s personality?

A

show signs of neuroticism (from loss of control over pain)
However, these s/s often go away if pain is relieved
Longer duration of pain= greater psychological changes

80
Q

What happens to pain fibers in chronic pain? What does this lead to?

A

tonic activity of C fibers: leads to enhanced postsynaptic effects by NMDA-receptor sensitization

81
Q

What electrolyte would you consider giving a patient w/ chronic pain before surgery? Why?

A

Magnesium: blocks NMDA receptors so they aren’t active

82
Q

Treatment of chronic pain

A

steroid epidural injections with or without trigger point injections, peripheral nerve blocks w/ neurolytics, acupunture
high levels of analgesics
rehabilitation: physically, psychosocially, psychologically

83
Q

What are 3 common causes of cancer pain?

A
  1. tumor invasion of bone: most common
  2. tumor compression of peripheral nerves: 2nd most common
  3. treatment: radiaion, chemo
84
Q

The physical effects are better/worse for cancer pain patients than for other chronic pain patients?

A

worse

loss of sleep, appetite, n/v

85
Q

Psychological effects of cancer pain

A

heightened anxiety, separation and loss, self esteem, life’s goals, effect on family, disfigurement

86
Q

Cancer patients w/ more emo disturbances & pain ________________ than those whose pain was controlled

A

died sooner

87
Q

How does the WHO recommend approaching cancer pain?

A
  1. Nonopiod analgesic (mild pain): inhibit prostaglandin syntetase and & antitumor effects in bone mets
    - -ASA, tylenol, NSAIDs
  2. “weak” oral opiods (moderate pain)
    - -codein, oxycodone
  3. “stronger” opiods (severe pain)
    - MSO4; hydromorphone
88
Q

What are some adjuncts to treating chronic/cancer pain?

A

corticosteroids: prevents release of steroids; stimulates appetite
antidepressants: elevate mood; help w/ sleep; block reuptake of serontonin, potentiate narcotic analgesics

89
Q

Tolerance of opiods is __________ in cancer patients. THey can require ___________ of morphine IV

A

normal

200mg/hr

90
Q

T/F: addiction to pain meds in ca pain patients is rare.

A

True

91
Q

What is the goal of chronic pain managment?

A

sustained pain relief w/ minimal side effects

92
Q

What are other treatment modalities of chronic pain?

A

regional: but short term relief only
Neurolytics: permanent destruction of nerve; often get some motor loss too but pts often willing to handle this

93
Q

What is a problem w/ using NSAIDS?

A

celiling effect on analgesia

94
Q

What parts of the brain are affected in acute stress?

A

RAS or thalamus
Arcuate nucleus; Locus coeruleus
PVN
Amygdala

95
Q

What happens when the amygdala, arcuate nucleus, and locus coerculeus are activated in acute stress?

A

Amygdala: behavioral changes

Arucate nucleus & Locus coeruleus: NPY, NE excretion

96
Q

What happens when the PVN is stimulated in acute stress?

A

increased CRH–>ACTH (pituitary)–>CORT; NPY/NE (adrenal glands)

97
Q

What happens at target tissues w/ acute stress?

A

increased BP/HR

decreased appetite, reproduction; immunity, growth & thyroid function

98
Q

What is the feedback mechanism w/ acute stress?

A

CORT inhibits ACTH which inhibits CRH

99
Q

How are target tissues affected w/ chronic stress?

A

?? BP/HR
?? appetite
decreased reproduction, immunity & growth/thyroid fx

100
Q

What is the feedback in chronic stress?

A

Maladaptive: no negative feedback like in acute

Instead more of the hormones are made

552 Pathophysiology (5 decks)

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