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NURA 662 Adv Pathophysiology > Pain > Flashcards

Pain Flashcards

1
Q

WHO definition of pain.

A

an unpleasant sensory AND emotional experience associated with actual or potential tissue damage

pain is a protective mechanism

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2
Q

Dyesthesia

A

any abnormal sensation described as UNPLEASANT by the patient

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3
Q

hyperalgesia

A

EXAGGERATED pain response from a normally painful stimulus; usually includes aspects of summation with repeated stimulus of constant intensity and after sensation (no longer normal, no longer protective)

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4
Q

hyperesthesia (hypesthesia)

A

exaggerated perception of TOUCH stimulus

hyper reactive response

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5
Q

allodynia

A

ABNORMAL PERCEPTION of pain from a normally NON - PAINFUL mechanical or thermal stimulus; usually has elements of delay in perception

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6
Q

hypoalgesia (hypalgesia)

A

DECREASED sensitivity and raised threshold to painful stimuli

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7
Q

anesthesia

A

reduced perception of all sensation, mainly touch

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8
Q

analgesia

A

reduced perception of pain stimulus

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9
Q

paresthesia

A

MAINLY SPONTANEOUS ABNORMAL sensation that is not necessarily unpleasant; usually described as “pins and needles”

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10
Q

causalgia

A

burning pain in the DISTRIBUTION OF ONE OR MORE PERIPHERAL NERVES

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11
Q

Are pain receptors adaptive or non-adaptive?

A

NON - ADAPTIVE: very little adaptation, or not at all

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12
Q

sensation: protopathic

A

noxious

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13
Q

sensation: epicritic

A

non - noxious

I.e. pressure, light touch, temperature, discrimination

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14
Q

Fast pain

A

thinly myelinated type A delta fibers

  • felt about .1 sec after stimulus
  • felt on surface of body: sharp, pricking, electric pain
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15
Q

slow pain

A

unmyelinated type C pain fibers

  • felt at 1 sec after stimulus
  • felt in deeper tissue and surface tissue: slow, burning, aching, throbbing, chronic
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16
Q

chemical burn

A
  • *bradykinin, acetylcholine, prostaglandins, substance P & proteolytic enzymes - inc permeability to ions like potassium
  • -slow pain only
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17
Q

four physiologic processes to nociceptive stimuli: transduction

A

noxious stimuli; causes cell damage with the release of sensitizing chemicals

  • prostaglandins
  • bradykinin
  • serotonin
  • substance p
  • histamine

these substances activate nociceptors and lead to generation of action potential

converted to electric activity at the sensory nerve ending

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18
Q

four physiologic processes to nociceptive stimuli: transmission

A

propagation of impulses thru the sensory nervous system

Action potential continues from:

  • -site of injury to spinal cord
  • -spinal cord to brainstem and thalamus
  • -thalamus to cortex for processing
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19
Q

four physiologic processes to nociceptive stimuli: modulation

A

process of transmission modified by neural influence

-neurons originating in the brainstem descend to the spinal cord and release substances (e.g. endogenous opioids) that inhibit nociceptive impulses

modulation can occur at the spinal cord AND the brain.

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20
Q

four physiologic processes to nociceptive stimuli: perception

A

above 3 interact with the psychology of the pt to create what is perceived as pain

“conscious experience of pain”

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21
Q

four physiologic processes to nociceptive stimuli

A
  1. transduction
  2. transmission
  3. modulation
  4. perception
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22
Q

Pain pathway: first order neurons

A
  • send their axons into the spinal cord via the dorsal (sensory) root
  • may synapse with inter-neurons, sympathetic neurons and ventral horn (motor) neurons
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23
Q

Pain pathway: second order neurons

A

in the gray matter of ipsilateral dorsal horn

24
Q

Pain pathway: spinothalamic tract

A

axons of most second order neurons cross midline and for the spinothalamic tract

major pain pathway to the thalamus, reticular formation (arousal and sleep), nucleus raphe magnus & periaqueductal gray

lies anterolaterally in white matter of spinal cord

25
Q

Pain pathway: third order neurons

A

located in the the thalamus

send fibers to somatosensory areas I and II in the parietal cortex, and the superior wall of the sylvian fissure

responsible for perception and localization of pain

26
Q

Alternate pain pathways: spinoreticular tract

A

insomnia due to pain

27
Q

Alternate pain pathways: spinomesencephalic tract

A

activates ANTI-NOCICEPTIVE, descending pathways

28
Q

alternate pain pathways: spinohypothalamic and spinotlencephalic tracts

A

activate the hypothalamus and evoke EMOTIONAL BEHAVIOR

29
Q

Fast pain pathway summary: neospinolthalamic tract

A

First order neurons - via type A delta fibers enter lamina I and V (lamina marginalis) of the dorsal horn of the spinal cord – synapse with 2nd order neurons

Second order neurons - cross the midline through the anterior white commissure and pass upwards in the anterolateral columns (STT).

  • few of these fibers terminate on the reticular formation
  • MOST - travel to ventrobasal complex (VBC) of the thalamus

Third order neurons - communicate with the somatosensory cortex

30
Q

Slow pain pathway summary: paleospinothalamic pathway

A

First order neurons - via type C fibers enter laminae II and III of the dorsal horns (substantial gelatinosa) - synapse with 2nd order neurons

Second order neurons - make synaptic connections in lamina IV - VIII, can go up WITHOUT crossing

-most 2nd order neurons join fibers from the fast pathway, crossing to the opposite side traveling upwards through the anterolateral pathway (STT).

They terminate widely in the brain stem with 1/10 of fibers stopping in the thalamus, and the rest stopping in the medulla, pons, and tectum of midbrain mesencephalon periaqueductal gray

31
Q

The analgesia system is mediated by 3 major components:

A

the periaqueductal grey matter (in the midbrain)

the nucleus raphe magnus (in the medulla)

and the nociception inhibitor neurons within the dorsal horns of the spinal cord

32
Q

What is the periaquaductal grey matter?

A

the epicenter of analgesia

It plays a role in the descending modulation of pain and in defensive behavior

33
Q

What is the nucleus raphe magnus

A

is afferently stimulated from axons in the spinal cord and cerebellum

the main function of the magnus - pain mediation

sends projections to the dorsal horn of the spinal cord to directly inhibit pain

34
Q

Pain cellular physiology: chemical mediators

A

substance P - released slower, building over few minutes (slow chronic pain)

glutamate - acts instantly; only lasts a few milliseconds (fast pain)

CGRP - calcitonin gene related peptide

35
Q

Pain cellular physiology: modulators

A

occurs peripherally at the nociceptors, int he spinal cord, or in supra spinal structures

this modulation can suppress or aggravate pain

NMDA receptor role

36
Q

Physiologic responses to acute pain

A

NEUROENDOCRINE RESPONSE

  • increase secretion of catabolic hormones
  • stress response
  • decrease anabolic metabolism
  • decrease anabolic metabolism, insulin, testosterone
  • ACTH release
  • hyperglycemia
37
Q

Cardiac responses to pain

A
  • inc HR (decreasing supply to coronaries), BP, SVR, CO
  • MI, CHF, dysrhythmias
  • decrease myocardial oxygenation - secondary to pulmonary dysfunction – atelectasis
  • coronary artery constriction - high catecholamines
  • —release of serotonin may induce coronary vasospasm

-increase plasma viscosity - platelet induced occlusion

38
Q

Pulm responses to pain

A
  • inc total body O2 consumption
  • inc CO2 production
  • inc minute ventilation
  • —dec TV, VC, FRC - most detrimental alteration in post surgical lung volume. As FRC decreases, resting lung volume approaches closing volume, as It continues, atelectasis results, VQ misact, and hypoxemia ensues
  • pulmonary function DECREASES with abd or thoracic incisions (splinting)
39
Q

Vascular system response to pain

A

stress mediated due to platelet adhesion and hyper - coagulability
—DVT, PE, edema

40
Q

GI and urinary systems: response to pain

A

INCREASED sympathetic tone, INCREASED sphincter tone, DECREASED gastric motility—-promoting ileum and urinary retention.

N/V COMMON

increased gastric juices - stress ulcers can occur!

41
Q

Pain response: other body systems

A

visceral pain is referred to somatic sites

periosteal and somatic irritation initiates reflex motor response leading to muscle spasm

without excellent pain control, some patient have increased anxiety and may get angry

42
Q

What is chronic pain?

A

pain which persists ONE MONTH longer than EXPECTED

chronic pain has NO time limit, often has NO apparent CAUSE, and serves NO apparent BIOLOGICAL PURPOSE

chronic pain was originally defined as pain that has lasted 6 months or longer – It is now defined as “THE DISEASE OF PAIN.”

associated with musculoskeletal disorders, chronic visceral disorders, lesions of peripheral nerves, nerve roots, dorsal root ganglia (including causalgia, phantom limb pain), lesions of the CNS and cancers invading the nervous system

43
Q

Which type of pain can have a psychosomatic or psychogenic cause?

A

chronic pain

44
Q

most common causes of chronic pain

A 
low back pain
headache
recurrent facial pain
cancer pain
arthritic pain
45
Q

Chronic pain: causes

A

chronic pathology in somatic or visceral structures

psychological mechanisms

peripheral mechanism

reflex role

peripheral central mechanism

the circle mechanism

chronic nerve compression

central pain mechanisms

psychophysiologic mechanisms

learned mechanisms

46
Q

Chronic pain causes: peripheral mechanisms

A

chronic pain syndromes associated with CHRONIC INFLAMMATION in the periphery respond to aspirin and NSAIDs which prevent synthesis of prostaglandins

47
Q

Chronic pain causes: reflex role

A

chronic pain can create excessive MUSCLE TENSION and tendon stretch. Sympathetic hyperactivity can create local ischemia and persistent disruption of the microcirculation

48
Q

chronic pain causes: peripheral - central mechanism

A

LESIONS of peripheral nerves, dorsal roots or dorsal ganglion cells

found in causalgia and other reflex sympathetic dystrophy, phantom pain

49
Q

chronic pain causes: the circle mechanism

A

suggests that INTENSE STIMULATION OF NERVE FIBERS IN THE CORD activate internuncial neurons creating an abnormal reverberatory activity in a closed loop

50
Q

chronic pain causes: central pain mechanisms

A

found in LESIONS TO THE THALAMUS AND SPINAL CORD injury as in paraplegia

51
Q

chronic pain causes: psychophysiologic mechanisms

A

SEVERE STRESS

usually seen in chronic tension headaches and chronic pain due to muscle spasms in the shoulder, back and chest

52
Q

chronic pain causes: learned mechanisms

A

SECONDARY GAIN

these patients frequently develop reactive depression and hypochondriasis

53
Q

effects of chronic pain

A

serotonin and endorphins become depleted, so minor injuries become intolerable

54
Q

psychologic profiles of chronic pain

A

the chronic pain pt shows significant differences on the MMPI, neuroticism.

However, when the pain is relieved the neurotic features dissipate. The longer the duration of the pain, the greater the psychological changes

55
Q

Chronic pain: treatment

A

must not only remove the pain and the cause of the pain but also rehabilitate the patient and family physically and psychosocially and psycholgogically

56
Q

examples of pain control

A

epidural injections with or without steroids

trigger point injections

peripheral nerve blocks with neurolytics

acupuncture

NURA 662 Adv Pathophysiology (7 decks)

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