Pain Flashcards

1
Q

Dysesthesia

A

Any abnormal sensation desc as unpleasant by pt

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2
Q

Hyperalgesia

A

Exaggerated pain response from a normally painful stimulus. Usually inc summation, repeated stimulus of constant intensity and aftersensation

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3
Q

Hyperpathia

A

Abnormally painful and exag rxn to a painful stim. R/t hyperalgesia

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4
Q

Hyperesthesia

A

Also hypesthesia. Exaggerated perception of touch stimulus

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5
Q

Allodynia

A

Abn 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

A

Decreased sensitivity and raised threshold to pain stim

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7
Q

Anesthesia

A

Reduced perception of all sensation, mainly touch

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8
Q

Pallanesthesia

A

Loss of perception of vibration

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9
Q

Analgesia

A

Reduced perception of pain

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10
Q

Parenthesia

A

Mainly spontaneous abnormal sensation that’s not always unpleasant, usually “pins and needles”

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11
Q

Causalgia

A

Burning pain in distribution of 1 or more peripheral nerves

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12
Q

Protopathic

A

Noxious stimuli

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13
Q

Epicritic

A

Non noxious stimuli. Pressure, light touch, temp discrimination

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14
Q

Fast pain
Fibers
Timing
Felt as

A

A delta. Myelinated
0.1 sec after stim
Felt on surface: sharp, pricking, electric pain

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15
Q

Slow pain
Fiber type
Timing
Felt where and how

A

C pain
1 sec after stimulus
Deeper tissue and surface tissue, slow burning/aching/throbbing/chronic

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16
Q

Chemical pain pathway mediated through what

What type of pain pathway is it

A

Bradykinin, acetylcholine, prostaglandins, substance P, proteolytic enzymes. Increased permeability to ions (potassium)

Slow pain only

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17
Q

4 physiologic processes to nociceptive stimuli

A

Transduction- noxious stim converted to electric activity at sensory nerve endings
Transmission- propagation of impulse through sensory NS
Modulation- transmission modified by neural influences
Perception- above 3 interact w psychology of pt to create pain percep

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18
Q

Transduction releases what and does what

A

Noxious stim causes cell damage, release of: prostaglandins, bradykinin, serotonin, sub p, and histamine. Activate nociceptors and generate action potential

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19
Q

Transmission

A

AP continues from site of injury to spinal cord, then to brainstem and thalamus, then to cortex for processing

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20
Q

Modulation

A

Neurons in brainstem descend to spinal cord and release endogenous opioids to inhibit pain

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21
Q

Primary afferrent neurons

A

1st order, send axons to SC via DRG, may synapse w interneurons, sympathetic neurons, and ventral horn neurons

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22
Q

Second order neurons

A

Gray matter of ipsilateral dorsal horn

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23
Q

Spinothalamic tract

A

Axons of 2nd order neurons cross midline. Pathway to thalamus, RG, nucleus Rachel, and periaqueductal gray. Anterolaterally in white matter of SC

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24
Q

3rd order neurons

A

In thalamus, send fibers to somatosensory areas I and II in parietal cortex and sup wall of Sylvian fissure. Perception and localization of pain.

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25
Q

Alternate pain pathways

A

Spinoreticular tract

Spinomesencephalic tract

Spinohypothalamic/spinotelencephalic tracts

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26
Q

Spinoreticular tract

A

Alt pain pathway, insomnia d/t pain

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27
Q

Spinomesencephalic tract

A

Activates anti-nociceptive descending pathways

28
Q

Spinohypothalamic/spinotelencephalic tracts

A

Activates hypothalamus and evokes emotional behavior

29
Q

Fast pain path: first order neurons

A

Enter lamina I and V (lamina marginalis) of dorsal horn of SC. Synapse w 2nd order

30
Q

Fast pain path: 2nd order neurons

A

Cross midline thru anterior white commissary and pass upwards in the anterolateral columns. Few of these terminate on reticular formation, most travel to ventrobasal complex of thalamus

31
Q

Fast pain: third order neurons

A

Communicate with somatosensory cortex

32
Q

Lamina where a delta fibers enter

A

I and V- lamina marginalis

33
Q

Slow pain path: first order neurons

A

Type C fibers enter lamina I and II or dorsal horns (substantia gelatinosa) synapse w 2nd order

34
Q

Slow pain path 2nd order neurons

A

Make synaptic connections in lamina 4-8, can go up without crossing. Most join fast pain path to opposite side thru anterrolateral path

35
Q

Where slow pain path fibers terminate

A

Brain stem. 1/10th of them stop in thalamus. Rest stop in medulla, pons, and rectum of midbrain mesencephalon periaqueductal grey

36
Q

Localization of pain

A

Fast pain- easily if a delta fibers stim together with tactile receptors

Slow pain poorly localized

37
Q

Analgesia system: 3 components

A

Periaqueductal gray matter (midbrain)

Nucleus raphe Magnus (medulla)

Nociceptors inhib neurons in dorsal horns of SC

38
Q

What periaquaductal gray matter does

A

Epicenter of analgesia. Role in descending modulation of pain and in defensive behavior

39
Q

Nucleus raphe Magnus role

A

Afferrent stim from axons in SC and cerebellum. Main func: pain mediation. Projections to dorsal horn of SC to inhibit pain

40
Q

Locus ceruleus

A

Where brain makes norepi, epi also stored

41
Q

Primary afferrent neuron axons synapse onto:

A

Spinothalamic neurons and onto inhibitory and excitatory neurons

42
Q

Substance p

A

Chemical mediator of pain. Released slowly, minutes, chronic pain

43
Q

Glutamate

A

Chemical pain mediator. Acts instantly. Only a few milliseconds, fast pain

44
Q

Cgrp

A

Chemical mediator of pain, calcitonin gene related peptide

45
Q

Modulators of pain

A

Peripheral at nociceptors. In SC or supraspinal structures. Suppresses or aggravates pain. NMDA receptor role

46
Q

Effects of chronic pain

A

Serotonin and endorphins depleted, minor injuries become intolerable. Diff in MMPI and neuroticism. Reversible w pain relief. Longer pain- greater changes

47
Q

Physiologic responses to acute pain: neuroendocrine

6

A

Inc secretion catabolic hormones
Decrease anabolic metab (esp insulin and testosterone)
ACTH release
Hyperglycemia

48
Q

Cv responses to acute pain

A
Inc hr, bp, SVR, co 
Mi, CHF, dysrhythmias 
Dec myo 02, atelectasis 
Coronary artery constrict from catecholamines 
Inc plasma viscosity, plt occlusion
49
Q

Pulmonary responses to acute pain

A

Inc total body o2 consumption, co2 production, inc minute vent
Decrease TV, VC, FRC. VQ mismatch and atelectasis- hypoxemia.

50
Q

Vascular response to acute pain

A

Plt adhesion and hypercoagulable. Dvt and PE

51
Q

GI and GU response to acute pain

A

Inc sympathetic tone, inc sphincter tone, dec gastric motility, promotion of ileus and urine ret. NV common. Stress ulcers

52
Q

Emotional and muscular responses to pain

A

Anxiety and anger

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

53
Q

Benefits of regional anesthesia

A

Less: morbidity, cv failure, infections, urinary cortisol, post op complications

54
Q

What cox inhibitors do

A

Inhibit prostaglandin synthesis

55
Q

Cox 1

A

Constitutive and widespread throughout body

56
Q

Cox 2

A

Expressed via inflammation

57
Q

Chronic pain

Definition

A

Persists 1 month longer than expected

58
Q

Chronic pain assoc with

A

Musculoskeletal disorders, chronic visceral disorders, lesions of peripheral nerves, nerve roots, DRG (causalgia, phantom limb pain), cns lesions, cancers invading NS

59
Q

Most common causes of chronic pain

A

Low back, HA, facial pain, cancer pain, arthritic pain

Psychomatic or psychogenic cause

60
Q

Peripheral mechanisms of chronic pain

A

Chronic inflammation

Give nsaids

61
Q

Reflex role in chronic pain

A

Excessive muscle tension and tendon stretch. Sympathetic hyperactivity can cause local ischemia and persistent disrup of micorcirculation

62
Q

Peripheral central mechanism- chronic pain

A

Lesions of peripheral nerves, dorsal roots, or DRG. Found in causalgia, reflex sympathetic dystrophy, phantom pain

63
Q

Circle mechanism (chronic pain)

A

Intense stim of nerve fibers in the cord activate internuncial neurons creating an abn reverbatory activity in closed loop

64
Q

Central pain mechanisms found where (chronic)

A

Lesions to thalamus and spinal cord, injury as in paralplegia

65
Q

Psychological mech of chronic pain

A

Severe stress- HA, muscle spasm in shoulder, back, chest

66
Q

Learned mechanisms of chronic pain

A

Secondary pain. Depression and hypochondria