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ARCHIVED: Pathophysiology > Exam 1: Pain > Flashcards

Exam 1: Pain Flashcards

1
Q

What is the point of pain?

A

Protective mechanism

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2
Q

Three types of pain:

A

Acute
Chronic
Cancer

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3
Q

Define dysesthesia:

A

Abnormal sensation described as unpleasant

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4
Q

Define hyperalgesia:

A

Exaggerated response from a painful stimulus; summation with repeated stimulus of constant intensity + aftersensation

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5
Q

Define hyperpathia:

A

Abnormally painful and exaggerated response to pain stimulus

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6
Q

Define hyperesthesia:

A

Exaggerated perception of touch stimulus

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7
Q

Define allodynia:

A

Abnormal perception of pain from a normally non-painful stimulus (often with delay in perception)

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8
Q

Define hypoalgesia/hypalgesia:

A

Decreased sensitivity/raised threshold for painful stimulus

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9
Q

Define anesthesia:

A

Reduced perception of all sensation, mainly touch

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10
Q

Define pallanesthesia:

A

Loss of perception of vibration

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11
Q

Define analgesia:

A

Reduced perception of pain stimulus

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12
Q

Define paresthesia:

A

Spontaneous abnormal sensation that is not painful (pins and needles)

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13
Q

Define causalgia:

A

Burning pain in the distribution of a peripheral nerve (i.e. diabetic neuropathy)

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14
Q

Are pain receptors adaptive?

A

No

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15
Q

Protopathic vs. epicritic:

A

Protopathic: noxious
Epicritic: non-noxious; pressure, light touch, temperature

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16
Q

Discuss fast pain:

A 
Thinly myelinated Aδ fibers
Perception 0.1 sec after stimulus
Very precise
Felt on surface of body
Sharp, pricking, electric pain
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17
Q

Discuss slow pain:

A

Unmyelinated C fibers
Perception 1 sec after stimulus
Felt in deeper tissue and surface tissue
Burning, aching, throbbing, chronic pain

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18
Q

Visceral pain is which type?

A

Slow pain

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19
Q

Mechanical, thermal, and chemical pain: fast and/or slow?

A

Mechanical: both
Thermal: both
Chemical: slow pain only

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20
Q

What causes chemical pain?

A

Release of pain mediators: bradykinin, ACh, prostaglandins, substance P, proteolytics

Increased permeability to ions like K+

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21
Q

Four physiologic processes that follow nociceptive stimulus:

A

Transduction
Transmission
Modulation
Perception

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22
Q

Describe transduction:

A

Stimulus converted to electrical activity at sensory nerve endings

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23
Q

Describe transmission:

A

Propagation of impulses through nervous system

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24
Q

Describe modulation and give an example:

A

Transmission is modified by neuronal influences; hyperalgesia or pain lessening with time

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25
Q

Describe perception and possible responses:

A

Transduction, transmission, and modulation interact with the pt’s psychology to produce the perception of pain

Responses can be crying, anger, nausea, etc

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26
Q

Sensitizing chemicals released by noxious stimulus:

A 
Prostaglandins
Bradykinin
Serotonin
Substance P
Histamine
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27
Q

How do neurons modulate pain transmission?

A

Neurons originating in brainstem descend to spinal cord and release endogenous opioids, etc to change nociceptive impulses

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28
Q

Describe pathway of first order STT neurons:

A

Send axons from tissue into spinal cord via dorsal (sensory) root

Synapse with interneurons, sympathetic neurons, and ventral horn/motor neurons

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29
Q

Brain destinations for STT neurons:

A

Thalamus
Reticular formation
Nucleus raphe magnus
Periaqueductal gray

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30
Q

Third order STT neurons terminate in:

A

Somatosensory areas I and II

Superior wall of Sylvian fissure

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31
Q

The STT is responsible for:

A

Perception and localization of pain

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32
Q

Pain pathway responsible for insomnia due to pain:

A

Spinoreticular tract

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33
Q

Pain pathway responsible for activating the endogenous opioid system:

A

Spinomesencephalic tract

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34
Q

Pain pathways responsible for evoking emotional behavior - and what part of the brain do they activate?

A

Spinohypothalamic and spinotelencephalic pathways

Activate the hypothalamus

35
Q

Describe the path of the neospinothalamic pathway:

A

First order: Type Aδ fibers enter the lamina marginalis of the dorsal horn of the spinal cord

Second order: Cross midline via anterior white commissure, travel up via anterolateral columns. Some terminate in reticular formation. Most terminate in thalamus.

Third order: Travel to the somatosensory cortex (areas I and II)

36
Q

Where do interneurons modulate the signals of the STT?

A

Between first and second order neurons

37
Q

Which lamina make up the lamina marginalis?

A

I and V

38
Q

Describe the path of the paleospinothalamic pathway:

A

First order: Type C fibers enter the substantia gelatinosa of the dorsal horn of the spinal cord

Second order: synapse in lamina IV-VIII; some travel up ipsilateral side; most join neospinothalamic fibers to cross and travel up contralateral side

Terminate throughout the brainstem:
10% in thalamus
Medulla, pons, midbrain, periaqueductal grey

No third order neurons

39
Q

What causes chronic pain after the stimulus is removed/injury is healed?

A

Reverberation within the spinal cord neurons

40
Q

Requirements for fast pain to be easily localized:

A

Aδ fibers are stimulated together with tactile receptors

41
Q

Requirements for slow pain to be easily localized:

A

Trick question - doesn’t happen

42
Q

3 components of CNS analgesia system:

A

Periaqueductal grey matter (midbrain)
Nucleus raphe magnus (medulla)
Nociception inhibitory neurons (spinal cord)

43
Q

What component is “the epicenter of analgesia”?

A

Periaqueductal grey matter

44
Q

Periaqueductal grey matter’s role in analgesia:

A

Descending modulation of pain

Guarding/defensive behavior

45
Q

Nucleus raphe magnus’s role in analgesia:

A

Sends projections to dorsal horn of SC to directly inhibit pain when afferent pain signals are recieved

46
Q

Where does the nucleus raphe magnus send projections to?

A

Throughout the cortex
Cerebellum
Spinal cord

47
Q

3 major chemical mediators of pain:

A

Substance P: slow pain (over a few minutes)
Glutamate: fast pain (few milliseconds)
Calcitonin gene-related peptide

48
Q

Which receptor has a role in pain modulation?

A

NMDA

49
Q

What receptors do substance P and glutamate activate?

A

Substance P: NK-1

Glutamate: AMPA

50
Q

Why are NMDA receptors typically inactive?

A

“Plugged” by Mg+ ions

51
Q

How do pain neurons respond to intense or prolonged stimulation?

A

Become sensitized and over-responsive

52
Q

What happens to NMDA receptors during prolonged pain stimulus?

A

Over-responsive neurons depolarize so much that the Mg+ leaves the NMDA channel and Ca++ ions can enter

53
Q

What occurs as a result of NMDA channels opening?

A

Ca++ influx activates cNOS, converting L-arginine to NO

NO diffuses out of neurons

54
Q

How does NO act in the synapse? (Pre and post)

A

Presynaptically: exaggerates release of sub. P and EAAs
Postsynaptically: makes neurons hyperexcitable, increased release of sub. P, ACh, etc

55
Q

What is the neuroendocrine response to pain? (5 responses)

A 
Increased catabolic hormones
Stress response
Decreased anabolic metabolism, insulin, testosterone
ACTH release
Hyperglycemia
56
Q

Cardiac parameters in response to pain:

A

Increased HR, BP, SVR, CO

57
Q

Potential cardiac pathology in response to pain:

A

MI, CHF, dysrhythmias

58
Q

Relationship between pain, myocardial demands, and pulmonary status:

A

Decreases myocardial oxygenation, which leads to secondary pulmonary dysfunction and atelectasis

59
Q

Effect of pain on coronary vasculature:

A

Coronary artery constriction 2ndary to high catecholamines and serotonin release

60
Q

Effect of pain on blood/vasculature:

A

Increases plasma viscosity leading to DVT, PE

61
Q

Pulmonary changes from pain:

A

Increased O2 consumption, CO2 production (inc. metabolism)

Increased minute ventilation - lower TV, higher RR

62
Q

Most detrimental post-op pulmonary effect of pain:

A

Decreased FRC leading to atalectasis, V/Q mismatch, hypoxemia

63
Q

GI/GU effects from pain:

A

Inc sympathetic tone, sphincter tone
Dec gastric motility
N/V
Stress ulcers

64
Q

Periosteal and somatic irritation lead to:

A

Muscle spasms from reflex motor response

65
Q

Considerations for pain relief methods:

A

Duration of relief
Patient hx
Goals of mgmt
Acute or chronic pain

66
Q

Best post-op pain management begins:

A

Pre-operatively

67
Q

Benefits of regional anesthesia for pain mgmt:

A 
Less morbidity
Less CV impact
Less infection
Less cortisol release
Lower overall post-op complication rate
68
Q

Types of analgesics:

A

NSAIDs/COX inhibitors

Opioids

69
Q

Drugs that affect the NMDA receptors for pain relief:

A

Ketamine

Magnesium

70
Q

Advantages of PCA:

A 
Cost-effective
More patient satisfaction
Lower overall consumption
Less overmedication
Shorter hospital stays
71
Q

Considerations for PCA dosing:

A

Relieve pain before starting PCA
Dose too small discourages pt
Dose too big causes adverse rxns/lowers trust

72
Q

Define chronic pain:

A

Pain which persists one month longer than expected

73
Q

Examples of conditions that cause chronic pain:

A 
Low-back pain
Headache
Facial pain
Cancer
Arthritis
74
Q

What is the reflex role in chronic pain?

A

Excessive muscle tension/tendon stretch creates sympathetic hyperactivity, local ischemia, interrupted microcirculation

75
Q

What is the circle mechanism of chronic pain?

A

Stimulation of nerve fibers in the spinal cord activate interneurons that lead to reverberatory loops

76
Q

What causes central chronic pain?

A

Lesions to the thalamus, spinal cord injury

77
Q

What are psychophysiologic sources of chronic pain?

A

Severe stress leading to chronic tension headaches and chronic pain in the shoulder/back/chest

78
Q

What are the peripheral-central causes of chronic pain?

A

Causalgias, phantom pain, sympathetic dystrophy

79
Q

Effect of chronic pain on pain tolerance:

A

Depletion of serotonin and endorphins leads to inability to tolerate minor injuries

80
Q

Causes of cancer pain:

A

Tumor invasion of bone (most common)
Tumor compression of peripheral nerves (2nd most common)
Treatment side effect

81
Q

Compared to other causes of pain, physical effects from cancer pain:

A

Much worse due to lack of sleep, appetite, N/V, etc

82
Q

Why is cancer pain so poorly treated?

A

Lack of physician knowledge

Fear of addiction from patients

83
Q

WHO recommendations for cancer pain treatment (3 steps):

A

Mild pain: non-opioid - ASA, APAP, NSAIDs
Moderate pain: “weak” opioids - codeine, oxy
Severe pain: “strong” opioids - morphine, dilaudid

84
Q

Cancer pain treatment adjuncts:

A

Corticosteroids - block prostaglandins, stimulate appetite

Antidepressants - psych effects, also potentiate opioids

ARCHIVED: Pathophysiology (18 decks)

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