Exam 1: Pain Flashcards
(84 cards)
1
Q
What is the point of pain?
A
Protective mechanism
2
Q
Three types of pain:
A
Acute
Chronic
Cancer
3
Q
Define dysesthesia:
A
Abnormal sensation described as unpleasant
4
Q
Define hyperalgesia:
A
Exaggerated response from a painful stimulus; summation with repeated stimulus of constant intensity + aftersensation
5
Q
Define hyperpathia:
A
Abnormally painful and exaggerated response to pain stimulus
6
Q
Define hyperesthesia:
A
Exaggerated perception of touch stimulus
7
Q
Define allodynia:
A
Abnormal perception of pain from a normally non-painful stimulus (often with delay in perception)
8
Q
Define hypoalgesia/hypalgesia:
A
Decreased sensitivity/raised threshold for painful stimulus
9
Q
Define anesthesia:
A
Reduced perception of all sensation, mainly touch
10
Q
Define pallanesthesia:
A
Loss of perception of vibration
11
Q
Define analgesia:
A
Reduced perception of pain stimulus
12
Q
Define paresthesia:
A
Spontaneous abnormal sensation that is not painful (pins and needles)
13
Q
Define causalgia:
A
Burning pain in the distribution of a peripheral nerve (i.e. diabetic neuropathy)
14
Q
Are pain receptors adaptive?
A
No
15
Q
Protopathic vs. epicritic:
A
Protopathic: noxious
Epicritic: non-noxious; pressure, light touch, temperature
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
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
18
Q
Visceral pain is which type?
A
Slow pain
19
Q
Mechanical, thermal, and chemical pain: fast and/or slow?
A
Mechanical: both
Thermal: both
Chemical: slow pain only
20
Q
What causes chemical pain?
A
Release of pain mediators: bradykinin, ACh, prostaglandins, substance P, proteolytics
Increased permeability to ions like K+
21
Q
Four physiologic processes that follow nociceptive stimulus:
A
Transduction
Transmission
Modulation
Perception
22
Q
Describe transduction:
A
Stimulus converted to electrical activity at sensory nerve endings
23
Q
Describe transmission:
A
Propagation of impulses through nervous system
24
Q
Describe modulation and give an example:
A
Transmission is modified by neuronal influences; hyperalgesia or pain lessening with time
25
Describe perception and possible responses:
Transduction, transmission, and modulation interact with the pt's psychology to produce the perception of pain
Responses can be crying, anger, nausea, etc
26
Sensitizing chemicals released by noxious stimulus:
```
Prostaglandins
Bradykinin
Serotonin
Substance P
Histamine
```
27
How do neurons modulate pain transmission?
Neurons originating in brainstem descend to spinal cord and release endogenous opioids, etc to change nociceptive impulses
28
Describe pathway of first order STT neurons:
Send axons from tissue into spinal cord via dorsal (sensory) root
Synapse with interneurons, sympathetic neurons, and ventral horn/motor neurons
29
Brain destinations for STT neurons:
Thalamus
Reticular formation
Nucleus raphe magnus
Periaqueductal gray
30
Third order STT neurons terminate in:
Somatosensory areas I and II
| Superior wall of Sylvian fissure
31
The STT is responsible for:
Perception and localization of pain
32
Pain pathway responsible for insomnia due to pain:
Spinoreticular tract
33
Pain pathway responsible for activating the endogenous opioid system:
Spinomesencephalic tract
34
Pain pathways responsible for evoking emotional behavior - and what part of the brain do they activate?
Spinohypothalamic and spinotelencephalic pathways
| Activate the hypothalamus
35
Describe the path of the neospinothalamic pathway:
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
Where do interneurons modulate the signals of the STT?
Between first and second order neurons
37
Which lamina make up the lamina marginalis?
I and V
38
Describe the path of the paleospinothalamic pathway:
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
What causes chronic pain after the stimulus is removed/injury is healed?
Reverberation within the spinal cord neurons
40
Requirements for fast pain to be easily localized:
Aδ fibers are stimulated together with tactile receptors
41
Requirements for slow pain to be easily localized:
Trick question - doesn't happen
42
3 components of CNS analgesia system:
Periaqueductal grey matter (midbrain)
Nucleus raphe magnus (medulla)
Nociception inhibitory neurons (spinal cord)
43
What component is "the epicenter of analgesia"?
Periaqueductal grey matter
44
Periaqueductal grey matter's role in analgesia:
Descending modulation of pain
| Guarding/defensive behavior
45
Nucleus raphe magnus's role in analgesia:
Sends projections to dorsal horn of SC to directly inhibit pain when afferent pain signals are recieved
46
Where does the nucleus raphe magnus send projections to?
Throughout the cortex
Cerebellum
Spinal cord
47
3 major chemical mediators of pain:
Substance P: slow pain (over a few minutes)
Glutamate: fast pain (few milliseconds)
Calcitonin gene-related peptide
48
Which receptor has a role in pain modulation?
NMDA
49
What receptors do substance P and glutamate activate?
Substance P: NK-1
| Glutamate: AMPA
50
Why are NMDA receptors typically inactive?
"Plugged" by Mg+ ions
51
How do pain neurons respond to intense or prolonged stimulation?
Become sensitized and over-responsive
52
What happens to NMDA receptors during prolonged pain stimulus?
Over-responsive neurons depolarize so much that the Mg+ leaves the NMDA channel and Ca++ ions can enter
53
What occurs as a result of NMDA channels opening?
Ca++ influx activates cNOS, converting L-arginine to NO
| NO diffuses out of neurons
54
How does NO act in the synapse? (Pre and post)
Presynaptically: exaggerates release of sub. P and EAAs
Postsynaptically: makes neurons hyperexcitable, increased release of sub. P, ACh, etc
55
What is the neuroendocrine response to pain? (5 responses)
```
Increased catabolic hormones
Stress response
Decreased anabolic metabolism, insulin, testosterone
ACTH release
Hyperglycemia
```
56
Cardiac parameters in response to pain:
Increased HR, BP, SVR, CO
57
Potential cardiac pathology in response to pain:
MI, CHF, dysrhythmias
58
Relationship between pain, myocardial demands, and pulmonary status:
Decreases myocardial oxygenation, which leads to secondary pulmonary dysfunction and atelectasis
59
Effect of pain on coronary vasculature:
Coronary artery constriction 2ndary to high catecholamines and serotonin release
60
Effect of pain on blood/vasculature:
Increases plasma viscosity leading to DVT, PE
61
Pulmonary changes from pain:
Increased O2 consumption, CO2 production (inc. metabolism)
| Increased minute ventilation - lower TV, higher RR
62
Most detrimental post-op pulmonary effect of pain:
Decreased FRC leading to atalectasis, V/Q mismatch, hypoxemia
63
GI/GU effects from pain:
Inc sympathetic tone, sphincter tone
Dec gastric motility
N/V
Stress ulcers
64
Periosteal and somatic irritation lead to:
Muscle spasms from reflex motor response
65
Considerations for pain relief methods:
Duration of relief
Patient hx
Goals of mgmt
Acute or chronic pain
66
Best post-op pain management begins:
Pre-operatively
67
Benefits of regional anesthesia for pain mgmt:
```
Less morbidity
Less CV impact
Less infection
Less cortisol release
Lower overall post-op complication rate
```
68
Types of analgesics:
NSAIDs/COX inhibitors
| Opioids
69
Drugs that affect the NMDA receptors for pain relief:
Ketamine
| Magnesium
70
Advantages of PCA:
```
Cost-effective
More patient satisfaction
Lower overall consumption
Less overmedication
Shorter hospital stays
```
71
Considerations for PCA dosing:
Relieve pain *before* starting PCA
Dose too small discourages pt
Dose too big causes adverse rxns/lowers trust
72
Define chronic pain:
Pain which persists one month longer than expected
73
Examples of conditions that cause chronic pain:
```
Low-back pain
Headache
Facial pain
Cancer
Arthritis
```
74
What is the reflex role in chronic pain?
Excessive muscle tension/tendon stretch creates sympathetic hyperactivity, local ischemia, interrupted microcirculation
75
What is the circle mechanism of chronic pain?
Stimulation of nerve fibers in the spinal cord activate interneurons that lead to reverberatory loops
76
What causes central chronic pain?
Lesions to the thalamus, spinal cord injury
77
What are psychophysiologic sources of chronic pain?
Severe stress leading to chronic tension headaches and chronic pain in the shoulder/back/chest
78
What are the peripheral-central causes of chronic pain?
Causalgias, phantom pain, sympathetic dystrophy
79
Effect of chronic pain on pain tolerance:
Depletion of serotonin and endorphins leads to inability to tolerate minor injuries
80
Causes of cancer pain:
Tumor invasion of bone (most common)
Tumor compression of peripheral nerves (2nd most common)
Treatment side effect
81
Compared to other causes of pain, physical effects from cancer pain:
Much worse due to lack of sleep, appetite, N/V, etc
82
Why is cancer pain so poorly treated?
Lack of physician knowledge
| Fear of addiction from patients
83
WHO recommendations for cancer pain treatment (3 steps):
Mild pain: non-opioid - ASA, APAP, NSAIDs
Moderate pain: "weak" opioids - codeine, oxy
Severe pain: "strong" opioids - morphine, dilaudid
84
Cancer pain treatment adjuncts:
Corticosteroids - block prostaglandins, stimulate appetite
| Antidepressants - psych effects, also potentiate opioids
