Exam 1: Pain Flashcards
What is the point of pain?
Protective mechanism
Three types of pain:
Acute
Chronic
Cancer
Define dysesthesia:
Abnormal sensation described as unpleasant
Define hyperalgesia:
Exaggerated response from a painful stimulus; summation with repeated stimulus of constant intensity + aftersensation
Define hyperpathia:
Abnormally painful and exaggerated response to pain stimulus
Define hyperesthesia:
Exaggerated perception of touch stimulus
Define allodynia:
Abnormal perception of pain from a normally non-painful stimulus (often with delay in perception)
Define hypoalgesia/hypalgesia:
Decreased sensitivity/raised threshold for painful stimulus
Define anesthesia:
Reduced perception of all sensation, mainly touch
Define pallanesthesia:
Loss of perception of vibration
Define analgesia:
Reduced perception of pain stimulus
Define paresthesia:
Spontaneous abnormal sensation that is not painful (pins and needles)
Define causalgia:
Burning pain in the distribution of a peripheral nerve (i.e. diabetic neuropathy)
Are pain receptors adaptive?
No
Protopathic vs. epicritic:
Protopathic: noxious
Epicritic: non-noxious; pressure, light touch, temperature
Discuss fast pain:
Thinly myelinated Aδ fibers Perception 0.1 sec after stimulus Very precise Felt on surface of body Sharp, pricking, electric pain
Discuss slow pain:
Unmyelinated C fibers
Perception 1 sec after stimulus
Felt in deeper tissue and surface tissue
Burning, aching, throbbing, chronic pain
Visceral pain is which type?
Slow pain
Mechanical, thermal, and chemical pain: fast and/or slow?
Mechanical: both
Thermal: both
Chemical: slow pain only
What causes chemical pain?
Release of pain mediators: bradykinin, ACh, prostaglandins, substance P, proteolytics
Increased permeability to ions like K+
Four physiologic processes that follow nociceptive stimulus:
Transduction
Transmission
Modulation
Perception
Describe transduction:
Stimulus converted to electrical activity at sensory nerve endings
Describe transmission:
Propagation of impulses through nervous system
Describe modulation and give an example:
Transmission is modified by neuronal influences; hyperalgesia or pain lessening with time
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
Sensitizing chemicals released by noxious stimulus:
Prostaglandins Bradykinin Serotonin Substance P Histamine
How do neurons modulate pain transmission?
Neurons originating in brainstem descend to spinal cord and release endogenous opioids, etc to change nociceptive impulses
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
Brain destinations for STT neurons:
Thalamus
Reticular formation
Nucleus raphe magnus
Periaqueductal gray
Third order STT neurons terminate in:
Somatosensory areas I and II
Superior wall of Sylvian fissure
The STT is responsible for:
Perception and localization of pain
Pain pathway responsible for insomnia due to pain:
Spinoreticular tract
Pain pathway responsible for activating the endogenous opioid system:
Spinomesencephalic tract
Pain pathways responsible for evoking emotional behavior - and what part of the brain do they activate?
Spinohypothalamic and spinotelencephalic pathways
Activate the hypothalamus
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)
Where do interneurons modulate the signals of the STT?
Between first and second order neurons
Which lamina make up the lamina marginalis?
I and V
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
What causes chronic pain after the stimulus is removed/injury is healed?
Reverberation within the spinal cord neurons
Requirements for fast pain to be easily localized:
Aδ fibers are stimulated together with tactile receptors
Requirements for slow pain to be easily localized:
Trick question - doesn’t happen
3 components of CNS analgesia system:
Periaqueductal grey matter (midbrain)
Nucleus raphe magnus (medulla)
Nociception inhibitory neurons (spinal cord)
What component is “the epicenter of analgesia”?
Periaqueductal grey matter
Periaqueductal grey matter’s role in analgesia:
Descending modulation of pain
Guarding/defensive behavior
Nucleus raphe magnus’s role in analgesia:
Sends projections to dorsal horn of SC to directly inhibit pain when afferent pain signals are recieved
Where does the nucleus raphe magnus send projections to?
Throughout the cortex
Cerebellum
Spinal cord
3 major chemical mediators of pain:
Substance P: slow pain (over a few minutes)
Glutamate: fast pain (few milliseconds)
Calcitonin gene-related peptide
Which receptor has a role in pain modulation?
NMDA
What receptors do substance P and glutamate activate?
Substance P: NK-1
Glutamate: AMPA
Why are NMDA receptors typically inactive?
“Plugged” by Mg+ ions
How do pain neurons respond to intense or prolonged stimulation?
Become sensitized and over-responsive
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
What occurs as a result of NMDA channels opening?
Ca++ influx activates cNOS, converting L-arginine to NO
NO diffuses out of neurons
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
What is the neuroendocrine response to pain? (5 responses)
Increased catabolic hormones Stress response Decreased anabolic metabolism, insulin, testosterone ACTH release Hyperglycemia
Cardiac parameters in response to pain:
Increased HR, BP, SVR, CO
Potential cardiac pathology in response to pain:
MI, CHF, dysrhythmias
Relationship between pain, myocardial demands, and pulmonary status:
Decreases myocardial oxygenation, which leads to secondary pulmonary dysfunction and atelectasis
Effect of pain on coronary vasculature:
Coronary artery constriction 2ndary to high catecholamines and serotonin release
Effect of pain on blood/vasculature:
Increases plasma viscosity leading to DVT, PE
Pulmonary changes from pain:
Increased O2 consumption, CO2 production (inc. metabolism)
Increased minute ventilation - lower TV, higher RR
Most detrimental post-op pulmonary effect of pain:
Decreased FRC leading to atalectasis, V/Q mismatch, hypoxemia
GI/GU effects from pain:
Inc sympathetic tone, sphincter tone
Dec gastric motility
N/V
Stress ulcers
Periosteal and somatic irritation lead to:
Muscle spasms from reflex motor response
Considerations for pain relief methods:
Duration of relief
Patient hx
Goals of mgmt
Acute or chronic pain
Best post-op pain management begins:
Pre-operatively
Benefits of regional anesthesia for pain mgmt:
Less morbidity Less CV impact Less infection Less cortisol release Lower overall post-op complication rate
Types of analgesics:
NSAIDs/COX inhibitors
Opioids
Drugs that affect the NMDA receptors for pain relief:
Ketamine
Magnesium
Advantages of PCA:
Cost-effective More patient satisfaction Lower overall consumption Less overmedication Shorter hospital stays
Considerations for PCA dosing:
Relieve pain before starting PCA
Dose too small discourages pt
Dose too big causes adverse rxns/lowers trust
Define chronic pain:
Pain which persists one month longer than expected
Examples of conditions that cause chronic pain:
Low-back pain Headache Facial pain Cancer Arthritis
What is the reflex role in chronic pain?
Excessive muscle tension/tendon stretch creates sympathetic hyperactivity, local ischemia, interrupted microcirculation
What is the circle mechanism of chronic pain?
Stimulation of nerve fibers in the spinal cord activate interneurons that lead to reverberatory loops
What causes central chronic pain?
Lesions to the thalamus, spinal cord injury
What are psychophysiologic sources of chronic pain?
Severe stress leading to chronic tension headaches and chronic pain in the shoulder/back/chest
What are the peripheral-central causes of chronic pain?
Causalgias, phantom pain, sympathetic dystrophy
Effect of chronic pain on pain tolerance:
Depletion of serotonin and endorphins leads to inability to tolerate minor injuries
Causes of cancer pain:
Tumor invasion of bone (most common)
Tumor compression of peripheral nerves (2nd most common)
Treatment side effect
Compared to other causes of pain, physical effects from cancer pain:
Much worse due to lack of sleep, appetite, N/V, etc
Why is cancer pain so poorly treated?
Lack of physician knowledge
Fear of addiction from patients
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
Cancer pain treatment adjuncts:
Corticosteroids - block prostaglandins, stimulate appetite
Antidepressants - psych effects, also potentiate opioids
