1.5.2 Pain I Flashcards
How would analgesics shift the pain threshold?
-Analgesics allow pain threshold to be raised (shifted right)
What are the central events of pain?
- Central sensitization caused by prolonged activation of nociceptors and projection pathways
- Secondary Hyperalgesia (peripheral & central events)
- Recruitment of adjacent neurons (cord)
- Changing of central pharmacology – via glutamate activation of NMDA receptors
- Neuronal plasticity
- “Memories of Pain”
How do opoids cause neuronal influence?
- Bind GABA alpha and delta receptors on nociceptors
- Inhibit transmission of painful stimuli
-A nociceptive stimulus will activate two component systems of pain perception what are they and what is the result?
1) Sensory/Discriminative Component
Via the neospinothalamic tract (VPL)
Carries information regarding:
- Location
- Intensity
- Modality
2) Emotional Component
Via the paleospinothalamic tract (limbic/brainstem)
- Carries information regarding:
- Affective/motivational impact
- Cognitive/evaluative impact
-Information from both systems is processed to produce a conscious perception of pain
What are the characteristics of mixed pain?
- Has both nociceptive & neuropathic components
- Ex: failed low-back surgery, complex regional pain syndrome
What is the primary and secondary sites of action for opoids?
-Primary: brainstem/medullary centers
- Periaqueductal Grey Matter
- Nucleus Raphe Magnus
-Secondary:
- Limbic system
- Spinal cord (dorsal horn)
- Periphery
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Injured cells will do what and how will this affect A delta and C fibers?
- Injury to tissue will cause cellular spilling of contents
- Molecules like ATP and potassium are stimulators of A delta and C fibers
What is the role of substance P and CGRP in pain?
- Substance P and CGRP (Calcitonin gene-related peptide) are synthesized in DRG and preferentially shipped to periphery where they act on mast cells and blood vessel
- Serve an important efferent function in the afferent processing of pain
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Describe the relationship between pain sensation vs stimulus intensity.
- Pain is a threshold phenomenon – stimulus intensity must surpass a particular threshold in order to be perceived
- Dotted vertical line = pain threshold
- Above the threshold, pain sensation will increase with increased stimulus (solid line)
Allodynia: central pain sensitization (increased response of neurons)
Hyperalgesia: an increased sensitivity to pain, which may be caused by damage to nociceptors or peripheral nerves
Afferent APs will reach branch points, what will happen at these branch points?
- As afferent AP are transmitted through nerves, they will reach branch points
- Some AP will be sent up to the brain, others sent to adjacent neurons (recruitment)
What is Gate Control Theory?
large nerve fibers (touch) can over-power the small pain fibers
From Wikipedia: The gate control theory of pain asserts that non-painful input closes the “gates” to painful input, which prevents pain sensation from traveling to the central nervous system. Therefore, stimulation by non-noxious input is able to suppress pain.
Can the threshold of pain be shifted based on circumstances? If yes, describe what can occur and the important terms to describe the phenomenom.
- Pain threshold can be shifted higher or lower based on other situations
- Two phenomena occur when pain threshold is lowered (shifted left)
- Allodynia: pain produced from a stimulus that would normally not cause pain
- Ex: clothing touching sunburnt skin vs clothes touching non-burnt skin
- Hyperalgesia: increased pain produced from a stimulus normally causing mild pain
- Ex: slapping sunburnt skin vs slapping non-burnt skin
What are the peripheral events associated with pain?
- Nociceptors:
- Direct activation
- Indirect sensitization
- Inflammation
- Primary Hyperalgesia (peripheral sensitization)
- Triple Response of Lewis: flare, wheal, heat
What is important about the endogenous opiates?
“-phins”, periaqueductal grey matter in the midbrain, nucleus magnus → descending fibers to inhibit pain fibers in the spinal cords
