SS25 Pain Pathways (Exam 2) Flashcards
(48 cards)
Differentiate the sensory-discriminative & motivational-affective aspects of pain.
- Sensory-discriminative - Ascending pathways via spinothalamic & trigemino-thalamic tracts and cerebral cortex → perception of pain (location, intensity, sensation, etc.)
- Motivational-affective - responses to painful stimuli (Ex. Attention/ Arousal, Somatic/ Autonomic reflexes, Endocrine responses, and Emotional changes)
What is nociception?
- The experience of pain through a series of complex neurophysiologic processes.
- Medications target causes of pain by actions on transduction, transmission, interpretation, & modulation in both PNS and CNS
What are the four stages of pain perception?
- Transduction (tissue level)
- Transmission (via nerve impulses)
- Modulation (via spinal cord)
- Perception (CNS)
Where does the modulation of pain impulses occur?
- What drugs work here?
- Dorsal horn of the spinal cord and produces reflex reactions
- Afferent fibers project signals to brain
- LAs, opioids, ketamine, A-2 agonist
What drugs are used to affect the transduction of pain?
What specifically is being affected by these drugs?
- Local anesthetics & NSAIDs
- Peripheral nociceptors - mechanical, thermal, and chemical stimuli
What drugs are used to affect the transmission of pain?
What specifically is being affected by these drugs?
- Local anesthetics
- Αδ and C fibers
What drugs are used to affect the perception of pain?
What specifically is being affected by these drugs?
- General anesthetics, opioids, α2 agonists
- Brain
Where are nociceptors located?
- Skin
- Muscles
- Joints
- Viscera
- Vasculature
What characterizes afferent C-fibers?
- Unmyelinated
- Burning pain from heat
- Sustained pressure
- Slow (less than 2 m/s)
What characterizes Alpha fibers?
- Myelinated
- Type I: Aβ & Aδ (heat,mechanical, chemical)
- Type II: Aδ (heat)
- Fast (>2 m/s)
What chemical mediators of pain are targeted with spinal anesthetics?
Peptides
- Substance P
- Calcitonin
- Bradykinin
- CGRP
Which chemical mediator is released first in response to injury?
- Bradykinin
What chemical mediators of pain are inhibited by NSAIDs?
- Lipids (Prostaglandins &Thromboxanes)
What chemical mediators of pain are inhibited by cannabis?
- Lipids (Endocannabinoids)
What is sensitization?
- Decreased pain threshold (likely due to upregulation of receptors)
Differentiate hyperalgesia and allodynia.
- Hyperalgesia - ↑ pain sensations to normally painful stimuli.
- Allodynia - perception of pain to things that aren’t normally painful.
What characterizes primary hyperalgesia?
Hyperalgesia at original site of injury.
- Lower pain threshold
- Spontaneous pain
- Expansion of receptive field (upregulation of receptors)
What characterizes secondary hyperalgesia?
- Sensitization of CNS → hyperalgesia from uninjured skin surrounding injury.
What area of the brain accounts for the perception (location & intensity) of pain?
- Somatosensory Cortex I & II (SI & SII)
What is the relay center for nociceptive and sensory activity?
How does sensory activity travel from this area to the cerebrum?
- Spinal Dorsal Horn
- Ascending pathways
What areas of the brain may depress or facilitate the integration of painful information in the spinal dorsal horn?
- PAG - Peraqueductal Gray Matter
- RVM - Rostral Ventral Medulla
Where are afferent C-fibers located in the spinal column?
- Dorsal horn: Lamina I (marginal layer) & Lamina II (Substantia Gelantinosa)
What is another name for Lamina II?
What drugs work here?
- Substantia gelatinosa
- Opioids act on chronic pain here (afferent C-fibers)
What nerve fibers are associated with an “open-gate” for pain?
What nerve fibers can shut this gate?
- Aδ & C-fibers = open
- Aβ fibers = closed (numbs, pressure)