The Phys Of Pain - K Flashcards
How can pain be characterized? Why do the characteristics differ?
Fast/sharp (time of injury)
Slow/dull/achy (occurs after injury)
By location: deep (bone or ligaments), muscle, visceral, cutaneous
Pain differs based on the physiological and anatomical variables
Describe the characteristics of the nociceptor. What fibers do they run with? What are the 5 R types?
Bare n endings with ion channels that open to specific stimuli under the pain umbrella (one R for temp..)
Attach to two types of fibers: A-delta (fast/sharp), C fibers (slow/dull)
R types: thermal, mechanical, mixed, silent/sleeping, ligand-gated
What are the characteristics of the A-delta fibers?
Transmits fast/sharp pain
Somewhat myelinated (faster conduction)
Releases EAA into synapse on non-NMDA R’s
High threshold
What are the characteristics of the C fibers?
Transmit dull/slow pain
Unmyelinated (slow conduction)
Synapse on interneurons
Release Substance P, EAA in synapse on non-NMDA R’s
What is significant about some of the channels on a mixed pain R?
They’re mechanosensitive Na channels that can be mutated leading to either an absence in pain sensation d/t non-function thus preventing AP creation/depolarization, or hyperactivity and an abundance of pain senstaion
What is the purpose of ligand-gated R’s in association with the nociceptive pathway? What ligands bind here? What R are they most associated with?
Ligands can activate these altering the sensitivity of nociceptors
Substance P, Kinins, ATP (indicates cell membrane dmg), H, K
Silent/sleeping R’s
What’s the avg speed of an AP?
1.5 - 3m/sec
Why is visceral pain different from other pain? What’s the same? Where is the pain processed?
Its signals travel with autonomic nerves, and not in the fast or slow pathways
Nociceptors are same, just wired a different way
“Lower”
What is the significance of the insular cortex? What occurs if it’s damaged?
Important in interpretation of nociceptive inputs coming from the innards of the body
Integrates all signals to pain (above the thalamus)
If damaged, one has a physiologic response to pain and is aware of hurt.. But can’t describe it
What is the significance of the amygdala in the nociceptive pathway?
Gives certain pain an emotional component
What are the steps regarding the gate theory of pain?
Step 1: alpha-beta fibers release EAA upon activation (rubbing close to an injured area)
Step 2: brach within SC releases EAA and activates inhibitory interneuron within SC
Step 3: inh interneuron releases glycine (not GABA, we’re in the SC), which inhibits a secondary neuron in the pain pathway
What structures is deep pain associated with? Is it fast or slow? What fibers predominantly transmit this pain? What’s a sx of this pain?
Periosteum/bone, ligaments
Slow/dull/achy
C fibers > A-delta
Muscle spasms
What are some causes of muscle pain? What fibers are associated with this pain? Is the pain fast or slow?
Injury, ischemia
A-delta AND C-fibers
Fast AND slow
What’s the important, discerning aspect about visceral pain? What fibers are at work here and what do they travel with? How many R’s? What R’s are most prominent with this pain? What’s another name for this pain?
Poorly localized
C-fibers, autonomics (not fast or slow)
Very few R’s
Stretch R’s
Referred pain
What do cutaneous and visceral pre-synaptic nociceptor fibers do sometimes?
Converge on the same post-synaptic fibers, leading to referred pain.
