Pain Flashcards
Pain
Pathway
Initiation/Propagated/Perception
- initiation = injury site pain receptor
- Propagation = spinal cord (spinothalamic) –> thalamus
- Perception = somatosensory, emotional, cognitive brain areas
Pain fibers w/ ______ fibers
Temp
Temp that sets off pain fibers
37 degrees C (tissue damage)
Nociceptor - adaptation
Slow
Pain pathway
Injured tissue
Releases glutamate to C fibers , next fiber releases substance P onto paleo, cascade, depole paleo neurons
Differences b/w C + A pain fibers?
LOOK UP, NOT SURE
C
*unmyelinated
*second pain = dull/aching, chronic
A
- myelinated
- “first pain” = sharp/stingin, intense
Painful stimulus derived from external stimulus
Nociceptive pain
Pain receptors
trauma, burning, temp, cold = each has DIFF receptor
Nociceptive pain affected by
- local anesthetics
- Cox 2 inhibitors
- opioids
TRPV1 Receptor
- Nociception
- activated by Heat/Capsaicin/Acid
*Non-selective Ca2+ channels
Pain from internal stimulus
Inflammatory Pain
Mediators activate: Histamine, serotonin, bradykinin, prostaglandins, protons
= bind to specific receptors on the nerve
Inflammatory pain
Tx w/
Local anesthetics
Cox 2 blocker
Opiates
Sensitizing pain fibers
Inflammatory + nociceptive
Hyperalgesia
Inflammatory mediators activating pain fiber receptors phosphorylate (phosph A2), sensitize fibers, increased AP firing, up pain
Allodynia
Inflammatory mediators sensitize receptors , non-painful even leads to pain
Damaged elements of PNS/CNS
Neuropathic pain
Neuropathic Pain
tx
NO NSAIDS
- Opioids (some respond, if no ……
- ->*Atypical analgesics: TCA, Anti-convulsants, CCBs
Neuropathic pain
Causes
Metabolic
Injury
Infections
Neurotoxins
DAMAGE/REWIRE pain pathway ABeta fibers (non-mechanical pain) = now activate w/ touch
2 components of pain processing
- Discriminative = Where, how much
* affective - emotional
Descending pain pathway
- endogenous + exogenous opioids = inhibit ascending pain pathway (A+C fibers and spinothalamic neurons)
- Local anesthetics = (C+A only)
Pain with unexplained source?
Think referred pain!
*visceral + cutaneous afferents converge into same spinothalamic tract
Rub bumped elbow and it hurts less?
Gate theory
*rub area activates ABeta fibers–>activate inhibitory local circuit n. –> supress paleospinothalamic n.
Phantom pain
Amputation = movement neurons gone/degenerate
Spinothalamic n. Rewire to another mechanostimulus in intact body part, rubbing body part gives pain
How do nociceptive AND inflammatory pain both lead to Hyperalgesia / Allodynia?
Both lead to release of inflammatory mediators (prostaglandins) at injury site
- nociceptive = recruited immune cells
- allodynia = local tissue release (immune cells at site) of inflammatory mediators
