NURS 549 Final Exam Questions and Correct
Answers| Latest Update
4 steps of pain pathway
transduction, transmission, perception, modulation
Transduction
Stimulus converted to nerve impulse
Travels from most distal nerve ending toward CNS
Transmission
Impulse carried to brain/CNS
Through Neospinothalamic tract (fast) or Paleospinothalamic tract (slow)
Perception
message from periphery interpreted by brain
Alterations in neural circuitry in brain can cause change in pain perception
--> Mood, stress, rest
Modulation
Brain sends signals that cause pain signals from periphery to be suppressed or
amplified
,Fast pain receptors
Type A-delta fibers
Felt <0.1 second of stimulus: sharp, acute
Mechanical, acute thermal pain
Not in deep tissues
Slow pain receptors
Type C fibers
Felt 1+ second of stimulus: aching, throbbing, burning
Chemical pain
Neospinothalamic tract
Type A-delta fibers
Mechanical and thermal pain
Spine --> Thalamus fibers, pain localized precisely
Paleospinothalamic tract
Type C fibers
Chemical pain
Terminates in brain stem, only 10-25% terminate in thalamus, cannot localize pain
Endogenous pain modulation/suppression
Serotonergic and enkephalin neurons BLOCK pain
, Analgesia signals can block pain from peripheral neurons - from both Type A-delta
and C fibers
NSAIDS: COX inhibitors
Inhibit transduction of TYPE C pain fibers
COX-1: constitutive (occurs all the time)
COX-2: induced by cytokines in presence of inflammation --> localized to pain
NSAIDS Side Effects
GI ulceration and bleeding d/t decreased platelet aggregation
Decreased renal function, not good for CKD or ARF pts
Acetaminophen
COX inhibitor (COX-3?), better for fever than inflammation or pain
Opioids
Block transmission of pain, binds to Mu receptors
S/S: suppresses respiratory center of brain stem, Chemoreceptor Trigger Zone
(CTZ) - N/V, constipation, urinary retention
Answers| Latest Update
4 steps of pain pathway
transduction, transmission, perception, modulation
Transduction
Stimulus converted to nerve impulse
Travels from most distal nerve ending toward CNS
Transmission
Impulse carried to brain/CNS
Through Neospinothalamic tract (fast) or Paleospinothalamic tract (slow)
Perception
message from periphery interpreted by brain
Alterations in neural circuitry in brain can cause change in pain perception
--> Mood, stress, rest
Modulation
Brain sends signals that cause pain signals from periphery to be suppressed or
amplified
,Fast pain receptors
Type A-delta fibers
Felt <0.1 second of stimulus: sharp, acute
Mechanical, acute thermal pain
Not in deep tissues
Slow pain receptors
Type C fibers
Felt 1+ second of stimulus: aching, throbbing, burning
Chemical pain
Neospinothalamic tract
Type A-delta fibers
Mechanical and thermal pain
Spine --> Thalamus fibers, pain localized precisely
Paleospinothalamic tract
Type C fibers
Chemical pain
Terminates in brain stem, only 10-25% terminate in thalamus, cannot localize pain
Endogenous pain modulation/suppression
Serotonergic and enkephalin neurons BLOCK pain
, Analgesia signals can block pain from peripheral neurons - from both Type A-delta
and C fibers
NSAIDS: COX inhibitors
Inhibit transduction of TYPE C pain fibers
COX-1: constitutive (occurs all the time)
COX-2: induced by cytokines in presence of inflammation --> localized to pain
NSAIDS Side Effects
GI ulceration and bleeding d/t decreased platelet aggregation
Decreased renal function, not good for CKD or ARF pts
Acetaminophen
COX inhibitor (COX-3?), better for fever than inflammation or pain
Opioids
Block transmission of pain, binds to Mu receptors
S/S: suppresses respiratory center of brain stem, Chemoreceptor Trigger Zone
(CTZ) - N/V, constipation, urinary retention
