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55 Cards in this Set

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difference btwn Primary and secondary hyperalgesia?
Primary = peripheral sensitization, -local tissue damage
-due to chemical mediators
Secondary = central sensitizatoin
-C fiber activity
-due to increased EPSP in dorsal horn
5 types of chemical mediators that can be responsible for primary hyperalgesia?
1)K+ from cell interior
2)5-hydroxytryptamine (5-HT, serotonin) from platelets
3)histamine from Mast cells
4)bradykinin from plasma
5)prostaglandins from cells
neurogenic inflammation
-type of primary hyperalgesia
-subtance P and CGRP are released and cause histamine release from mast cells. Cause vasodilation and edema.
Function of substance P
-produces slow, long lasting depolarization
describe the "wind up" phenomenon
-secondary hyperalgesia
-glutamate released from C fibers acting on NMDA receptors on dorsal horn
-If persists: Long-term potentation
-Substance P + CGRP involved
-NMDA receptor activation --> nociceptive neurons in dorsal horn--> increase in transmitter receptors. This causes supersensitivity and hyperexcitability= spontaneous pain
allodynia
pain in response to a stimulus which does not normally produce pain
How is allodynia caused by mechanoreceptors projecting to neurons in the nociceptive pathway?
-after injury, central nociceptive neurons become sensitized (central sensitization) and now mechanoreceptors input excites second order nociceptive neurons
allodynia only occurs if ______ is present
central sensitization
Allodynia vs hyperalgesia?
-allodynia= painful response due to mechanoreceptive fibers A(beta)
-hyperalgesia= enhanced pain due to nociceptive fibers A(delta)
visceral pain receptors are especially sensitive to what?
distention
How are silent receptors activated in visceral pain?
-inflammation or hyperemia produces primary hyperalgesia which reduces threshhold of regular nociceptors and activates the silent nociceptors
guarding
-visceral pain which initiates contraction of overlying skeletal muscle
-this is accomplished thru a reflex pathway
How does neuropathic pain arise?
-results form injury to neurons in the PNS (peripheral neuropathic pain) or CNS (central neuropathic pain) and NOT from activation of nociceptors
Deaffernatation (neuropathic pain)
-loss of afferent input to cord (as brachial plexus avulsion)
-produces burning pain in denervated dermatomes
-due to sensitivity and hyperactivity of dorsal neurons in denervated region
causalgia
-reflex sympathetic dystrophy syndrome
-after a peripheral nerve injury, damaged sensory fibers trigger spontaneous burning which gets worse with time.
Why does causalgia happen?
-Due to expression of alpha receptors on damaged sensory fibers
-sympathetic efferent activity stimulates these damaged fibers producing severe pain (sympathetically mediated pain)
How can you stop causalgia?
By blocking sympathetic activity or depleting catecholamines
dorsal root irritation
-compression or inflammation of dorsal roots
-abnormalities of sensation in dermatomes
1)pain
2)parathesia
3)hypesthesia
4)anesthesia
parathesia
spontaneous sensations of prickling, tingling or numbness
hyperesthesia
diminished sensitivity due to loss of afferents
Thalamic syndrome
-usually produced by vascular accident-blockade of a branch of the posterior cerebral artery (thalamogeniculate arterties)
-produces intense intractable pain on contralateral side of body
What is the difference between nociceptive pain and referred pain
nociceptive pain involves stimulation of nociceptors

neurogenic pain involves nerve injury. This pain does not involve the activation of nociceptors,
visceral pain receptors are especially sensitive to what type of stimulus?
stretch
When patients feel pain in the amputated limb it in part to what?
Secondary (central) hyperalgesia.
causalgia is also know as
reflex sympathetic dystrophy syndrome
neuropathic pain caused by bullet wound or shrapnel.
causalgia
3 causes of Trigeminal neuralgia
1)mcc enlarged looping vessel pressing on the trigeminal. the repeated pulses
2)multiple sclerosis
3)tumor
intermittent claudication
pain produced during muscular exertion because of occlusive vascular disease.
What chemical agent is thought to be involved in muscle pain of vascular origen: intermittent claudication & angina pectoris
K+ reslased during contraction, that accumulates in the absence of normal blood flow and cause pain. K+ depolarizes nociceptors,
what is the most most prominent and best studied tract for pain?
lateral spinothalamic tract
nalaxone
mu receptor opiate antagonist
T/F Direct brain stimulation (periaqueductal gray matter) may result in either analgesia or hyperalgesia
T, It is like that both the analgesic and hyperalgesic pathways are activated simultaneously.
opiate-induced hyperalgesia
ween patient of opiate they have a much lower threshold for pain.
Does opiate induced analgesia has a direct actions on ______
CNS (not on peripheral receptors)
Chronic inflammatory pain
-pains extending beyond the time of healing
-occurs in response to tissue injury or invading foreign substances
-damaged tissue --> release inflammatory mediators that sensitize/activate local nociceptors
-prostaglandins
-bradykinin
-histamine
-adenosine
-resulting in hypersensitivity and spontaneous persistent pain.
-Ex: arthritis
Chronic neuropathic pain
?
Prialt the synthetic version of w-conotoxin is useful in the treatment of what channel associated with chronic pain?
Preialt is N-type Ca channel blocker
"The most painful disease in all of medicine" or suicide disease
Trigeminal Neuralgia
cause of Trigeminal Neuralgia?
1)enlarged artery/vein pressing on Trigeminal nerve root in brain stem. The pulsations cause irritation and abnormal signals.

2) tumor
3) multiple sclerosis
What pain type can manifest as a tooth ache?
Trigeminal Neuralgia
Cause of Muscle pain?
occlusion of blood supply to muscle which results in K+ accumulation (no blood flow to move it out). K+ depolarizes nociceptors.
Causalgia
1) peripheral nerve injury by gunshot.

2) alpha receptors incorporated into membrane of damaged sensory fibers and sympathetic efferent innervate.

3) When sympathetic nerves fire it stimulates injured neruron causing sympathetic mediated pain.
Pain, Paresthesia, hypesthesia, anesthesia are associated with what type of pain
Dorsal root irritation

compression/irritation of dorsal root by slipped disks, disk degeneration, bone spurs

Basically anything that puts pressure on the dorsal roots, likelihood increases with age
Paresthesia
pins/needles
hypesthesia
diminished sensitivity due to loss of afferents.

diminished sensation
anesthesia
absence of sensation
If you have pain on the right side and suspect Thalamic syndrome...what is the cause?
Thalamic syndrome is caused by cranial artery compression of the thalamus which manifests pain on the the contralateral side.

So the thalamus on the left side would be of interest.
Why should you suspect there is a problem with the diaphram when the patient has pain in his neck and shoulder.
The diaphragm (visceral) and cutaneous nociceptors (somatic) of the neck and shoulders converge on the same spinothalamic neurons in the spinal cord (C3,C4). The brain interprets the pain as more likely coming from the skin leading to referred visceral pain
What is the dematomal rule and what type of pain is associated.
The dematomal rule states:
pain is referred to a cutaneous structure innervated by the dame dermatome as the visceral organ.

Referred visceral pain
Neuropathic pain vs. Nociceptive pain
Neuropathic pain results from injury to neruons of the PNS or CNS. Pain is not produced by direct activation of nociceptors.

Nociceptive pain: Pain produced by direct activation of nociceptors.
Phantom limb syndrome

1) cause of pain
2) why can you feel the phantom thumb on your cheek?
1) pain is caused by super-sensitivity and hyperactivity of dorsal horn neurons

2)Cortical remapping occurs where the cortical neurons innervate the dormant phantom limb neurons
sympathetic mediated pain is associated with
causalgia
The gate control theory states that spinal modulation of pain can occur by large afferent inputs.

What are these large afferent inputs?
If you burn yourself small C-fiber afferents will
1) inhibit inhibitory interneurons
2) stimulate 2nd order Projections neruons that cross the midline and send the pain signal up to the thalamus.

To reduce nociceptor c-fiber acitivity a person can rub the boo-boo and stimulate mechanorecptors. Signal then travels through their "large A-Beta afferent fibers" and stimulate the inhibitory interneuron which will inhibit the second order projection neuron that is sending the pain signal. This reduces
3)
Why should you suspect there is a problem with the diaphram when the patient has pain in his neck and shoulder.
The diaphragm (visceral) and cutaneous nociceptors (somatic) of the neck and shoulders converge on the same spinothalamic neurons in the spinal cord (C3,C4). The brain interprets the pain as more likely coming from the skin leading to referred visceral pain
What is the dematomal rule and what type of pain is associated.
The dematomal rule states:
pain is referred to a cutaneous structure innervated by the dame dermatome as the visceral organ.

Referred visceral pain