Block 2 Neurobiology Of Pain

Front 1

allodynia?
hypoalgesia?
hyperalgesia?
radiculopathy?
vasomotor changes?
sudomotor changes?

Back 1

"allo!"=pain in response to non-painful stim

hypoalgesia=decreased response to painful stim

hyperalgesia=increased response to painful simt

radiculopathy=func abn of sensation, motor/atuonomic actvity of spinal nerve root

vasmotor=temp/skin coloration abn
subomotor=abn sweating

Front 2

pain is a ____ process

Back 2

complex

Front 3

acute nociceptive pain is what? what nerve endings? what is its purpose?
two different types?

Back 3

pain in response to tissue injury/inflammation
-peripheral nociceptors=free nerve endings of A-delta and C fibers
-protect organism from further injury and allows healing
-somatic vs. visceral

Front 4

Acute somatic pain vs. acute visceral pain

Back 4

somatic=skin, subcut, mucous memb (sharp, well localized, burning, throbbing)
muscles, tendons, bone (dull aching)

visceral=viscera (dull diffuse) and pleura, pericardium peritoneum (sharper, localized) -getting kicked in the balls!

Front 5

referred pain happens becuase...?

Back 5

because visceral nociceptors share the same spinal root origin at the dorsal horn as somatic nociceptors=>>pain is coming from skin surface of somewhere else

ex) heart pain in upper left shoulder

Front 6

where are the visceral structures on the homunculus?

Back 6

they aren't!

Front 7

chronic pain is when? is pain a symptom?

Back 7

chronic pain is pain that persists for 1-6 months after healing. is no longer a symptom! is a disease state.

Front 8

4 elements of pain?

Back 8

transduction
transmission
perception
modulation (affects the first 3)

Front 9

neuropathic pain is what?

Back 9

results of injury/acquired abnormality of peripheral/central neural structures. wide variety.

Front 10

First order neurons are made up of what types of fibers?

Back 10

A-delta (first pain/fast) and C fibers (Second pain/slow). cell bodies in dorsal root ganglion. synapse in dorsal horn with 2nd order neurons

Front 11

first order neurons for the cranial nerves for the head

Back 11

5, 7,9, 10synapse in brainstem

Front 12

Third order neurons can go from the thalamus to where?

Back 12

1) Anterior Cingulate Gyrus (ACG) for emotional responses=pain affect

2) Sensory Cortex-perception/discrete localization=cognitive appreciation of pain

Front 13

Modulation. how can it affect pain? 2 ways in 4 locations

Back 13

increase painful sensation (facilitation)
or
decrease painful sensation (inhibition)

1)peripherally (peripheral sensation)
2)dorsal horn (exc/inhib interneurons)
3)descending inhib pathways
4)higher centers (culture, conditioning, emotions, judgements)

Front 14

peripheral modulation facilitation. primary and secondary hyperalgesia

Back 14

1) injury->release of algogenic substances (histamine, serotonin, prostaglandins etc.) which sensitize periph nociceptors=increased pain

2) inflammation in surrounding tissues->edema, erythema, sensitzation to noxious stimuli

Front 15

where do the act?

opoids?
local anesthetics?
antihistamines?
NSAIDS?

Back 15

opoids: dorsal horn
local anesthetics: nerve axon/sodium, channels
antihistamines: injured/inflammed tissues
NSAIDS: prostaglandin synthesis

Front 16

modulation inhibition. segmental inhibition and gate control theory. what does the A-beta do vs. the C?

Back 16

A-beta stimulates an exciatory signal to the inhibitory interneuron (Adding a inhibitory signal) which inhibits projection neuron/WDR/spinothalamic tract=gate closed

C fiber inhibits the inhibitory interneuron=gate open=projection neuron transmits pain signal

Front 17

gate control theory. TENS/Distraction do what exactly?

Back 17

tingling/distraction sensation decrease the pain sensation by overriding the pain sensory via activing the inhibitory interneuron

Front 18

neurotransmitters of descending inhibitory pathways. all synapse where?

Back 18

adrenergic (a2)=norephinephrine
serotonergic (5HT)=serotonin
Opiod (u, d, k receptor sites)

all synapse at dorsal horn at 1st-2nd order synapse (pre/post synaptic)

pre synpaptic=decrease Ca movement (kappa)

post synp=open potassium channels=hyperpolarization=Mu and Delta

Front 19

opiod receptors. which is the strongest?

Back 19

mu="u"=strongest analgesia/strongest side effects. includes u1 (analgesia brady, sedation) and u2 (hypovent, nausea, constip, tachy, dependence, euphora, muscle rigid)

kappa=k=modest, dysphoria, antagonizes mu

delta=d=modulate mu receptor activity