Pain Flashcards

1
Q

where does pain transmission and processing occur

A

Peripheral - at site of injury

Central - spinal dorsal horn; midbrain and cortex

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2
Q

Pathway of pain transmission

A

nociceptor -> DRG -> spinal cord -> processed -> relayed to brain

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3
Q

What are nociceptive fibers

A

nerve fibers located in skin and deep tissue that detect pain (not called pain until brain registers it as pain)

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4
Q

Two types of nociceptive fibers

A

A-delta and C-fibers

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5
Q

A-delta fibers

A

myelinated, fast conducting, involved in 1st pain sensation

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6
Q

C-fibers

A

non-myelinated, slower conducting, involved in 2nd/continuous pain sensation

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7
Q

Do A-delta and C-fibers go to the brain?

A

NO. Only located in periphery. Cell bodies located in DRG

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8
Q

Pain travels through _____ and causes the release of _____ in the _______

A
  1. nociceptive fibers
  2. neurotransmitters
  3. spinal cord
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9
Q

Primary neurotransmitters released into the spinal cord upon activation of nociceptive fibers

A

Glutamate and Substance P

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10
Q

What does NT release activate

A

projection neurons of spinal cord

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11
Q

Is glutamate excitatory or inhibitory

A

excitatory

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12
Q

Main neuronal pathway involved in nociceptive transmission from spinal cord to brain

A

spinothalamic pathway

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13
Q

where do projection neurons from spinal cord send information

A

to the brain

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14
Q

Pathway of pain processing in the brain

A

Ascending pathway: signal goes to primary somatic sensory cortex -> homunculous, lets the brain know where pain is coming from –> projection neurons stimulate specific parts of the brain.

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15
Q

what is the primary sensory cortex involved in

A

awareness of pain

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16
Q

what is the amygdala involved in

A

affective components of pain (emotional aspect)

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17
Q

what part of the brain is constantly activated in chronic pain

A

the amydala

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18
Q

the descending pain pathway is also known as the

A

bulbospinal pathway

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19
Q

The descending patheway consists of several synaptic connections where in brain (2)

A

midbrain and brainstem

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20
Q

prominent NT of descending pathway (2)

A

NE and 5HT

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21
Q

What is the mechanism by which you can inhibit pain

A

descending pathway

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22
Q

where are NT and 5HT released

A

spinal cord

23
Q

descending pathway

A

cell bodies in brain release NE and 5HT into spinal cord –> make synaptic connection with interneuron –> interneuron synapses with projection neuron and releases NE and enkephalin –> this inhibits projection neuron –> stops pain transmission

24
Q

NT with inhibitory effect

A

NE, 5HT, Enkephalin

25
Nociception
physiological perception of pain
26
hyperalgesia
enhanced sensitivity to painful stimuli
27
allodynia
enhanced sensitivity to non-painful stimuli
28
What causes peripheral sensitization
A-delta and C-fibers
29
What causes central sensitization
neurons in spinal cord
30
peripheral sensitization pathway
1. tissue damage 2. prostaglandins (PG) and bradykinin )BK) released 3. this stimulates release of substance P from local fibers --> causes MORE release of PG, BK, histamine, 5HT, etc. 4. Leads to sensitization of nociceptive fibers: sensitized fibers transmit more intense messages to spinal cord; fire multiple AP; can contribute to primary hyperalgesia
31
central sensitization pathway
1. projection neurons sensitized when large amts of glutamate and substance P constantly released. 2. sensitization of neurons in the spinal dorsal horn magnify pain signal to brain
32
what receptors are believed to play a role in central sensitization
NMDA
33
Can you have central sensitization without first having peripheral sensitization
No
34
What lasts longer: central or peripheral sensitization
central
35
does central sensitization always occur?
No - depends on severity of injury
36
Primary and secondary hyperalgesia are due to central sensitization
True
37
What is neurokinin receptor 1 (NK1r)
player in central sensitization | activated by substance P
38
What do interneurons release
Enkephalin and NE
39
Describe the tissue inflammation pathway
Injury -> PLA2 activation leads to increase in AA -> COX and AA released -> increases PG release -> increases PG -> terminal sensitization and pro-inflammation
40
What to block to treat pain
block enzymes that convert AA to PG --> COX 1 and 2
41
Does COX 1 or 2 have minimal constitutive activity
COX 2
42
Inhibitors of Cox 1 and 2
``` Acetylsalacylic Acid (Aspirin) Ibuprofen (Advil) Naproxen (Aleve) Ketoprofen Indomethacin Ketorolac (Toradol) Meloxicam (Mobic) ```
43
NSAIDs with LOW potency and FAST elimination
``` Acetylsalacylic Acid (Aspirin) Ibuprofen ```
44
NSAIDs with INTERMEDIATE potency and INTERMEDIATE elimination
Naproxen (Aleve)
45
NSAIDs with HIGH potency and FAST elimination
Ketoprofen Indomethacin Ketorolac
46
NSAIDs with HIGH potency and SLOW elimination
Meloxicam
47
Which NSAID is most selective for COX 2
Meloxicam
48
Selective COX-2 inhibitors
Celecoxib (Celebrex) Valdecoxib (Bextra) -> off market Rofecoxib (Vioxx) -> off market
49
COX 1 and 2 inhibitors SE profile
Lung: can exacerbate asthma sx (esp aspirin) Stomach: can induce ulcers and stomach bleeds (mainly COX1 property) Platelets: inhibits platelet aggregation (good for pt at risk for clots) Anti-coagulant properties -> can be good or bad
50
Selective Cox 2 inhibitors SE profile
just as effective as COX1/2 inhibitors in reducing pain reduced risk of ulcers and modest decrease in stomach bleeds no effect on platelet aggregation no long term use risk
51
Para-aetylaminopenol
Acetaminophen (Tylenol)
52
Is Tylenol an NSAID
NO! It is an analgesic/antipyertic
53
What does acetominophen increase?
endogenous NT
54
What can disable acetominophens anti-inflammatory properties
peroxidases