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PBT 3 Exam 2 > Pain > Flashcards

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
Q

Nociception

A

physiological perception of pain

26
Q

hyperalgesia

A

enhanced sensitivity to painful stimuli

27
Q

allodynia

A

enhanced sensitivity to non-painful stimuli

28
Q

What causes peripheral sensitization

A

A-delta and C-fibers

29
Q

What causes central sensitization

A

neurons in spinal cord

30
Q

peripheral sensitization pathway

A
  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
Q

central sensitization pathway

A
  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
Q

what receptors are believed to play a role in central sensitization

A

NMDA

33
Q

Can you have central sensitization without first having peripheral sensitization

A

No

34
Q

What lasts longer: central or peripheral sensitization

A

central

35
Q

does central sensitization always occur?

A

No - depends on severity of injury

36
Q

Primary and secondary hyperalgesia are due to central sensitization

A

True

37
Q

What is neurokinin receptor 1 (NK1r)

A

player in central sensitization

activated by substance P

38
Q

What do interneurons release

A

Enkephalin and NE

39
Q

Describe the tissue inflammation pathway

A

Injury -> PLA2 activation leads to increase in AA -> COX and AA released -> increases PG release -> increases PG -> terminal sensitization and pro-inflammation

40
Q

What to block to treat pain

A

block enzymes that convert AA to PG –> COX 1 and 2

41
Q

Does COX 1 or 2 have minimal constitutive activity

A

COX 2

42
Q

Inhibitors of Cox 1 and 2

A 
Acetylsalacylic Acid (Aspirin)
Ibuprofen (Advil)
Naproxen (Aleve)
Ketoprofen 
Indomethacin
Ketorolac (Toradol)
Meloxicam (Mobic)
43
Q

NSAIDs with LOW potency and FAST elimination

A 
Acetylsalacylic Acid (Aspirin)
Ibuprofen
44
Q

NSAIDs with INTERMEDIATE potency and INTERMEDIATE elimination

A

Naproxen (Aleve)

45
Q

NSAIDs with HIGH potency and FAST elimination

A

Ketoprofen
Indomethacin
Ketorolac

46
Q

NSAIDs with HIGH potency and SLOW elimination

A

Meloxicam

47
Q

Which NSAID is most selective for COX 2

A

Meloxicam

48
Q

Selective COX-2 inhibitors

A

Celecoxib (Celebrex)
Valdecoxib (Bextra) -> off market
Rofecoxib (Vioxx) -> off market

49
Q

COX 1 and 2 inhibitors SE profile

A

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
Q

Selective Cox 2 inhibitors SE profile

A

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
Q

Para-aetylaminopenol

A

Acetaminophen (Tylenol)

52
Q

Is Tylenol an NSAID

A

NO! It is an analgesic/antipyertic

53
Q

What does acetominophen increase?

A

endogenous NT

54
Q

What can disable acetominophens anti-inflammatory properties

A

peroxidases

PBT 3 Exam 2 (8 decks)

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