Pain Flashcards

1
Q

How do non-nociceptors respond at higher temps?

A

At the same rate

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2
Q

What do nociceptors respond to?

A

Higher temperatures

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3
Q

What are the two temporal elements of pain, and what fibers are they transmitted by?

A

1: sharp quick (A delta)
2: more long lasting, less sharp (C)

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4
Q

How do local anesthetics block pain?

A

Block Na+ channels to prevent conduction of impulses along C fibers

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5
Q

What are the components of pain?

A

Sensory discriminative component
Affective motivational component
Sensitization
Desc. control/central modulation

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6
Q

What is the sensory discriminatory component of pain? What does it depend on?

A

Location, quality and intensity of noxious stimulation

Pathways that target somatosensory areas

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7
Q

What is the affective motivational component of pain?

What does it depend on?

A

Unpleasant quality of experience –> autonomic

Additional cortical/brainstem pathways

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8
Q

What is the sensitization of pain?

A

Hypersensitivity to protect injured area, promote healing and prevent infection

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9
Q

What is the descending control/central modulation of pain?

A

Reduces pain perception

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10
Q

What does the spinothalamic tract transmit about nociceptive pain?

A

Discriminative aspects of pain/temp: who, what, when

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11
Q

What does the spinoreticular tract transmit about nociceptive pain?

A

Emotional/arousal aspects of pain

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12
Q

What does the spinomesencephalic tract transmit about nociceptive pain?

A

central modulation of pain: start to feel better

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13
Q

What is the destination of the spinomesencephalic tract?

A

Periaqueductal gray, superior colliculus

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14
Q

What is the destination of the spinoreticular tract?

A

Amygdala, hypothalamus, reticular formation

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15
Q

What is the destination of the spinothalamic tract?

A

Somatosensory cortex

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16
Q

What are the thalamic relays of the spinoreticular and spinomesencephalic tracts?

A

Midline thalamic nuclei, intralaminar nuclei

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17
Q

What are the symptoms of a lesion of the parietal lobe or primary sensory cortex?

A

contralateral numb tingling or pain

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18
Q

What are the symptoms of a lesion of the thalamus?

A

contralateral burning pain

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19
Q

What are the symptoms of a lesion of the DCMLS?

A

tingling, numb sensation
tight band-like sensation around trunk or limbs
feeling of gauze on fingers
electricity sensation down back and extremities upon neck flexion = Lhermite’s sign

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20
Q

What are the symptoms of a lesion of the STT pathway?

A

sharp, burning or searing pain

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21
Q

What are the symptoms of a lesion of the nerve roots?

A

Radicular pain with numbness and tingling in dermatomal distribution = radiculopathy

22
Q

What are some causes of sensory neuropathies?

A
Diabetes
Immune disorders
Mechanical
Varicella/Herpes Zoster
Infectious disorders
HIV, CMV, Hep B, toxins, malnutrition
23
Q

How does Guillain Barre cause sensory neuropathy?

A

Demyelination following viral infection –> paresthesia

24
Q

What is neurapraxia?

A

Mild insult causing temporary impairment of nerve conduction

25
Q

What is Causalgia/complex regional pain syndrome?

A

incomplete regeneration causing burning sensation, edema

26
Q

What is neuralgia?

A

Severe persistent pain in the distribution of a cranial or spinal nerve

27
Q

What are the symptoms of trigeminal neuralgia?

A

Lancinating paroxysms, trigger zones, unilateral, symptom free between attacks

28
Q

How does varicella/herpes zoster cause sensory neuropathy?

A

Increases excitability of sensory neurons in DRG resulting in low threshold of firing and spontaneous activity

29
Q

What do recessive mutations in sodium channels cause?

A

Loss of function: congenital insensitivity to pain (CIP)

30
Q

What do dominant mutations in sodium channels cause?

A

Gain of function: inherited erythromelalgia (IEM) and paroxysmal extreme pain disorder (PEPD)

31
Q

What is sensitization?

A

Following repeated application of noxious stimuli, neighboring nociceptors that were not responsive, now become responsive

32
Q

What is hyperalgesia?

A

phenomenon of stimuli that are normally perceived as slightly painful as signficantly more painful

33
Q

What is allodynia?

A

The induction of pain by what is normally an innocuous stimulus

34
Q

What is the goal of sensitization?

A

Protects injured area
promotes healing
prevents infection

35
Q

What causes sensitization?

A

Changes in sensitivity of:

  • peripheral nociceptive receptors
  • central targets
36
Q

What is peripheral sensitization?

A

interaction of nociceptors with the “inflammatory soup” of substances to decrease threshold of activation for nociceptors (fire more easily)

37
Q

How do prostaglandins interact with nociceptors?

A

Increase response of nociceptive fibers

38
Q

How does capsaicin work?

A

Repeated application of capsaicin causes desensitization of C fibers and depletes substance P to block peripheral sensitization

39
Q

What are some therapeutic uses of capsaicin?

A

Arthritis
Mastectomy
Neuralgia
Shingles

40
Q

What channels in C fibers can be moderated for an analgesic effect?

A

VR1 / TRPV1 channels in C fibers are activated by moderate heat (45 degrees C) and capsaicin

41
Q

What is central sensitization?

A

immediate, activity dependent increase in excitability of neurons in dorsal horn of SC following high levels of activity in nociceptive afferents to increase pain sensitivity

42
Q

What is the transcription-independent mechanism of central sensitization?

A

Windup = lasts only during stimulation (acute)

43
Q

What is the transcription-dependent mechanism of central sensitization?

A

Allodynia: outlasts stimulus for hours and can be mediated by COX (chronic)
- development/increase in spontaneous activity
reduction of threshold of activation by peripheral stimuli
- expansion of receptive field size (respond to innocuous and noxious stimuli)

44
Q

What are two ways that the descending control of pain perception works?

A

1 stress induced analgesia

2 placebo effect - physiological response following administration of inert remedy

45
Q

How can one block the effects of a placebo effect?

A

Naloxone: inhibitor of opiate receptors

46
Q

How do endogenous opioids work?

A

Inhibit nociceptors

47
Q

What is the gate theory of pain?

A

local modulation of nociceptive information: pain results from the balance of activity in nociceptive and non-nociceptive afferents

48
Q

How does visceral pain transmit to the cortex? What is the pathway?

A

DRG
relay point 1: dorsal column ipsilaterally of SC
relay point 2: medulla via gracile nucleus
DECUSSATES in medulla, crossing medial lemniscus
relay point 3: ventral posterior nuclear complex of thalamus
Terminates in insular cortex

49
Q

What are 2 surgical interventions for intractable pain, and what are they used for?

A

1 midline myelotomy: visceral pain

2 cordotomy for cutaneous pain

50
Q

What is a midline myelotomy and what is it used for?

A

1 midline myelotomy for visceral pain: cut neurons

51
Q

What is a cordotomy and what is it used for?

A

2 cordotomy for cutaneous pain: lateral funiculus from dentate ligaments to line of ventral rootlets several segments rostral to the highest dermatomal level of pain

52
Q

Why does referred pain occur?

A

Visceral pain is also conveyed centrally by neurons that contain cutaneous pain!