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Flashcards in Section 3 Pain Deck (153):
1

The detection and localization of a stimulated pain receptor:

nociception

2

The emotional (affective) and arousal aspects of such stimulation:

pain

3

T or F? Pain and temperature are transmitted along different pathways.

F. same pathway

4

T or F? All thermoreeptors are specialized for non-noxious temperature ranges.

F. Some (same for noxious)

5

Temp range bw 50' and 140' stimulates:

TRPA1, M8, V4, V3, V3, TRPV1, TRPV2 (low temp to high temp)

6

At what temp do thermoceptors plateau out?

after 140'

7

Fire at a high rate of increase at the 45' C range:

TRPV1

8

Fire at a high rate of increase at 50' C:

TRPV2

9

Fire at a higher rate at decreasing temperatures:

TRPV4, TRPM8, TRPA1

10

How do thermoceptors respond to increasing temps?

by changing their conformation

11

TRPM8:

increases firing as things get cool and activated by menthol

12

Why is menthol cool?

transmitted via TRPM8, temps under 25 'C

13

Which are activated by capsaicin:

TRPV1 fibers, active as it gets hotter normaly, 45' C

14

Medical tx using capsaicin:

arthritis ointment, gradually hyperactivates nociceptor axons, depleting its NT (substance P) and blasts them out, making nonfxnal, TRPV1

15

What is the NT for arthritis?

Substance P

16

A-delta nocioceptors:

thinly-my, fast conducting, fast pain (sharp, prickling, localized)

17

C nocioeptors:

unmy, slower conducting, slow pain (diffuse, burning)

18

A nocipceptor that responds to all types of stimuli:

polymodal (therm, mechanical, heat and cold)

19

Localized response to stepping on a tack, and then diffuse later:

differentiation comes bc we have 2 types of fibers that transmit at different rates

20

What activates nocioceptors?

Heat, cold, mechanical, chemical

21

T or F? Some nociceptors respond to only one type of stimulus.

T

22

What gives rise to the inflammatory soup?

Damage cells leak contents which activates the nocio endings giving rise to the inflammatory soup

23

Contents of the inflammatory soup:

ATP, serotonin (5-HT), histamine, bradykinin, H+, prostaglandins

24

Reduce pain by taking:

an aspirin, reduces prostaglandin production

25

What does tissue damage lead to?

the release of substances that activate nociceptors

26

What is 5-HT?

Serotonin

27

Both aspirin and IB profin block:

COX-2

28

Which is more selective, aspirin or Ibuprofen?

Ibuprofin

29

Pwy from tissue damage to pain:

Cut, arachidonic acid, COX-2, prostaglandins, pain

30

Ibuprofin only blocks:

COX-2

31

Aspirin blocks:

both Cox-1 and Cox-2

32

Blocking Cox-1 is associated with?

GI symptoms

33

Selectively blocks pain and not other sensations:

Analgesic

34

Anesthetics block:

non-selectively, not just pain

35

Lidocaine blocks:

voltage gated Na channels, blocks all n. conduction, unable to move nearby mm. as well)

36

Name an analgesic.

Aspirin

37

T or F? APs can't invade non-stimulated nociceptor branches.

F. they can

38

What NT increases activation of nearby nocioceptors?

Histamine

39

How can pain lead to edema and more pain?

APs invade non-stimulated branches, nociceptor endings release Sub P and CGRP (calcitonin Gene-Related Peptide), Sub P activates mast cells, macros, and neutrophils, which release pain producing substances. CGRP and SubP cause vasoldilation, plasma leaks out, including bradykinin, edema and more pain

40

Increased sensitivity to painful stimuli:

hyperalgesia (prone to heightened pain if area has already been hurt (soup and other aspects of CNS)

41

Pain due to a stimulus that deos not normally provoke pain:

allodynia

42

Painful, inflammatory condition usually caused by carious bacteria penetrating dentin:

pulpitis

43

Early events in inflammatory pain:

vasodilation, inc interstitial fluid P, pain

44

Early symptoms of pulpits:

hypersensitivity of tooth (cold, hot evoke a stab of short lasting pain)

45

Type of receptors peripheral neurons have:

Opioid

46

Major source of peripheral opioids:

Immune cells

47

Endorphins:

bind receptors in the brain

48

"endorphin" stands for:

Endogenous morphine

49

Types of endorphins:

enkephalins, endo(mo?)rphins, dynorphins

50

Endogenous opioid receptors:

delta-OR, kappa-OR, mu-OR, nociceptin/orphanin FQ peptide receptor

51

Synthetic ligands for ORs:

codeine, oxycodone, morphine, heroin, methadone, usually similar to opium

52

Effects of peripheral opioid receptors:

Change levels of 2nd msgs (i.e. cAMP), reduce Ca channel opening, cell depolarizes, Sub P, CGRP, and other nasty things leak out. Less Na channel opening, leads to less pain conduction to CNS

53

What differentiates pain fibers from others?

Na channel type (1.8 and 1.9 for damage sensing?) for AP transmission to s.c. (sometimes overexpressed making the axon hyperexcitable)

54

What may develop after traumatic damage to a peripheral nerve?

causalgia, improper n. regeneration, excess Na channels, easier to generate APs even wo pain stimulus

55

T or F? Strong analgesics can tx causalgia.

T. ish. Sometimes not enough

56

Hypothesized mechanism of causalgia:

upregulation of Na channels

57

How does an Inflamed nerve differ from a normal nerve?

less my, more voltage sensitive Na channels, easier to get APs when they should be firing, cross-talk, new kinds of Na channels can appear

58

What starts to get expressed in pulpits?

New kinds of Na channels on my polymodal A-delta fibers

59

What happens to my polymodal A-delta fibers if they start to loose their my?

cross-talk

60

What controls how much pain info reaches consciousness?

Descending projections

61

What can lead to hypersensitivity to pain or the damping down of pain?

Local changes in the s.c.

62

Where does modulation of pain transmission take place?

s.c.

63

Why do you instinctively rub a site of pain?

Activation of touch fibers activates interneurons that inhibit pain, this reduces the amount of pain info going to higher levels

64

What determines how much pain gets up to consciousness?

interneurons

65

What can activate the inhibitory neurons that can damp pain?

touch and pressure

66

T or F? Endorphins work in both the CNS and PNS.

T

67

The gate control theory of pain:

Stimulate pain fiber, depolarize terminal, Ca enters, glutamate and Sub P released, excite projection neuron

68

Presynaptic mech to reduce pain transmission:

release endorphins that shut down voltage gated Ca channels. Little transmitter coming out of the pain fiber, less transission of pain

69

Postsynaptic mech to reduce pain transmission:

increase K channel activity via binding of Sub P to receptor, K channels open, K leaves, hyperpolarizing cell, less pain transmission (lower endorphin firing rate)

70

What does morphine mimic?

effects of dorsal horn inhibitory interneurons

71

What are the key to understanding opiate analgesia?

opioid interneurons

72

Disadvantage to (dorsal horn inhibitiory interneurons?)

opioid receps are all over the brain that are not involved w pain

73

Opioid overdose leads to:

depression of breathing

74

What happens with prolonged use of opioids?

Brain desensitized, higher and higher doses required

75

TENS stands for:

Transcutaneous Electrical Nerve Stimulation

76

To relieve pain after surgery:

TENS

77

How does TENS work?

Place electrode bw pain and s.c., inc amp until activating touch and not pain fibers.

78

Which have a lower threshold of activation, touch or pain fibers?

Touch, can be stimulated to decrease pain transmission

79

How long does TENS therapy last?

hours beyond the tx

80

Wide dynamic range of nociceptor dorsal horn projection cells:

signal presence of mild to extreme pain, there to signal the somatosensory cortex, primarily factual info

81

2 kinds of nociceptor dorsal horn projection cells:

Wide dynamic range (WDR) and Nociceptor specific (NS)

82

What do WDR dorsal horn projection cells respond to?

both touch and pain

83

WDR dorsal horn projection cells provide input primarily about:

the location and magnitude of the stimulus to the pwys, such as somatosensory cortex

84

Fxn of nociceptive inputs:

give you the emotional (affective) aspects of the pain experience

85

What do nociceptive specific cells respond to?

nociceptive inputs only

86

Nociceptive specific dorsal horn projection cells provide input primarily to:

the pwys associated w the affective (emotional) aspects of pain

87

Central sensitization:

CNS neurons that prone to firing bc of repeated or extremely painful stimuli (i.e. extreme activation of NMDA-type glutamate receptors, making the synapse stronger)

88

reinforce connection, making it permenantely stronger by the NMDA receptors:

Memory formation/ long term potentiation:

89

Pain that doesn't have a visible cause:

neuropathic pain ie phantom limb pain.

90

Phantom limb pain generally starts with:

peripheral pain

91

What is the trigger for phantom limb pain?

Peripheral pain

92

What does phantom-limb pain set off?

over-stimulation w in s.c.

93

Causes of Phantom limb pain:

post-synaptic NMDA recep open bc of excess release of glutamate triggering long-term increases in strength of synapses OR trauma induces Sub P release from C fibers inhibiting post-synaptic K channels: extreme excitation

94

Other probable aspects of the causes of phantom limb pain:

gene transcription, new axon terminals, changes that propagate to higher levels of the brain

95

Mirror box therapy:

Look at normal arm mirroring the other arm moving it as if the damaged arm were in tact. Pain goes in a few weeks or months

96

Why are pain levels felt so variable depending on your emotional state?

Gating from higher levels

97

Descending pain-control pathways:

PAG activates rostral medulla, the off switch cells (in the RVM) activate dorsal horn opiate interneurons, pain transmission is reduced

98

T or F? Off cells project to dorsal horn making them less excitable, reducing the transmission of pain.

F. MORE excitable

99

Fxn of PAG:

Pain modulation

100

Locus Coreruleus:

projects to dorsal horn, releases NE, this reduces pain transmission, much like opioids do, inhibitory effect on dorsal horn

101

What activates the Locus Coreruleus?

PAG

102

These cells make it easier for pain info to reach higher levels:

proprioceptive cells in the rostal ventral medulla

103

T or F? The RVM has both on and off cells.

T

104

Fxn of on cells of the RVM:

pro-nociceptive action

105

What determines how much pain reaches consciousness?

Balance bw the 2 pain-control pathways, the on and off cell activity

106

Why should pain transmission pwys be open?

To keep protective reflexes at a useful level, in case you get cut, etc.

107

Where are opioid receps found?

on peripheral and central ends of pain fibers, on projection neurons, and now here in the RVM

108

T or F? Opiates inhibit the OFF cells.

F. Facilitate the off cells, opioids hit these cells and turns off pain

109

T or F? Opiates inhibit ON cells.

T

110

How do systemic opioids work?

by activating off cells at the RVM and mimicking inhibitory interneurons in the dorsal horn

111

Role of opiates under conditions of morphine tolerance:

they bc pronociceptive, causing pain

112

PAG has (few/many) opioid receptors.

many

113

PAG is turned on by:

the dorsal horn (turn antipain system on), anterior cinguate (emotional component of pain), and other ascending connections form the s.c.

114

Slow pain is assoc with what part of pain

the emotional aspect

115

Fast pain goes (here) and localizes where the pain is from.

to the somatosensory cortex

116

Is slow or fast pain associated with the localization of pain?

fast

117

T or F? Fast pain transmits a great deal of info regarding the magnitude of pain.

F. little or no info about this

118

The anterior cingulate is associated with this type of pain:

slow, perception of the emotional component of pain

119

Cingulate and the insula cortex is involved in:

mediating pain

120

Viscera sends pain to:

the insula

121

What is the insular cortex connected to?

the amygdala, for the emotional connection

122

The insular cortex is involved in:

pain consciousness, esp. visceral pain

123

Cannabinoids are similar in effects to:

opioids

124

How do cannabinoids work?

via G-protien coupled cannabinoid receptors

125

What is anandamide (AEA)?

One of several endocannabinoids (endogenous)

126

How do cannabinoids act on their target?

Increase in Ca++ in postsynaptic cell, if this synapse has a cannabis component, there will be a release of cannabinoids which go backwards to act on the cannabinoid receptors on the presynaptic cell (CB1 receptor), inhibiting their targets, reducing voltage sensitive Ca++ activity and NT release

127

Do cannabinoids work on the pre or postsynaptic cell?

pre, backwards transmitters "retrograde", released from postsynaptic cell

128

2 ways cannabinoids inhibit their targets:

activate K channel activity or reduce voltage-sensitive Ca channel activity

129

How can we treat persistent neuropathic pain?

Cannabinoids

130

Where in the CNS are cannabinoids found?

Dorsal horn, RVM, and PAG

131

T or F? Cannabinoids and opioids are part of the same system.

F. seem to be 2 distinct systems: different sites in the PAG

132

T or F? Cannabinoids are coextensive with opioids.

F. They exist in a different locations and are 2 different systems.

133

What role do cannabinoids play in the periphery?

anti-nociceptive, nociceptors have cannabinoid receps

134

Inflammatory skin disease is related to:

renal failure, liver disease, and some cancers

135

T or F? Itch is a separate sense.

T

136

How is itch inhibited in the body?

s.c. has a set of inhibitory interneurons that inhibit itch (unresponsvie to pain)

137

Itch is a prominent feature of:

inflammatory skin disease

138

2 types of itch:

Chemical and mechanical itch

139

What fiber type is chemical itch stimulated by?

C-fibers

140

Examples of chemical itch:

allergic reactions, bug bites

141

Examples of mechanical itch:

scratchy sweater, bug walking on skin

142

What is mechanical itch mediated by?

C-fibers and low-threshold A-fibers

143

Migraine may be a result of:

cortical dysfunction

144

Where do migraines likely begin?

Trigeminal complex in cortex

145

Are men or women more prone to migraines?

women 18% vs. 6%

146

What do migraines lead to?

Change in blood flow in and around the brain

147

Rx for acute migraines:

agonist of serotoinin (5-HT(1B) and 5-HT(1D) receptors, BV constriction and prevents extravasation (reduce the inflammatory soup and decreaese the release of CGRP and substance P)

148

Long-term mgmt of migraines:

diet, lifestyle (i.e. chocolate can give some people migraines)

149

Phase 2 trials to treat migraines:

ABs to CGRP or CGRP receps

150

Tx for migraines involving behavioral techniques:

condition pts to activate their own anti-pain circuits

151

What can be used to reduce the intensity of migraine attacks?

Sympathetic system cues: temperature, sweating to reduce tension from pain (Biofeedback)

152

cyclooxygenase is aka:

COX-2

153

Fxn of COX-1:

Key player in inflammation, protects the GI tract, kidneys, and platelets, induced by injury