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PMCOL 343 > pain 1 > Flashcards

pain 1 Flashcards

1
Q

what are the 2 main types of local anesthetics

A

amide and ester

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2
Q

what are the 3 types od fibres that are involved in sensation

A

Adelta
Abeta
C

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3
Q

what do Abeta fibres detect

A

gentle stimulus, non-noxious mechanical stimulus

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4
Q

how fast are Abeta fibres

A

very fast

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5
Q

which of the fibres conduct pain

A

Adelta

C

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6
Q

what do Adelta fibres detect

A

immediate pain (hammer), noxious mechanical stimulus

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7
Q

what do C fibres detect

A

noxious heat and chemical stimuli - slower and longer lasting

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8
Q

which are the slowest fibres

A

C

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9
Q

which are the fastest fibres

A

A beta

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10
Q

what is nociception

A

neural encoding of a noxious stimulus (neurophysiological)

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11
Q

what does a stronger stimulus do to action potentials

A

makes it a higher frequency of APs

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12
Q

what is pain

A

an unpleasent sensory and emotional experience associated with actual or potential tissue damage (psychological)

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13
Q

is nociception or pain neurophysiological

A

nociception

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14
Q

is nociception or pain psychological

A

pain

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15
Q

what is an analgesic

A

selectively blocks the sensation of pain without blocking other sensations

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16
Q

what is a local anesthetic

A

blocks nerve conduction and all sensation (pain too)

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17
Q

what is a general anesthetic

A

cause unconsciousness but do not always cause analgesia

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18
Q

is this analgesia or anesthetic:

blocks nerve conduction and all sensation (pain too)

A

anesthetic

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19
Q

is this analgesia or anesthetic:

selectively blocks the sensation of pain without blocking other sensations

A

analgesia

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20
Q

what is hyperalgesia

A

enhanced response to a painful stimuli

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21
Q

what is : enhanced response to a painful stimuli

A

hyperalgesia

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22
Q

what is allodynia

A

generation of a painful response by a non-painful stimulus (like a feather)

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23
Q

what term would describe a phenomenon when a feather on the skin would feel very painful

A

allodynia

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24
Q

what term would describe a phenomenon when the hot shower hurts a lot more when you have a sunburn

A

hyperalgesia

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25
Q

what is the “first pain” carried out by (which fibres) and where is it carried to

A

A-delta, carried to CNS

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26
Q

why is pain good

A

serves biological purpose - protects from tissue injury

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27
Q

what fibre carries inflammation and chronic pain

A

c fibres

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28
Q

what is chronic pain

A

mild, musculoskeletal pain

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29
Q

how do you treat or prevent acute pain

A

local anesthetics

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30
Q

how do you treat or prevent chronic pain

A

NSAIDs

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31
Q

what 4 things cause chronic pain

A

bradykinin, histamine, acid metabolites, prostaglandins

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32
Q

what role does chronic pain serve

A

still serves a protective role like acute pain

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33
Q

how do you treat deep pain

A

major analgesics like opioids

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34
Q

what is deep pain

A

deep aching pain, deep to body surface, poorly localized

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35
Q

what is deep pain associated with (what causes it)

A

major trauma, car accidents, childbirth, post-operative pain, heart attacks, cancer

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36
Q

is chronic pain still good pain

A

yes, it is protective

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37
Q

is deep pain still good pain

A

yes, it is protective and allows the healing process to progress

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38
Q

what is neuropathic pain

A

pain induced by injury to or disease of the somatosensory system

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39
Q

what can cause neuropathic pain

A

nerve injury or infections of the nervous system

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40
Q

what are 5 examples of neuropathic pain

A

phantom limb pain, trigeminal neuralgia, shingles, diabetic neuropathy, fibromyalgia

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41
Q

how fast does neuropathic pain develop in relation to injury

A

slowly, and outlasts healing of original injury

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42
Q

what causes diabetic neuropathy

A

too much sugar in blood for a long time

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43
Q

what is fibromyalgia

A

ideopathic pain (no reason), chronic muscle pain - neuropathic

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44
Q

what are 4 signs of neuropathic pain

A

allodynia, hyperalgesia, causalgia, shooting pains

45
Q

what is causalgia

A

ongoing burning pain

46
Q

what is neuropathic pain

A

when the thing heals but the pain stays

47
Q

what can alter perceptrion of pain

A

fear, rage, depression, etc

48
Q

how long typically do you consider something to be acute pain

A

less than 3 months

49
Q

how long typically do you consider something to be chronic pain

A

more than 3 months

50
Q

what is “centralization” of pain

A

when the pain becomes chronic and difficult to treat

51
Q

what causes “centralization” of pain

A

untreated pain due to peripheral nerve injury

52
Q

what does untreated pain due to peripheral nerve injury lead to

A

“centralization” of pain

53
Q

what are the structural requirements for local anesthetics

A

aromatic residue, amide or ester linkage to alkylamino group

54
Q

where on the pH scale would a local anesthetic be

A

somewhere where weak bases go

55
Q

what is the equilibrium equation for local anesthetics

A

R3-NH+ + A-

R3-N + H+ A-

56
Q

What are the 2 forms that local anesthetics can be in (ionization)

A

cationic and uncharged

57
Q

do you want local anesthetics to be cationic or uncharged

A

needs to be uncharged for it to work

58
Q

what are 2 examples of ester local anesthetic

A

cocaine and procaine

59
Q

is cocaine an ester or amide local anesthetic

A

ester

60
Q

is procaine an ester or amide local anesthetic

A

ester

61
Q

is lidocaine an ester or amide local anesthetic

A

amide

62
Q

what is an example of an amide local anesthetic

A

lidocaine

63
Q

what is the ratio of the neutral and cationic form of the local anesthetic given by (which formula)

A

henderson-hasselbach equation

64
Q

what is the henderson-hasselbach equation formula

A

Log(cationic/uncharged) = pKa-pH

65
Q

what is the mechanism of action of local anesthetics

A

interacts and blocks Na+ channels

66
Q

what are 3 things that local anesthetics do

A

block Na+ channels
increases threshold
blocks conduction

67
Q

what do local anesthetics do to threshold

A

increase

68
Q

what do local anesthetics do to conduction

A

block

69
Q

how do local anesthetics block conduction

A

nerve impulses propagate via Na+ channel opening, so this way it cant propagate

70
Q

what state must a local anesthetic be in to enter the membrane

A

neutral

71
Q

what happens once the local anesthetic gets across the membrane

A

it re-ionizes and enters the channel from the inside

72
Q

why do local anesthetics work so great mainly in pain nerves

A

because of use dependent block (if nerve is giving pain signals, it is actively opening and letting Na+ through. so when it is open more it has more chance that it can be blocked)

73
Q

what enables access to the receptor by local anesthetics

A

activation and opening of the channel

74
Q

what is the efficacy of local anesthetics in damaged/ infected tissues and why

A

not good because they would have a lower pH - that would push the reaction towards cationic form that can’t enter the membrane

75
Q

how is pKa related to the rate of onset

A

smaller pKa is a faster rate of onset

76
Q

what does a small pKa do to rate of onset

A

fast rate of onset

77
Q

what does a large pKa do to rate of onset

A

slow rate of onset

78
Q

would a drug with a henderson-hasselbach equation answer of 1 or 2 have a faster rate of onset and why

A

1 because there is a smaller difference in pKa, meaning that 1 in 10 molecules are charged and ready to enter (instead of 1 in 100 being ready)

79
Q

why is the block use dependent

A

because the channel needs to open to let R3-NH+ in from the inside, so the more active the nerve is, the more rapidly block develops

80
Q

where would local anesthetic administration pose a threat to systemic toxicity

A

if it it administered to a highly vascularized area

81
Q

how can you offset potential toxicity of local anesthetic

A

by co-administering with a vasoconstrictor

82
Q

what are 3 reasons to mix local anesthetics with vasoconstrictors

A

1-limit systemic absorption
2-increase local anesthetic at site of action
3-counteracts local anesthetic’s tendency to cause vasodilation

83
Q

do local anesthetics tend to cause vasoconstriction or vasodilation

A

vasodilation

84
Q

what is the half life of procaine

A

less than 1 min in blood

85
Q

what metabolizes procaine

A

plasma cholinesterases

86
Q

are plasma cholinesterases more or less selective than acetylcholinesterases

A

less

87
Q

what metabolizes lidocaine

A

microsomal cytochrome p450 enzymes in liver

88
Q

what does liver disease do to lidocaine

A

extend its toxicity

89
Q

which nerve fibres are most susceptible to local anesthetics

A

C and A-delta (thin ones)

90
Q

which nerve fibres are least susceptible to local anesthetics

A

A-fibres

91
Q

what 3 things determine nerve fibre susceptibility

A

1-which fibre (Ab d or C)
2-firing frequency
3-AP duration

92
Q

what does firing frequency do to nerve fibre susceptibility

A

nerves that fire at high frequency are more likely to block (use dependent)

93
Q

what does AP duration/ spike width do to nerve fibre susceptibility

A

broader spikes have channels in activated state longer so mre chances for local anesthetic to enter

94
Q

why are C and A-delta fibres most susceptible

A

because they have less Na+ channels i think

95
Q

why are A-beta fibres less susceptible

A

because they have more Na+ channels i think

96
Q

do A-beta or C-fibres have a longer AP duration

A

C-fibres

97
Q

what happens with systemic absorption of local anesthetics (2 toxic effects)

A
  • hypotension

- cardiac depression

98
Q

how do local anesthetics cause vasodilation

A

direct action on blood vessel smooth muscle

99
Q

how do local anesthetics cause cardiac depression

A

action on Na+ channels in the heart

100
Q

is a higher dose needed for anti-dysrhythmia or local anesthetic for lidocaine

A

higher dose needed for anesthetic

101
Q

what are 4 CNS effects of local anesthetics

A

sleepiness, light-headedness, auditory disturbances, restlessness

102
Q

are there Na+ channels in the brain

A

yes

103
Q

why do local anesthetics cause restlessness

A

loss of cortical inhibition

104
Q

what do local anesthetics do at high concentrations (3)

A

nystagmus, shivering, convulsions

105
Q

what is nystagmus

A

quivering of eyes back and forth

106
Q

what do local anesthetics do at very high concentrations

A

CNS depression - no heart or brain

107
Q

do some practice calculation questions and the questions at the end of the lecture

A

yes

108
Q

what metabolizes cocaine

A

plasma cholinesterases

PMCOL 343 (31 decks)

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