pain 1 Flashcards
(108 cards)
1
Q
what are the 2 main types of local anesthetics
A
amide and ester
2
Q
what are the 3 types od fibres that are involved in sensation
A
Adelta
Abeta
C
3
Q
what do Abeta fibres detect
A
gentle stimulus, non-noxious mechanical stimulus
4
Q
how fast are Abeta fibres
A
very fast
5
Q
which of the fibres conduct pain
A
Adelta
C
6
Q
what do Adelta fibres detect
A
immediate pain (hammer), noxious mechanical stimulus
7
Q
what do C fibres detect
A
noxious heat and chemical stimuli - slower and longer lasting
8
Q
which are the slowest fibres
A
C
9
Q
which are the fastest fibres
A
A beta
10
Q
what is nociception
A
neural encoding of a noxious stimulus (neurophysiological)
11
Q
what does a stronger stimulus do to action potentials
A
makes it a higher frequency of APs
12
Q
what is pain
A
an unpleasent sensory and emotional experience associated with actual or potential tissue damage (psychological)
13
Q
is nociception or pain neurophysiological
A
nociception
14
Q
is nociception or pain psychological
A
pain
15
Q
what is an analgesic
A
selectively blocks the sensation of pain without blocking other sensations
16
Q
what is a local anesthetic
A
blocks nerve conduction and all sensation (pain too)
17
Q
what is a general anesthetic
A
cause unconsciousness but do not always cause analgesia
18
Q
is this analgesia or anesthetic:
blocks nerve conduction and all sensation (pain too)
A
anesthetic
19
Q
is this analgesia or anesthetic:
selectively blocks the sensation of pain without blocking other sensations
A
analgesia
20
Q
what is hyperalgesia
A
enhanced response to a painful stimuli
21
Q
what is : enhanced response to a painful stimuli
A
hyperalgesia
22
Q
what is allodynia
A
generation of a painful response by a non-painful stimulus (like a feather)
23
Q
what term would describe a phenomenon when a feather on the skin would feel very painful
A
allodynia
24
Q
what term would describe a phenomenon when the hot shower hurts a lot more when you have a sunburn
A
hyperalgesia
25
what is the "first pain" carried out by (which fibres) and where is it carried to
A-delta, carried to CNS
26
why is pain good
serves biological purpose - protects from tissue injury
27
what fibre carries inflammation and chronic pain
c fibres
28
what is chronic pain
mild, musculoskeletal pain
29
how do you treat or prevent acute pain
local anesthetics
30
how do you treat or prevent chronic pain
NSAIDs
31
what 4 things cause chronic pain
bradykinin, histamine, acid metabolites, prostaglandins
32
what role does chronic pain serve
still serves a protective role like acute pain
33
how do you treat deep pain
major analgesics like opioids
34
what is deep pain
deep aching pain, deep to body surface, poorly localized
35
what is deep pain associated with (what causes it)
major trauma, car accidents, childbirth, post-operative pain, heart attacks, cancer
36
is chronic pain still good pain
yes, it is protective
37
is deep pain still good pain
yes, it is protective and allows the healing process to progress
38
what is neuropathic pain
pain induced by injury to or disease of the somatosensory system
39
what can cause neuropathic pain
nerve injury or infections of the nervous system
40
what are 5 examples of neuropathic pain
phantom limb pain, trigeminal neuralgia, shingles, diabetic neuropathy, fibromyalgia
41
how fast does neuropathic pain develop in relation to injury
slowly, and outlasts healing of original injury
42
what causes diabetic neuropathy
too much sugar in blood for a long time
43
what is fibromyalgia
ideopathic pain (no reason), chronic muscle pain - neuropathic
44
what are 4 signs of neuropathic pain
allodynia, hyperalgesia, causalgia, shooting pains
45
what is causalgia
ongoing burning pain
46
what is neuropathic pain
when the thing heals but the pain stays
47
what can alter perceptrion of pain
fear, rage, depression, etc
48
how long typically do you consider something to be acute pain
less than 3 months
49
how long typically do you consider something to be chronic pain
more than 3 months
50
what is "centralization" of pain
when the pain becomes chronic and difficult to treat
51
what causes "centralization" of pain
untreated pain due to peripheral nerve injury
52
what does untreated pain due to peripheral nerve injury lead to
"centralization" of pain
53
what are the structural requirements for local anesthetics
aromatic residue, amide or ester linkage to alkylamino group
54
where on the pH scale would a local anesthetic be
somewhere where weak bases go
55
what is the equilibrium equation for local anesthetics
R3-NH+ + A-
R3-N + H+ A-
56
What are the 2 forms that local anesthetics can be in (ionization)
cationic and uncharged
57
do you want local anesthetics to be cationic or uncharged
needs to be uncharged for it to work
58
what are 2 examples of ester local anesthetic
cocaine and procaine
59
is cocaine an ester or amide local anesthetic
ester
60
is procaine an ester or amide local anesthetic
ester
61
is lidocaine an ester or amide local anesthetic
amide
62
what is an example of an amide local anesthetic
lidocaine
63
what is the ratio of the neutral and cationic form of the local anesthetic given by (which formula)
henderson-hasselbach equation
64
what is the henderson-hasselbach equation formula
Log(cationic/uncharged) = pKa-pH
65
what is the mechanism of action of local anesthetics
interacts and blocks Na+ channels
66
what are 3 things that local anesthetics do
block Na+ channels
increases threshold
blocks conduction
67
what do local anesthetics do to threshold
increase
68
what do local anesthetics do to conduction
block
69
how do local anesthetics block conduction
nerve impulses propagate via Na+ channel opening, so this way it cant propagate
70
what state must a local anesthetic be in to enter the membrane
neutral
71
what happens once the local anesthetic gets across the membrane
it re-ionizes and enters the channel from the inside
72
why do local anesthetics work so great mainly in pain nerves
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
what enables access to the receptor by local anesthetics
activation and opening of the channel
74
what is the efficacy of local anesthetics in damaged/ infected tissues and why
not good because they would have a lower pH - that would push the reaction towards cationic form that can't enter the membrane
75
how is pKa related to the rate of onset
smaller pKa is a faster rate of onset
76
what does a small pKa do to rate of onset
fast rate of onset
77
what does a large pKa do to rate of onset
slow rate of onset
78
would a drug with a henderson-hasselbach equation answer of 1 or 2 have a faster rate of onset and why
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
why is the block use dependent
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
where would local anesthetic administration pose a threat to systemic toxicity
if it it administered to a highly vascularized area
81
how can you offset potential toxicity of local anesthetic
by co-administering with a vasoconstrictor
82
what are 3 reasons to mix local anesthetics with vasoconstrictors
1-limit systemic absorption
2-increase local anesthetic at site of action
3-counteracts local anesthetic's tendency to cause vasodilation
83
do local anesthetics tend to cause vasoconstriction or vasodilation
vasodilation
84
what is the half life of procaine
less than 1 min in blood
85
what metabolizes procaine
plasma cholinesterases
86
are plasma cholinesterases more or less selective than acetylcholinesterases
less
87
what metabolizes lidocaine
microsomal cytochrome p450 enzymes in liver
88
what does liver disease do to lidocaine
extend its toxicity
89
which nerve fibres are most susceptible to local anesthetics
C and A-delta (thin ones)
90
which nerve fibres are least susceptible to local anesthetics
A-fibres
91
what 3 things determine nerve fibre susceptibility
1-which fibre (Ab d or C)
2-firing frequency
3-AP duration
92
what does firing frequency do to nerve fibre susceptibility
nerves that fire at high frequency are more likely to block (use dependent)
93
what does AP duration/ spike width do to nerve fibre susceptibility
broader spikes have channels in activated state longer so mre chances for local anesthetic to enter
94
why are C and A-delta fibres most susceptible
because they have less Na+ channels i think
95
why are A-beta fibres less susceptible
because they have more Na+ channels i think
96
do A-beta or C-fibres have a longer AP duration
C-fibres
97
what happens with systemic absorption of local anesthetics (2 toxic effects)
- hypotension
| - cardiac depression
98
how do local anesthetics cause vasodilation
direct action on blood vessel smooth muscle
99
how do local anesthetics cause cardiac depression
action on Na+ channels in the heart
100
is a higher dose needed for anti-dysrhythmia or local anesthetic for lidocaine
higher dose needed for anesthetic
101
what are 4 CNS effects of local anesthetics
sleepiness, light-headedness, auditory disturbances, restlessness
102
are there Na+ channels in the brain
yes
103
why do local anesthetics cause restlessness
loss of cortical inhibition
104
what do local anesthetics do at high concentrations (3)
nystagmus, shivering, convulsions
105
what is nystagmus
quivering of eyes back and forth
106
what do local anesthetics do at very high concentrations
CNS depression - no heart or brain
107
do some practice calculation questions and the questions at the end of the lecture
yes
108
what metabolizes cocaine
plasma cholinesterases
