pain 1 Flashcards
what are the 2 main types of local anesthetics
amide and ester
what are the 3 types od fibres that are involved in sensation
Adelta
Abeta
C
what do Abeta fibres detect
gentle stimulus, non-noxious mechanical stimulus
how fast are Abeta fibres
very fast
which of the fibres conduct pain
Adelta
C
what do Adelta fibres detect
immediate pain (hammer), noxious mechanical stimulus
what do C fibres detect
noxious heat and chemical stimuli - slower and longer lasting
which are the slowest fibres
C
which are the fastest fibres
A beta
what is nociception
neural encoding of a noxious stimulus (neurophysiological)
what does a stronger stimulus do to action potentials
makes it a higher frequency of APs
what is pain
an unpleasent sensory and emotional experience associated with actual or potential tissue damage (psychological)
is nociception or pain neurophysiological
nociception
is nociception or pain psychological
pain
what is an analgesic
selectively blocks the sensation of pain without blocking other sensations
what is a local anesthetic
blocks nerve conduction and all sensation (pain too)
what is a general anesthetic
cause unconsciousness but do not always cause analgesia
is this analgesia or anesthetic:
blocks nerve conduction and all sensation (pain too)
anesthetic
is this analgesia or anesthetic:
selectively blocks the sensation of pain without blocking other sensations
analgesia
what is hyperalgesia
enhanced response to a painful stimuli
what is : enhanced response to a painful stimuli
hyperalgesia
what is allodynia
generation of a painful response by a non-painful stimulus (like a feather)
what term would describe a phenomenon when a feather on the skin would feel very painful
allodynia
what term would describe a phenomenon when the hot shower hurts a lot more when you have a sunburn
hyperalgesia
what is the “first pain” carried out by (which fibres) and where is it carried to
A-delta, carried to CNS
why is pain good
serves biological purpose - protects from tissue injury
what fibre carries inflammation and chronic pain
c fibres
what is chronic pain
mild, musculoskeletal pain
how do you treat or prevent acute pain
local anesthetics
how do you treat or prevent chronic pain
NSAIDs
what 4 things cause chronic pain
bradykinin, histamine, acid metabolites, prostaglandins
what role does chronic pain serve
still serves a protective role like acute pain
how do you treat deep pain
major analgesics like opioids
what is deep pain
deep aching pain, deep to body surface, poorly localized
what is deep pain associated with (what causes it)
major trauma, car accidents, childbirth, post-operative pain, heart attacks, cancer
is chronic pain still good pain
yes, it is protective
is deep pain still good pain
yes, it is protective and allows the healing process to progress
what is neuropathic pain
pain induced by injury to or disease of the somatosensory system
what can cause neuropathic pain
nerve injury or infections of the nervous system
what are 5 examples of neuropathic pain
phantom limb pain, trigeminal neuralgia, shingles, diabetic neuropathy, fibromyalgia
how fast does neuropathic pain develop in relation to injury
slowly, and outlasts healing of original injury
what causes diabetic neuropathy
too much sugar in blood for a long time
what is fibromyalgia
ideopathic pain (no reason), chronic muscle pain - neuropathic
what are 4 signs of neuropathic pain
allodynia, hyperalgesia, causalgia, shooting pains
what is causalgia
ongoing burning pain
what is neuropathic pain
when the thing heals but the pain stays
what can alter perceptrion of pain
fear, rage, depression, etc
how long typically do you consider something to be acute pain
less than 3 months
how long typically do you consider something to be chronic pain
more than 3 months
what is “centralization” of pain
when the pain becomes chronic and difficult to treat
what causes “centralization” of pain
untreated pain due to peripheral nerve injury
what does untreated pain due to peripheral nerve injury lead to
“centralization” of pain
what are the structural requirements for local anesthetics
aromatic residue, amide or ester linkage to alkylamino group
where on the pH scale would a local anesthetic be
somewhere where weak bases go
what is the equilibrium equation for local anesthetics
R3-NH+ + A-
R3-N + H+ A-
What are the 2 forms that local anesthetics can be in (ionization)
cationic and uncharged
do you want local anesthetics to be cationic or uncharged
needs to be uncharged for it to work
what are 2 examples of ester local anesthetic
cocaine and procaine
is cocaine an ester or amide local anesthetic
ester
is procaine an ester or amide local anesthetic
ester
is lidocaine an ester or amide local anesthetic
amide
what is an example of an amide local anesthetic
lidocaine
what is the ratio of the neutral and cationic form of the local anesthetic given by (which formula)
henderson-hasselbach equation
what is the henderson-hasselbach equation formula
Log(cationic/uncharged) = pKa-pH
what is the mechanism of action of local anesthetics
interacts and blocks Na+ channels
what are 3 things that local anesthetics do
block Na+ channels
increases threshold
blocks conduction
what do local anesthetics do to threshold
increase
what do local anesthetics do to conduction
block
how do local anesthetics block conduction
nerve impulses propagate via Na+ channel opening, so this way it cant propagate
what state must a local anesthetic be in to enter the membrane
neutral
what happens once the local anesthetic gets across the membrane
it re-ionizes and enters the channel from the inside
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)
what enables access to the receptor by local anesthetics
activation and opening of the channel
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
how is pKa related to the rate of onset
smaller pKa is a faster rate of onset
what does a small pKa do to rate of onset
fast rate of onset
what does a large pKa do to rate of onset
slow rate of onset
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)
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
where would local anesthetic administration pose a threat to systemic toxicity
if it it administered to a highly vascularized area
how can you offset potential toxicity of local anesthetic
by co-administering with a vasoconstrictor
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
do local anesthetics tend to cause vasoconstriction or vasodilation
vasodilation
what is the half life of procaine
less than 1 min in blood
what metabolizes procaine
plasma cholinesterases
are plasma cholinesterases more or less selective than acetylcholinesterases
less
what metabolizes lidocaine
microsomal cytochrome p450 enzymes in liver
what does liver disease do to lidocaine
extend its toxicity
which nerve fibres are most susceptible to local anesthetics
C and A-delta (thin ones)
which nerve fibres are least susceptible to local anesthetics
A-fibres
what 3 things determine nerve fibre susceptibility
1-which fibre (Ab d or C)
2-firing frequency
3-AP duration
what does firing frequency do to nerve fibre susceptibility
nerves that fire at high frequency are more likely to block (use dependent)
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
why are C and A-delta fibres most susceptible
because they have less Na+ channels i think
why are A-beta fibres less susceptible
because they have more Na+ channels i think
do A-beta or C-fibres have a longer AP duration
C-fibres
what happens with systemic absorption of local anesthetics (2 toxic effects)
- hypotension
- cardiac depression
how do local anesthetics cause vasodilation
direct action on blood vessel smooth muscle
how do local anesthetics cause cardiac depression
action on Na+ channels in the heart
is a higher dose needed for anti-dysrhythmia or local anesthetic for lidocaine
higher dose needed for anesthetic
what are 4 CNS effects of local anesthetics
sleepiness, light-headedness, auditory disturbances, restlessness
are there Na+ channels in the brain
yes
why do local anesthetics cause restlessness
loss of cortical inhibition
what do local anesthetics do at high concentrations (3)
nystagmus, shivering, convulsions
what is nystagmus
quivering of eyes back and forth
what do local anesthetics do at very high concentrations
CNS depression - no heart or brain
do some practice calculation questions and the questions at the end of the lecture
yes
what metabolizes cocaine
plasma cholinesterases
