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Pain Control > L3- Local Anesthetics > Flashcards

L3- Local Anesthetics Flashcards

1
Q

Esters

A

not used in dentistry use as much - ones we will use are benzocaine - which is topical or maybe tetracain

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2
Q

benzocaine

A

type of LA that is an ester and is used as a topical

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3
Q

first anesthetics?

A

1884

- cocaine

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4
Q

amides

A

ones we are more familiar with and have more clinical importance

  • articaine
  • lidocaine
  • mepivacaine
  • prilocaine (sometimes)
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5
Q

most potent vasodilator?

A

procaine - used to get rid of a spasm - but not used in dentistry

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6
Q

all LA?

A

possess a degree of vasoactivity - most producing vasodilation

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7
Q

only LA that produces vasoconstriction?

A

Cocaine - vasodialates first and the does constriction

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8
Q

anesthetics with the least vasodialating properties? implicatins?

A

mepivicaine and prilocaine
- meaning they do not need the addition of a vasoconstrictor as much because they are not doing vasodialtion (more diffuse and will leave area with more dilation)

so given without a vasoconstrictor

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9
Q

oral route of LA

A

besides cocaine - these are poorly absorbed from the gastrointestinal tract following oral administration
not as effective because of first pass effect at liver
50-90% are taken up by liver so little left systemically to do anything

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10
Q

topical route of LA

A

absorbed at differeing rates after the application

used as topicals at certain concentration

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11
Q

tracheal mucosa

A

does work - almost as rapid uptake as IV administration

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12
Q

LA applied to intact skin?

A

does NOT WORK - they do not have an anesthetic action

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13
Q

EMLA?

A

‘Eutectic mixture of Local Anesthetic’
- surface anesthesia for intact skin

put on skin - wrap it and it has some effect as LA on the skin

can be effective before giving an injection or IV

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14
Q

intravenous pharmokinetics of LA

A

Iv administration provides the most rapid elevation of blood levels and is used in the primary treatment of ventricular dysrhythmias

  • but wont get a ‘local’ effect
  • used in medical emergencies
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15
Q

Pharmacokinetics - distribution once absorbed

A

vasodilating factors – more blood into area an LA reuptake into bloodstream (vasoconstrictor would prevent this)

once absorbed into the blood, local anesthetics are distributed throughout the body to all tissues

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16
Q

blood levels of LA depend on?

A

whereever most blood going - more LA

  1. rate of absorption into CVS
  2. rate of distribution
  3. elimination of the drug

wherever most blood goes - where you get most LA at first

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17
Q

ALL LA cross?

A

blood brain barrier AND the placenta - give local to pregnant make sure no effect - like class A? B is not as bad

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18
Q

more cardiac output =?

A

more blood flow and thus more LA to the area

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19
Q

Percentages/rank of Cardiac output distributed to different organ systems

A
  1. kidney - 22%
  2. GI system/spleen - 21%
  3. Skeletal muscle 15%
  4. Brain -14%
  5. skin - 6 %
  6. Liver - 6%
  7. bone
  8. heart muscle
  9. other
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20
Q

General first steps in LA once injected

A
  1. Uptake
  2. Distribution
  3. Biotransformation
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21
Q

Biotransformation of Esters

A

Ester LA are hydrolyzed in the PLASMA by the enzyme pseudocholinesterase

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22
Q

Biotransformation example of esters

A

procaine –> hydrolysis by pseudocholinesterase to para-aminobenzoic acid (PABA) – this can be excreted unchanges in the urine or to diethylamino alcohol then excretion

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23
Q

most common reason allergies to esters?

A

due to the PABA that is produced by the pseudocholinesterase –> THESE METABOLITES - not the parent compound (like procaine)

24
Q

atypical pseudocholinesterase

implicatoins?

A

inability to hydrolyze the ester LA

incidence is 1 out of every 2800 persons

avoid esters
- so use amides

25
Q

how do you know if patient has a pseudocholinesterase deficiency?

A

after they had exposure - not an allergic reaction

if first time had it - may have taken them a long time to come out of it but succinyl choline – used for general anesthetic

26
Q

Amide Biotransformation and difference with them compared to esters

A

LIVER - primary site of biotransformation
*amidea have a more complex biotransformation and amides are usually present as the parent compound in greater precentage than esters

metabolized in liver – what effects liver will effect this

27
Q

what would be effects and reasons for slower biostransformation of amides?

A

slower than normal biotransformation can lead to increased levels of LA in the blood stream (since less being metabolized) and can lead to increased toxicity

  • hypotension
  • congestive heart failure
  • poor liver function like cirrhosis
28
Q

take things to liver?

A

if slower rate – less LA to liver – less load to liver and longer time for metabolize

29
Q

how many half lives does it usually take to eliminate a drug from the system?

A

about 6 half lives (not same thing as 6 hours)

30
Q

normal half life for lidocaine?
with heart failure?
hepatic disease?
renal disease?

A 
normal - 1.8 
heart failure - 1.9
hepatic disease * - 4.9
- has almost double effect
renal disease 1.3
31
Q

defintion t 1/2

A

is the time necessary for a 50% reduction in the blood level

one half life = 50 % reduction, two half lives = 75 % reduction

32
Q

two half lives is how much reduction?

A

75%
(50% = first)
second is half of 50 (25) so 50 + 25 = 75

33
Q

pharmokinetics with excretion

A
  • KIDNEYS
  • the kidneys are the primary excretory organ for both the local anesthetics and its metabolites.

A percentage of a given dose local anesthetic drug will be excreted unchanged in the urine

what we will find is that the amide ones - parent compound will be excreted and esters the metabolites would be

34
Q

systemic actions of LA

A

any membrane / nerve function is effected - so CNS and CVS are susceptible to their action and relates to the plasma levels of LA
- CNS is more susceptible

35
Q

CNS effect systemic action

A

Anticonvulsant properties and preconvulsive phase

36
Q

anticonvulsant properties

A

CNS systemic effect of LA
- raise the seizure threshold
doses 2-3 mg/kg given at a rate of 40-50 mg/min (0.-4 ug/ml
here there is a balance between inhibitory and facilitory impulses
then…. preconvulsive stage

37
Q

preconvulsive phase

A

CNS effect
direct depressant action of the local anesthetic on the CNS (4.5-7ug/ml).

  • slurred speech
  • shivering
  • muscular twitching
  • tremor in muscle of face and distal extremities

FIRST there is a balance between inhibitory and facilitory impulses and then in the PRECONVULSIVE STAGE - inhibitory impulsee depressed-
selectively blocks out the inhibitory impulses – so the fascilitated takes over and gets shaking

then convulsive – could get to seizure

more? - both inhibitory and stimilatory are depressed

38
Q

convulsive stage

A

with further elevation of the LA blood level produces clinical signs and symptoms consistent with a generalized tonic-clonic convulsive episode
*inhibitory impulses inhibited (vs. pre they are depressed)
greater that 7.5 ug/ml

39
Q

Final stage in systemic effect of LA on CNS

A

Both the inhibitory and facilitory impulses are totally depressed, producing general CNS depression

  • CVS will be effected next
40
Q

effect of pCO2 on the convulsive threshold of various LA

A

with higher pCO2 – lower pH and more acidic so you need LESS of the LA to produce a toxic effect
- with seizure increase in metabolism is also occurring- so more acidic

with lower pH DURATION IS LONGER AND TAKES LESS TO REACH CONVULSIVE STATE

41
Q

LA systemic effect on Cardiovascular system

A

LA drug action decreases electrical excitability of the myocardium, decreases conduction rate, and decreases the force of contraction

42
Q

intravenous dose of LA agents required for Convulsive activity of CNS vs. Irreversible cardiovascular collapse

A

*effects to CNS will occur FIRST WITH LOWER AMOUNT NEEDED to produce toxic effect

so seizure CNS effects are going to occur at lower doses than CVS
example lidocain = 22 for CNS and 76 mg/kg for CNS

43
Q

Step 1 - Sequence of LA - induced actions on CVS

A

(5 total steps)

  1. at non-overdose levels, a slight increase to no change in BP occurs because of increased CO and HR as a result of enhanced sympathetic activity -
    - some vasoconstriction in peripheral vascular beds
44
Q

Step 2 - Sequence of LA - induced actions on CVS

A

Levels are approaching but still below the overdose threshold - a mild degree of HYPOTENSION is noted - this is produced by a direct relaxant action on the vascular smooth muscle (due to vasodilation)

45
Q

Step 3 - Sequence of LA - induced actions on CVS

A

AT OVERDOSE LEVELS - profound hypotension is caused by direct decreased myocardial contractility, cardiac output, and peripheral resistance

46
Q

Step 4 - Sequence of LA - induced actions on CVS

A

AT LETHAL LEVELS - cardiovascular collapse is noted. this is caused by massive peripheral vasodilation and decreased myocardial contractility and heart rate
- sinus bradycardia

47
Q

Step 5 - Sequence of LA - induced actions on CVS + which LA most associated with this - implications/why associated?

A

Bupivacaine (and lesser degree ropivacaine and etiodocaine) may precipitate potentially FATAL ventricular fibrillation

  • these are LONG LASTING and can cause more problems with arrhythmia
  • pt history of v-fib would not want to use
48
Q

duration of anesthesia dependent on?

general

A
  1. individual patient variation
  2. accurate administration
  3. anatomical variation (IAN - look where mandibular canal is)
  4. type of injection administered (block lasts longer than infiltration)
49
Q

doses of LA- given by? reflects?

A

manufacturer will give you the maximum dose for a specific drug usually in mg/kg or mg/lb/
these numbers reflect approximate values for there is a wide range in patient responses to blood levels of LA

50
Q

maximum calculated dose should be decreased in who?

A

medically compromised, debilitated, or elderly patients

51
Q

Factors in selection of LA and expand on each

A
  1. length of time that pain control is required
  2. potential for discomfort in the post-treatment period – *use a longer lasting LA
  3. requirement for hemostasis during treatment -*think about vasoconstrictors
  4. medical status of patient -*do not use ones that can cause adverse side effects
52
Q

patient that ‘took a long time to wake up’ when went under general anesthesia

A

*atypical pseudocholinesterase
pseudocholinesterase deficiency?
- cannot effectivly break down the esters in the plasma – so use an amide which is metabolized in the liver - amide LA when working on the patient

53
Q

absolute contraindication

A

implies that under no circumstance should the drug be administered to the patients because of the possibility of potentially toxic or lethal reactions is increased

54
Q

relative contraindication?

A

the drug in question may be administered to the patient after carefully weighing the risk of using the drug to its potential benefit - and if an acceptable alternative drug is not an option - may use

55
Q

benzocaine is? if contraindicated what can you use?

A

an ester- used as a topical anesthetic

could use lidocaine?

56
Q

metabolism of articaine? Use it in patient with CHF?

A

LIVER AND BLOOD
90% liver
10% blood
not going to find articaine WITHOUT A VASOCONSTRICTOR
- but if use without it is okay to use in patient with history of CHF

57
Q

use prilocaine in patient with CHF?

A

probably not - because takes longer to metabolize - higher risk of developing side effects

Pain Control (12 decks)

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