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Local Anesthesia > Exam 1 > Flashcards

Exam 1 Flashcards

1
Q

Lidocaine composition that we use

A

2% lidocaine with 1:100,000 epinephrine

Halflife: 1.6

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2
Q

Short duration anesthetic we use

A

3% mepivicaine without vasoconstrictor

Halflife: 1.9

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3
Q

Intermediate duration anesthetic we use

A

4% articaine with 1:100,000 epinephrine

Halflife: 0.5

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4
Q

Long duration anesthetic we use

A

0.5% bupivacaine with 1:200,000 epinephrine

Halflife: 3.5

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5
Q

Antioxidant used in anesthetics

A

(with vasoconstrictors only)

sodium metabisulfite

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6
Q

Preservative used in anesthetics

A

(multidose vials only)

methylparaben

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7
Q

pH adjusting agents

A

HCl, NaOH

pH is usually acidic (4-6) especially with vasoconstrictors

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8
Q

What gylcoprotein has a higher protein binding affinity for lidocaine?

A

Alpha1-acid Glycoprotein (AGP, AAG)

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9
Q

What conditions increase alpha1-acid glycoprotein?

A

uremia, jaundice, pregnancy, or HIV infection

but might not have any clinical significance in binding of lidocaine

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10
Q

Unbound Drug Tissue Distribution

A

Rapid uptake by lungs (1 minute)
Brain, heart, liver, kidneys (5 minutes)
Muscle (15 minutes)
Fat (1-2 hours)

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11
Q

Ester-type anesthetics metabolism and excretion

A

circulating plasma pseudocholinesterase, renal excretion

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12
Q

Amide-type metabolism and excretion

AND EXCEPTIONS

A

hepatic metabolism, renal excretion
Exceptions:
-prilocaine has significant extrahepatic metabolism
-articaine is partly metabolized by pseudocholinesterase

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13
Q

Effects of lidocaine on CNS:

General Effects

A

Sedation
Disinhibition
-But low doses act like excitation

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14
Q

Effects of lidocaine on CNS:

Low doses

A

anticonvulsant activity
mild relaxation/sedation
generalized analgesia

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15
Q

Effects of lidocaine on CNS:

Moderate doses

A 
euphoria
lightheadedness
dysphoria
slurred speech
drowsiness
sensory changes (blurred, double vision)
twitching
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16
Q

Effects of lidocaine on CNS:

Moderate to high doses

A

disorientation
tremor
unconsciousness
seizures

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17
Q

Effects of lidocaine on CNS:

high doses

A

Coma

Respiratory arrest

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18
Q

Effects on vasculature (LOCAL)

A

Vasodilation at local injection site
direct inhibition of vascular smooth muscle tone
bupivacaine > lidocaine > mepivacaine

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19
Q

Effects on vasculature (SYSTEMIC)

A

Low concentrations - mild increase in peripheral vascular resistance
Moderate concentrations - central effects predominate
decreased heart rate, cardiac output, PVR
Higher concentrations - systemic vasodilation and decreased resistance

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20
Q

Do more lipophillic drugs have a higher rxn with CV effects or CNS?

A

more lipophilic drugs have proportionally greater cardiovascular than CNS effects

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21
Q

Cardiac effects

A 
Higher concentrations decrease:
conduction velocity
automaticity
myocardial contractility
cardiac output
blood pressure
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22
Q

Are systemic effects of local anesthetics overshadowed by vasoconstrictor effects?

A

yes

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23
Q

Presynaptic Reuptake and metabolism

A

Leakage out of vesicles into cytoplasm – an active equilibrium
Degradation by MAO within the neuron

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24
Q

Hepatic degradation

A

by COMT

Now thought to be a relatively minor pathwa

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25
Q

alpha1 receptor

Area, Action, clinical effect

A 
Vascular system (excitatory)
Action: Vasoconstriction 
Clinical effect: increase BP
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26
Q

Beta1

Area, Action, clinical effect

A

– Heart (and small intestine)
Action: Increased heart rate and force of contraction
Clinical effect: increase heart rate

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27
Q

Beta2

Area, Action, clinical effect

A

– Vascular, pulmonary systems (inhibitory)
Action: Vasodilation in skeletal muscle
Clinical effect: Decrease BP

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28
Q

Alpha 2

Only action

A

Action: Inhibits release of norepinephrine

(presynaptic feedback inhibition)

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29
Q

Why do we use a vasoconstrictor?

3 reasons

A
  • Improve local retention of anesthetic
    - enhance local anesthetic effect
    - prolong duration
  • Provide local hemostasis for surgery
  • (Reduce systemic toxicity)
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30
Q

Effects of vasoconstrictor on Heart

A

Heart - increase contractility, rate, output

BUT net decrease in efficiency

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31
Q

If you take vasoconstrictor with:

Alpha blockers

A

Alpha1 - Blocked
B1 - Increased Heart Rate
B2 - Decreased Blood Pressure

Effect: Hypotension and Tachycardia

32
Q 
If you take vasoconstrictor with:
Beta blockers (NON-SELECTIVE)
A

Alpha1 – Increased Blood Pressure
B1 – Blocked
B2 – Blocked

Effect: Hypertension & Bradycardia

33
Q 
If you take vasoconstrictor with:
Beta blockers (SELECTIVE)
A

Alpha1 – Increased Blood Pressure
B1 – Blocked
B2 – Decreased BP

Effect: None

34
Q

If you take vasoconstrictor with:

Tricyclic Antidepressants

A

Block reuptake of norepinephrine & epinephrine

Exogenous epinephrine may produce exaggerated effects

35
Q

If you take vasoconstrictor with:

MAO inhibitor

A

Inhibit monoamine oxidase

But epinephrine is also metabolized by COMT

36
Q

If you take VC with:

d-Amphetamine

A

Stimulates CNS adrenergic system

May be potentiated by epinephrine

37
Q

Cocaine and Vasoconstrictors

A 
Stimulates NE release
Inhibits NE reuptake
Causes tachycardia, hypertension
Increased cardiac oxygen demand
Decreased efficiency
Leads to dysrhythmias, ischemia
Sensitizes patient to epinephrine!
Defer elective dental care 24 hours
38
Q

What is “Special Care?”

A
  1. stress reduction
  2. limit epinephrine use
  3. limited treatment
39
Q

How to treat people with Stable vs Unstable Angina:

A

Stable: cautious with stress and epinephrine
Unstable: monitored setting

40
Q

How to treat people with Myocardial Infarction:

  1. recent
  2. 6 months ago
A
  1. recent: cautious with stress and epinephrine
  2. 6 months ago (6-8 weeks in recent studies):
    controlled: low risk
    uncontrolled: cautious with stress and epi
41
Q

How to treat people with Coronary Artery Bypass Surgery

  1. Recent
  2. > 3 months ago
A

Recent: caution with stress, epinephrine

More than 3 months ago: Variable, similar to MI

42
Q

How to treat people with Arrthymia

A

SUPER DIFFICULT TO ASSESS: Need PCP/Cardiologist consultation

  1. Controlled: caution with epinephrine
  2. Refractory/Uncontrolled: treat in monitored setting
43
Q

How to treat people with hypertension:

  1. controlled
  2. uncontrollable
A
  1. Controlled:
    Consider drug interactions, monitor pressure
    may need to reduce epinephrine use
  2. Severe, untreated, uncontrollable
    limit epinephrine use
    consider monitored setting
44
Q

How to treat people with Congestive Heart Failure

  1. controlled
  2. uncontrolled
A
  1. Controlled
    Low risk
  2. Uncontrolled, untreated
    stress, time in chair are major issues
45
Q

How to treat people with strokes

A
  1. variable presentation
    May be low risk; watch BP

2.Variable risk for recurrence
monitor pressure
may need to reduce epinephrine

46
Q

How to treat people with diabetes

  1. controlled
  2. uncontrolled
A

controlled: you’re good
uncontrolled: monitor for other diseases

47
Q

How to treat people with hyperthyroidism

  1. controlled
  2. uncontrolled
A 
Controlled:
      no problem
Uncontrolled Hyperthyroidism:
       Recognize (see text), defer treatment
       avoid stress, epinephrine
48
Q

Pheochromocytoma

A

rare tumor in medulla of adrenal gland that secretes cathecholamines and such: defer treatment, avoid stress and epinephrine

49
Q

How to treat people with Coagulopathy

A

congenital or acquired

alter technique to avoid deep blocks

50
Q

How to treat people with Methemoglobinemia:

no oxyhemoglobin cuz Fe3+ instead of Fe2+

A

avoid prilocaine

lidocaine may be a trigger but is lowest risk anesthetic

51
Q

How to treat people with asthma:

A

no treatment necessary

52
Q

How to treat people with COPD (Chronic Obstructive Pulmonary Disease )

A

Time in chair may be issue

53
Q

How to treat people with liver disease:

A

unlikely to cause issue

54
Q

How to treat people with renal disease

A

Unlikely to be an issue unless they have dialysis in which case treat the day after

55
Q

How to treat people with pregnancy

A

limit care generally

local anesthetics are ok

56
Q

Conditions that beckon you use amide esters:

A

Malignant Hyperthermia
no problem with amide anesthetics
Atypical Plasma Pseudocholinesterase
delayed metabolism of esters
amide anesthetics are not a problem

57
Q

Issues with tricyclic antidepressants or MAO inhibitors?

A

No just monitor blood pressure

58
Q

Issues with Beta Blockers

A

selective:
little concern

nonselective:
monitor pressure with epinephrine use

59
Q 
Possible allergies to local anesthetics :
1. Amide
2. Esters 
Preservatives/stabilizing agents
3. Parabens 
4. Sulfites
A

Amide – very rare but possible
Esters – possible, but we aren’t injecting them any more

Preservatives/stabilizing agents
Parabens – we don’t use
Sulfites – possible (in epi.-containing anesthetics)

60
Q

ADA criteria for dental Syringe (FOUR)

A

1- Should provide effective aspiration
2- Durable and withstand repeated sterilization
3- Inexpensive, light weight and simple to use
4- permit the use of wide variety of cartilages and needles of different manufacturers

61
Q

1- Infiltration

A

1- Infiltration - local area where treatment will be

62
Q

2- Field block

A

2- Field block - Local anesthetic is deposited toward larger nerve terminal branches
Treatment is done away from the site of local anesthetic injection
Maxillary injections administered above the apex of the tooth to be treated are properly referred to as field blocks not local infiltrations

63
Q
  1. nerve block
A

3- Nerve block -Local anesthetic is deposited close to a main nerve trunk, usually at a site removed from the area of treatment (PSA, IANB, NPB)

64
Q

A nerve fibers

A 
A: Large, myelinated
alpha (Aα), beta (Aβ), gamma (Aγ)
          motor, proprioception
delta (A)
          sensory
65
Q

B and C nerve fibers

A

B: Preganglionic autonomic (otherwise like A)
C: Small, unmyelinated
sensory, postganglionic autonomic

66
Q

Sodium channel (how to activate and gates)

A

Gating
activation (m) gate
inactivation (h) gate

Initial depolarization opens activation gate
Rapid depolarization closes inactivation gate

67
Q

Refractory Period of Na+ Channel

A

Channel must “reset” before reopening

determined by the time needed for the axon to repolarize

68
Q

What is responsible for repolarization of axons?

A

Na+ channel inactivation is responsible for repolarization

69
Q

Do K+ channels play a large role in conduction along axon?

A

K+ channels in between nodes play a very small role in conduction but is more important in unmyelinated

70
Q

Where are Na+channels concentrated?

A

at nodes of Ranvier

71
Q

Specific Receptor Theory

A

anesthetic agent receptor in channel
accessed from intracellular side
charged agents not effective unless nerve is stimulated (=phasic block)
uncharged agents not stimulation dependent

72
Q

Membrane Interaction Theory

A

agent molecules associate with hydrophobic membrane
membrane is “disordered”
channel conformational changes are prevented

73
Q

Anesthetic structure:

A

Aromatic (hydrophobic) group
Intermediate chain (ester or amide)
Amino (hydrophilic) group

74
Q

Organic:Aqueous Distribution Constant: Q

A

reflects ability to penetrate hydrophobic tissue

correlates with duration (protein binding?)

75
Q

Dissociation Constant: pKa

A

Proportion of ionized to un-ionized molecules

correlates with onset

76
Q

In order of last to go and first to come back:

Sensations of anesthetics

A 
dull pain
warmth
cold
sharp pain
 touch
pressure
proprioception

Local Anesthesia (1 decks)

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