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Local Anesthesia > Exam 1 > Flashcards

Exam 1 Flashcards

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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
alpha1 receptor | Area, Action, clinical effect
``` Vascular system (excitatory) Action: Vasoconstriction Clinical effect: increase BP ```
26
Beta1 | Area, Action, clinical effect
– Heart (and small intestine) Action: Increased heart rate and force of contraction Clinical effect: increase heart rate
27
Beta2 | Area, Action, clinical effect
– Vascular, pulmonary systems (inhibitory) Action: Vasodilation in skeletal muscle Clinical effect: Decrease BP
28
Alpha 2 | Only action
Action: Inhibits release of norepinephrine | (presynaptic feedback inhibition)
29
Why do we use a vasoconstrictor? | 3 reasons
- Improve local retention of anesthetic - enhance local anesthetic effect - prolong duration - Provide local hemostasis for surgery - (Reduce systemic toxicity)
30
Effects of vasoconstrictor on Heart
Heart - increase contractility, rate, output | BUT net decrease in efficiency
31
If you take vasoconstrictor with: | Alpha blockers
Alpha1 - Blocked B1 - Increased Heart Rate B2 - Decreased Blood Pressure Effect: Hypotension and Tachycardia
32
``` If you take vasoconstrictor with: Beta blockers (NON-SELECTIVE) ```
Alpha1 – Increased Blood Pressure B1 – Blocked B2 – Blocked Effect: Hypertension & Bradycardia
33
``` If you take vasoconstrictor with: Beta blockers (SELECTIVE) ```
Alpha1 – Increased Blood Pressure B1 – Blocked B2 – Decreased BP Effect: None
34
If you take vasoconstrictor with: | Tricyclic Antidepressants
Block reuptake of norepinephrine & epinephrine | Exogenous epinephrine may produce exaggerated effects
35
If you take vasoconstrictor with: | MAO inhibitor
Inhibit monoamine oxidase | But epinephrine is also metabolized by COMT
36
If you take VC with: | d-Amphetamine
Stimulates CNS adrenergic system | May be potentiated by epinephrine
37
Cocaine and Vasoconstrictors
``` 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
What is “Special Care?”
1. stress reduction 2. limit epinephrine use 3. limited treatment
39
How to treat people with Stable vs Unstable Angina:
Stable: cautious with stress and epinephrine Unstable: monitored setting
40
How to treat people with Myocardial Infarction: 1. recent 2. 6 months ago
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
How to treat people with Coronary Artery Bypass Surgery 1. Recent 2. >3 months ago
Recent: caution with stress, epinephrine | More than 3 months ago: Variable, similar to MI
42
How to treat people with Arrthymia
SUPER DIFFICULT TO ASSESS: Need PCP/Cardiologist consultation 1. Controlled: caution with epinephrine 2. Refractory/Uncontrolled: treat in monitored setting
43
How to treat people with hypertension: 1. controlled 2. uncontrollable
1. Controlled: Consider drug interactions, monitor pressure may need to reduce epinephrine use 2. Severe, untreated, uncontrollable limit epinephrine use consider monitored setting
44
How to treat people with Congestive Heart Failure 1. controlled 2. uncontrolled
1. Controlled Low risk 2. Uncontrolled, untreated stress, time in chair are major issues
45
How to treat people with strokes
1. variable presentation May be low risk; watch BP 2.Variable risk for recurrence monitor pressure may need to reduce epinephrine
46
How to treat people with diabetes 1. controlled 2. uncontrolled
controlled: you're good uncontrolled: monitor for other diseases
47
How to treat people with hyperthyroidism 1. controlled 2. uncontrolled
``` Controlled: no problem Uncontrolled Hyperthyroidism: Recognize (see text), defer treatment avoid stress, epinephrine ```
48
Pheochromocytoma
rare tumor in medulla of adrenal gland that secretes cathecholamines and such: defer treatment, avoid stress and epinephrine
49
How to treat people with Coagulopathy
congenital or acquired | alter technique to avoid deep blocks
50
How to treat people with Methemoglobinemia: | no oxyhemoglobin cuz Fe3+ instead of Fe2+
avoid prilocaine | lidocaine may be a trigger but is lowest risk anesthetic
51
How to treat people with asthma:
no treatment necessary
52
How to treat people with COPD (Chronic Obstructive Pulmonary Disease )
Time in chair may be issue
53
How to treat people with liver disease:
unlikely to cause issue
54
How to treat people with renal disease
Unlikely to be an issue unless they have dialysis in which case treat the day after
55
How to treat people with pregnancy
limit care generally | local anesthetics are ok
56
Conditions that beckon you use amide esters:
Malignant Hyperthermia no problem with amide anesthetics Atypical Plasma Pseudocholinesterase delayed metabolism of esters amide anesthetics are not a problem
57
Issues with tricyclic antidepressants or MAO inhibitors?
No just monitor blood pressure
58
Issues with Beta Blockers
selective: little concern nonselective: monitor pressure with epinephrine use
59
``` Possible allergies to local anesthetics : 1. Amide 2. Esters Preservatives/stabilizing agents 3. Parabens 4. Sulfites ```
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
ADA criteria for dental Syringe (FOUR)
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
1- Infiltration
1- Infiltration - local area where treatment will be
62
2- Field block
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
3. nerve block
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
A nerve fibers
``` A: Large, myelinated alpha (Aα), beta (Aβ), gamma (Aγ) motor, proprioception delta (A) sensory ```
65
B and C nerve fibers
B: Preganglionic autonomic (otherwise like A) C: Small, unmyelinated sensory, postganglionic autonomic
66
Sodium channel (how to activate and gates)
Gating activation (m) gate inactivation (h) gate Initial depolarization opens activation gate Rapid depolarization closes inactivation gate
67
Refractory Period of Na+ Channel
Channel must “reset” before reopening | determined by the time needed for the axon to repolarize
68
What is responsible for repolarization of axons?
Na+ channel inactivation is responsible for repolarization
69
Do K+ channels play a large role in conduction along axon?
K+ channels in between nodes play a very small role in conduction but is more important in unmyelinated
70
Where are Na+channels concentrated?
at nodes of Ranvier
71
Specific Receptor Theory
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
Membrane Interaction Theory
agent molecules associate with hydrophobic membrane membrane is “disordered” channel conformational changes are prevented
73
Anesthetic structure:
Aromatic (hydrophobic) group Intermediate chain (ester or amide) Amino (hydrophilic) group
74
Organic:Aqueous Distribution Constant: Q
reflects ability to penetrate hydrophobic tissue | correlates with duration (protein binding?)
75
Dissociation Constant: pKa
Proportion of ionized to un-ionized molecules | correlates with onset
76
In order of last to go and first to come back: | Sensations of anesthetics
``` dull pain warmth cold sharp pain touch pressure proprioception ```

Local Anesthesia (1 decks)

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