Lecture 1 Flashcards
1
Q
5th vital sign:
A
pain
2
Q
What creates pain?
A
noxious stimulus
3
Q
2 components of pain:
A
perception, reaction
4
Q
What component of pain is the same bw people:
A
perception
5
Q
La will not work in this case:
A
hot tooth
6
Q
4 ways to stop pain pw:
A
initiation, propagation, integration, stimulation of descending inhibitory pw
7
Q
How does la intercede in pain pw?
A
prevent propagation
8
Q
poorly myelinated fibers, diffuse pain, la will interact well with:
A
C
9
Q
fibers for sharp pai, huge myelinated nerves, more difficult to anesth with la
A
A beta, a delta
10
Q
LA must cross:
A
he ct, epinerum, perinerum, endoneureum, middle of nerve bundle:
11
Q
Fraction of mandibular blocks that will not be effective even when good, due to alterations in pt anatomy
A
1/5
12
Q
anelgesics and narcotics intercede in the part of the pain pw:
A
Integration: still sense pain (not as much), you just don’t care, brain nad s.c.
13
Q
drug for stimulation of the descending pain inhibitory pw:
A
serotonin, increase cns serotonin levels to decrease pain
14
Q
A-delta/ beta fibers:
A
fast, sensitive to mechanical stimuli, small, myelinated, high conductance speed, acute, sharp, well localized pain
15
Q
c fibers:
A
slow, sensitive to many stimuli, small, unmyelinated, slow conductance speed, dull, achy, poorly localized
16
Q
What explains the phenomenon of double pain?
A
2 sets of pain fibers: a-delta and C
17
Q
Which type of pain fibers do we want to knock out?
A
All 3: A-d, A-beta and C
18
Q
Most heavily myelinated nerves:
A
Motor nerves
19
Q
Pain travels up via:
A
spinothalamic track (anterior/ ventral and lateral)
20
Q
Anterior/ ventral spinothalamic track:
A
immediate warning of the presence, location, and intensity of an injury
21
Q
Lateral spinothalamic track:
A
slow, aching reminder that tissue damage has occured
22
Q
Where do the lateral and anterior/ ventral spinothalamic tracks decusate?
A
level of sc
23
Q
Pain ends here in the brain:
A
Somatosensory cortex
24
Q
Responsible for affective sensation:
A
descending pathways
25
Ex of affective sensation:
compulsion to act
26
anelgesia:
pain relief
27
Ways to produce local pain:
Mechanical trauma, low temperature, low O2, chemical irritants, neurolytic agents, chemical agents
28
Ex's of neurolytic agents:
alcohol, phenol (inject alcohol so it can no longer transmit)
29
Ex's of chemical agents:
local ensthestics
30
Only la with intrinsic vasoc props:
cocaine
31
Koller first use cocaine to:
anesthetize the cornea
32
Benefit of the vasoc properties of cocaine:
absorption, duration, absorption rate, decrease chance of systemic serum levels, diffusion
33
First synthesized local anesthetic:
procaine
34
What type of anesthetic is procaine?
ester anesthetic
35
First non-ester type la used in dentistry:
lidocaine (amide)
36
What type of anesthetic is lidocaine:
amide
37
Lidocaine is aka:
xylocaine
38
3 parts of la:
aromatic ring, amine group, ester or amide linkage
39
La's with ester linkages (5):
cocaine, procaine, tetracaine,2-chlorprocaine, benzocaine
40
La's with amide linkages:
mepivicaine, lidocaine, prilocaine, bupivacaine, etidocaine, ropivacaine
41
What determines the classifiaction of La?
linkage
42
lipophilic portion of La's:
aromatic ring
43
hydrophilic portion of La's:
3'/ 4' amine
44
We need to the hydrophilic end to:
diffuse through interstitial tissue
45
We need the hydrophobic end to:
pass through myelin and L.B.
46
Properties of an ideal anesthetic:
Reversible, non-irritating, low systemic toxicity, rapid onset, required duration, high potency, absorb through skin/mucosa for topical use, free from allergic reactions, stable in solution, readily metabolized, sterile or capable of being sterilized
47
TF? Some LA’s permanently interfere with the ability of a nerve to produce an AP.
T
48
Ion channels that Ap's depend upone:
Na, K, Cl, Ca
49
Ion channel that la's primarily work on:
Na
50
States of the Na channel that la's work on:
resting, open, inactivated
51
Which are open for a longer duration, Na channels or K channels?
K
52
Chemicals that inhibit Na channels besides La:
Toxins, CCBA's, Alpha-2 adrenergic agents, meperdine, volatile anesthetics
53
la's are classified based on:
How strong they are (potency), how long they work, how fast they work, what they block
54
Potency of La tends to increase with:
increasing molecular size
55
Potency is directly proportional to:
lipid solubility
56
Duration of action is related to:
lipid solubility
57
Higher lipid solubility,
longer lasting effects
58
Duration of action is indirectly related to:
protein-binding
59
Speed of onset is inversely related to:
pKa (ionization constant) and lipid solubility
60
Only form of La that can interact w membrane:
non-ionized, uncharged form
61
Highly lipid soluble La:
etidocaine
62
La with a high pKa:
chlorprocaine
63
Rate of onset is controlled by:
aqueous diffusion
64
How fast LA works is inversely related to:
molecular size
65
Two local anesthetics that are “relatively” selective for sensory blockade:
bupivicaine, ropivacaine
66
Additional factors that affect la activity:
Dosage, site of administration, additives (same as preservatives?) - vasoconstrictor, temperature, pregnancy
67
Properties of all la's:
synthetic (weak B, strong A), tertiary amino groups, form salts with strong acids, salts are water soluble, weak alkaloid base is soluble in lipids, reversible, compatible with vasoc's, incompatible with metal salts, little to no direct irritating affects on tissue, similar systemic toxic effect, all metabolized in the body
68
3 moa of La:
receptor binding, membrane swelling, channel blockade
69
Salts fo weak base w strong acid:
stable, soluble in water, the farther the pH from the pKa, the more water soluble and less lipid soluble
70
La is present in these 2 forms in the tissues:
ionized and un-ionized (same as associated/ dis?)
71
More of the ionized form will be present if:
higher pKa of La or lower pH of body
72
higher pKa or lower pH are good for this and bad for this:
water solubility, anesthesia
73
Required to produce a nerve blockade:
free, uncharged base, diffuse into nerve, bind receptor
74
Effectiveness of a local anesthetic depend on:
Chemical structure, concentration, rate of diffusion of the salt and free base, vasoconstrictors, anatomy of nerve
75
Toxic effects of local anesthetics:
Mutagenicity, carcinogenicity, fetotoxicity, effect on geriatric/pediatric populations, A, D, M, E, Drug interactions, adverse reactions
76
Is absorption a factor in La?
not really
77
Proteins that La bind:
alpha 1 acid glycoprotein, albumin
78
What does protein binding effect?
duration of action
79
Distribution is dependent upon:
direct application, dose, vasculature, vasoconstrictor
80
Effect of metabolism on la:
convert lipid soluble agents to water soluble agents for excretion by the kidneys
81
These are involved in ester hydrolysis of la's:
cholinesterases
82
This is responsible for allergic reactions in ester hydrolysis:
PABA
83
How are amide La's metabolized?
liver
84
Liver enzymes for la metabolism:
cytochrome P450 system
85
Toxic by-products metabolism of La's can produce:
O-toluidine and methemoglobinemia
86
Clearance of amide LA’s depends on (3):
Hepatic blood flow and extraction, cytochrome P450 enzyme system function
87
Factors/drugs that can reduce hepatic blood flow:
Beta adrenergic blocking agents, Histamine-2 blocking agents, Heart failure, Liver failure
88
What can increase the chance of LA toxicity?
reduced blood flow to the liver
89
Toxic effects of LA's:
CNS, Cardiovascular, allergic (usually to the preservative, right?), direct neurotoxic
90
What type of response is there to LA?
biphasic, CNS stimulation/ depression, seizures/ respiratory depression or arrest
91
Seizure generating ability of LA is directly related to:
potency
92
Factors that would make a person have seizures at a lower dose:
elevated CO2 levels (COPD), Acidosis (from aspirin use)
93
Which requires higher doses to produce, seizures ro CV depression?
CV depression, 3X more
94
There is a higher incidence of CV depression with this LA:
bupivicaine (one of the 2 sensory specific)
95
How do La's depress the CV system:
bind and inhibit myocardial Na channels
96
Which isomer binds to myocardial Na channels more strongly?
right handed
97
Left-handed La's:
levobupivacaine (is this sensory specific?) and ropivacaine (one of two sensory specific)
98
Are true allergic reactions to LA common?
no
99
Anaphylaxis related to LA:
IgE mediated anaphylaxis to esters or amides (allergy to preservative)
100
How to test for allergic reactions to LA:
skin testing
101
Tx for minor allergic reaction:
nothing
102
Tx for non-minor allergic reactions:
Benadryl, epi, steroids
103
Benadrly is aka:
diphenhydramine
104
Injection techniques:
Standard mandibular block, Gow-gates and akinosi
105
Standard mandibular block:
Jorgensen modification of Halsted tech, aim for w/in 1mm of target, 80% success
106
Landmarks for Stan Man block:
coronoid notch, pterygomandibular raphe, occlusal plane posteriorly, premolar dentition
107
how to give a stan man block:
Aim for lingula, midpoint of medial surface of ramus in both A-P and S-I directions, 2/3 - 3/4 of needle, may hit bone, may not
108
Why might the stan man block not work?
Lingula not in the middle, nerve branching variation
109
How to increase the success rate of the stan man block:
aim high (cephalad), Gow-Gates Technique
110
Gow-Gates Technique provides sensory anesthesia to:
entire man division of CN V
111
Advantages of Gow-Gates Technique:
Higher success rate, lower rate of positive aspiration, anesthetizes (7) inferior alveolar, lingual, mylohyoid, mental, incisive, auriculotemporal, buccal nerves – only one injection
112
Name all nerves anesthetized with Gow-Gates Technique
nferior alveolar, lingual, mylohyoid, mental, incisive, auriculotemporal, buccal nerves – only one injection
113
When to not use Gow-Gates Technique:
Patient can't open wide, must open 50-55mm
114
Pt positioning for Gow-Gates Technique:
reclines, supine position
115
Why is there a higher success rate with the Gow-Gates Technique?
uses extraoral landmarks as well, commisure of lip, tragus/intertragic notch
116
Explain Gow-Gates Technique:
inject lateral to raphe but medial to temporalis tendon from opposite commissure, along visualize commissure-intertragus line and parallel with angulation of ear to face, go until bone/ condyle, about 25mm, deposit after negative aspiration or "walk" the needle toward the medial
117
Closed mouth technique:
Akinosi Technique
118
Primary indication to use the Akinosi technique:
pts with trismus
119
Explain Akinosi technique:
buccal mucogingival junction of the maxillary second/third molar, intraoral reference: coronoid notch, teeth in occlusion, syringe parallel with maxillary occlusal plane
120
three operative factors:
Avoid (issue), recognize, manage (if it occurs)
121
This is when action taken is not action intended:
Technical error, ie intra-vascular administration
122
Are system errors common with LA?
no
123
Anesthesai complications: Recognition:
NETCC: Necessary, efficacy, toxicity, compliance, cost (?)
124
What to check when monitoring and managing anesthesia complications:
ABC's, BP, P, RR, OMI/ MONA
125
CN V originates from these three sensory nuclei in the midbrain:
Mesencephalic, principle sensory nucleus, spinal nucleus
126
What merge to form the sensory root?
sensory nuclei
127
Where do the sensory nuclei merge to form the sensory root?
pons
128
What forms the motor route?
motor nucleus
129
The trigeminal ganglion is in this fossa:
middle cranial fossa
130
The trigeminal ganglion is adjacent to:
cavernous sinus
131
The trigeminal ganglion is aka:
Gasserian ganglioin
132
Trigeminal ganglion is at the level of the:
pons
133
In which portion of the brainstem is the mesencephalic nuceus?
midbrain (m-m)
134
In which portion of the brainstem is the Principle sensory nucleus?
Pons (p-p)
135
In which portion of the brainstem is the spinal nucleus?
medulla
136
The opthamlic division exits via the:
superior orbital fissure
137
Terminal branches of the opthalmic dividision:
Frontal, lacrimal, and nasociliary
138
Besides the main three terminal brances, what else does the opthalimic division carry?
Also carries postganglionic parasympathetic fibers from the pterygopalatine ganglion (via facial nerve) which initially travel with the zygomatic branch of the maxillary division then join the lacrimal branch of the ophthalmic division
139
Which branch of the opthalmic division carries parasympathetic fibers?
lacrimal
140
What does the opthalmic division innervate?
skin and mucous membrane derivatives of the frontonasal process: Forehead and scalp, Frontal and ethmoid sinuses, Upper eyelid and conjunctiva, Cornea, Dorsum of nose
141
Maxillary division of the trigeminal nerve exits the skull via:
the foramen rotundum
142
How many branches does the maxillary division give rise to?
14
143
Maxillary division innervates:
the skin, mucous membranes and sinuses that are derived from the maxillary prominence of the first pharyngeal arch
144
Does the maxillary branch carry parasympathetic?
Yes, to the lacrimal and the nasal glands
145
7 of the 14 maxillary branches that we care about:
Anterior superior alveolar nerve, middle superior alveolar nerve, posterior superior alveolar nerve, infraorbital nerve, nasopalatine nerve, greater palatine nerve, lesser palatine nerve(s)
146
Sensory branches of V3 innervate:
skin, mucous membranes and striated muscle derivatives of the mandibular prominence of the first pharyngeal arch Mucous membranes and floor of the oral cavity, external ear, lower lip, chin, anterior 2/3 of the tongue with special taste sensation from the chorda tympani branch from the facial nerve, all lower teeth, gingiva and bone
147
4 terminal branches of V3:
Buccal, Inferior alveolar (mental nerve/incisive nerve extensions), Auriculotemporal, Lingual
148
How many muscles does V3 supply motor innervation to? and name:
8: Muscles of mastication (masseter, temporalis, Internal/medial pterygoid, external/lateral pterygoid), anterior belly of the digastric, mylohyoid, tensor veli palatini, tensor tympani
149
What innervation does the mylohyoid often carry?
accessory sensory innervation to mandible
150
Does the mandibular branch carry parasympathetic?
Yes, supply to the salivary glands – sublingual, submandibular, parotid
151
Infraobital block:
MaxRCI to MR2P and the MB aspect of MR1M, including the lip in that area
152
Anterior superior alveolar block:
MaxLCI to the MaxLC and the lip area
153
Middle superior alveolar block:
MaxL1P and MaxL2P, the MB aspect of the MaxL1M AND the lip of that area
154
Posterior superior alveolar block:
The Max L molars except the MB aspect of the Max1M and the surrounding gingiva
155
Nasopalatine block:
Hard palate region from canine to canine, comes to a point on the hard palate
156
Greater palatine block:
MaxL hard palate from Max1P and posterior
157
inferior alveolar block:
All man R teeth, right half of tongue, lips from the D aspect of the 2nd premolar to the midline
158
Incisive block:
ManLCI to the Man2P and the lip in that region
159
Buccal block:
The gingiva and lip adjacent to the mandibular molars
160
What does the anterior superior alveolar nerve supply?
pulp & investing structures & labial mucoperiosteum of anterior teeth
161
What does the middle superior alveolar nerve supply?
The pulp & investing structures & buccal mucoperiosteum of mromoplars and MB root of 1st molar
162
What does the greater palatine nerve supply?
palatal mucoperiosteum of maxillary molars and premolars
163
What does the nasopalatine nerve supply?
palatal mucoperiosteum of maxillary anterior teeth
164
Which is more anterior on the lateral side of the ramus, the inferior alveolar nerve or artery?
nerve
165
You want the needle to be bw these structures:
medial surface of the ramus and medial pterygoid muscle/ lingual nerve
166
Injection point in the mucosa:
pterygomandibular raphe
167
How can local anesthetics interfere with the excitation process?
Alter the resting membrane potential, alter the threshold potential, decrease the rate of depolarization, prolong the rate of repolarization
168
80-58% of LA work in this manner:
Interfering with depolarization, decrease rate of polarization, let it leak in slowly
169
Which LA's alter the threshold potential?
none
170
Which LA's arrest the membrane potential?
none
171
Does LA prevent Na from entering or leaving the cell?
entering
172
Which ion does LA not really affect?
chloride
173
Where is the specific Na channel receptor that LA reacts with?
either outer or inner cell membrane surface
174
Primary mechanism of action of LA:
via specific receptor binding at the Na channel, decreasing permeability of Na channel, slight decrease in K conductance (insignificant)
175
Where does venom interact with the cell?
inside of cell membrane
176
Do most LA's react with the outer or inner membrane?
outer
177
Typical anesthetics react with specific receptor sites here:
within the channel itself
178
Snake venom react with specific receptor sites here:
outer surface of the channel
179
Scorpion venoms react with specific receptor sites here:
the fast or slow sodium gates
180
Class A:
receptor on external surface of membrane
181
Class B:
receptor on internal surface of membrane (not clinically usable, venoms)
182
Class C:
receptor independent
183
Class D:
combination of receptor dependent and independent mechanisms
184
Topical anesthetic is what class anesthetic?
3
185
Recommended injection rate for anesthetic:
1mL per minute
186
Why is it painful for pt if you inject quickly?
Rippinng interstitial tissue
187
Class C drugs exist only in this form:
uncharged dissociated form
188
Ex of Class C drug:
benzocaine
189
Class D drugs exist in this form:
both charged, undissociated form and the uncharged dissociated form
190
Most acitivity of Class D drugs is due to:
uncharged form and 10% is due to the charged form
| RNH+ or RN
191
Which form of LA has the most effect?
Uncharged dissociated form (check) (due to pH the charged form is what has the efffect?)
192
TF? The moa is dependent onthe nerve fiber itself.
T
193
Where does LA interact with my nn.?
Na channels in the nodes
194
TF? Na channels are only found at the nodes of Ranvier.
F. mainly found there
195
All LA's are toward this end of the pH scale:
basic end (7.6-8.0)
196
Is the body's pH higher or lower than LA?
lower, more acidic
197
We need to silence about this many nodes in order to stop the AP:
6-12 (1 cm or more of distance) at LEAST 3 adjacent nodes, can be up to 8-10mm
198
If you inject LA 1 cm away from the intended target will it work?
no, not enough to get the desired effect
199
Small, unmyelinated nerves have about __ sodium channels per square micrometer.
35
200
Nodes of Ranvier may contain sodium channels per square micrometer.
20,000
201
Why won't the AP be stopped if you block only one node?
saltatory conduction
202
Which has more nodes, a small unmy n. or or node or ranvier?
node
203
TF? The goal in anesthesia is to block the transmission of all nerve fibers.
F. This will never happen
204
Even if pain is blocked a pt may still experience these senses:
proprioception, sense of direction
205
What effect is calcium bound in the membrane thought to exert?
regulatory effect on movement of sodium ions across membrane
206
Proposed mech of LA:
LA displaces Ca rom Na channel (competitive antagonism), LA then binds receptor, blocking it (conduction blockade)
207
Whether the A is short or long duration depends on:
it's structure
208
Short acting LA's last:
30 min
209
Lidocaine without vasoconstrictor will only give pulpal A for:
5min
210
Lidocaine with vasoconstrictor will give pulpal A for:
1.5-2hours
211
TF? The rate of LA metabolism is altered with the addition of vasoconstrictor.
T
212
Where are amide A's metabolized?
liver
213
If a pt has liver disease what LA should you not gibe?
any amide
214
Hw are ester LA's metabolized?
enzyme in blood, pseudocholinesterase in serum, ester is metabolized by esterase, Some ppl have hereditary issues with esterases. Know MxHistory
215
A LA will be less lipid soluble if:
the pH is fa from the pKa (more ionized, more water soluble)
216
90% of molecuels of LA are in this form:
undis charged form, highly water soluble, poorly lipid soluble (other 10% can't get to n.)
217
Would infection drive the equation to the charged or uncharged side?
uncharged (highly water soluble)
218
pH of infected tissue:
4-5 (check)
219
2 competing factors of LA:
diffusibility and binding
220
Which factor of LA is more important clinically, diffusibility or binding
difusibiity
221
LA with pKa of 7.9 will have this % water and lipid soluble:
75% water, 25% lipid
222
What happens as a local anesthetic diffuses into a nerve?
increasingly diluted by tissue fluids and absorption, tissue/protein binding
223
nerve blockade:
free, uncharged base must interact with the nerve membrane, diffuse into and bind receptor site
224
3 factors that decrease effectivity as the LA diffuses
Decease volume, decreased concentration, protein binding
225
Related to intrinsic potency of LA:
Lipid solubility
226
LA with low lipid solubility, La with high lipid solubility:
Procaine = 1, etidocaine = 140
227
This is related to the duration of action of LA:
protein binding
228
TF? Increased protein binding to receptor = decreased duratio
F. increased
229
factors that influence the clinical effectiveness of LA:
Chem struct, diffusibility, vasoc, conc, anatomy of n., location of n.
230
Will mepevocaine be present more in the assoc or disocciated form?
dis
231
Lipid solubility theoretically leads to:
more rapid onset of action, longer duration, slower recovery
232
What differs bw each LA?
carrier protein molecules
233
All LA's bind this:
albumin
234
TF? The more LA binds to protein, the better,
T
235
TF? Most LA's have intrinsic vasodilating abilities.
T. except coke
236
Moderate duration anesthetic lasts:
up to 3 hours
237
Long lasting anesthetic lasts:
up to 12 hours
238
Why is recovery slower than the onset of action?
because LA is bound to receptor and is released more slowly than it is bound
239
Posterior sup alveolar artery, thin or thick fibers?
very thin, to upper premolar
240
Sequence of sense loss with anesthesia:
Pain and temp lost at same time, then touch/ prop, then motor
241
If prop sensors are still there they will feel:
pressure and vibrations
242
in what order do you gain sense back as anesthesia wears off?
reverse
243
What to do if you accidentally anesthetize CN 7:
nothing, it will come back in minutes
244
physiologic effects of local anesthesia are dependent on :
concentration
245
Amt of fluid in each carpule:
1.7ml
246
3 components in each carpule:
LA, vasoc, preservative
247
When is a preservative needed?
if there is vasoc
248
1% solution =
1gm in 100 ml, 1000 mg in 100 ml, 00 mg in 10 ml, 10 mg in 1ml
249
1.7 ml of a 1% solution =
17 mg
250
1.7 ml of a 2% solution =
34mg
251
1.7 ml of a 3% solution =
51 mg
252
How is LA conc reported?
weight/volume molar solution
253
How is vasoc concentration reported?
fraction in weight/volume
254
In one 1.7 ml carpule how much epinephrine is injected if everything is delivered?
0.017 mg of
255
In very ml of 2% lidocaine with .. Epi there will be __mg of lido in every ML of the injection and __ mg of epi in every ml of the injection
20, 0.01
256
Be aware of this with a patient that has COPD:
Increased likelihood of seizure at lower dose of LA
