Lecture 1 Flashcards
5th vital sign:
pain
What creates pain?
noxious stimulus
2 components of pain:
perception, reaction
What component of pain is the same bw people:
perception
La will not work in this case:
hot tooth
4 ways to stop pain pw:
initiation, propagation, integration, stimulation of descending inhibitory pw
How does la intercede in pain pw?
prevent propagation
poorly myelinated fibers, diffuse pain, la will interact well with:
C
fibers for sharp pai, huge myelinated nerves, more difficult to anesth with la
A beta, a delta
LA must cross:
he ct, epinerum, perinerum, endoneureum, middle of nerve bundle:
Fraction of mandibular blocks that will not be effective even when good, due to alterations in pt anatomy
1/5
anelgesics and narcotics intercede in the part of the pain pw:
Integration: still sense pain (not as much), you just don’t care, brain nad s.c.
drug for stimulation of the descending pain inhibitory pw:
serotonin, increase cns serotonin levels to decrease pain
A-delta/ beta fibers:
fast, sensitive to mechanical stimuli, small, myelinated, high conductance speed, acute, sharp, well localized pain
c fibers:
slow, sensitive to many stimuli, small, unmyelinated, slow conductance speed, dull, achy, poorly localized
What explains the phenomenon of double pain?
2 sets of pain fibers: a-delta and C
Which type of pain fibers do we want to knock out?
All 3: A-d, A-beta and C
Most heavily myelinated nerves:
Motor nerves
Pain travels up via:
spinothalamic track (anterior/ ventral and lateral)
Anterior/ ventral spinothalamic track:
immediate warning of the presence, location, and intensity of an injury
Lateral spinothalamic track:
slow, aching reminder that tissue damage has occured
Where do the lateral and anterior/ ventral spinothalamic tracks decusate?
level of sc
Pain ends here in the brain:
Somatosensory cortex
Responsible for affective sensation:
descending pathways
Ex of affective sensation:
compulsion to act
anelgesia:
pain relief
Ways to produce local pain:
Mechanical trauma, low temperature, low O2, chemical irritants, neurolytic agents, chemical agents
Ex’s of neurolytic agents:
alcohol, phenol (inject alcohol so it can no longer transmit)
Ex’s of chemical agents:
local ensthestics
Only la with intrinsic vasoc props:
cocaine
Koller first use cocaine to:
anesthetize the cornea
Benefit of the vasoc properties of cocaine:
absorption, duration, absorption rate, decrease chance of systemic serum levels, diffusion
First synthesized local anesthetic:
procaine
What type of anesthetic is procaine?
ester anesthetic
First non-ester type la used in dentistry:
lidocaine (amide)
What type of anesthetic is lidocaine:
amide
Lidocaine is aka:
xylocaine
3 parts of la:
aromatic ring, amine group, ester or amide linkage
La’s with ester linkages (5):
cocaine, procaine, tetracaine,2-chlorprocaine, benzocaine
La’s with amide linkages:
mepivicaine, lidocaine, prilocaine, bupivacaine, etidocaine, ropivacaine
What determines the classifiaction of La?
linkage
lipophilic portion of La’s:
aromatic ring
hydrophilic portion of La’s:
3’/ 4’ amine
We need to the hydrophilic end to:
diffuse through interstitial tissue
We need the hydrophobic end to:
pass through myelin and L.B.
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
TF? Some LA’s permanently interfere with the ability of a nerve to produce an AP.
T
Ion channels that Ap’s depend upone:
Na, K, Cl, Ca
Ion channel that la’s primarily work on:
Na
States of the Na channel that la’s work on:
resting, open, inactivated
Which are open for a longer duration, Na channels or K channels?
K
Chemicals that inhibit Na channels besides La:
Toxins, CCBA’s, Alpha-2 adrenergic agents, meperdine, volatile anesthetics
la’s are classified based on:
How strong they are (potency), how long they work, how fast they work, what they block
Potency of La tends to increase with:
increasing molecular size
Potency is directly proportional to:
lipid solubility
Duration of action is related to:
lipid solubility
Higher lipid solubility,
longer lasting effects
Duration of action is indirectly related to:
protein-binding
Speed of onset is inversely related to:
pKa (ionization constant) and lipid solubility
Only form of La that can interact w membrane:
non-ionized, uncharged form
Highly lipid soluble La:
etidocaine
La with a high pKa:
chlorprocaine
Rate of onset is controlled by:
aqueous diffusion
How fast LA works is inversely related to:
molecular size
Two local anesthetics that are “relatively” selective for sensory blockade:
bupivicaine, ropivacaine
Additional factors that affect la activity:
Dosage, site of administration, additives (same as preservatives?) - vasoconstrictor, temperature, pregnancy
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
3 moa of La:
receptor binding, membrane swelling, channel blockade
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
La is present in these 2 forms in the tissues:
ionized and un-ionized (same as associated/ dis?)
More of the ionized form will be present if:
higher pKa of La or lower pH of body
higher pKa or lower pH are good for this and bad for this:
water solubility, anesthesia
Required to produce a nerve blockade:
free, uncharged base, diffuse into nerve, bind receptor
Effectiveness of a local anesthetic depend on:
Chemical structure, concentration, rate of diffusion of the salt and free base, vasoconstrictors, anatomy of nerve
Toxic effects of local anesthetics:
Mutagenicity, carcinogenicity, fetotoxicity, effect on geriatric/pediatric populations, A, D, M, E, Drug interactions, adverse reactions
Is absorption a factor in La?
not really
Proteins that La bind:
alpha 1 acid glycoprotein, albumin
What does protein binding effect?
duration of action
Distribution is dependent upon:
direct application, dose, vasculature, vasoconstrictor
Effect of metabolism on la:
convert lipid soluble agents to water soluble agents for excretion by the kidneys
These are involved in ester hydrolysis of la’s:
cholinesterases
This is responsible for allergic reactions in ester hydrolysis:
PABA
How are amide La’s metabolized?
liver
Liver enzymes for la metabolism:
cytochrome P450 system
Toxic by-products metabolism of La’s can produce:
O-toluidine and methemoglobinemia
Clearance of amide LA’s depends on (3):
Hepatic blood flow and extraction, cytochrome P450 enzyme system function
Factors/drugs that can reduce hepatic blood flow:
Beta adrenergic blocking agents, Histamine-2 blocking agents, Heart failure, Liver failure
What can increase the chance of LA toxicity?
reduced blood flow to the liver
Toxic effects of LA’s:
CNS, Cardiovascular, allergic (usually to the preservative, right?), direct neurotoxic
What type of response is there to LA?
biphasic, CNS stimulation/ depression, seizures/ respiratory depression or arrest
Seizure generating ability of LA is directly related to:
potency
Factors that would make a person have seizures at a lower dose:
elevated CO2 levels (COPD), Acidosis (from aspirin use)
Which requires higher doses to produce, seizures ro CV depression?
CV depression, 3X more
There is a higher incidence of CV depression with this LA:
bupivicaine (one of the 2 sensory specific)
How do La’s depress the CV system:
bind and inhibit myocardial Na channels
Which isomer binds to myocardial Na channels more strongly?
right handed
Left-handed La’s:
levobupivacaine (is this sensory specific?) and ropivacaine (one of two sensory specific)
Are true allergic reactions to LA common?
no
Anaphylaxis related to LA:
IgE mediated anaphylaxis to esters or amides (allergy to preservative)
How to test for allergic reactions to LA:
skin testing
Tx for minor allergic reaction:
nothing
Tx for non-minor allergic reactions:
Benadryl, epi, steroids
Benadrly is aka:
diphenhydramine
Injection techniques:
Standard mandibular block, Gow-gates and akinosi
Standard mandibular block:
Jorgensen modification of Halsted tech, aim for w/in 1mm of target, 80% success
Landmarks for Stan Man block:
coronoid notch, pterygomandibular raphe, occlusal plane posteriorly, premolar dentition
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
Why might the stan man block not work?
Lingula not in the middle, nerve branching variation
How to increase the success rate of the stan man block:
aim high (cephalad), Gow-Gates Technique
Gow-Gates Technique provides sensory anesthesia to:
entire man division of CN V
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
Name all nerves anesthetized with Gow-Gates Technique
nferior alveolar, lingual, mylohyoid, mental, incisive, auriculotemporal, buccal nerves – only one injection
When to not use Gow-Gates Technique:
Patient can’t open wide, must open 50-55mm
Pt positioning for Gow-Gates Technique:
reclines, supine position
Why is there a higher success rate with the Gow-Gates Technique?
uses extraoral landmarks as well, commisure of lip, tragus/intertragic notch
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
Closed mouth technique:
Akinosi Technique
Primary indication to use the Akinosi technique:
pts with trismus
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
three operative factors:
Avoid (issue), recognize, manage (if it occurs)
This is when action taken is not action intended:
Technical error, ie intra-vascular administration
Are system errors common with LA?
no
Anesthesai complications: Recognition:
NETCC: Necessary, efficacy, toxicity, compliance, cost (?)
What to check when monitoring and managing anesthesia complications:
ABC’s, BP, P, RR, OMI/ MONA
CN V originates from these three sensory nuclei in the midbrain:
Mesencephalic, principle sensory nucleus, spinal nucleus
What merge to form the sensory root?
sensory nuclei
Where do the sensory nuclei merge to form the sensory root?
pons
What forms the motor route?
motor nucleus
The trigeminal ganglion is in this fossa:
middle cranial fossa
The trigeminal ganglion is adjacent to:
cavernous sinus
The trigeminal ganglion is aka:
Gasserian ganglioin
Trigeminal ganglion is at the level of the:
pons
In which portion of the brainstem is the mesencephalic nuceus?
midbrain (m-m)
In which portion of the brainstem is the Principle sensory nucleus?
Pons (p-p)
In which portion of the brainstem is the spinal nucleus?
medulla
The opthamlic division exits via the:
superior orbital fissure
Terminal branches of the opthalmic dividision:
Frontal, lacrimal, and nasociliary
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
Which branch of the opthalmic division carries parasympathetic fibers?
lacrimal
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
Maxillary division of the trigeminal nerve exits the skull via:
the foramen rotundum
How many branches does the maxillary division give rise to?
14
Maxillary division innervates:
the skin, mucous membranes and sinuses that are derived from the maxillary prominence of the first pharyngeal arch
Does the maxillary branch carry parasympathetic?
Yes, to the lacrimal and the nasal glands
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)
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
4 terminal branches of V3:
Buccal, Inferior alveolar (mental nerve/incisive nerve extensions), Auriculotemporal, Lingual
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
What innervation does the mylohyoid often carry?
accessory sensory innervation to mandible
Does the mandibular branch carry parasympathetic?
Yes, supply to the salivary glands – sublingual, submandibular, parotid
Infraobital block:
MaxRCI to MR2P and the MB aspect of MR1M, including the lip in that area
Anterior superior alveolar block:
MaxLCI to the MaxLC and the lip area
Middle superior alveolar block:
MaxL1P and MaxL2P, the MB aspect of the MaxL1M AND the lip of that area
Posterior superior alveolar block:
The Max L molars except the MB aspect of the Max1M and the surrounding gingiva
Nasopalatine block:
Hard palate region from canine to canine, comes to a point on the hard palate
Greater palatine block:
MaxL hard palate from Max1P and posterior
inferior alveolar block:
All man R teeth, right half of tongue, lips from the D aspect of the 2nd premolar to the midline
Incisive block:
ManLCI to the Man2P and the lip in that region
Buccal block:
The gingiva and lip adjacent to the mandibular molars
What does the anterior superior alveolar nerve supply?
pulp & investing structures & labial mucoperiosteum of anterior teeth
What does the middle superior alveolar nerve supply?
The pulp & investing structures & buccal mucoperiosteum of mromoplars and MB root of 1st molar
What does the greater palatine nerve supply?
palatal mucoperiosteum of maxillary molars and premolars
What does the nasopalatine nerve supply?
palatal mucoperiosteum of maxillary anterior teeth
Which is more anterior on the lateral side of the ramus, the inferior alveolar nerve or artery?
nerve
You want the needle to be bw these structures:
medial surface of the ramus and medial pterygoid muscle/ lingual nerve
Injection point in the mucosa:
pterygomandibular raphe
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
80-58% of LA work in this manner:
Interfering with depolarization, decrease rate of polarization, let it leak in slowly
Which LA’s alter the threshold potential?
none
Which LA’s arrest the membrane potential?
none
Does LA prevent Na from entering or leaving the cell?
entering
Which ion does LA not really affect?
chloride
Where is the specific Na channel receptor that LA reacts with?
either outer or inner cell membrane surface
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)
Where does venom interact with the cell?
inside of cell membrane
Do most LA’s react with the outer or inner membrane?
outer
Typical anesthetics react with specific receptor sites here:
within the channel itself
Snake venom react with specific receptor sites here:
outer surface of the channel
Scorpion venoms react with specific receptor sites here:
the fast or slow sodium gates
Class A:
receptor on external surface of membrane
Class B:
receptor on internal surface of membrane (not clinically usable, venoms)
Class C:
receptor independent
Class D:
combination of receptor dependent and independent mechanisms
Topical anesthetic is what class anesthetic?
3
Recommended injection rate for anesthetic:
1mL per minute
Why is it painful for pt if you inject quickly?
Rippinng interstitial tissue
Class C drugs exist only in this form:
uncharged dissociated form
Ex of Class C drug:
benzocaine
Class D drugs exist in this form:
both charged, undissociated form and the uncharged dissociated form
Most acitivity of Class D drugs is due to:
uncharged form and 10% is due to the charged form
RNH+ or RN
Which form of LA has the most effect?
Uncharged dissociated form (check) (due to pH the charged form is what has the efffect?)
TF? The moa is dependent onthe nerve fiber itself.
T
Where does LA interact with my nn.?
Na channels in the nodes
TF? Na channels are only found at the nodes of Ranvier.
F. mainly found there
All LA’s are toward this end of the pH scale:
basic end (7.6-8.0)
Is the body’s pH higher or lower than LA?
lower, more acidic
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
If you inject LA 1 cm away from the intended target will it work?
no, not enough to get the desired effect
Small, unmyelinated nerves have about __ sodium channels per square micrometer.
35
Nodes of Ranvier may contain sodium channels per square micrometer.
20,000
Why won’t the AP be stopped if you block only one node?
saltatory conduction
Which has more nodes, a small unmy n. or or node or ranvier?
node
TF? The goal in anesthesia is to block the transmission of all nerve fibers.
F. This will never happen
Even if pain is blocked a pt may still experience these senses:
proprioception, sense of direction
What effect is calcium bound in the membrane thought to exert?
regulatory effect on movement of sodium ions across membrane
Proposed mech of LA:
LA displaces Ca rom Na channel (competitive antagonism), LA then binds receptor, blocking it (conduction blockade)
Whether the A is short or long duration depends on:
it’s structure
Short acting LA’s last:
30 min
Lidocaine without vasoconstrictor will only give pulpal A for:
5min
Lidocaine with vasoconstrictor will give pulpal A for:
1.5-2hours
TF? The rate of LA metabolism is altered with the addition of vasoconstrictor.
T
Where are amide A’s metabolized?
liver
If a pt has liver disease what LA should you not gibe?
any amide
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
A LA will be less lipid soluble if:
the pH is fa from the pKa (more ionized, more water soluble)
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.)
Would infection drive the equation to the charged or uncharged side?
uncharged (highly water soluble)
pH of infected tissue:
4-5 (check)
2 competing factors of LA:
diffusibility and binding
Which factor of LA is more important clinically, diffusibility or binding
difusibiity
LA with pKa of 7.9 will have this % water and lipid soluble:
75% water, 25% lipid
What happens as a local anesthetic diffuses into a nerve?
increasingly diluted by tissue fluids and absorption, tissue/protein binding
nerve blockade:
free, uncharged base must interact with the nerve membrane, diffuse into and bind receptor site
3 factors that decrease effectivity as the LA diffuses
Decease volume, decreased concentration, protein binding
Related to intrinsic potency of LA:
Lipid solubility
LA with low lipid solubility, La with high lipid solubility:
Procaine = 1, etidocaine = 140
This is related to the duration of action of LA:
protein binding
TF? Increased protein binding to receptor = decreased duratio
F. increased
factors that influence the clinical effectiveness of LA:
Chem struct, diffusibility, vasoc, conc, anatomy of n., location of n.
Will mepevocaine be present more in the assoc or disocciated form?
dis
Lipid solubility theoretically leads to:
more rapid onset of action, longer duration, slower recovery
What differs bw each LA?
carrier protein molecules
All LA’s bind this:
albumin
TF? The more LA binds to protein, the better,
T
TF? Most LA’s have intrinsic vasodilating abilities.
T. except coke
Moderate duration anesthetic lasts:
up to 3 hours
Long lasting anesthetic lasts:
up to 12 hours
Why is recovery slower than the onset of action?
because LA is bound to receptor and is released more slowly than it is bound
Posterior sup alveolar artery, thin or thick fibers?
very thin, to upper premolar
Sequence of sense loss with anesthesia:
Pain and temp lost at same time, then touch/ prop, then motor
If prop sensors are still there they will feel:
pressure and vibrations
in what order do you gain sense back as anesthesia wears off?
reverse
What to do if you accidentally anesthetize CN 7:
nothing, it will come back in minutes
physiologic effects of local anesthesia are dependent on :
concentration
Amt of fluid in each carpule:
1.7ml
3 components in each carpule:
LA, vasoc, preservative
When is a preservative needed?
if there is vasoc
1% solution =
1gm in 100 ml, 1000 mg in 100 ml, 00 mg in 10 ml, 10 mg in 1ml
1.7 ml of a 1% solution =
17 mg
1.7 ml of a 2% solution =
34mg
1.7 ml of a 3% solution =
51 mg
How is LA conc reported?
weight/volume molar solution
How is vasoc concentration reported?
fraction in weight/volume
In one 1.7 ml carpule how much epinephrine is injected if everything is delivered?
0.017 mg of
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
Be aware of this with a patient that has COPD:
Increased likelihood of seizure at lower dose of LA
