Term
| how are ester local anesthetics eliminated |
|
Definition
| via metabolism by plasma cholinesterase. Except for cocaine which is eliminated in the liver. |
|
|
Term
| The most toxic ester LA is? Why? |
|
Definition
| Tetracaine is most toxic b/c it is metabolized the slowest out of all the esters |
|
|
Term
| Which lcoal anesthetic is least toxic? Why |
|
Definition
| Chloroprocaine since it is eliminated the FASTEST. |
|
|
Term
| When should chloroprocaine, tetracaine and procaine not be administered to apatient |
|
Definition
| Since all these ester LA are eliminated via plasma cholinesterase then anyone with a deficiency in plasma cholinesterase should not get them. |
|
|
Term
| which ester LA is not eliminated via plasma choilnesterase |
|
Definition
|
|
Term
| what is the local agent that produces vasoconstriction |
|
Definition
|
|
Term
| How are amides eliminated |
|
Definition
|
|
Term
| What the least toxic amide local anesthetic |
|
Definition
|
|
Term
| What is the max dose of lidocaine for a 70 kg patient without epi |
|
Definition
|
|
Term
| which amide is most cardiotoxic and why |
|
Definition
| Bupivacaine is most cardiotoxic. R/T its more intense binding to gated Na channels. |
|
|
Term
| what is the difference of ropivicaine and bupivicaine |
|
Definition
| ropivicaine and bupivicaine are both long acting, similar pKa, protein bindnig, potency, and clinical use. The difference is that ropivicaine is less cardiotoxic and produces LESS motor block. (which makes ropivicaine better for labor patients) |
|
|
Term
|
Definition
| the pKa is the pH at which 50% of a weak acid or weak base is ionized and 50% is un-ionized. |
|
|
Term
| The local anesthetics are prepared as what kind of salts |
|
Definition
|
|
Term
| Are local anesthetics weak acids or weak bases |
|
Definition
|
|
Term
| what LA with this kind of pKa ___ be the most IONIZED at physiological pH of 7.4 |
|
Definition
| a high pKA will be mostly ionized at a pH of 7.4. |
|
|
Term
| typically LA injected into body are in the ionized or un-ionized form? |
|
Definition
| Ionized! B/c Most pKas are higher than the body's pH therefore they become ionized. |
|
|
Term
| if LA is injected into an aeaa of trauma or infection will its onset increase or decrease or no effect? Why? |
|
Definition
| Decrease onset b/c prevailing acidosis increases the ionization of the LA. |
|
|
Term
| how does adding bicarb to LA increase its onset |
|
Definition
| bicarb is alakaline and addign it to local makes more un-ionized LA. This form of LA will be more likely to cross axon membranes to produce its affects. |
|
|
Term
| How does a local anesthetic work |
|
Definition
| They produce a conduction blockade of neural impulses in the affect nerve. This is accomplished by preventing passage of Na ions through ion-selective Na channels. By slow the rate of depolarization you prevent threshold from being reached. |
|
|
Term
| what state of the Na-Ion channel do Local anesthetics have the highest affinity to bind to |
|
Definition
1. activated state
2. inactivated states.
Those conformations are most susceptible to LA binding. |
|
|
Term
| what is myelin (which surrounds the nerves) made up of |
|
Definition
myelin is made from specialized schwanna cells that wrap around the axon. Myelin's purpose is:
1. insulation
2. increases speed of conduction. |
|
|
Term
| How many Nodes Ranvier are needed to be blocked in order for an effected LA administration |
|
Definition
|
|
Term
which is more sensitivt to LA
1. myelinaed nerves
or
2. unmyelinated |
|
Definition
| Myelinated nerves are more sensitive than nonmyelinated like C fibers |
|
|
Term
| which LA seems to be more selective for motor blockade versus sensory |
|
Definition
|
|
Term
| Most local Anesthetics have pKa that are |
|
Definition
|
|
Term
| the primary determinant of potency for local anesthetics is |
|
Definition
|
|
Term
in order from highest to lowest, what is the realtive order of peak plasma concentrations at
1. intercostal
2. sciatic/femoral
3. brachial plexus
4. caudal
5. epidural |
|
Definition
| Intercostal > caudal > epidural > brachial plexus > sciatica/femoral. |
|
|
Term
| What are the INITIAL manifestations of LA toxicity |
|
Definition
1. circumoral numbness
2. facial tingling
3. restlessness
4. vertigo
5. tinnitus
6. slurred speech |
|
|
Term
| what are two mechanisms of action on how LA may cause hypotension |
|
Definition
1. direct depression to the myocardium
2. relaxation of the peripheral smooth muscle |
|
|
Term
| what changes on the ECG may you see with LA toxicity |
|
Definition
| increase conduction time therefore increase PR and increase QRS. BC lidocaine is a class Ib antidys which causes early repolarization. |
|
|
Term
| what properties of bupivicaine that makes it a long acting LA |
|
Definition
| Its fast in, but slow out. |
|
|
Term
| the maximum recommended concentration of bupivicaine for epidural aneshtesia in obstetrics is |
|
Definition
| 0.5% because 0.75 is associated with more s/e |
|
|
Term
| which local is associated with methemoblobinemia |
|
Definition
| prilocaine, lidocaine and benzocaine |
|
|
Term
| how do you treat methemoglobinemia |
|
Definition
|
|
Term
| what is transient neurologic symptoms (TNS) |
|
Definition
| is a syndrome of pain/dysesthesia in the lower back, posterior thighs, or buttocks that generally occurs within 24 hours of recovery from a spinal anesthetic. |
|
|
Term
| Is TNS associated with sensory loss, motor weakness or bowel or bladder dysfunction? |
|
Definition
| NOOOOOOOOOO this is not cauda equina syndrome |
|
|
Term
| Name the three risk factors for transient neurologic symptoms TNS |
|
Definition
1. lidocaine use
2. lithotomy position
3. outpatient status |
|
|
Term
| cauda inquina syndrome is the result of damage to |
|
Definition
| nerve roots caudal to the conus. |
|
|
Term
| describe the SX of cauda equina syndrome |
|
Definition
1. perineal sensory loss
2. bowel dysfunction
3. bladder dysfunction
4. lower extremity muscle weakness |
|
|
Term
| what are the chances for a true allergic reaction to local anesthetic |
|
Definition
| <1 %!! SO RARE for a true allergic reactions. |
|
|
Term
| IF true allergic reactions are rare to LA than why do people have reactions |
|
Definition
|
|
Term
| Why do ester LA have higher incidence of allergic reactions |
|
Definition
| due to metabolite known as PABA. Para-aminobenzoic acid |
|
|
Term
| what perservativie in LA may cause allergic reactions |
|
Definition
| preservative methylparaben |
|
|
Term
| the ester with the least potency |
|
Definition
|
|
Term
| least toxic ester and why |
|
Definition
| chloroprocaine since it is eliminated faster than all other local anesthetics. |
|
|
Term
| cocaine is an ester of what group? |
|
Definition
|
|
Term
| why is bupivicaine most cardiotoxic |
|
Definition
| binds to gated sodium channels with great intensity. |
|
|
Term
| does ropivicaine or bupivicaine produce less motor blockade |
|
Definition
| ropivicaine. So better choice for pregnant people in labor. |
|
|
Term
| when would you expect a decrease in clearance of amide local anesthetics |
|
Definition
1. decrease liver blood flow states
2. inhibtion of hepatic cytochrome p450 system. |
|
|
Term
|
Definition
| a combination cream made up of lidociane 2.5% and prilocaine 2.5% |
|
|
Term
| local anesthetics are prepared as what kind of salts |
|
Definition
| hydrochloride salts. lidocaine hydrochloride as an example. |
|
|
Term
| target range for local anesthetics is |
|
Definition
|
|
Term
| are local anesthetics weak bases or weak acids |
|
Definition
|
|
Term
| do locals become more or less ionized as the pH increases. |
|
Definition
| Local are weak bases. AS pH goes up then Base + base = non-ionized. |
|
|
Term
| what local anesthetics, those with high pKa or low Pka are most ionized at physiological pH (7.4) |
|
Definition
| Those with Highest pKa are most ionized at pH of 7.4 |
|
|
Term
| if a local is injected into an area of infection will it speed or slow onset |
|
Definition
| SLOW bc acidosis increases ionization of local |
|
|
Term
| what are some drugs that may decrase clearance of amide local anesthetics? Remember how do amides get cleared? |
|
Definition
Amides are cleared via oxidation and the P450 system in the liver. Drugs such as
1. volatiles
2. propanolol
3. Cimetidine
ALL INHIBIT P450 or reduce blood flow and therefore increase duration of amide locals. |
|
|
Term
| why are preservative contianing solutions of local anesthetics not used for neuroaxial anesthesia |
|
Definition
| First of all preservatives in LA such as paraben family are highly culpable in allergic reactions. Secondily if used for neuraxial anesthesia they ARE NEUROTOXIC |
|
|
Term
| which two local anesthetics are administered as racemic mixtures? |
|
Definition
| bupivicaine and mepivcaine. |
|
|
Term
| what are the three stages of fast, voltage gated sodium channels |
|
Definition
1. closed
2. open
3. inactivated |
|
|
Term
| what part of the nerve cell is actually the site of action for local anesthetics |
|
Definition
| THE AXON. Thats whats lined with Fast, voltage gated Na receptors. The soma and nerve endings is different. |
|
|
Term
| Since lipid solubility determines potency of a local anesthetic then what characteristic of the local is making it more lipid soluble |
|
Definition
| More carbon atoms than MORE lipid soluble THEN more POTENT. |
|
|
Term
| What six factors determine the absorption of local anesthetic into the surrounding vasculature and therefore increasing blood levels |
|
Definition
1. Total Dose
2. pH
3. Use of vasoconstrictor
4. Amt of blood flow to that area
5. Lipid solubility of the agent
6. Protein binding of agent. |
|
|
Term
| What kind of pH would influence MORE local anesthetic levels in blood (toxicity) |
|
Definition
| The higher the pH means more non-ionized local. = more local getting absorbed into blood stream and causing toxicity. |
|
|
Term
| The greater or lower lipid solubility will result in faster blood levels and toxicity |
|
Definition
| Lower solubility b/c less drug in lipophilic tissues and instead will go into hydrophillic which is blood. |
|
|
Term
| which local anesthetic has the least protein binding |
|
Definition
| Chloroprocaine. HEnce why its so fast acting b/c none of it remains on proteins to slowly come off and keep localizing the area. |
|
|
Term
| speed of onset of a local anesthetic is determined by? |
|
Definition
|
|
Term
| what is the max dose of epi for use with a local anesthetic for infiltration, brachial plexus, epidural, caudal or intrapleural anesthesia |
|
Definition
|
|
Term
| the opitmal epi concnetration in a local anesthetic is |
|
Definition
|
|
Term
| 1:100,000 is how many epi per mL |
|
Definition
|
|
Term
| 1:200,000 of epi is how much epi per mL |
|
Definition
|
|
Term
| how does prilocaine convert Hb to methemoglobin |
|
Definition
| prilocaine, an amide local anesthetic, is metabolized to orthotoluidine. Orthotouidine is an oxidizing agent capable of converting Hb tgo methemoglobin. |
|
|
Term
|
Definition
| Oxidization of Hb which really means oxidizing of the Fe 2+ component to Fe 3+ makes it incapable of carrying oxygen. |
|
|
Term
| name two active metabolites of lidocaine |
|
Definition
1. monoethylglycinexylidide (MEGX)
2. glycine xylidide (GX) |
|
|
Term
| The most susceptible fibers to local anesthetic blockade are? |
|
Definition
|
|
Term
| What is the menumonic for what sensory / motor elements are blocked by LA in order |
|
Definition
ATP, TP, MVP ATP:
or AUdrey TEll PAul TO PRay for MOre VIagra PRoducts
Autonomic - Temperature - Pain TP: Touch - Pressure MVP: Motor - Vibratory - Propioception. |
|
|
Term
| Name the three main chemistry components of a local anesthetics |
|
Definition
| Aromatic ring - intermediate linkage which is either an amide or ester - terminal amine. |
|
|
Term
| metabolism of esters result in what metabolite |
|
Definition
|
|
Term
| name in order where LA get absorbed the fastest in what tissue areas |
|
Definition
tracheal > intrapleural > intercostal > caudal > epidural >
brachial (or other major nerve) plexus > intradermal > spinal |
|
|
Term
| A faster onset would be expected from a pKa of a LA that is closer or futher from physiologic pH |
|
Definition
| closer. so pKa of 7.9 would be faster onset than a pKa of 8.4. |
|
|
Term
| pKa of LIdocaine, chloroprocaine, and bupivicaine |
|
Definition
1. lidocaine 7.9
2. Chloroprocaine 8.7
3. Bupivicaine 8.1 |
|
|
Term
| Main determinant of duration of action of a LA is? Second component of DOA of action of LA is? |
|
Definition
1. Protein binding #1
2. Lipid solubility #2 |
|
|
Term
|
Definition
you can BET on them
Bupivicaine
Etidocaine
T: Tetracaine |
|
|
Term
| what local has a respiratory side effect of blunting ventilatory drive to hypoxemia |
|
Definition
|
|
Term
| early Sx of digoxin toxicity are? What should the therapuetic levels be? |
|
Definition
Early Sx of digoxin toxciity are Anorexia, nausea, and vomiting.
Digoxin levels should be < 0.5ng/L |
|
|
