(a) Procaine is the only ester listed — all the rest are amides

(a) this is basically a true-false type question. (a) is the only statement that is true

(ii) another ester vs. amide type identification question. Lidoccaine is an amide, thus other amides will be crossallergenic – mepivacaine, prilocaine and dibucaine are the other amides listed. Procaine and tetracaine are esters and will not be cross-allergenic.

(c) procaine is an ester; esters are metabolized predominately by pseudocholinesterases in the plasma.

(c) esters are metabolized by plasma esterases – tetracaine is the only ester listed, all the rest are amides

(d) remember #9 above? see the word “mainly”? same question, but worded a little differently to throw you off. Again, procaine is an ester; esters are metabolized predominately by pseudocholinesterases in the plasma, but also to some extent by esters in the liver.

(c) the word “EXCEPT” should alert you that this is basically a true-false type question with 4 true statements and 1 false statement; you just have to figure out which one! In this case, you just have to remember that plasma cholinesterase levels are only important for the duration of action of ester-type LAs, not amides, which are metabolized in the liver. All the other statements are variables which affect duration of the block, but apply to both esters and amides.

c) again, just another question that requires you to be able to pick out an ester or an amide from a list. Since procaine is an ester, only another ester LA would be cross-allergenic. In this list the only ester listed is tetracaine.

(d) According to textbooks, local anesthetics fall into the following classes in terms of duration of action:

short: procaine;
moderate: prilocaine, mepivacaine, lidocaine;
long: bupivacaine, tetracaine, etidocaine.

Statements (a), 3, and 4 would be true if the question was comparing mepivacaine to bupivacaine, which are structurally similar; but the comparison is to lidocaine. Bupivacaine (Marcaine) is more toxic, has a slower onset of action and has a longer duration of action compared to lidocaine. However, both are amide-type local anesthetics which makes answer choice B.

(b) don’t forget: esters in plasma; amides in liver

(b) this is an interaction I tested you on several times – now you know why! Propranolol interacts with lidocaine in two ways. By slowing down the heart via beta receptor blockade, blood delivery (and lidocaine) to the liver is reduced, thus lidocaine remains in the systemic circulation longer, and can potentially accumulate to toxic levels. Propranolol and lidocaine also compete for the same enzyme in the liver, thus metabolism of lidocaine can be reduced.

(b) Answer is (b)- You should be able to recognize that all of these drugs are local anesthetics. Local anesthetics are of one of two types, either sters or amides. Ester types are subject to hydrolysis in the plasma and thus have short half lives. Amides are metabolized primarily in the liver and have longer half lives. Thus the biotransformation (e.g., metabolism; again, the rats are using a different word to confuse you, even though they are asking the same basic question) of an amide type local anesthetic would be the most altered in the presence of sever liver disease. The key word here is “least”. Of the drugs listed, only procaine is an ester. The rest are amides.

(b) strictly memorization

(d) same as above but asked backwards. Methemoglobinemia may result from a toluidine metabolite of prilocaine, orthotoluidine.

(e) Most toxic reactions of a serious nature are related to excessive blood levels arising from inadvertent intravascular injection. Hypersensitivity reactions (options b & c) are rare, but excessive blood levels will induce toxic reactions like CNS stimulation in most everyone. This is a case where option (e) is the “best” answer, because it is more likely than the other alternatives, which might be true, but are not as likely (e.g, “most probable”) to happen.

(d) Initially LAs inhibit central inhibitory neurons, which results in CNS stimulation, which can proceed to convulsions. At higher doses, they inhibit both inhibitory and excitatory neurons, leading to a generalized state of CNS depression which can result in respiratory depression and death.

(c) same question as above just worded differently. The intraarterial injection would result in the high plasma levels mentioned in the previous question.

(c) it is a sympathomimetic after all. All the other reactions are related to elevated lidocaine levels

(a) Grave’s disease is an autoimmune disease that causes hyperthyroidism – the resulting high levels of circulating thyroid hormone result in a hypermetabolic state with heightened sympathetic activity, which combined with injected epinephrine could result in a hypertensive crisis.

(d) Cardiovascular collapse is due to a direct action of the local anesthetic on the heart muscle itself (LA’s in toxic doses depress membrane excitability and conduction velocity), thus (d) is the correct answer. All of the other alternatives are indirect ways to affect the heart

(e) Of the options listed, this is the one that will kill the patient, which I guess makes it the most serious.

(a) All the listed local anesthetics except cocaine are vasodilators, especially ester-ctype drugs such as proccaine and the amide lidocaine. Cocaine is the only local anesthetic that predictably produces vasoconstriction. Cocaine is also the only local anesthetic to block the reuptake of NE into adrenergic neurons, and thus potentiate the NE that has been released from nerve endings

(a) see explanation above

(e) didn’t I make you memorize this? You should at keast remember Na+ ions are involved, which limits your choices to (c) and (e). (c) would increase or facilitate nervous impulse conduction, which is the opposite of what you want the local anesthetic to do, so pick (e).

(b) this should be really obvious!

(c) Answer is (c)- straight memorization- nerve impulses are generated by the influx of sodium resulting in depolarization. repolarization and inactivity occurs when potassium moves out. (sodium-potassium pump). LAs act by blocking Na+ movement.

(a) see how many different ways they can ask the same question?

(d) the next three or four questions are all versions of the same thing – see the explanation below

(a) while some of the other alternatives sound plausible, think about the factoids you were taught about local anesthetics and variables that affect their action. An important one was the role of pH and ionization factors. Remember, the free base or nonionized form is the form that passes through membranes, yet once inside the neuron only the ionized form is effective. Inflamed tissue has a lower pH than normal tissue and will shift the equilibrium of the LA solution such that most of it remains ionized and thus unavailable to penetrate

(c) only options (b) and (c) are relevant here – the others have nothing to do with LA penetration into membranes. Membrane permeability is affected by whether or not the molecule is “charged” or ionized or not (e.g., unionized). Only the latter form passes readily through membranes. See, they’re asking the same thing they asked in the previous question, just coming at it from another angle. Remember the fact and you can cover the angles.

(c) the ratio of ionized to unionized forms is given by the formula log A/AH= pH-pKa. In this instance the difference between pH and pKa is 0. Thus lidocaine will exist as an equal mixture ( so (c) is correct). Most local anesthetics are weak bases with pKa ranging from 7.5 to 9.5. LA’s intended for injection are usually prepared in salt form by addition of HCl. They penetrate as the unionized form into the neuron where they re-equilibrate to both charged and uncharged forms inside the neuron – the positively charged ion blocks nerve conduction.

Who knows? Who cares? probably the answer is (b) – the theory goes that there is a size dependent critical length of anesthetic exposure necessary to block a given nerve. Small fibers will be blocked first because the anesthetic
concentration to h critical length in a small fiber will be reached faster than the critical length in a larger fiber. You have to block three nodes of ranvier, and they are farther apart in larger fibers than they are in small diameter fibers. Make sense?

(ii) if you knew the fact above about small nerves, then this question basically becomes a true false type thing, and (c) is the false statement. (a) and (d) make logical sense so you are stuck picking between (b) and (c). You have your pick of memorizing the small nerve thing or the myelinated nerve nodes of ranvier thing.

(d) 2% solution = 20 mg/ml X 1.8 ml = 36 mg lidocaine. And you thought you would never have to do this stuff again!

(d) 2% lidocaine = 20 mg/ml x 3 = 60 mg lidocaine 1:100,000 epi = 0.01 mg/ml x 3 = 0.03 mg epi

(c) 2% mepivacaine = 20 mg/ml, so 300 mg / 20 mg/ml = 15 ml

(d) 0.05% = 0.5 mg/ml . To give 30 mg, you have to give 30mg/0.5 mg/ml or 60 ml. 1 cartridge = 1.8 ml, thus 60ml /1.8ml = 33.3 cartridges. – first express the percentage of solution as a fraction of 100, then add the units gm/ml. 0.05% equals 0.5 or 1/2 gms per 100 ml. The cartridge is 1.8 ml which you can round off to almost 2 mls total. In this 2 ml you would have 1 gm of the local anesthetic. You need to give 30 gms, which would require 30 cartridges. The alternative that meets this answer is (d). Don’t get tricked by the placement of the decimal pointmany people read the 0.05% as being the same as 5 gms rather than 0.5 gms.

(d) the AHA limit is 0.04 mg, compared to 0.2 mg in the healthy patient. 1:200,000 equals 0.005 mg/ml or 0.009 per 1.8 ml carpule. 4 carpules would thus contain 0.036 mg, which is just below the 0.04 mg limit