Block 15 Local Anesthetics MCQ's

Local anesthetics primarily work by blocking inactivated, voltage-gated Na+ channels. When these channels are inactivated, they are unable to open and allow the influx of sodium ions, which is necessary for the propagation of action potentials. By blocking these channels, local anesthetics prevent the generation and conduction of nerve impulses, resulting in temporary loss of sensation in the localized area.

Bupivacaine is mainly metabolized by the liver. This is because it undergoes extensive hepatic metabolism, primarily through the process of ester hydrolysis. The liver enzymes break down bupivacaine into various metabolites, which are then eliminated from the body through urine. In contrast, cocaine is primarily metabolized by enzymes in the blood and other tissues, while procaine, tetracaine, and benzocaine are mainly metabolized in plasma and tissues other than the liver.

When a local anesthetic is applied to a nerve, it blocks the transmission of nerve signals. Motor function refers to the ability of muscles to contract and move. Since the local anesthetic blocks the nerve signals, it will affect the motor function last, as the other functions such as pain sensation, muscle tone, temperature sensation, and sympathetic activity will be blocked before the motor function.

Bupivacaine is the most cardiotoxic local anesthetic drug. Cardiotoxicity refers to the potential of a drug to cause harmful effects on the heart. Bupivacaine has a higher affinity for sodium channels in cardiac tissues, which can lead to the inhibition of cardiac conduction and potentially result in arrhythmias, cardiac arrest, or other cardiovascular complications. This makes it more cardiotoxic compared to other local anesthetics such as benzocaine, procaine, tetracaine, and lidocaine.

Lidocaine would be appropriate for this patient because it is a local anesthetic that does not contain para-aminobenzoic acid, which the patient had an anaphylactic reaction to in the past. Therefore, using lidocaine for spinal anesthesia would minimize the risk of another allergic reaction in this patient.

In infected tissues, the presence of bacteria and inflammation causes a decrease in extracellular pH, making it more acidic. This acidic environment hinders the diffusion of the local anesthetic drug into the cell, slowing down its onset of action.

The ionized form of local anesthetics is mainly responsible for receptor binding. When local anesthetics are ionized, they are able to bind to specific receptors in the body, blocking the transmission of nerve signals and producing their anesthetic effects. This binding to receptors is crucial for the local anesthetics to exert their desired pharmacological effects.

Lidocaine is the most appropriate drug to use for lumbar epidural anesthesia during a lithotripsy procedure. Lidocaine is a local anesthetic that provides rapid onset and intermediate duration of action. It is commonly used for procedures of short to moderate duration, such as this 30-minute procedure. Cocaine, procaine, benzocaine, and tetracaine are also local anesthetics but are not typically used for epidural anesthesia.

When a local anesthetic is applied to a nerve fiber, the refractory period of the nerve is most likely to increase. The refractory period is the time during which the nerve is unable to generate another action potential. By increasing the refractory period, the local anesthetic prolongs the time it takes for the nerve to recover and generate another action potential. This can help block pain signals and prevent the transmission of nerve impulses.

After the administration of lidocaine near the brachial plexus for peripheral nerve block, the most likely adverse effect to occur would be drowsiness. Lidocaine is a local anesthetic that can cause systemic effects when administered in larger doses or when it enters the bloodstream. Drowsiness is a common side effect of lidocaine and is typically a result of its central nervous system depressant properties. Ventricular tachycardia, abdominal colic, tonic-clonic convulsions, and nystagmus are less likely to occur as adverse effects of lidocaine administration in this scenario.

Rapidly firing fibers are most sensitive to the action of local anesthetics because these fibers have a higher frequency of action potentials. Local anesthetics work by blocking sodium channels and preventing the generation and propagation of action potentials. Since rapidly firing fibers have a higher frequency of action potentials, they are more likely to be affected by the blocking action of local anesthetics compared to resting fibers, fibers with high conduction velocity, unmyelinated fibers, or fibers of large diameter.

Benzocaine would be appropriate for this boy because it is a local anesthetic that is commonly used for topical application to relieve pain and itching caused by minor skin irritations, such as abrasions. It works by numbing the affected area and providing temporary relief from discomfort. Benzocaine is often used in over-the-counter products such as creams, ointments, and sprays for skin conditions. It is generally considered safe and effective for use in children and adolescents.

Lidocaine is a weak base with a pKa of 7.9. The pKa is the pH at which half of the drug is in its ionized form and half is in its non-ionized form. In extracellular fluids with a pH of 7.4, which is lower than the pKa, more of the drug will be in its non-ionized, lipid soluble form. Since the pH is closer to the pKa, we can expect that a significant fraction of the drug will be in its non-ionized form. The closest option is 24%, which suggests that approximately 24% of the drug will be in the lipid soluble form in extracellular fluids at pH 7.4.

An increased extracellular concentration of K+ makes the nerve membrane more sensitive to the action of local anesthetics. Local anesthetics work by blocking sodium channels, preventing the generation and conduction of nerve impulses. Increasing the extracellular concentration of potassium ions (K+) depolarizes the nerve membrane, making it more likely for sodium channels to open and allowing local anesthetics to have a greater effect on blocking these channels. This increased sensitivity to local anesthetics can lead to a more potent and prolonged anesthetic effect.

When a toxic dose of a local anesthetic is given intravenously, it can have severe effects on the cardiovascular system and the central nervous system (CNS). The cardiovascular system is likely involved because the local anesthetic can cause changes in heart rate, blood pressure, and rhythm, leading to cardiovascular collapse. The CNS is also likely involved because the local anesthetic can cause seizures, respiratory depression, and central nervous system depression. The other systems listed (gastrointestinal, respiratory, urinary, and immune) are not directly involved in the immediate effects of a toxic dose of a local anesthetic given IV.

Local anesthetics work by blocking sodium channels, which are responsible for the conduction of nerve impulses. The voltage dependency of local anesthetics means that their affinity for binding to these channels is influenced by the membrane potential. In this case, the more negative the membrane potential (hyperpolarization), the lower the affinity for local anesthetics. This means that local anesthetics are less likely to bind to sodium channels and block nerve conduction when the membrane potential is more negative.

Adding a vasoconstrictor drug to a local anesthetic serves the purpose of increasing the duration of the anesthetic effect by constricting the blood vessels at the site of administration, thus reducing the systemic absorption and prolonging the local effect. It also helps decrease the risk of systemic overdose toxicity by limiting the amount of drug that enters the bloodstream.