One prime factor involved in the termination of action of local anesthetics used for pain control is their redistribution from the nerve fiber into the (...).

All local anesthetics possess a degree of vasoactivity, most producing (...) of the vascular bed into which they are deposited.

(...) is the most potent vasodilator among local anesthetics.

(...) is the only local anesthetic that consistently produces vasoconstriction.

Cocaine induces vasodilation by inhibiting (...) into tissue binding sites.

Local anesthetics are absorbed poorly, if at all, after (...) administration.

In 1984 Astra Pharmaceuticals and Merck Sharp & Dohme introduced an analogue of lidocaine, (...), that is effective orally.

Topically applied local anesthetics can produce an anesthetic effect wherever there is no (...) present.

(...) is a mixute of lidocaine and prilocaine capable of providing surface anesthesia of intact skin.

What type of local anesthetics are the following?

1. butacaine
2. cocaine
3. benzocaine
4. piperocaine
5. tetracaine

What type of local anesthetics are the following?

1. articaine
2. bupivacaine
3. lidocaine
4. mepivacaine
5. prilocaine

(...) administration of local anesthetics provides the most rapid elevation of blood levels

IV administration of local anesthetics is used clinically in the primary management of (...).

Once absorbed into the blood, local anesthetics are distributed throughout the body to all tissues; (...) organs initially have the highest anesthetic blood levels.

(...) contains the greatest percentage of local anesthetic of any tissue or organ in the body.

What three factors influence the blood level of the local anesthetic?

The rate at which a local anesthetic is removed from the blood is described as its (...).

The elimination half-life is the time necessary for a 50% reduction in the blood level:

1. one half-life represents a (...)% reduction
2. two half-lives represents a (...)% reduction
3. three half-lives represents a (...)% reduction
4. four half-lives represents a (...)% reduction
5. five half-lives represents a (...)% reduction
6. six half-lives represents a (...)% reduction

Can local anesthetics cross the blood-brain barrier?

Can local anesthetics cross the placenta?

The significant difference between the two major groups of local anesthetics, the esters and the amides, is mean by which they are (...).

Ester local anesthetics are hydrolyzed in the plasma by the enzyme (...).

The rate of hydrolysis of ester local anesthetic has an impact on the (...) of a local anesthetic.

(...), the most rapidly hydrolyzed ester local anesthetic, is the least toxic.

(...), a slowly hydrolyzed ester local anesthetic, has the greatest potential toxicity.

Allergic reactions that occur (rarely) in response to ester local anesthetic are usually related to (...), which is a major metabolic product of many ester local anesthetics.

(...) is a short-acting muscle relaxant commonly used during the induction phase of general anesthesia.

Persons with (...) are unable to hydrolyze succinylcholine at a normal rate, resulting in the duration of apnea being prolonged.

An (...) implies that under no circumstance should the drug in question be administered to the patient.

A (...) means that the drug in question may be administered to the patient after careful weighing of the risk versus the potential benefit.

The primary site of biotransformation of amide local anesthetics is the (...).

(...) contains both ester and amide components, and undergoes metabolism in both the blood (primarily) and the liver.

Which two conditions represent relative contraindications to the administration of amide local anesthetic drugs?

The (...) of certain local anesthetics can possess significant clinical activity if they are permitted to accumulate in the blood.

Due to its biotransformation products high doses of prilocaine may cause (...).

A primary metabolite of prilocaine, (...), induces the formation of methemoglobin, which is responsible for orthotoluidine.

The (...) are the primary excretory organ for both the local anesthetic and its metabolites.

Which conditions represents a relative contraindication to the administration of all local anesthetic drugs?

Most of the systemic actions of local anesthetics are related to their (...) in a target organ.

The quinoline derivative (...) has proved to be more potent than lidocaine, but does not adversely affect the CNS or CVS.

The major pharmacologic action of local anesthetics on the CNS is one of (...).

Individual reactions to local anesthetics lie on a (...)-shaped curve.

The “classic” overdose reaction to a local anesthetic is a generalized (...).

Epileptic patients possess hyperexcitable cortical neurons at a site within the brain where the convulsive episode originates, called the (...).

Local anesthetics, by virtue of their depressant actions on the CNS, raise the seizure threshold by decreasing the (...).

A blood level of (...) μg/mL lidocaine appears to be the “dividing line” before signs of minor toxicity (i.e. drowsiness) occur.

At a normal arterial partial pressure of CO2, a lidocaine blood level between (...) μg/mL usually results in a convulsive episode.

When CO₂ levels are increased, the blood level of the local anesthetic necessary for seizures (...), while the duration of the seizure (...).

If anesthetic blood levels continue to rise, beyond the cessation of seizure activity (...) depression also occurs, culminating in (...).

Local anesthetics produce clinical signs and symptoms of CNS excitation through selective blockade of (...) in the cerebral cortex.

The cerebral cortex has pathways of neurons that are essentially (...) and others that are (...) normally maintained in a state of balance.

At preconvulsant local anesthetic blood levels, balance is tipped in favor of excessive (...) input, leading to symptoms including tremor and slight agitation.

At higher (convulsive) blood levels, (...) neuron function is completely depressed, allowing unopposed function of (...) neurons.

In the final stage of local anesthetic action, both the facilitatory pathway and the inhibitory pathway are depressed, producing (...).

In the 1940s and 1950s the local anesthetic (...) was administered intravenously for the management of chronic pain and arthritis.

The local anesthetic (...) has long been used for its euphoria-inducing and fatigue-lessening actions.

The major pharmacologic action of local anesthetics on the CVS is one of (...).

Local anesthetics (...) the electrical excitability of the myocardium, (...) conduction rate, and (...) the force of contraction.

Therapeutic advantage is taken of the depressant action of local anesthetics on the myocardium in management of (...).

(...), a chemical analogue of lidocaine, was introduced in 1981 as an oral antidysrhythmic drug because lidocaine is ineffective after oral administration.

(...) is the only local anesthetic drug that consistently produces vasoconstriction at commonly used dosages.

All injectable local anesthetics produce a peripheral (...) through (...) in the walls of blood vessels.

The primary effect of local anesthetics on blood pressure is (...).