Local Anesthetics Flashcards
What are local anesthetics, and what is their primary function?
Local anesthetics are drugs that reversibly block voltage-gated sodium channels to provide analgesia and patient safety, improve operating conditions, and control intraoperative and postoperative pain.
What are the two main types of local anesthetics based on their chemical structure?
Ester-type (e.g., procaine, tetracaine) and amide-type (e.g., lidocaine, bupivacaine).
Name five ester-type local anesthetics.
Cocaine, procaine (Novocain), chloroprocaine, tetracaine (Pontocaine), benzocaine.
Name five amide-type local anesthetics.
Lidocaine (Xylocaine), bupivacaine (Marcaine), mepivacaine (Carbocaine), prilocaine (Citanest), ropivacaine (Naropin).
Name two ether-type and one ketone/ether-type local anesthetic.
Ethers: Pramoxine, Phenacaine. Ketone/Ether: Dyclonine (found in Sucrets and some forms of Cepacol).
How does pH affect the effectiveness of local anesthetics?
Lower extracellular pH (e.g., in infected tissues) reduces their effectiveness because the uncharged form penetrates membranes, but the cationic form is active at the binding site.
How are ester-type local anesthetics metabolized?
Hydrolyzed in the blood by butyrylcholinesterase (pseudocholinesterase) and some are converted to p-aminobenzoic acid (PABA), which can cause allergic reactions.
How are amide-type local anesthetics metabolized?
Hydrolyzed by liver microsomal cytochrome P450 enzymes. Liver disease or reduced hepatic blood flow increases toxicity risk.
Which local anesthetics are short-, intermediate-, and long-acting?
Short-acting: Procaine, chloroprocaine. Intermediate-acting: Lidocaine, mepivacaine, prilocaine. Long-acting: Bupivacaine, ropivacaine, tetracaine.
Why are vasoconstrictors like epinephrine added to local anesthetics?
To decrease regional blood flow, reduce systemic absorption, and prolong anesthetic effects, especially for short-acting drugs like procaine and lidocaine.
How do local anesthetics block nerve conduction?
They bind to sites near the intracellular end of voltage-gated sodium channels, blocking sodium influx and preventing action potential generation.
What four factors determine how sensitive a nerve is to local anesthetics?
Size (smaller = more sensitive), myelination (myelinated = more sensitive), frequency of depolarization (higher frequency = more sensitive), and location in the nerve bundle (outer fibers = blocked first).
What are the early and severe signs of CNS toxicity from local anesthetics?
Early: Numbness around the mouth, metallic taste, tinnitus, dizziness. Severe: Convulsions, CNS depression, respiratory arrest.
What are the effects of local anesthetics on the cardiovascular system?
Depress cardiac pacemaker activity, excitability, and conduction → hypotension, arrhythmias, and in high doses, cardiac arrest.
Which local anesthetic is most cardiotoxic?
Bupivacaine is the most cardiotoxic. Ropivacaine (levobupivacaine) is a safer alternative.
What are the unique properties of cocaine as a local anesthetic?
Unlike other local anesthetics, cocaine causes vasoconstriction by blocking norepinephrine reuptake, leading to hypertension and potential arrhythmias.
Which local anesthetic can cause methemoglobinemia and how?
Prilocaine (>10 mg/kg) is converted to o-toluidine, which oxidizes hemoglobin to methemoglobin. Antidotes: reducing agents (e.g., methylene blue).
Which local anesthetic should be avoided during labor and why?
Bupivacaine should be avoided due to its high cardiotoxicity. Pregnant women require lower doses and are more susceptible to toxicity.
What are some common clinical applications of local anesthetics?
Topical: Benzocaine, pramoxine, dyclonine (e.g., Sucrets). Ophthalmology: Proparacaine, tetracaine. Peripheral nerve block: Lidocaine, mepivacaine, prilocaine, ropivacaine. Spinal anesthesia: Tetracaine, bupivacaine, ropivacaine.
What are key drug interactions with local anesthetics?
All LAs: Increased CNS & respiratory depression with alcohol, opioids, antidepressants. Amides: Beta-blockers and cimetidine reduce metabolism, increasing toxicity. Esters: Anticholinesterases reduce metabolism, and esters inhibit sulfonamide action.
