How do local anesthetics block nerve conduction?

They cross the nerve membrane in the uncharged form, become charged inside the axon, and block voltage-gated sodium channels from the intracellular side.

Why do acidic infections need more local anesthetic?

Acidic tissue protonates the drug, trapping more of it in the charged form outside the nerve. Charged drug cannot cross the membrane well, so less reaches the inside of the sodium channel.

What is the board pattern for benzocaine methemoglobinemia?

Endoscopy spray, dyspnea, cyanosis or chocolate-colored blood, low pulse oximetry, and normal PaO2. Treat with methylene blue.

What separates succinylcholine from nondepolarizing neuromuscular blockers?

Succinylcholine is a depolarizing Nm agonist that causes fasciculations before paralysis and has no phase I reversal. Rocuronium, vecuronium, and related drugs are competitive Nm antagonists that paralyze without the fasciculation phase.

Pharmacology signal map

Anesthesia Pharmacology

Start with the blocked signal. Local anesthetics block the axon from the inside, benzocaine oxidizes hemoglobin iron, paralytics freeze the NMJ, and malignant hyperthermia is calcium trapped open inside muscle.

Opening board trap

A patient with a draining finger abscess needs incision and drainage. Lidocaine is injected, but the first cut still hurts. Which explanation fits the failed block?

VIGNETTE 1 OF 12

Screen 2

The Sodium Channel Door

Local anesthetics work only after they cross the membrane and sit inside the voltage-gated sodium channel. The board exam keeps changing the wrapper, but the lock is always inside the axon.

Charged form blocks from inside

The uncharged base crosses the membrane. Inside the axon, the charged form binds the inner sodium channel pore. No sodium upstroke means no nerve impulse.

Drug family sorter

Tap each drug into the right family. Amides usually have an extra "i" before "caine"; esters are the older bench.

Amides

Esters

Differential blockade

Tap the sensory losses in order. Small fibers go before large fibers, and pain disappears before pressure.

Screen 3

The Two Toxicity Rooms

One room steals oxygen from hemoglobin. The other overstimulates brain and heart before it crashes them. The sign decides which room you are in.

Methemoglobin triage

A patient becomes short of breath after benzocaine throat spray. Blood drawn from the IV looks chocolate brown. Pulse oximetry stays in the 80s, but PaO2 on arterial blood gas is normal. Pick the mechanism.

1

CNS excitation first

Talkative, anxious, confused, stuttering speech. The brakes are wobbling, not fully gone.

2

CNS depression later

Drowsiness, seizure risk, coma. The nervous system is no longer conducting cleanly.

3

Cardiac conduction fails

Hypotension, arrhythmia, bradycardia, heart block. Bupivacaine is the board-famous cardiotoxic one.

4

Cocaine is the exception

Cocaine blocks sodium channels too, but vasoconstriction and catecholamines push hypertension.

Use case lock

Choose the clinical use that fits local anesthetics directly.

Lidocaine chemical structure — Lidocaine: the common amide local anesthetic.

Benzocaine chemical structure — Benzocaine: endoscopy spray plus chocolate blood.

Suxamethonium succinylcholine chemical structure — Succinylcholine: fasciculations, then paralysis.

Dantrolene chemical structure — Dantrolene: the RyR1 rescue drug.

Screen 4

Paralytic Bay

At the NMJ, the exam asks whether the receptor is being forced open, competitively blocked, or bypassed entirely by a calcium fire inside muscle.

Pick the bay

Succinylcholine forces the receptor open

It acts like acetylcholine at the Nm receptor. Phase 1 is sustained depolarization, so fasciculations can happen before paralysis.

Phase 1 has no reversal and cholinesterase inhibitors can worsen it. The board also ties it to hyperkalemia, burns, dialysis, pseudocholinesterase deficiency, and malignant hyperthermia.

Keep the map simple: sodium channel, hemoglobin iron, NMJ receptor, or RyR1 calcium channel.

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