1.14 Neuromuscular Junction (physiology

Muscle relaxants don't make the person sleep, they just paralyze the muscles. So, first things first, how does a muscle work?

1. Action potential hits the nerve ending.
2. Calcium enters, and Acetylcholine is released.
3. Acetylcholine travels across the synapse.
4. Sodium enters the muscle -> Depolarization -> Contraction.

The two types of Blockers:

1. Depolarizing
   1. Succinylcholine: attaches to the receptors on the muscles, depolarizes them and keeps them depolarized.
2. Non-Depolarizing:
   1. Steroids: Vecuronium and Rocuronium (one memory aid is that in a case in the united states, a nurse was sent to jail over accidently injecting vecuronium to a patient).
   2. Isoquinolines: Atracurium and Cisatracurium (Cisatracurium sounds a bit like 'sisters sat' at the start).
      1. An important fact about cisatracurium is that it is broken down by blood esterases. So it is the best choice for patients with liver and renal failure.

Now, to reverse these effects, we could use:

1. Neostigmine: The acetylcholine booster. It works by inhibiting acetylcholine esterase so acetylcholine is not broken down.
2. Sugammadex is the antidote for rocuronium and vecuromium. It encapsulates them to make them unavailable.

Okay, enough about drugs that act at the muscular junction, we can also centrally inhibit the muscular neurons.

1. Dantrolene: It doesn't work on the nerve, it blocks Calcium release from muscle so is the only antidote to malignant hyperthermia.
2. Baclofen: GABA-B agonist. Used for MS.

Lastly, when we give anesthetics, first the small muscles of the eyes and face, then the rest of the muscles in the limbs and the trunk and lastly the muscles for respiration get paralysed.