Hello and welcome to the Zero to Finals podcast. My name is Tom and in this episode I'm going to be

talking to about Myasenia Gravis. If you want to follow along with written notes on this topic,

you can follow along at zero definals.com slash myasenia gravis or in the neurology section of the Zero De Finals Medicine book. Let's get straight into it.

Myasthenia Gravis is an autoimmune condition that causes muscle weakness and gets progressively

worse with activity and improves with rest. Interestingly, myosinagravus affects men and women at different ages,

so a typical patient is either a woman under the age of 40 or a man over the age of 60.

There's a strong link with myasenia gravis and thymomas,

which are tumors of the thymus gland.

Around 10 to 20% of patients with myosenia gravis will have a thymoma,

and around 20 to 40% of patients with a thymoma will develop myasenia gravis.

Let's talk about the pathophysiology.

First, we need to look at motor nerves and how they communicate with muscles.

And this is done at something called the neuromuscular junction.

At the neuromuscular junction, axons of the motor nerves are situated across a synapse

from the post-synaptic membrane on the muscle cell.

The axons release a neurotransmitter from the pre-synaptic membrane,

and this neurotransmitter at these junctions is called acetylcholine,

and this acetylcholine travels across the synapse and attaches itself to receptors on the post-synaptic

membrane. The acetylcholine stimulates the receptors and this leads to muscle contraction. So in order for

the motor nerves to communicate with the muscle cells, they need to release acetylcholine and this needs

to bind to receptors on the post-synaptic membrane.

In around 85% of patients with myosenia gravis, acetylcholine receptor antibodies are produced by the immune system.

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