You explained this better than any doc I've seen since being diagnosed, while I knew the basics and then I still learnt more here, thank you

My dad has been diagnosed with this, but it took quite a while because it's quite rare... Thank you for giving it some attention!

Thank you...I learned so much with this video!

Great explanation.

Fantastic video. Thankyou 🙌👏🏻👏🏻

Thanks. I appreciated your presentation of MG. Very informative.

great explanation 🙌

Thank you I thought the Tensilon test could be added, could you elaborate on this?

Informative video.. 🌷🌷👍👍

Very well explained.... thankyou🙂

A few years ago, I was being tested for this condition but I only tested positive for an anti striated antibody, which was “Titin”, but I was also negative for thymoma. Not sure what to make of it

Thanks

Thank you for the information, does a patient have cramps throughout their body with this disease?

In medications section, you might have meant ACETYLCHOLINESTERASE INHIBITORS, not anticholinesterase inhibitors, since ACETYLCHOLINESTERASE breaks down ACH, while ANTICHOLINESTERASE inhibits the function of acetylcholinesterase.

Please move your videos to playlist

My transcript notes of the video: 00:00 hi everyone this lesson is on the condition known as myasthenia gravis so mycenae gravis is an acquired autoimmune condition involving neuromuscular blockade and subsequent muscle weakness we're going to talk about this in more 00:12 detail when we talk about the pathophysiology in the next slide my senior gravis is considered a type 2 hypersensitivity condition and it is the most common neuromuscular junction disorder affecting skeletal muscles 00:25 it is estimated to have a prevalence of 1 in 5 000 people and this data comes from north america and there are different age predispositions for this condition so for instance female patients outnumber male patients with 00:38 this condition below the age of 40 but after the age of 50 male patients outnumber female patients so as a patient gets older the age of onset will change depending on the patient and this is roughly what will happen with patient 00:51 characteristics who have this condition now let's talk about the pathophysiology behind why myasthenia gravis occurs so as mentioned before it is an autoimmune condition and it involves auto antibodies being produced against 01:04 acetylcholine receptors and other muscle components so auto antibodies are antibodies that are produced against the patient's own tissues so before we actually talk about what those antibodies do let's talk about 01:17 what's supposed to happen when a patient wants to contract one of their muscles so if a patient wants to contract one of their muscles they have motor neurons that contain acetylcholine neurotransmitter so motor neurons 01:29 contain vesicles of acetylcholine so when a patient wants to contract one of their muscles acetylcholine is released from the motor neuron and attaches to what are known as nicotinic acetylcholine receptors on the target 01:43 muscle the binding of acetylcholine to these nicotinic acetylcholine receptors leads to contraction of that particular muscle however in the case of mycenia gravis there are these antibodies that are 01:55 formed against particular parts of this apparatus so as you mentioned before one of these autoantibodies is anti-acetylcholine receptor so antibodies against this particular nicotinic acetylcholine receptor another 02:08 auto antibody that can be formed is anti-muscle specific kinase and there are other auto antibodies that we will talk about later on when we talk about diagnosing this condition nevertheless what will happen is that these auto 02:20 antibodies will bind to the nicotinic acetylcholine receptors or other parts of the muscle which will then prevent acetylcholine from binding to those receptors so what essentially happens is in the 02:34 case of anti-acetylcholine receptor antibodies those antibodies actually compete against acetylcholine for those acetylcholine receptors on the target muscle and because of that acetylcholine can't bind to those acetylcholine 02:46 receptors can't activate the target muscle and this will lead to issues like muscle weakness and fatigue other auto antibodies can bind to other parts of the muscle also preventing the proper contraction of that muscle so ultimately 03:00 those auto antibodies can lead to muscle weakness and fatigue and the worst part of this is that as a patient goes through the day and continues to try to contract their muscles their motor neuron will start to deplete 03:11 acetylcholine neurotransmitter leading to less and less acetylcholine being released and less competition for those auto antibodies so those auto antibodies start to win the battle so as the day goes on the patient becomes weaker and 03:26 weaker and has more muscle fatigue this is going to be important when we talk about the signs and symptoms in the next upcoming slides now let's talk about those signs and symptoms so now that we know the pathophysiology we can better 03:37 understand why we see fluctuating muscle weakness and fatigue of heavily used muscle groups heavily used muscle groups because those are the muscle groups that are going to utilize more acetylcholine and it's going to deplete those motor 03:51 neurons so what can often be noted is that the muscle weakness and fatigue worsens with activity and improves with rest so what will be noted is that the weakness gets worse in the afternoon hours into the evening hours and is 04:03 better in the morning and there are particular muscle groups that are more commonly affected in myosinian gravis including the muscles of the eyes the extremities and the throat and we're going to break it down 04:13 and get into more specific details as to each of these muscle groups here in a moment so the first group of muscles we're going to look at are the extra ocular muscles so they're going to be extra ocular muscle weakness so this can 04:24 present as ptosis which is drooping of the eyelid and diplopia which is double vision so you can see here this is ptosis so this would be unilateral poses one-sided and what's important about this ptosis in diplopia or double vision 04:36 is that it is often not present in the morning so a patient wakes up they don't have ptosis or double vision but as the day goes on into the afternoon and evening hours they start to have ptosis in double vision again as we mentioned 04:47 before the ptosis can be unilateral or bilateral so if it is bilateral both eyelids would be affected both would be drooping but oftentimes it's going to be asymmetric meaning that one of them is going to droop more than the other and To get the full transcript and PDF notes with screenshot - try Askify chrome extension tool

Is there any perfect treatment for curing it permanently for 65 aged male person?

My MG started in June of ‘21. Cancerous mass found on my thymus in August of ‘21. Had chemo then thymectomy followed by radiation. Two years no MG symptoms. The double vision has returned… back on Mestinon and had IVIg. No improvement. Now back on prednisone. This sucks

I realized this because I m patient of Mysethnia gravis

few week ago I felt some pains and I went to the hospital my doc told me I had Herpes about 1 yr and I need to start the treatment early from dr oigiangbe 💯

So if you have weak limps that cause falling regularly and arms and hands that can't lift much weight and get fatigued fast and breathing problems that can last weeks; could that be MG ? When you fall on the ground in front of strangers, that's one thing but in front of your employer that's another thing. You can only laugh it off and blame it on the mat once but 3 times in a week and they are wanting a medical examination performed. I managed to get out of it by producing a doctors report that says it's all in my head.

Reverse

Thanks

few week ago I felt some pains and I went to the hospital my doc told me I had Herpes about 1 yr and I need to start the treatment early from dr oigiangbe 💯