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Myasthenia Gravis - case study

Bukidnon state university.

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Preview text, mabini extension, cabanatuan city 3100 nueva ecija, college of nursing, myasthenia gravis: a case presentation, a case presented to college of nursing of wesleyan university-philippines, submitted by: bsn 2-3 (group 2), in partial fulfillment of the requirements for the ncm 104 (lec) community health nursing, cuadra, mica dr., cudal, yvette nicole, daclag, jasmin d., del mundo, angel alexa, diaz, jianna cailee d., dionisio, ivan b., encarnacion, gail, engaran, trisha joyce, estabillo, geumi p., ferry, john kenley db., december 5, 2022, table of contents, title page................................................................................................................................., table of contents................................................................................................................, case overview............................................................................................................., problem cues and family nursing diagnosis............................................................, definition.........................................................................................................................., synonyms.............................................................................................................................., causative agent........................................................................................................., risk factors (modifiable)................................................................................................., risk factors (non-modifiable) ......................................................................................, clinical manifestations..................................................................................................., diagnostic tests........................................................................................................., phatophysiology............................................................................................................, objective of management........................................................................................., medication management............................................................................................., surgical management......................................................................................................, complications.................................................................................................................., signs that the illness is under control according to patient....................., prevention............................................................................................................................., doh program........................................................................................................................, references....................................................................................................................., risk factors (modifieble),  emotional stress and excitement,  some medications,  pregnancy and delivery,  menstrual periods, risk factors (non-modifieble),  autoimmune reaction,  age of 20-30y/o (female),  age of 60-70y/o (male),  abnormalities of the thymus gland,  genes – having specific genetic markers called hla-b8 or dr,  neonates with mothers who have abnormal antibodies – entered the baby’s body, via the placenta during pregnancy., clinical manifestations, manifestations to look out for,  weakness of the eye muscles (called ocular myasthenia),  drooping of one or both eyelids (ptosis),  blurred or double vision (diplopia),  a change in facial expression,  difficulty swallowing,  shortness of breath,  impaired speech (dysarthria),  weakness in the arms, hands, fingers, legs, and neck., manifestations that the patient experienced,  ang pogi ni kenley, diagnostic test, neurological exam.

• This may include testing your reflexes, muscle strength, muscle tone, senses of

touch and sight, gait, posture, coordination, balance and mental skills. Impaired

Eye movement or muscle weakness may prompt a doctor to evaluate further., blood tests.

• The main test for myasthenia gravis is a blood test to look for a type of antibody

(produced by the immune system) that stops signals from being sent between

The nerves and muscles. a test like the anti-acetylcholine receptor antibody is a, great example..

• If you have a droopy eyelid, your doctor might place a bag filled with ice on your

eyelid. After two minutes, your doctor removes the bag and analyzes your droopy

Eyelid for signs of improvement., edrophonium test.

• A short-acting drug called edrophonium chloride (Tensilon®) is given

intravenously. If weakness, especially in the eye muscles, briefly and temporarily

Improves, it indicates you may have mg., nerve conduction studies, o normally, the acth binds with nachr to produce muscle contraction, but, patients with myasthenia gravis have abnormalities in terms of how they, bind or transmit certain signals. here comes,  the impaired transmission takes place because the antibodies block, alter, or, destroy the receptors that acth was supposed to bind within the neuromuscular,  fewer receptors occur because of how the antibodies block the supposedly, binding of acetylcholine and the nicotinic receptors.,  if not enough acth and nachr bind, it will not be enough to support muscle, contraction and will therefore lead to muscle weakness which is a number one, symptom and impact of myasthenia gravis., further explanation of the impaired transmission,  acetylcholine is released by the cholinergic fibers, in fact, are neurons.,  immediately after acth is released, it will travel down or diffuse across the,  since the antibodies already blocked or destroyed the nicotinic receptors,,  depolarization and muscle contraction don't occur and neuromuscular, transmission is a block, o what is the involvement of depolarization in this situation,  because the activation or the presence of the nachr leads to the, flow of cations (sodium and calcium) that causes depolarization of, the muscle cell membrane. in turn, depolarization results in muscle, contractions.,  neuromuscular blocking or disturbance results in muscle weakness/paralysis., objective of management, 1. increase general muscle function, a. moderate physical activity, b. the type and intensity of systematic training are adapted by the patient., 2. intake of any of these medications to relieve signs and symptoms, a. cholinesterase inhibitors, b. corticosteroids, c. immunosuppressants, 3. minimize the neuromuscular disease, a. thymectomy (surgical), b. intravenous therapy, 4. dietary considerations, a. eats during periods when patients have more strength..

• 5-6 smaller meals throughout the whole day rather than 3 larger meals.

b. A low-sodium, high-potassium diet may be advised to prevent fluid retention,

As well as supplements to maintain bone health..

• Vitamin D, Calcium, Astragalus, Creatine

MEDICATION MANAGEMENT

Pyridostigmine,  it can reduce muscle weakness, but the effect only lasts for a few hours so, the patient needs to take it several times a day, myasthenic crisis.

• A complication of myasthenia gravis that is life-threatening. This arises

whenever the respiratory muscles an individual employs become so poor

That one cannot breathe the air either into or out of the lungs. due to the, respiratory muscles' weakening, respiratory failure happens, necessitating, mechanical ventilation., cholinergic crisis.

• Once edrophonium is administered to the patient, a cholinergic crisis

occurs when such weakness does not resolve but rather worsens.

Edrophonium - anticholinesterase agent and injection used to help, diagnose myasthenia gravis and may help select the proper treatment. it, is also used to reverse the effects of certain muscle relaxants., heart disease.

• Heart muscle is a target for autoimmune inflammation in myasthenia

gravis. Symptoms overlap with myasthenia and may result in failure to

Recognize cardiac involvement. people with mg are at risk of muscle, weakness spreading to their heart muscles..

• The thymus gland is crucial to the immune system's functionality. The

thymus gland is frequently hyperactive, and excessively big, or MG

Patients frequently have immune cell concentrations in their thymus gland, and it may develop or result in thymomas. these are tumors, which are, located on the thymus gland, and could or could not be cancerous., signs that the illness is under control according to the, multidisciplinar teams, - presentations are communication tools that can be used as, demonstrations, lectures, speeches, reports, and more. it is mostly, presented before an audience., electronic medical records, 24/7support, there is no way to prevent myasthenia gravis. however, if you have the condition, there, are steps you can take to prevent your symptoms from worsening, including:,  reduce stress.,  prevent infections.,  avoid getting too hot or too cold,  don’t overdo it,  seek accommodations at work if necessary, doh program, medical management.

• nhs/conditions/myasthenia-gravis/treatment/#:~:text=The

%20first%20medicine%20used%20for,it%20several%20times%20a

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The Biology Corner

Biology Teaching Resources

Case Study – The Mystery of Muscle Weakness

Bring neuromuscular disorders to life in your high school anatomy classroom with this case study on myasthenia gravis! Designed to illustrate the complex interactions between nerves, muscles, and the immune system, this resource uses the story of a relatable character, Elena, to make advanced anatomy concepts accessible and engaging. Discover why Elena is feeling tired and has muscle weakness.

Through Elena’s journey with muscle fatigue and her ultimate diagnosis, students will understand how anatomy concepts apply to real-life medical cases. They’ll explore symptoms, testing methods, and treatment options in the context of an authentic patient scenario.

The case study introduces myasthenia gravis, giving students insight into how autoimmune diseases can impact muscle function. Each section builds on their understanding of anatomy and physiology in a way that’s both educational and relatable.

Note: This resource is similar to a previous case study, “ The Tired Swimmer .” This updated version includes access to answer key on TpT and more details on the diagnostics of myasthenia gravis.

Step-by-Step Guided Sections

1 : Introduces Elena and her symptoms, helping students recognize signs of muscle weakness and fatigue.

2 : Diagnostic testing, including electromyograms (EMGs), antibody tests, and the ice pack test, emphasizing how doctors assess neuromuscular function.

3 : Explains the anatomy of the neuromuscular junction and the autoimmune mechanism behind myasthenia gravis.

4 : Focuses on treatment options and outcomes, highlighting how medications and lifestyle changes can manage symptoms.

Each section includes targeted questions that reinforce key concepts and prompt critical thinking. This activity is ideal for units on muscle physiology, nervous system function, and immune disorders.

By following Elena’s experiences, students will gain a better understanding of how medical professionals diagnose and treat disorders, building both scientific knowledge and empathy for individuals with chronic illnesses.

Engage your students in a story-driven, scientific exploration of myasthenia gravis with our expertly crafted case study—an interactive resource that bridges textbook learning with real-world application. Perfect for high school anatomy and health science teachers looking to enrich their curriculum and captivate their students!

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Shannan Muskopf

Myasthenia Gravis: A Neurologist’s Perspective

Jun 28, 2013

570 likes | 943 Views

Myasthenia Gravis: A Neurologist’s Perspective. M. Nicolle MD FRCPC D. Phil. Introduction. This PowerPoint presentation is based on one given to the Myasthenia Gravis Ontario Chapter in Etobicoke Ontario, Canada.

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Presentation Transcript

Myasthenia Gravis: A Neurologist’s Perspective M. Nicolle MD FRCPC D. Phil.

Introduction • This PowerPoint presentation is based on one given to the Myasthenia Gravis Ontario Chapter in Etobicoke Ontario, Canada. • Many of the products discussed in this presentation are not ‘officially’ approved to treat Myasthenia Gravis. However, most are widely used by neurologists who manage patients with MG. In many cases investigations are underway. • The material in this presentation is intended for patient educational purposes only. It should not be used in place of advice from your neurologist or family physician. • Acknowledgements:I thank Talecris Biotherapeutics for making this educational CD possible through an unrestricted education grant. M. Nicolle MD FRCPC D. Phil.

Overview • What is MG - an introduction • Treatment of MG • Management issues • Future

Myasthenia Gravis • An autoimmune disease in which the immune system attacks a protein on the surface of muscle • Autoimmune disease = a disease in which parts of the immune system are overactive and start to damage the body tissues • A normal immune system attacks ‘foreign’ organisms - for example infections • In an autoimmune disease the immune system inappropriately damages normal body tissues antibodies

Cause of Myasthenia Gravis • Unknown • One of many “autoimmune diseases” • A basic problem with the immune system - parts of it are overactive • Individuals with MG and their family members more likely to have one of these other autoimmune diseases

What are Antibodies (Immunoglobulins)? • Antibodies are proteins that play an important role in the immune system. • They are normally directed at foreign proteins called antigens that attack the body. • Such foreign proteins include bacteria and viruses. • Antibodies help the body to protect itself from these foreign proteins.

Autoimmune Antibody Molecular Mimicry Infection “Foreign protein” e.g.“Self protein” bacteria Acetylcholine receptor

Myasthenia Gravis - the symptoms • Weakness • Fluctuates • Worse with use, at end of day • Periods of remission, periods of worsening • Involving • Eyes - double vision and droopy eyes • Usually the first symptom • Face - facial weakness • Speech - slurred or hoarse • Swallowing problems • Breathing problems • Arm weakness - carrying, lifting • Leg weakness - stairs and chairs

But.... • Many other diseases can cause weakness, tiredness and fatigue - even if you have myasthenia • Not all symptoms in someone who has MG are directly related to MG • Sometimes treatments for MG can worsen the symptoms of weakness if the weakness is caused by something other than MG. • Important to know the cause of weakness

These are not symptoms of Myasthenia Gravis: • Pain • Memory loss • Numbness • Sleepiness (at least directly)

Other things that can bring out or worsen the symptoms of Myasthenia Gravis • Pregnancy • Stress • Operations • Medications • Some • Many lists - none are absolutely contra-indicated

Cause of Myasthenia Gravis • No evidence that MG is caused by: • Mercury fillings in teeth • Poor diet • Environmental exposure • Accidents or trauma • Not contagious

Cause of Myasthenia Gravis • There are non-immune hereditary forms of MG • Congenital myasthenic syndromes • Very rare - 1/1,000,000 • Most start at birth - some later

Neuromuscular junction • Normally, nerves ‘talk’ to muscles to make them move • This occurs at the junction between nerves and muscles • The neuromuscular junction

Normal Neuromuscular junction • Acetylcholine (ACh), a chemical messenger, is formed in the motor nerve terminal and stored in vesicles • When an action potential (signal) travels down a motor nerve and reaches the nerve terminal, ACh is released and combines with ACh receptors on muscle fibers, triggering muscle contraction. • The process is terminated by the breakdown of ACh by acetylcholinesterase.

Myasthenia Gravis • The most prevalent cause of myasthenia gravis is an autoimmune disorder in which thepatient produces antibodies that attack the(acetylcholine)receptorat the neuromuscular junction. • In MG, the key defect is a decrease in the number of available ACh receptors at the muscle membrane. • This results in decreased efficiency of neuromuscular transmission, leading to weak muscle contractions.

Receptors blocked by antibodies Acetylcholine Nerve Neuron Ach receptor Muscle Reduced transmission Normal Muscle Contraction Impaired Muscle Contraction Myasthenia Gravis Normal neuromuscular junction Neuromuscular junction in myasthenia gravis

Diagnosis of Myasthenia Gravis • Suspect it • Tensilon test • Electrical studies - repetitive nerve stimulation or single fiber EMG • Anti-acetylcholine receptor antibodies or other antibodies

Diagnosis of Myasthenia Gravis • Suspect it - often the biggest delay • Characteristic pattern of weakness • Everyone is different - some don’t have characteristic pattern • Fluctuation in weakness • No other cause • On average 1-2 years between first symptoms and diagnosis • Weakness fluctuates - now you see it now you don’t • Uncommon disease

Diagnosis of Myasthenia Gravis • Anti-acetylcholine receptor antibodies • Measured in the blood • Positive in 50% with “ocular MG” and 85% with “generalized MG” • Expensive ($150) • 4-6 Weeks for results

Seronegative Myasthenia Gravis • Some patients don’t have antibodies against the acetylcholine receptor • 50% of those with only eye symptoms - “ocular MG” • 15% of those with generalized MG • Seronegative MG” • Not MG • MG but non-immune • Congenital myasthenic syndromes • Immune MG but autoimmune attack is against something other than the acetylcholine receptor • MuSK • Others?

Treatment of Myasthenia Gravis • Individualized • Don’t compare your drugs/doses to the person beside you • The treatment changes over time • Which drugs used, and doses of these drugs depends on your disease severity and other health problems • In most people involves combinations of drugs

Treatment of Myasthenia Gravis • The overall goal is to get you better and then start reducing the drugs to try and avoid side effects • Attempts at reducing drugs while you still have MG symptoms are usually not successful • Although we try it sometimes if side effects are a problem • For this to work your neurologist must know which symptoms are a result of MG and which are not

Treatment of Myasthenia Gravis--Disclaimer • Many of the products discussed in this presentation are not ‘officially’ approved to treat Myasthenia Gravis. However, most are widely used by neurologists who manage patients with MG. In many cases investigations are underway.

Treatment of Myasthenia Gravis • Treat the symptoms • Mestinon (pyridostigmine) • Treat the immune problem - immunosuppression • Prednisone • Imuran (azathioprine) • Mycophenolate mofetil (Cellcept) • Cyclosporine (Neoral) • others • Short term fixes • Long term fixes?

Treating the symptoms - Mestinon • Increases the amount of acetylcholine available to make the muscles move • If it works, improvement within hours • Inexpensive • Few serious side effects • Doesn’t treat underlying problem with immune system

Immunosuppression - Prednisone • Suppresses immune system • Works in most people • Takes months • 1 month minimum • 3-6 months optimum • Sometimes 12 months • Many side effects - some serious • Smallest dose for shortest time possible • When going through this -remember the light at the end of the tunnel

Immunosuppression - Imuran (Azathioprine) • Works well in MG • Allows the use of lower doses of prednisone • However, takes 12 months or longer • Fewer side effects but needs monitoring with blood tests • Flu-like • Liver • Blood counts • ? Cancer of lymph glands (probably not in MG)

Immunosuppression - Mycophenolate mofetil (Cellcept) • First used to suppress immune system after transplants • Expensive • $15-20/day • No proof that it is any better than prednisone • May have fewer side effects compared to either prednisone or Imuran • Onset of benefits fairly rapid - 2-4 months

Immunosuppression - Other drugs • Any medication which suppresses the immune system • Cyclosporine (Neoral) • Methotrexate • Cyclophosphamide ....others

Short term fixes - What if I really get in trouble and the medications aren’t working?

Temporary treatments in Myasthenia Gravis • Plasma exchange (PLEx) • Removes the antibodies which cause weakness • Benefits in 70% of patients within two weeks • Few serious side effects • More difficult to arrange short notice Plasma exchange (PLEx)

Temporary treatments in Myasthenia Gravis • Intravenous immunoglobulin (IVIg) • A blood product – safe • IVIGs are a concentrated preparation of human antibodies, produced from plasma pooled from thousands of blood donors • Modulates the immune system - ? How • Benefit in 70% of patients within two weeks • Common side effects are mild • IVIg = PLEx in terms of benefit in MG • Neither are recommended for long term treatment of MG • Both are expensive : $8-10,000 per round of treatment

What is IVIG?

Blood Components Blood contains: Red Blood Cells, White Blood Cells, Platelets, and Plasma

Separation of Blood Components Centrifugation: a way to separate out particles

Useful Blood Components

Useful Blood Products Albumin ATIII Shock, plasma exchange, burn therapy Coagulation Disorders plasma Alpha1-proteinase inhibitor FVIII Hemophilia Immunoglobulins PI-deficiency IVIG Hyperimmunes Tetanus, rabies, HepB IVIGs are a concentrated preparation of antibodies

How does IVIg work in MG?Possible mechanisms • The infused antibodies will, for a time, dilute the abnormal host antibodies that are causing the diseases • The presence of large amounts of IgG will also suppress the production of host IgG and increases its breakdown • The donated antibodies will also bind to the other components of the immune system, thereby using up resources, resulting in fewer immune resources to do damage • The infused antibodies may bind to host antibodies, including those causing disease, and take them out of action

IVIg infusion ‘Good’ antibodies against bad antibodies How does IVIg work in MG?One possible mechanism Acetylcholine receptor ‘Bad’ antibody against AChR

Mechanism of Immune Suppression with IVIg • The infused antibodies will, for a time, dilute the abnormal host antibodies that are causing the diseases • IVIg also increases the breakdown of host immunoglobulin “good” antibodies in IVIG “bad” auto- antibodies in MG

Y Y The presence of large amounts of IgG will also suppress the production of host IgG Auto-Antibody Production in Myasthenia Gravis Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y B-cell Plasma cell Autoantibody production Y Y IVIG Infusion Y Y Y Y Y Y Y Y Y Y Y Suppression of autoantibody production Adapted from Israels & Israels (2002) Mechanisms in Hematology (3rd Edition)

The infused antibodies may bind to host antibodies, including those causing disease, and take them out of action Autoimmune antibodies IVIG Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y Y

The infused (IVIG) antibodies may bind to host autoantibodies, including those causing disease, and take them out of action

Long-term - Is there a cure? • Although MG is highly treatable - there is no cure (yet) • Most patients end up on medications for years or forever, but do very well • With medical (pills) treatment over 90% of individuals will get better • Expense, life-long treatment, side effects

Long term - Is there a cure? • Thymectomy may offer chance for drug-free remission in some patients • Early onset (< 50 years) • Generalized (not just ocular) • Within 2-3 years of disease onset • Seropositive (AChR antibodies) • Trans-sternal thymectomy • ? Cervical ? Video-assisted • What we think (not what we know) • Without treatment 20% of MG patients will have a sustained (years) remission • After thymectomy in young MG patients it doubles to about 40% • Another 30-40% are better, but not off medications and therefore not “cured” • …………..Current international research trial may answer this

? Management issues • You’re not getting better • Where do you get information? • What about other drugs - what is safe to take?

You’re not getting better - why? • You don’t have MG • Not all weakness = MG • If you’re going to take drugs which can cause side effects, make sure you have MG first • I see 1-2 patients a year who have been diagnosed with, and treated for MG which I don’t think they ever had. • Many GPs will never see a case • MG is a rare disease - affects roughly 1 in 10,000 individuals • 4-5 GPs X 2-3,000 patients in each practice = one case of MG • Even some neurologists may only see 1-2 cases in a year

You’re not getting better - why? • You do have MG • You aren’t on the right drugs or on the right doses • You’re not taking your medications • You haven’t been on them long enough • Although you have MG, it isn’t the cause of your symptoms • ‘Weakness’ ≠ weakness • Other diseases • Side effects of medications • Depression • You have severe MG

You’re not getting better • You do have MG • Although you have MG, it isn’t the cause of your symptoms • `Weakness’ ≠ weakness

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