39
Navigating Myasthenia Gravis
An Interactive Infographic Journey by Group 39
GO!
Index
Introduction
What is myasthenia gravis?
Pathogenesis
What is the cause of MG?
Objectives
Contextualize your topic
Quiz
Test your knowledge!
Bibliography
References
Symptoms & Treatments
Objectives
Learning Objectives:
- Understand the basis of Myasthenia Gravis
- Understand the pathogenesis of Myasthenia Gravis
- Be able to identify the symptoms of Myasthenia Gravis and relate them back to the pathogenesis.
- Be able to explain the different treatment options for Myasthenia Gravis
What is Myasthenia Gravis?
What is Myasthenia Gravis?
What is Myasthenia Gravis?
Myasthenia Gravis
Healthy
Myasthenia gravis (MG) is a chronic autoimmune neuromuscular disorder characterized by muscle weakness and fatigue, particularly in muscles that control eye movements, facial expressions, chewing, swallowing, and speaking.
What is Myasthenia Gravis?
Etiology of Myasthenia Gravis
In myasthenia gravis, the body's immune system produces antibodies that target and attack proteins involved in communication between nerve cells and muscle cells at the neuromuscular junction. These proteins include the acetylcholine receptors or other proteins such as muscle-specific tyrosine kinase (MuSK). The attack on these proteins interferes with the normal transmission of nerve impulses to the muscles, leading to weakness and fatigue, which worsens with activity and improves with rest.
What is Myasthenia Gravis?
Risk Factors
The severity and distribution of muscle weakness can vary widely among individuals with myasthenia gravis. Risk factors include genetics, other dieseases, and environmental factors.
Age and Sex
Family History
Thymus Abnormalities
Autoimmune Diseases
Pathogenesis
Pathogenesis
What causes Myasthenia Gravis?
Myasthenia Gravis
Pathogenesis Overview
The pathogenesis of myasthenia gravis involves an immune-mediated attack on the neuromuscular junction which is where nerve cells communicate with muscles.Click the button to see an overview of the key steps.
+ Key steps
Pathogenesis
Key Steps of Myasthenia Gravis
1. Autoimmune Response
In MG, the immune system mistakenly identifies the acetylcholine receptors (AChR) on the muscle cells as foreign or abnormal. The majority of MG cases (around 85%) involve antibodies directed against the AChR, which is crucial for transmitting nerve signals to muscles.
2. Formation of Auto-Antibodies
The immune system produces autoantibodies, specifically immunoglobulin G (IgG) antibodies, against the AChR. These antibodies bind to the AChR on the surface of muscle cells, particularly at the neuromuscular junction.
Pathogenesis
Key Steps of Myasthenia Gravis
3. Blocking of Acetylcholine Receptors
The binding of autoantibodies to AChR leads to the blocking or destruction of these receptors. As a result, the normal communication between nerve cells and muscles is impaired because acetylcholine, the neurotransmitter responsible for transmitting signals, cannot effectively bind to its receptors.
4. Reduced Signal Transmission
With fewer functional acetylcholine receptors, the transmission of nerve impulses to muscles is compromised. This impairment results in muscle weakness and fatigue, especially during repetitive or sustained muscle activity.
Pathogenesis
Key Steps of Myasthenia Gravis
Other Autoantibodies
Thymus Involvement
+INFO
+INFO
Symptoms & Treatments
Symptoms
Six Prelevent Markers
Treatments
To manage myasthenia gravis
Monitoring and Support - Avoid medications that may worsen symptoms - Adequate rest - Nutritional support
Thymectomy Surgical removal of the thymus gland
Medications - Cholinesterase inhibitors - Immunosuppressants - Intravenous immunoglobin (IVIG) or plasma exchange
Syptomatic Treatment - Physical therapy - Respiratory Support
+INFO
+INFO
+INFO
+INFO
Quiz
Question 1/5
Symptoms
Question 2/5
Pathogenesis
Question 3/5
Treatments
Question 4/5
Treatments
Question 5/5
Basis of Myasthenia Gravis
Bibliography
01
02
03
Bibliography
04
05
06
Bibliography
07
08
09
Bibliography
10
11
12
13
Lesson learned!
Individuals with other autoimmune diseases, such as rheumatoid arthritis, lupus, or thyroid disorders, may have an increased risk of developing myasthenia gravis.
People with abnormalities of the thymus gland are at higher risk. This includes individuals with thymomas (tumors of the thymus gland) or those with thymic hyperplasia (overgrowth of the thymus gland).
Although myasthenia gravis is not usually inherited, there can be a familial predisposition, meaning that multiple members of the same family may be affected, though not necessarily in a predictable pattern.
Myasthenia gravis can affect people of any age, but it's most commonly diagnosed in women under 40 and men over 60.
Other Antibodies
Can contribute to Myasthenia Gravis
While AChR antibodies are most common, some individuals with MG have antibodies against other components of the neuromuscular junction, such as muscle-specific kinase (MuSK) or lipoprotein receptor-related protein 4 (LRP4).
Key Steps
Pathogenesis of MG
- Autoimmune Response
- Formation of Autoantibodies
- Blocking of Acetylcholine Receptors
- Reduced Signal Transmission
Thymus Involvement
Myasthenia Gravis Pathogenesis
The thymus, a gland located in the chest, plays a role in the development of MG in some cases. In individuals with MG, the thymus may be abnormal and could contain clusters of immune cells.
Thymomas are found in a small percentage of MG patients, but the exact relationship between thymic abnormalities and MG is not fully understood.
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Transcript
39
Navigating Myasthenia Gravis
An Interactive Infographic Journey by Group 39
GO!
Index
Introduction
What is myasthenia gravis?
Pathogenesis
What is the cause of MG?
Objectives
Contextualize your topic
Quiz
Test your knowledge!
Bibliography
References
Symptoms & Treatments
Objectives
Learning Objectives:
What is Myasthenia Gravis?
What is Myasthenia Gravis?
What is Myasthenia Gravis?
Myasthenia Gravis
Healthy
Myasthenia gravis (MG) is a chronic autoimmune neuromuscular disorder characterized by muscle weakness and fatigue, particularly in muscles that control eye movements, facial expressions, chewing, swallowing, and speaking.
What is Myasthenia Gravis?
Etiology of Myasthenia Gravis
In myasthenia gravis, the body's immune system produces antibodies that target and attack proteins involved in communication between nerve cells and muscle cells at the neuromuscular junction. These proteins include the acetylcholine receptors or other proteins such as muscle-specific tyrosine kinase (MuSK). The attack on these proteins interferes with the normal transmission of nerve impulses to the muscles, leading to weakness and fatigue, which worsens with activity and improves with rest.
What is Myasthenia Gravis?
Risk Factors
The severity and distribution of muscle weakness can vary widely among individuals with myasthenia gravis. Risk factors include genetics, other dieseases, and environmental factors.
Age and Sex
Family History
Thymus Abnormalities
Autoimmune Diseases
Pathogenesis
Pathogenesis
What causes Myasthenia Gravis?
Myasthenia Gravis
Pathogenesis Overview
The pathogenesis of myasthenia gravis involves an immune-mediated attack on the neuromuscular junction which is where nerve cells communicate with muscles.Click the button to see an overview of the key steps.
+ Key steps
Pathogenesis
Key Steps of Myasthenia Gravis
1. Autoimmune Response
In MG, the immune system mistakenly identifies the acetylcholine receptors (AChR) on the muscle cells as foreign or abnormal. The majority of MG cases (around 85%) involve antibodies directed against the AChR, which is crucial for transmitting nerve signals to muscles.
2. Formation of Auto-Antibodies
The immune system produces autoantibodies, specifically immunoglobulin G (IgG) antibodies, against the AChR. These antibodies bind to the AChR on the surface of muscle cells, particularly at the neuromuscular junction.
Pathogenesis
Key Steps of Myasthenia Gravis
3. Blocking of Acetylcholine Receptors
The binding of autoantibodies to AChR leads to the blocking or destruction of these receptors. As a result, the normal communication between nerve cells and muscles is impaired because acetylcholine, the neurotransmitter responsible for transmitting signals, cannot effectively bind to its receptors.
4. Reduced Signal Transmission
With fewer functional acetylcholine receptors, the transmission of nerve impulses to muscles is compromised. This impairment results in muscle weakness and fatigue, especially during repetitive or sustained muscle activity.
Pathogenesis
Key Steps of Myasthenia Gravis
Other Autoantibodies
Thymus Involvement
+INFO
+INFO
Symptoms & Treatments
Symptoms
Six Prelevent Markers
Treatments
To manage myasthenia gravis
Monitoring and Support - Avoid medications that may worsen symptoms - Adequate rest - Nutritional support
Thymectomy Surgical removal of the thymus gland
Medications - Cholinesterase inhibitors - Immunosuppressants - Intravenous immunoglobin (IVIG) or plasma exchange
Syptomatic Treatment - Physical therapy - Respiratory Support
+INFO
+INFO
+INFO
+INFO
Quiz
Question 1/5
Symptoms
Question 2/5
Pathogenesis
Question 3/5
Treatments
Question 4/5
Treatments
Question 5/5
Basis of Myasthenia Gravis
Bibliography
01
02
03
Bibliography
04
05
06
Bibliography
07
08
09
Bibliography
10
11
12
13
Lesson learned!
Individuals with other autoimmune diseases, such as rheumatoid arthritis, lupus, or thyroid disorders, may have an increased risk of developing myasthenia gravis.
People with abnormalities of the thymus gland are at higher risk. This includes individuals with thymomas (tumors of the thymus gland) or those with thymic hyperplasia (overgrowth of the thymus gland).
Although myasthenia gravis is not usually inherited, there can be a familial predisposition, meaning that multiple members of the same family may be affected, though not necessarily in a predictable pattern.
Myasthenia gravis can affect people of any age, but it's most commonly diagnosed in women under 40 and men over 60.
Other Antibodies
Can contribute to Myasthenia Gravis
While AChR antibodies are most common, some individuals with MG have antibodies against other components of the neuromuscular junction, such as muscle-specific kinase (MuSK) or lipoprotein receptor-related protein 4 (LRP4).
Key Steps
Pathogenesis of MG
Thymus Involvement
Myasthenia Gravis Pathogenesis
The thymus, a gland located in the chest, plays a role in the development of MG in some cases. In individuals with MG, the thymus may be abnormal and could contain clusters of immune cells.
Thymomas are found in a small percentage of MG patients, but the exact relationship between thymic abnormalities and MG is not fully understood.