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Type I hypersensitivity
Autoimmune hemolytic anemia
Hemolytic disease of the newborn
Rheumatic heart disease
Type II hypersensitivity
Systemic lupus erythematosus
Type III hypersensitivity
Type IV hypersensitivity
Common variable immunodeficiency
Hyperimmunoglobulin E syndrome
IgG subclass deficiency
Isolated primary immunoglobulin M deficiency
Selective immunoglobulin A deficiency
Adenosine deaminase deficiency
Hyper IgM syndrome
Severe combined immunodeficiency
Cytomegalovirus infection after transplant (NORD)
Post-transplant lymphoproliferative disorders (NORD)
Chronic granulomatous disease
Leukocyte adhesion deficiency
Blood transfusion reactions and transplant rejection: Pathology review
Immunodeficiencies: Combined T-cell and B-cell disorders: Pathology review
Immunodeficiencies: Phagocyte and complement dysfunction: Pathology review
Immunodeficiencies: T-cell and B-cell disorders: Pathology review
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Myasthenia Gravis - My Symptoms
Myasthenia Gravis & Lambert-Eaton Myasthenic Syndrome
myasthenia gravis p. 480
myasthenia gravis diagnosis p. 479
autoantibody p. 113
diagnosis of p. 239
neostigmine for p. 239
as paraneoplastic syndrome p. 219
pyridostigmine for p. 239
restrictive lung disease p. 696
thymoma association p. 96
type II hypersensitivity p. 110
myasthenia gravis p. 479
myasthenia gravis treatment p. 480
myasthenia gravis association p. 479
myasthenia gravis and p. 219, 479
Myasthenia gravis, is a Latin expression that literally means “grave muscle weakness,” which perfectly describes the weakness that happens when this autoimmune disease affects the skeletal muscles.
People with myasthenia gravis might wake up feeling fine, but get progressively weaker as the day goes on and by the end of the day they might feel very weak, sometimes even getting weaker with repetitive movements like chopping vegetables.
Myasthenia gravis can affect the extraocular muscles, which control movement of the eye as well as the eyelids, so individuals might have diplopia or double vision, as well as ptosis, or drooping eyelids.
Myasthenia gravis preferentially affects young women in their 20s and 30s and older men in their 60s and 70s, but the cause of this odd “bimodal” distribution of age-of-onset isn’t quite clear.
To better understand myasthenia gravis, let’s review normal muscle contraction but at the cellular level.
First you’ve got your motor neurons that release the neurotransmitter acetylcholine at the neuromuscular junction, which then binds to nicotinic acetylcholine receptors on muscle cell membranes.
Binding of acetylcholine to its receptor activates a chain reaction in the muscle cell that ultimately results in muscle contraction.
But what happens in myasthenia gravis though? Well remember that it’s an autoimmune disease, specifically one that’s categorized as a type II hypersensitivity which causes cytotoxic injury meaning that it results in the lysis or death of host cells, which is mediated by autoantibodies, which are antibodies that are specific for our own cells or proteins.
Alright, so in this case, the patient’s B cells inappropriately make antibodies that bind to nicotinic acetylcholine receptors on the muscle cells.
Myasthenia gravis is an autoimmune disease, specifically a type II hypersensitivity disorder, which is characterized by autoantibodies against nicotinic acetylcholine receptors on the surface of muscle cells.
The antibodies block the receptors which means the signal to contract isn't received. Those antibodies also activate the complement pathway which leads to muscle cell destruction.
Symptoms can range from mild to severe and may include drooping eyelids, difficulty speaking or swallowing, and muscle weakness in the arms and legs. Treatment involves immunosuppressive drugs like prednisolone, and acetylcholinesterase inhibitors like neostigmine. The purpose is to reduce the immune system's attack on the muscle and to increase muscle strength.
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