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Type I hypersensitivity
Type II hypersensitivity
Immune thrombocytopenic purpura
Autoimmune hemolytic anemia
Hemolytic disease of the newborn
Rheumatic heart disease
Type III hypersensitivity
Systemic lupus erythematosus
Type IV hypersensitivity
Cytomegalovirus infection after transplant (NORD)
Post-transplant lymphoproliferative disorders (NORD)
Selective immunoglobulin A deficiency
Common variable immunodeficiency
IgG subclass deficiency
Hyperimmunoglobulin E syndrome
Isolated primary immunoglobulin M deficiency
Severe combined immunodeficiency
Adenosine deaminase deficiency
Hyper IgM syndrome
Leukocyte adhesion deficiency
Chronic granulomatous disease
Blood transfusion reactions and transplant rejection: Pathology review
Immunodeficiencies: T-cell and B-cell disorders: Pathology review
Immunodeficiencies: Combined T-cell and B-cell disorders: Pathology review
Immunodeficiencies: Phagocyte and complement dysfunction: Pathology review
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myasthenia gravis p. 484
myasthenia gravis diagnosis p. 483
autoantibody p. 113
diagnosis of p. 241
neostigmine for p. 241
as paraneoplastic syndrome p. 221
pyridostigmine for p. 241
restrictive lung disease p. 700
thymoma association p. 96
type II hypersensitivity p. 110
myasthenia gravis p. 483
myasthenia gravis treatment p. 484
myasthenia gravis association p. 483
myasthenia gravis and p. 221, 483
Tanner Marshall, MS
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.
Once acetylcholine receptors are bound by the antibody, they are unable to bind to acetylcholine, and therefore don’t respond to the “contract” signal from the central nervous system.
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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