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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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Graves' Disease│Hyperthyroidism│My Story
Graves' Disease Characteristics
Graves' Disease Labs and Treatment
Hyperthyroidism: Overview & Graves' Disease
Graves disease and p. 346
Graves disease p. 346
autoantibody p. 113
goiter caused by p. 346
HLA-DR3 and p. 98
hyperthyroidism p. 346
type II hypersensitivity p. 110
First described by Irish surgeon Robert James Graves, Graves disease is an autoimmune disorder that causes hyperthyroidism.
In hyperthyroidism, ‘hyper’ refers to having too much, and ‘thyroid’ refers to thyroid hormone, so Graves disease refers to a condition where there’s excess thyroid hormones.
Normally, the hypothalamus, which is located at the base of the brain, detects low blood levels of thyroid hormones and releases thyrotropin-releasing hormone into the hypophyseal portal system - which is a network of capillaries linking the hypothalamus to the anterior pituitary.
The anterior pituitary then releases thyroid-stimulating hormone, also called thyrotropin or simply TSH.
TSH stimulates the thyroid gland which is a gland located in the neck that looks like two thumbs hooked together in the shape of a “V”.
The thyroid gland is made up of thousands of follicles, which are small spheres lined with follicular cells.
Follicular cells convert thyroglobulin, a protein found in follicles, into two iodine-containing hormones, triiodothyronine or T3, and thyroxine or T4.
Once released from the thyroid gland, these hormones enter the blood and bind to circulating plasma proteins.
Only a small amount of T3 and T4 will travel unbound in the blood, and these two hormones get picked up by nearly every cell in the body.
Once inside the cell T4 is mostly converted into T3, and it can exert its effect.
T3 speeds up the basal metabolic rate.
So as an example, they might produce more proteins and burn up more energy in the form of sugars and fats.
It’s as if the cells are in a bit of frenzy.
T3 increases cardiac output, stimulates bone resorption - thinning out the bones, and activates the sympathetic nervous system, the part of the nervous system responsible for our ‘fight-or-flight’ response.
Graves' disease is an autoimmune disorder in which the body produces thyroid-stimulating antibodies, leading to the overproduction of thyroid hormone. People with Graves' disease present with ophthalmopathy, weight loss, anxiety, tremors, irritability, muscle weakness, and diarrhea.
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