Hypersensitivities I-IV Flashcards
What is the mechanism for type II hypersensitivities?
Either IgG or IgM is made against normal self antigens or a foreign antigen resembling some molecule on the surface of host cells enters the body
What does the binding of antibodies to the surface of host cells lead to?
Opsonization of the host cells. Activation of the classical complement pathway.ANTIBODY-DEPENDENT CELLULAR CYTOTOXICITY (ADCC) destruction of the host cells
What are some examples of antibody-dependent cytotoxicity (type II hypersensitivities) diseases?
transfusion rxns, ITP, Hastiomoto’s thyroiditis, Grave’s, myasthenia gravis, goodpasture’s, MS
What is the most common adverse rxn to a blood transfusion?
febrile non-hemolytic transfusion rxn. fever and dyspnea
What are symptoms of an acute hemolytic transfusion rxn?
feeling of doom, chills, fever, and pain in the back and flanks
What is delayed hemolytic transfusion rxn?
donor RBCs are destroyed by the recipient’s antibodies, but the hemolysis is “delayed” because the antibodies are only present in low amounts initially.
Why is a delayed hemolytic transfusion rxn difficult to prevent?
by the time a cross match is done, the level of antibody in the recipient’s plasma is too low to cause agglutination
What do IgG antibodies bind to in immune thrombocytopenic purpura?
platelet membrane glycoproteins IIb-IIIa
What happens as a result of IgG coating of platelets in ITP?
renders them susceptible to opsonization and phagocytosis by splenic macrophages. also damage megakaryocytes
What is the stimulus for auto-antibody production in ITP?
abnormal T cell activity
What is Hashimoto’s thyroiditis?
chronic autoimmune thyroiditis that eventually leads to goiter and hypothyroidism
What does a patient have antibodies to in Hashimoto’s thyroiditis?
Thryoglobulin, thyroid peroxidase, TSH receptor
What happens to the thyroid at the cellular level if a patient has Hashimoto’s thyroidits?
diffuse lymphocytic infiltrate with thyroid-specific B & T cells and follicular destruction
What happens due to auto-Antibodies to TSHR (thyroid stimulating hormome receptor) seen in Grave’s disease?
Activation of the receptor stimulates thyroid hormone synthesis, secretion and leads to thyroid growth due to an overproduction and overactivation of T3 and T4
What are symptoms of Graves?
hyperthyroidism, goiter, bulging eyes, anxiety
What is the targeted antigen in myasthenia gravis?
Nicotinic Acetylcholine Receptor (AChR)
What happens as a result of myasthenia gravis?
AChR becomes blocked over time. muscle fatigues and can become paralyzed
What is one of the first symptoms of myasthenia gravis?
eyelid droop
Describe type III hypersensitivity rxns.
Antigen-antibody complexes form circulating immune complexes that are deposited in vessel walls or at extra-vascular sites & induce inflammation directly or by activating complement.
Where do antigen-antibody complexes lodge in type III hypersensitivites?
between the endothelial cells and the basement membrane (glomeruli, joints, skin, heart, serosal surfaces & small blood vessels)
What can glomerulonephritis occur secondary to?
Systemic infection (Hep B, malaria). Neoplasm (tumor antigens). Autoimmune. Systemic illness such as Lupus
What do AB-AG complexes target in glomerulonephritis?
GBM, Bowman’s space, endothelium. Result is destruction of glomeruli and progression to renal compromise and renal failure
Where do immune complexes get deposited in Rheumatoid arthritis?
in the synovial lining
What are extra-articular diseases seen with RA?
cardiopulmary, renal, skin, vasculitis, ocular, Rheumatoid nodules
