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Hypersensitivity type 2 3 4

1. Type 2 HS disease is caused by inducing inflammation at the site of deposition; opsonizing cells for phagocytosis; and interfering with normal cellular functions, such as hormone receptor signaling.
2. How is T2 Autoimune hemolytic anemia caused Rh blood group antigens cause distruction of RBC by complement and phagocytosis. Leads to anemia
3. How is T2 Goodpasture syndrome caused collagen antigens cause glomulonephritis and pulmonary hemorrhage.
4. How is T2 Pemphigus Vulgaris caused antigens to cadherin cause blistering skin
5. How is T2 Acute Rheumatic Fever caused strep wall antigens make antibodies cross react with cardiac cells. Cause Arthritis, Myocarditis, cardiac scarring
6. T2 Graves disease is caused by TSH receptor antibody binding causing STIMULATION = hyperthyroidism
7. T2 Myasthenia gravis is caused by Ach antibody binding leading to BLOCKING = progressive weakness
8. Child receives antibodies from mother across placenta hemolytic disease of the newborn
9. Examples of Antibodies produced against the microbial antigens cross react with host tissue Acute Rheumatic fever (ARF) & Acute glomerulonephritis (AGN)
10. The ABO locus is located on chromosome 9
11. The A allele encodes a glycosyltransferase that bonds α-N-acetylgalactosamine to the D-galactose end of the H antigen, producing the A antigen
12. . The B allele encodes a glycosyltransferase that bonds α-D-galactose to the D-galactose end of the H antigen, creating the B antigen.
13. The H antigen is an essential precursor to the ABO blood group antigens. The H locus, that produces the H antigen on RBCs, is located on chromosome 19, encodes a fucosyltransferase
14. ABO groups are carbohydrates, genes code for enzymes, IgM binds, complement pathway
15. Rh groups are polypeptides, directly coded, have IgG which can cross placenta
16. Coomb assay Rh D antigens
17. Anti-D polyclonal antibodies (Rhogam- IgG)
18. Drug treatment damage via drug absorption to surface proteins antibodies, made to the now immunogenic drug epitope on carrier cell, bind, and complement-mediated lysis occurs.
19. drug absorbs to cell (RBCs) surface proteins antibodies made to the now immunogenic drug epitope on carrier cell, bind, and complement-mediated lysis occurs.
20. IgG mediated HS disease Type 3 HS
21. Pemphigus vulgaris is an example of a type 2 HSR where IgG against desmoglein proteins in desmosomes
22. In type 3HS complexes activate complement, platelet secretion of CXCL-8 which attracts neutrophils and macrophages to the site. These cells may exocytose their granule contents and release reactive oxygen and nitrogen intermediates to cause local tissue damage
23. Serum sickness occur 7-10 days after injection
24. Stevens-Johnson syndrome (SJS) caused by a type 4 HSR to haptenized drugs
25. IgE-mediated reactions occur within 5-30 minutes (Type I)
26. Immune complexes cause symptoms after 12 hours (Type III); Arthus reactions..
27. T cell-mediated reactions develop 2 to 3 days after re-exposure (Type IV).
28. SLE criteria acute cutanieus lupus, oral or nasal ulcers]
Created by: splashgreen