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MUA M2B2 IDR 05
Hypersensitivity type 2 3 4
Term | Definition |
---|---|
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] |