Hypersensitivity Flashcards

Question

Examples of type II hypersensitivity

Answer 1

- AB and Rh blood group rxns - Autoimmune diseases like: Idiopathic Thrombocytopenia Purpura (ITP), Hashimoto's thyroiditis, Graves Disease, Myasthenia Gravis, Goodpasture's syndrome, MS - Some drug rxns

Answer 2

Febrile non-hemolytic transfusion reastion symtoms- fever, dyspnea This is clinically benign, causing no long lasting side effects.

Answer 3

- Type II - within 24 hours of the transfusion - sense of impending doom, burning at site of infusion, chills, fever, and pain (back and flanks) - results from rapid destruction of the donor RBCs by host antibodies. Factor P then binds to C3 in the donor blood facilitating the reaction through the alternate pathway.

Answer 4

1. How much incompatible antigen was transfused. 2. the nature of the antigen 3. the nature of the recipients antibodies

Answer 5

Type II Occurs 1-14 days after blood transfusion Clinical outcomes depend of the rate at which the patient can produce antibodies and destroy donor RBCs. Usually much less severe than acute hemolytic rxns. Recipient formed antibodies during a previous sensitization. During the blood transfusion the ab levels are too low to cause acute transfusion reaction. As the blood infuses, the antigen is re-encountered and the immune system is stimulated to rapidly produce more antibodies. Over days, the abs bind to the donor RBCs, which are removed.

Answer 6

Type II - idopathic or autoimmune (antibodies are against platelet membrane glycoproteins Ilb-Illa (IgG type). Platelets coated with IgG renders them more susceptible to opsonization and phagocytosis (increase in C3 and C4 adherence on platelets). - abnormal T-cell activity

Answer 7

TypeII chronic autoimmune thyroiditis- eventually hypothyroidism and/or goiter antibodies to: - Thyroglobulin (Tg) - Thyroid peroxidase (TPO) - TSH receptor (TSHR) - ---> B cells in thyroid are a major site of ab secretion---> T cells become activated and secrete cytokines---> cytokines have a role in antibody production and activate Tc cells which destroy thyroid cell

Answer 8

Type II Auto antibodies to TSHR causing: - Activation of the recpetor - stimulating thyroid synthesis, secretion, and thyroid growth (over production/activation of T3 and T4) hyperthyroidism, goiter, bulging eye and anxiety

Answer 9

Type II Nicotinic Acetylcholine Receptor (AChR) is the target antigen. ACh released from the nerve causes muscle to contract and over time, the receptor is blocked. the muscle fatigues and become paralyzed. Eyelid droop

Answer 10

Antigen-antibody complexes form and enter the circulation forming circulating immune complexes. Immune complexes are deposited in vessel walls (between the endothelial cells and the basement membrane) and induce inflammation directly or by activating compliment Neutrophils and mfgs are recruited and produce tissure damage

Answer 11

Type III ab-ag complexes can target GBM, bowmans space, endothelium. Results in destruction of glomeruli and prgression to renal compromise and renal failure. If secondary to infection, treating infection can halt progress but immunosuppressive drug is best hope

Answer 12

Type III Immune complexes get deposited in the synovial lining and the cascade of leukocyte migration, phagocytosis, edema, and inflammation occurs, resulting in cartilage and joint injury Extra-articular disease (outside the joint)- cariopulmonary, renal, skin, vasculitis, ocular, rheumatiod nodules

Answer 13

Type III - involves many organ systems, wide clinical spectrum with variable course - presence of antinuclear-antibodies (ANA) - persistence of pathogenic B cells: - --- polyclonal hyperactivity - ---pathogenic, auto-antibody IgG has high affinity from encoded mutated Ig genes - failure of regulatory networks to interrupt the process. - antibodies form the immune complexes with antigens to cause the disease environmental: sex hormones, sun exposure, drugs, dietary factors, infections, stress

Answer 14

CELL-MEDIATED rather then antibody-mediated Initiated by antigen activated (sensitized) T lymphocytes Type 1- delayed type hypersensitivity reactions mediated by CD4+ T cells that secrete cytokines which recruit leukocytes and stimulate inflammation and phagocytosis Type 2- direct cell cytotoxicity mediated by CD8+ T cells that directly kill tissue cells *both lead to lymphocyte infiltrates and granuloma formation

Answer 15

Type IV Lymphocytes and monocytes infiltrate upper dermis first. T cells activated by antigen. Once Induced, the CD4+ T cells start releasing cytokines It only takes one exposure because the first exposure sensitizes, then a small amount remains to elicit the contact dermatitis. Lesions vary from mild erythema to edematous papules, can be vesicular, itching is hallmark

Answer 16

Type IV headache, visual distrubances, tender or enlarged temporal artery, elevated ESR --can cause blindness T cell mediated. CD4+ and CD8+ T cells infiltrate vessel wall

Answer 17

Type IV hypersensitivity to cereal grain proteins (gluten or gliadin) lymphocitic inflitrate in the lamina propria beneath the epithelial layer. Causes tissue swelling---> villous atrophy of small intestine resulting in malabsorption, steatorrhea (lipid poop), and weight loss.