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48 Cards in this Set
- Front
- Back
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type II immune reactant
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IgG Ab
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type III immune reactant
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IgG Ab
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type II Ag
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cell surface R's
Ab specificity to Ag's autoAb related to tissue damaged |
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type III Ag
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Ag/Ab trapped
Ab specificity to Ag unrelated to tissue damage |
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type II effector mechanism
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cytotoxic Ab and complement
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type III effector mechanism
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complement and neutrophils
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chemotaxis for type II and III
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neutrophils
complement: C3a, C5a, C3b |
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type II clinical sig
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anemia/cytopenia
- hemolytic - thrombocytopenia R's - M. gravis - Grave's disease organ - thyroid : hashimoto's - theumatic fever: heart - pemphigoid: skin - kidney: goodpasture's |
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type III clinical sig
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arthus rxn
allergic pneumonitis lupus nephritis immune complex glomerulonephritis |
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type II time
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20-30 min
neutrophil chemotaxis |
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type III test
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serum sickness
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type II & III therapy
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non specific anti-inflammatory drugs
immunosupressive - cyclophosphamide - corticosteroids decrease Ab production |
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characteristics of type II
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Ab specificity is related to clinical presentation of disease
- may cause disease useful in dx and pt monitoring |
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mechanisms of injury in type II
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cytotoxic mechanism
circulation vs tissue |
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type II mechanism in circulation
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Ab to "self" cells/ protein
fixed phagocytic system; Ab and C3b |
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type II mechanism in tissue
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Ab to "self" tissue
inflammation PMN infiltration C3a, C5a opsonization PMNs, C3b block organ function activate R's |
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tytotoxic Ab rxns specificity to Ag's on
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foreign circulating cells
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RBC transfusion Rxns
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ABO blood groups and polysaccharide Ag's (almost all IgM; anti-ABO)
exposed to bacterial polysaccharides that mimic our ABO Ag's: make IgM Ab's if have: - Ag A: Anti-B Ab's - Ag B: Anti-A Ab's - Ag's A & B: no Ab's - no Ag: both anti-A and anti-B Ab's |
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hemolytic disease of newborn
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Rhd (rhesis monkey Ag) Ag on fetal RBC
sensitization of Rhd neg mother in 1s pregnancy IgG Ab to Rhd crosses placent in 2nd pregnancy Rhd + fetus at risk prevent with RhoGam: commercial anti-Rhd; IgG Ab against Rhd) IgG can cross placenta |
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cytotoxic Ab rxns to autoantigens on own circulating cells causes
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autoimmune hemolytic anemia and cytopenia
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types of autoimmune hemolytic anemia and cytopenia
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idiopathic, association with infections
drug induced hemolytic anemia pernicious anemia Ab specificity to autoantigens on membranes in tissue |
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idiopathic autoimmune hemolytic anemia/cytopenia
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usually RBC but granulocytes can be involved
- anemia warm: IgG react at 37 degrees C or cold: IgM react at 30 degrees C or lower - either one reactive Ab - Raynaud's syndrome: ppl cold and circ problems; cold IgM Ab's bind RBC and agglute; blocks circ; tx: wam them up platelets: idiopathic thrombocytopenia purpura |
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idiopathic thrombocytopenia purpura
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IgM1Ab aainst platelets
must have splenectomy don't want to treat with corcitosteroids b/c that will dampen immune system seen in lupus and kids |
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drug induced hemolytic anemia
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Ab's: penicillin and sulfa drugs
Quinidine Methyldopa others kids mostly |
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pernicious anemia
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Ab specific to intrinsic factor
- in gut, for absorption of B12; from bacteria or supplement block vitamin B12 utake from intestine - can lead to anemia b/c dont develop RBCs |
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frustrated phagocyosis
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neutrophil adherence
type II hypersensitivity rxn frustrated phagocytosis ec enzyme release : toxic: causes memranitis |
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autoAb specificity to glomerular basement membrane
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goodpasteur's syndrome
immune comlexes "actively" fromed in BM complement, PMN activation; membrane damaged from focused localized release enzymes, etc. |
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goodpasteur's syndrome from Ab to
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glomerular BM
- glomerulonephritis |
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pancreatitis Ab to
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islet cell
- diabetes type I |
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rheumatic fever makes Ab to
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heart and joint tissue
- Ab to streptococcus (M protein); molecular mimicry |
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myocarditis can make Abs to
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heart muscle
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thyroiditis can make Abs to
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thyroglobulin
- hashimoto's - hypo |
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pemphigold make Ab to
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skin BM
- blisters |
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primary biliary cirrhosis can make Ab to
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mitochondria
- primarily in bile duct - digestive problems |
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Sjogren's syndrome make Abs to
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salivary gland
- or mito - dry mouth |
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type II disease that block R's
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myassthenia gravis
- blocks Ach R - autoimmune |
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type II disease that activates R's
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grave's disease
- thyroid stimulatin hormone R - opposite of hashimoto's - hyperthyroidism |
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summary of type II
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specificity of Ab (idiotype) associated with clinical presentation of disease
- may be underlying etiology Ab mediated and complement amplified - C3b, C3a, C5a, PMNs, lysis |
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characteristcs of type III
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IC mediated
complication of primary disease Ab specificity creating disease condition is unrelated to clinical presentation of disease IC's trapped (non-speciically deposited) in tissue - may form locally in tissue or accumulate from circulation |
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localized Rxn types in type III
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skin on dermis
- direct deposit of Ag in highly sensitized individual : arthus rxn: Ag-Ab causing edeme and errythemia: wheel & flare from histamine - treat with corticosteroid or benedryl to block histamine internal organs - kidney - lung |
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type III localized rxn in kidney
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IC mediated
glomerulonephritis results from high circulating IC's : CIC - stick nonspecifically in kidney and makes glomerulus lumpy and bumpy - high viral infections; lupus |
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type III localized rxn in lung
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Ag generally bacteria, fungi and/or spores
- in alveolar spaces hypersensitive allergic pneumonitis: Ab, complement, neutrophiles Th-2: secondary lymphoid tissue, makes Ab occupational disease - can become type IV if persistent == T cell, mac, Th1 |
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type III systemic rxns
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IC clearance from circulation
serum sickness CIC and tissue deposition complication of many autoimmune diseases |
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IC clearance from circ in type III systemic rxn
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Ab immune rxns exist as Ag or Ab excess, equivalence efficient cleareance at Ag-Ab equivalence
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serum sickness in type III systemic Rxns
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massive systemic complement activation
- persistent Ag and Ab, don't get cleaved transfusion Rxns xenoserum anti-toxins massive release of histamine: anaphylaxis |
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CIC and tissue deposition in type III systemic rxns
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persistent Ag accumulation and persistent Ab production
complication of primary disease non-specific IC deposition |
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complication of autoimmune diseases that causse type III systemic rxns
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systematic lupus erythematosis
- Ab to DNA and RNA rheumatoid arthritis - rheumatoid factor - IgM anti IgG; altered in Fc and make IgM against it chronic hepatitis - viral Ag, persistent Ag, liver damage - kupffer cells can't do their job alcoholic cirrhosis - liver damage and impeded CIC clearance Sjogren's syndrome - Ab to mito, salivary glands |
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summary of type III
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Ab not related to clinical presentation of disease
Ag-Ab complexes non-specifically deposited in tissues - formed locally - from circulation Ab mediated and complement amplified C3b, C3a, C5a, PMN's, lysis |
