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25 Cards in this Set
- Front
- Back
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Types Hypersensitivty
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Type I Hypersensitivity
Anaphylactic type Allergy & Anaphylaxis Type II Hypersensitivity Antibody Dependent Antibody to Fixed Tissue Antigen Type III Hypersensitivity Immune Complex-Mediated Type IV Hypersensitivity Cell-mediated Delayed |
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Type I Hypersnsitivity
Involves? Requires? |
Allergy & Anaphylaxis
Seasonal Rhinitis or hay fever (Lung) Asthma (Lung) Anaphylaxis (System) Requires “primed” immune system |
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Type I hypersensitivity pathway
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-Pollen Antigen processed by DCs
-Activate T-Helper2 -Th2 Secrete IL-4-->B cells to class switch and form IgE antibody -B-Cells activated -B cells IgE antibody binds to mast cells/eosinophils which then complex with antigen to activate *explains why priming is necessary, B-cells must have IgE antibody |
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Type I hypersensitivity:
Immune Mechanism: Phases: |
-Allergen cross-links IgE antibody
-Initial phase (5 to 30 minutes) -Release of vasoactive amines & other mediators from basophils and mast cells -opening of circulatory system -Late-phase (2 to 8 hours & lasts for days) -Recruitment of other -inflammatory cells Mucosal epithelial cell damage -takes hours/days, initial phase recruits inflammatory cells |
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Activating a Mast Cell
Resting contains? Activated by? Release granules by? |
-granules containing histamine and inflammatory mediators(proteases and vasocative amines)
-Mast cells have FcE Receptor I which binds to IgE antibodies. -once these IgE antibodies encounter/bind antigens mast cell will become activated and will release its granules -Complement componenets C5a and C3a can also activate Mast cells(and basophils) |
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Initial Phase of Type I Hypersenstivity
Kinds of mediators? Antibody assoicated? What cells are affected? Releases? Granules contain? Histamine causes what symptoms? physiological effects? |
-Primary
-vasoactive amines and other mediators -Granules contain histamine, proteases and chemotactic factors -Histamine is a vasoactive amine which causes hay fever sx -Increase vascular permeability -vasodilation -bronchoconstriction -mucus production |
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Protease released?
effect? |
-tryptase
-degrade -generate clotting components(kinins) -cleave C' components |
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Chemotactic Factors
kinds? functions? |
-Eosinophil CF, Neutrophil CF
- bring in other innate cells-eosinophils and neutrophils |
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Initial Phase Type I hypersensitivity
-kind of mediator? -receives signals for? -secretions of what types of things? fxns of these things? |
-Secondary
-Cytokine gene activation and activation of phospholipase A2 -Cytokines -TNFa, IL-1,4,5,6 -recruit and activate inflammatory cells -Membrane Phospholipids - PAF -Arachidonic acid -leukotrienes B4, C4, D4 -Prostaglandin D2 - cause pain, activate nerves |
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Leukotrienes types? fxns?
Prostaglandin D2 effects? PAF effects? |
-C4/D4: potent vasoactive/spasmogenic agents
-B4: chemotactic for Eosinophils, Neutrophils, Monocytes -Prostaglandin -bronchospasm -mucuous secretion -PAF -platelet aggregation -histamine release -bronchospasm -chemotactic for eosinophil and neutrophils |
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Type I Hypersensitivity Allergy
Causes? Pathway? other causes of granules release? initial response consists of?time period? late phase reaction consist of? time period? |
-Rhinitis/Hives/Urticaria
-APC activates TH2 -TH2 secretes IL-4 helping activate IgE B cell(along with antigen/antibody complex) -IL-3,5,GMCSF-recruit eosinophil IgE B Cell -secertes IgE antibody which binds to IgE FcE receptor on mast cells -Antigen binds IgE antibodies bound to IgE FcE receptors-activates mast cell to release granules leading to initial phase and late phase response -release IL-3,5 which activates Eosinophils -Activated Eosinophils release granules leading to late phase rxn -other causes of granules: C' activation(C5a, C3a), cytokines from MQ(infection), drugs, physical stimuli(bee stings, plants, fruits, vegis) -initial response: vasodilation, vascular leakage, ssmooth muscle spasm, minutes -Late phase: mucosal edema, mucus secretion, leukocyte infiltration, epithelial damage, bronchospasm -hr/days |
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Type I hypersensitivity Recruitment of Inflammatory Cells:
-can cause? -leads to? -role of mast cells? -chemotactic factors? -fxn of chemotactic factors? |
-laryngeal edema
-mucosal epithelial dammage -CF: ECF, NCF, Leukotriene B4, PAF, TNF A -mast cells produce CF which bring in innate cells such as basophils,eosinophils, neutrophils by adhesion molecules -gets them out into lamina propria to help destroy epithelial cells |
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Atopic Asthma
Type of hypersensitivity? Mediated by? Triggered by? epidemiology? Initial/late phase responses? |
-type I
-mediated by type I IgE -triggered by allergen and good -positive family history of asthma is common -initial airway sensitization to antigen leads to synthesis of IgG that binds mucosal mast cells -Initial response: exposed of IgE coasted mast cells to same antigen releases mediators that open mucosal intercellular jxns which leads to even more antigens reaching mast cells -leads to bronchoconstriction, edema(vascular permeability), mucus secretion Late Phase Response: -inflammatory cells recruited including eosinophils which amplify and sustain inflammatory response -this is anaphylactic shock, stab with epi or take benadryl b4 laryngeal response |
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Atopic Asthma chronically causes?
treatment? |
-Airway remodeling:
-thickening of basement membrane of the bronchial epithelium -edema and inflammatory infiltrate in bronchial walls with a prominence of eosinopils and mast cells -increase in size of submucosal glands -hypertrophy of bronchial muscle walls -epi for bronchospasm -anti-inflammatory deal with mucosa itself |
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Clinical Course of Asthma attack:
Asthma attack is due to? |
-last severl hrs, and recurrent episodes
-chest tightness, breathlessness, wheezing -cough w/o sputum -difficulty exhaling as air is trapped distal to bronchi Asthma attack due to: -intermittent and reversible airway obstruction -chronic bronchial inflammation with eosinophils -bronchial smooth muscle cell hypertropy and hyperreactivity(bronchoconstriction) |
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Testing for Type I Hypersensitivity
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-Systemic admin of protein antigens or drugs(bee venom, penicillin)
-leads to systemic anaphylaxis(minutes) -urticaria, pulmonary bronchoconstrcition, laryngeal edema, GI tract musculature -Anaphylactic shock -systemic vasodilation -Process: Inject a bit of antigen under the skin through 7 layers of epi/dermis -if antigen present: mast cells activate release vasoactive amines and chemotactic factors-->fluid accumulation in first 24 hr-squsihy -24-48 hrs: swtich from fluid to innate immune cells-->hard on touch |
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Type II Hypersensitivity
Dependent on? Specific to? evokes? |
-antibodies
-antibody specific for target antigens on cells/tissues -normal cell surface molecule -eg. goodpastures disease-antigolmerular basement mb dis(drug/metabolite bind epithelial cell which draws an AB against it) -adsorbed exogenous antigens -drug or metabolite 3 mechanisms: -complement(C')- dependent rxns -antibody-dependent cell mediated cytotoxicity(ADCC) -antibody-mediated cellular dysfxn |
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Goodpastures:
type of disease? in which organs? cause? initiate? |
-autoimmune
-kidney and lung -kidney/lung injury caused by circulating autoantibodies against the basement membrane type Iv collagen -inflammatory destruction of BM in renal glomeruli and pulmonary alveoli leading to proliferative and rapidly progessive glomerulonephrities and necroticizing hemorhhagic interstiital pneumonia in teans-20s males |
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Renal finidngs in goodpastures
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-IgG
-glemorulonephritis-thicking of bm |
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Goodpastures Complement Dependent Reactions:
mechansims? after tissue binding-->? |
-direct cell lysis
-Ab binds RBC -complement binds RBC -MAC forms-->osmotic lysis -opsonization --aB coats RBC -complement binds to C3bR activating - macrophage/phagocyte eats -3 mechanisms: -complement -lysis of RBCs(as in RH disease/ABO incompatibility-a |
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Complement Dependent Reactions
-transfusion reactions? -erythroblastosis fetalis -autoimmune hemolytic anemia, neutropenia(agranulocytosis), thrombocytopenic purpura -drug reactions -pemphigus vularis |
Transfusion reactions
-Blood group antigens Erytroblastosis fetalis -Rh incompatibility -ABO incompatibility Autoimmune hemolytic anemia, Autoimmune neutropenia (agranulocytosis), Autoimmune thrombocytopenic purpura -Ab produced against self-blood cells-->lysis Drug reactions -Penicillin adsorbed to cell surface -aB-->new epitope-->immune response Pemphigus vularis -Abs against desmosomal proteins in oral epithelial layer that lead to disruption of epidermal intercellular junctions |
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Pemphigus Vulagaris
-type of disorder -caused by -most common type, lesions seen in -characterized by? |
-blistering
-IgG Ab directed against cadherin molecules in cadherin molecules in desmosome attachments in epidermis and mucosa -oral and genital mucoa -superficial blisters that rupture easily |
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Bullous Pemphigoid
-caused by? -characterized by? -oral involvement? -common in? |
-IgG Abs disrupt Basl Cell-basement membrane attachments(hemidesmosomes)
-blisters that do not ruptusre easily -1/3 of patients -elderly |
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Antibody-dependent-cell mediated cyotoxicity
-mediated by? pathway? -presence of phag/complement fixaiton? |
-leukocytes(neutrophils, eosinophils, macrophages, NK)
-Ab binds antigen on surface of target cells -Fc Receptors on NK cells recognize bound antibody -cross-linking of Fc receptors signals the NK cell to kill target cell -target cell dies by apoptosis -none -NK is the key |
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Antibody Mediated Cellular Dysfxn
-types? -fxnality? |
-impair cell fxn, and not cause cell injury or inflammation: myasthenia gravis
-stimulate cell fxn: graves disease(anti-TSHR ab) hypthyroidism -essentially antibodies bind receptors by either impairing their cell fxn or overstimulate fxn |
