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58 Cards in this Set
- Front
- Back
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Type I Hypersensitivity
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IgE mediated (immediate hypersensitivity, allergy, atopy, anaphlyaxis)
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Type II hypersensitivity
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IgG, IgM mediated (cytotoxic rxn)
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Type III hypersensitivity
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IgG mediated (immune complex disease)
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Type IV hypersensitity
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T Lymphocyte mediated (delayed type hypersensitivity); happens with TB*
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the players in Type I hypersensitivity
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allergen, basophil and mast cells (histamine and other mediators), IgE, TH2 cells
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Ways to get allergens
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inhalation, ingestion, touch, injection/sting
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Basophils quick facts
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in peripherial blood, 1% of circulating blood
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Mast cell quick facts
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found in vascularized tissues; especially in skin, mucous membrane of respiratory and Gi tracts
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IgE
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< .001% of serum Ig's; serum half-life is 2.5 days; binds to mast cells up to *12 weeks; *high affinity FceRI receptors on basophils and mast cells;*FceRI and lower affintiy FceRII on eosinophils; TH2 response*
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IL-4
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is produced by TH2; this is needed to produce IgE; required for type I hypersensitvity
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Factors that lead to Type I hypersensitivity
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IL-4, IL-5, IL-6, IL-10, TGF-Beta
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What causes release of granulocytes from mast cell?
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IgE crosslinking of FceR
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Type 1 hypersensitivity phases
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immediate, delayed
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Immediate pahse of Type 1
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5-30 min after exposure to allergen; peripherial dialation, vascular leakage, smooth muslce spasm (bronchospasm); *subject cannot breathe, may go into shock
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Delayed phase of type 1
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2-8 hrs later and lasts for several days; intense infiltration of tissues w/ inflammatory cells; muscosal epithelial cell damage
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Granules contain
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histamin, proteases, chemotactic factors ( for eosinophila dn neutrophils) (primary mediators)
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Arachidonic acid is metabolized
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Leukotrienes (B4, C4, D4) and prostoglandin (D2); these are ecosonoids (secondary mediators)
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Primary mediators
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repsonsible for immediate effects of Type I; granule contents; *Histamine, proteases, *eosinophil chemotactic factor, neutrophil chemotactic factor, heparin
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Histamine
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10% of granule weight; 4 types of histamine receptors: H1, H2, H3, H4
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H1 receptors*
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mediates contraction of bronchial and gut SM; systemic vasodilation; increased veule permeability
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H2 receptors
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stimulates gastric acid secretion
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H3 receptors
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modulates neurotransmitter release
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H4 receptors
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mediates mast cell chemotaxis
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Secondary medaitors
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Eicosanoids (products of arachidonic acid) (5-30 min), Leukotrienes (LT): SRS (LTC4 + LTD4), LTB4, Prostaglandins; Cytokines (late) (hours)
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SRS
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made up of LTC4 + LTD4 - increases vascular permeability, bronchoconstriction
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Etiology of type I
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20% population has; TH2 response; gentic factors; environmental factors (hygiene hypothesis )
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Local Type 1
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skin, mucous membranes, urticaria, eczema, conjunctivitis; URT - hay fever, acute laryngeal edema; LRT- asthma
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Systemin Type 1
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anaphylatic shock
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Hygiene Hypothesis
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the more infections kids have the less likley they will be allergic; and as people get clean more chances for allergy
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Urticaria
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Hives; generally made by ingested allergen
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When you see a bunch of eosinophils what does it mean?
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Mean you have a type 1 hypersensitivity or a parasitic worm; that is why snot is green due to eosinophils?
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Anaphylaxis
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systemic rxn, massive degranulation of blood basophils (bee sting, IV drug); bronchoconstriction, shock; Treat: establish airway, assist respiration, epinephrine, combat shock
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Hyposensitivity
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treatment most useful in patient w/single allergies; repeated injection of small doses of allergen; two potentiel effects: down regulates igE sysnthesis, increased synthesis of IgG blocking antibodies
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Type 1 treatment
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alpha-adrenergic agonists, inhaled Cromolyn, antihistamines, leukotriene inhibitors, corticosteroids (local/systemic)
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Alpha adrenergic agonists
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epinephrine, primatene, pseudophedrine
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Epinephrine, Primatene
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activate alpha, beta-1, beta 2 receptors; injected (epinehrine), Inhaled (primatene mist); onset (3-5) - duration (1-1.5 hrs)
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Pseudoephedrine
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vascular constriction, wide variation of patient tolerance due to insomnia and irritability, availability now limited
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Cromolyn Sodium
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Blocks Ca influx to mast cells, stabilized mast cell membranes (inhibits degranulation), prophylactic, nasal spray form, very safe
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Antihistamines
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*the current primary drug for nasal allergy treatment; competes w/ histamine for H! receptor; effective with prophylactically; effective at reducing sympotims of sneezing, nasal itching, and rhinorrhea
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Leukotriene inhibitors
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competitive inhibition of leukotriene D4 receptor; singulair*; successful in asthma; seasonl allergy rhinitis
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Corticosteroids
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block late phase rxn, small fraction absorbed locally, side effects w/ prolonged use
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Physiological role of IgE
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main fighting against parasites; eosinophils produce major basic protein and eosinophil cationic protein (toxic to helminths)
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Type II hypersensitivity
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IgM,IgG; cytotoxic rxns (complement mediated (lysis/phagocytosis) and antibody dependent cellular cytotoxicity)
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Examples of Type II
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blood fusions rxns; hemolytic disease of newborn; drug-induced hemolytic anemia
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Drug induced autoimmune hemolytic anemia
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alpha methyl dopa binds RBC which then attracks anti-D antibodies which kills RBC
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Type III hyper sensitivity
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immune complex diseases; complexes depositied in tissues results in complement activation, PMN chemotaxis and granule release; platlet aggregation ( local or systemic effects)
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Arthus rxn
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local Type III; common with vaccines; local antigen excess, pre-formed antibodies bind antigen and infalmmation; about 4-12 hrs after injection
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Systemic effect of Type III
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deposition of immune complexes especially where blood is slowed by tortuous vessels; glomerulitis (lupus), vasculitis (small blood vessels), arthritis (joint synovial vessels)
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Types of Type IV hypersensitivity
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contact (contact dermititus), tuberculin-type, and granulomatous hypersensitivities
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Type IV response
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TH1 response - activation of monocyte and macrophages w/ release of inflammatory mediators
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Th1 mediators for Type IV
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IL-2, IFN- gamma, TNFalpha, TNFbeta
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Type IV causative agents
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contact antigens (*nickel, poison ivy/oak, hair dyes, latex), intracellular bacteria (*mycobacteria, listeria), Intracellular fungi (candida, pneumocystsits, histoplasia), Intracellular parasites (leishmania), Viruses (herpes, measles)
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Type IV contact hypersenstivity
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aka contact dermititius; 48 hrs, low MW, acts as haptens; penetrate skin through sweat glands combine with self proteins and presented to T cells by langerhans; histology: MNC, edema
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Tuberculin t ype hypersensitivity
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48-72 hrs; antigens : dermal mycobacterial; lymphocytes and monocytes
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Granulomatous hypersensitivity
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4 weeks; antigens- persistent Ag or immune complexes or inert particles; epitheliod cells, giant cells, macrophages, fibrosis, necrosis
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Graft rejection
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rejection is due to TH1 induced CTL repsonse
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Latex hypersensitivity
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8-12 % HCW are sensitive; may be Type I or IV rxn (local - oral blisters, ulceration, pain, facial urticaria, rhinitis) systemic (bronchospasm or anaphylatic shock)
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Skin test rxn hypersentivity times*
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Type 1 ( minutes); Type III (Arthis) (4-12 hrs); Type IV (48-72 hrs); good test question
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