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84 Cards in this Set
- Front
- Back
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mediated by Ab vs T cells
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mediated by:
1. Ab: I, II, III 2. T cells IV - all types require previous sensitization |
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Type I gen
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Type I:
- immediate response: 2-30 min - mast cells, basophils, Th2, IgE, histamine |
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Type II gen
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Type II:
- cytolytic response: 5-8 hr - complement binds to IgG or IgM, causing cell lysis |
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Type III gen
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Type III gen:
- immune complexes: 2-8 hr - soluble Ab-Ag complex deposits of vessels in tissues - complement activation - chemotaxis of neutrophils |
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Type IV gen
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Type IV:
- delayed (DTH): 24-72 hr - macrophages, Th1, cytokines |
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atopy
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atopy:
- genetically determined predisposition to develop clinical (type-I) allergies |
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Type I examples
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Type I:
- localized or systemic - symptoms depend on site of Ag contact - hayfever (allergic rhinitis), eczema, asthma, urticaria |
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Type I and IgE
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Type I:
1. Ag in food or air 2. pre-existing IgE bound to surface of mast cells 3. acute inflammation: IgE (Th2 med) binds Ag, explosive release of mast cell contents - normally - |
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normal response to food and air Ag
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normal response to food and air Ag:
- production of IgG or IgA without clinical responses - IgE normally used to get rid of parasitic worms so is detrimental response to environmental Ag |
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first IgE response to Ag
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first IgE response to Ag:
1. stimulate Th2 response 2. production of IgE to Ag 3. IgE binds mast cell receptors 4. no obvious effect until next encounter |
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Type I: IgE-mast cell, basophil or eosinophil
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1. IgE-mast cell:
degranulation of mast cell--> vasoactive, chemotactic molecules, enzymes and cytokines--> acute inflammation and systemic effects 2.IgE- eosinophils or basophil: - stimulation and degranulation |
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Type I: products released by mast cells
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Type I: products released by mast cells:
1. histamine: smooth m contraction and vasodilation 2. heparin: inhibits clotting |
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inhaled allergens
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inhaled allergens:
- plants pollens - dander of dom animals - mold spores - feces of very small animals: eg dust mites |
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injected allergens
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injected allergens:
- insect venoms - vaccines - drugs - therapeutic proteins |
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Type I: early phase
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Type II early phase:
- immediate acute inflammation: 10-20 mins after mast cell degranulation - histamine and heparin: vasodilation, smooth m contraction, mucous production at some sites - skin: pruritis, "wheel and flare phase" |
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Type I: late phase
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Type I late phase:
- several hours later, peak 6-12 hours - redness, edema, pruritis - mediated by chemotactic factors from mast cells: attracts eosinophils and neutrophils, plus release of their factors |
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Type I: late phase asthma
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Type I late phase asthma:
- recruitment of inflammatory cells: eosinophils and neutrophils to epithelial sites - leads to tissue damage |
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Type I severity:
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Type 1 severity depends upon:
1. number and location of mast cells, eosinophils and basophils 2. degree of sensitization of animal 3. amount of Ag involved 4. route of admin: oral, inhaled, injected |
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Type I: nasal and sinus symptoms
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Type I symptoms:
1. nasal: swelling of mucosa (allergic rhinitis) - eg hay fever 2. sinus symptoms: - allergic sinusitis |
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Type I: eye and ear symptoms
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Type I symptoms:
1. eye: - allergic conjunctivitis: redness, itching of conjunctiva 2. ear: - feeling of fullness, pain, impaired hearing due to lack of eustacian tube drainage |
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type 1: airway symptoms
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type 1 airway symptoms:
- sneezing, coughing, wheezing - bronchoconstriction, dyspnea - asthma attacks - angioedema: airway constriction due to edema - eg feline asthma (lower airways) |
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type 1: skin symptoms
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type 1 skin symptoms:
- rashes, eczema, hives (urticaria) - eg parasite allegies: fleas - atopic dermatitis: cairn terriers, scotties, westies and irish setters |
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type 1: GI symptoms
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type GI symptoms:
- abdominal pain, bloating, vomiting, diarrhea - eg food allergies |
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systemic anaphylaxis
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systemic anaphylaxis (shock):
- generalized mast cell degranulation and massive mediator release - acute signs: 1. vasodilation: hypotension 2. vascular permeability: edema in shock organ 3. blood loss and pooling in shock organ: hypovolemia, smooth m contraction resulting in bronchial constriction - may result in death |
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primary shock organs of different spp
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primary shock organs of different spp:
1. horse: lung, intestine 2. cattle, sheep: pulmonary 3. dog: liver - excitement followed by vomiting, defecation, urination, muscular weakness and depressed respiration - massive blood pooling in liver, int 4. cats |
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vaccine reactions
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vaccine reactions:
- type I example - usually due to albumin adjuvants, not Ag |
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drug reactions
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drug reactions:
- type I - haptens: molecules too small to be Ag on own until bound to host proteins - eg Pen - acute, systemic or localized |
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urticaria
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urticaria (hives):
- many due to Type I - red, edema, plaque-like eruptions which are often pruritic - most in horses and dogs - inhaled or ingested Ag, drugs, insect bites |
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measure of total serum IgE
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measure of total serum IgE:
- measures Type I - ELISA with anti-dog IgE conjugated to enzyme |
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intradermal skin test
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intradermal skin test:
- small amount of suspected allergens into dermis - measure wheel and flare vs controls - controls: positive= histamine and negative= saline |
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treatments of type I
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tx of type I:
1. inhibit mast cell degranulation and effects 2. inhibit histamines 3. corticosteroids 4. anti-IgE to neutralize IgE 5. hyposensitization - promote Th1 cytokine response to inhibit Th2 and the production of IL4 and IgE |
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inhibition of mast cell degranulation and effects
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inhibition of mast cell degranulation and effects:
- type I tx - epi: stimulates beta adrenergic receptors - resulting in muscle relaxation and vasoconstriction - bovine: no epi, but norepi and dex |
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histamine inhibitors and corticosteroids
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tx for Type 1:
1. histamine inhibitors: antihistamines bind histamine receptors on cells 2. corticosteroids: stabilize cell membrances, prevents arachadonic acid breakdown and inflammation |
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hyposensitization
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hyposensitization:
- tx for Type I - switches Ab response to Ag away from IgE to an IgG response |
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Type III: immune complexes
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Type III immune complexes:
- Ab (usually IgG) and soluble Ag - only clinically significant when in excessive amounts - activate complement and cause acute inflammation of tissues |
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Type III local vs generalized
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Type III:
1. local: complexes form in tissues 2. generalized: - complexes form in circulation and are deposited in certain tissues, triggering inflammation - blood vessel walls, joints, kidneys |
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Type III mechanism
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Type III mechanism:
1. immune complezes activate complement and C' can bind mast cells 2. mast cell degranulation 3. products are chemotactic for neutrophils 4. neutrophils accumulate, releasing enzymes and other factors causing acute inflammation in tissue |
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blue eye (type III)
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blue eye (Type III):
1. small % of dogs infected or vaccinated with modified live canine adenovirus type 1 - 1-3 weeks after infection 2. lesion: anterior uveitis leading to corneal edma and opacity 3. resolution: usually spontaneous - virus-Ab complex, neutrophils |
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heaves in horses (Type III)
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heaves in horses (Type III):
- pathogenesis incompletely understood - triggered by inhalation of organic dusts (with molds) - older horses with genetic predisposition - smaller airway obstruction due to bronchoconstriction and excessive mucous production - severity varies |
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glomerulonephritis (Type III)
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glomerulonephritis (Type III):
- most due to immune complex dz - Ag from variety of sources: 1. dogs: Borrelia burgdorferi (Lyme), Ehrlichia, Canine adenovirus 1 and 2. cats: FLV, FIP 3. cattle: bovine viral diarrhea virus 4. horses: equine infectious anemia virus |
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tx of Type III
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tx of Type III/ immune complex conditions:
1. treat underlying conditions: anti-microbials 2. immune suppression: - glucocorticoids, cyclosphamide |
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strangles (Type III)
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strangles (Type III):
- after Streptococcus equi - purpura hemmorrhagica: skin vasculitis |
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Type IV components
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Type IV components:
1. Ag sensitized Th1 CD4 and CD8 lymphocytes 2. Th1 cytokines 3. activated macrophages 4. response peaks at 72 hours |
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Type IV delayed type hypersensitivity Ag
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Type IV delayed type hypersensitivity (DTH) Ag:
proteins such as 1. insect venom 2. Mycobacterial tuberculin or lepromin |
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Type IV: contact hypersensitivity Ag
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Type IV contact hypersensitivity Ag:
1. haptens: pentadecacatechol (poison ivy) 2. small metal ions: nickel, chromate |
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Type IV: contact hypersensitivity consequences
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Type IV contact hypersensitivity consequences:
local epidermal reaction: 1. erythema 2. cellular infiltrate 3. contact dermatitis |
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Type IV delayed type hypersensitivity results
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Type IV delayed type hypersensitivity results:
Local skin swelling (cellular infiltrate in dermis): 1. erythema 2. induration 3. cellular infiltrate 4. dermatitis |
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allergic contact dermatitis (Type IV)
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allergic contact dermatitis (Type IV):
- cellular infiltrate in epidermis 1. poison ivy 2. drug-induced contact dermatitis |
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drug-induced contact dermatitis (Type IV)
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drug-induced contact dermatitis (Type IV):
- variety of topical drugs act as haptens 1. neomycin: common in humans 2. Pen 3. sulfa meds 4. local anesthetics: novocaine - |
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formaldehyde (Type IV)
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formaldehyde (Type IV):
- acts as a hapten: binds proteins easily causing skin hypersensitivity and asthma - cosmetics, textiles, furniture, upholstery, newspaper dyes, paper |
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nickel (Type IV)
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nickel (Type IV):
- dissolves in weakly acidic environment of sweat - binds with high affinity to proteins (albumin, complement) - haptens binds to keratinocytes causing cytotoxic T cells to induce apoptosis - costume jewerly, collars |
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treatment for allergic contact dermatitis (Type IV)
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treatment for allergic contact dermatitis (Type IV):
1. avoid contact with chemical or substance 2. anti-inflammatory drugs: glucocorticoids 3. Ab if secondary infection |
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MHC molecules expressed by graft (Type IV)
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MHC molecules expressed by graft (Type IV):
1. TCR of recipient recognizes allogenic MHC molecules (class I) of graft 2. direct activation of cytotoxic T cells - acute rejection: by CTLs within 7days - chronic rejection: Th1 and macs induced by foreign MHC II, months later - chron |
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HY Ag expressed by male Y chromosome (Type IV)
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HY Ag expressed by male Y chromosome (type IV):
- graft from male to female - immune response to HY Ag expressed on tissues from male - observed in skin grafts |
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graft vs host (type IV)
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graft vs host (type IV):
- foreign lymphocytes in immunosupressed recipient destroy cells and tissues of recipient - bone marrow recipients |
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type II gen
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type II:
- IgG or IgM: binds Ag on surface of cells, causing their destruction= cytolytic - target cells: 1. foreign to host: eg ABO of RBCs -or- 2. autoimmune |
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type II mechanism
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type II mechanism:
1. Ab binds cell surface Ag 2. agglutination, hemolysis, or stimulate opsonization and phagocytosis of cells 3. cell destruction: a. complement binding Ab and triggering classical compliment pathway b. Ab-dependent cell cytotoxicity (ADCC): killing by NKs, macs, PMNs with surface Fc receptors for the Ab on the cell |
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Transfusion reactions (type II)
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transfusion reactions (type II):
- cats A, B, or AB - 75-95% A+: anti-B - 5-25% B+: anti-A - <1% AB+: no RBC Ag |
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monoclonal Ab (mAb)
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monoclonal Ab (mAb):
- make Ab to cat RBC A Ag: put RBCs from known A+ cat into a mouse = mouse-anti-cat RBC-A-Ab |
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neonatal isoerythrolysis (type II)
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neonatal isoerythrolysis (type II):
- humans, horses, cattle, carnivores 1. fetal RBCs leak into maternal circulation at birth 2. sensitization: maternal Ab produced against fetal RBC Ag, no problem 3. subsequent feti from same sire: ingest colostrum with these Ab, experiencing hemolysis |
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indicators of RBC destruction
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indicators of RBC destruction:
1. hemolysis in serum 2. low PCV 3. hematuria |
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immune-mediated cytopenia examples (type II)
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immune-mediated cytopenias (type II):
1. RBCs: often hemolytic anemia 2. platelets: thrombocytopenias 3. leukocytes: leukopenias (rare) |
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immune-mediated cytopenia mechanism (type II)
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immune-mediated cytopenia mechanism (type II):
1. Ab binds blood component 2. extravascular hemolysis: Ab and C3b coated cells are removed by macs in spleen or liver by binding to Fc and CR1 receptors 3. intravascular hemolysis: IgG, IgM activates complement and cells are lysed |
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primary and secondary immune-mediated cytopenia (type II)
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immune-mediated cytopenia (type II):
1. primary: animal makes Ab to RBC, platelets, or other BC surface Ag causing their destruction 2. secondary: Ab to cell are secondary to drug tx or infectious agent |
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secondary immune-mediated cytopenia (type II)
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secondary immune-mediated cytopenia (type II):
- hapten-carrier complex: drug too small to be Ag without binding cell 1. pen 2. triple sulfa antibiotics |
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secondary immune-mediated cytopenia (type II) complement mechanism
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secondary immune-mediated cytopenia (type II) complement:
1. complement- coated Pen RBC phagocytosed by macs 2. macs present peptides from pen-protein conjugate and activate specific CD4 T cells to become Th2 cells |
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secondary immune-mediated cytopenia (type II) B cell mechanism
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secondary immune-mediated cytopenia (type II) B cell mechanism:
1. B cells activated by Ag and by help from activated Th2 cells 2. plasma cells secrete Pen-specific IgG which binds to modified RBCs |
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secondary immune-mediated cytopenia (type II) final complement mechanism
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secondary immune-mediated cytopenia (type II) final complement mechanism:
1. RBC lysis: activation of complement components C1-C9 and formation of membrane-attack complexes 2. phagocytosis of Ab and complement-coated RBC: activation of complement components C1-C3 leads to covalent binding of C3b |
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secondary immune-mediated cytopenia (type II) infectious agents
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secondary immune-mediated cytopenia (type II) infectious agents:
- LPS, etc render RBCs foreign - equine infectious anemia virus: infects and replicates inside macs/ monos, Ag sticks to host RBC rendering foreign - infect RBCs, changing surface Ag expression: 1. Mycoplasma: canis, felis 2. rickettsias: Anaplasma 3. protozoa: Babesia |
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Coomb's Test
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Coomb's Test:
- tests for Ab on RBC surface: eg anti- dog IgG, M, A, or C3b - positive: RBC agglutination |
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treatment of primary immune-mediated cytopenia
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treatment of primary immune-mediated cytopenia:
- immunosupressive drugs - eg glucocorticoids |
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treatment of secondary immune-mediated cytopenia
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treatment of secondary immune-mediated cytopenia:
- treat underlying conditions: 1. remove drug 2. baterial infection: antibiotics |
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arthus reaction mechanism (localized Type III)
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arthus reaction (localized Type III):
1. SQ injection of Ag that already has Ab 2. IgG complexes form 3. activation of complement: release of mediators C3a, C4a and C5a 4. mast cell degranulation: inj site redness, edema, pain then hemmorrhage and thrombosis - severe: tissue necrosis 4. max rxn: 4-8 hours |
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arthus reaction (localized Type III) gen
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arthus reaction (localized Type III):
- vaccines, eg tetanus toxoid - complement activation not required, but may modify symptoms |
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generalized Type III
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generalized Type III:
1. complexes form in circulation 2. immune complex deposition in vessel walls 3. activation of complement 4. mast cells degranulation, neutrophil chemotaxis = vasculitis |
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serum sickness (type III)
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serum sickness (type III):
- reaction to IV injected Ag: usually proteins from other spp - eg anti-toxin, anti-venom, plasma 1. Ab made, form complexes: takes time 2. complexes lodge in small vessels of kidney, joints, etc. 3. type III inflammation: complement, mast cells, PMNs 4. fever, joint pain, proteinuria |
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serum sickness (type III) discovery
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- first recognized when humans injected with horse serum to provide passive immunity
- generalized vasculitis, erythema, edema, urticaria, neutrophenia, lymph node enlargement, joint selling, proteinuria after 10 days - subsided a few days later |
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Type I overview
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Type 1:
1. immediate, IgE mediated 2. time: 2-30min 3. Ag: induce cross-linking of IgE bound to mast cells with release of vasoactive mediators 4. examples: systemic anaphylaxis, local rxn (hay fever, asthma) |
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type II overview
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type II:
1. Ab-mediated cytotoxic 2. time: 5-8 hr 3. examples: blood transfusion rxns, hemolytic dz of newborn, IMHA |
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type II mechanism overview
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type II mechanism overview:
- IgG and IgM - Ab directed against cell surface Ag mediates cell destruction via ADCC or complement - Ag: cell surface Ag of platelets, RBCs, WBCs |
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type III overview
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type III overview:
1. immune-complex 2. time: 2-8 hr 3. localized: arthus, blue eye, heaves 4. generalized: serum sickness, glomerulonephritis, SLE, wet form FIP |
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Type III mechanism overview
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Type III:
- IgG and IgM - Ag-Ab complexes deposited at various sites induces mast cell and PMN degranulation = tissue damage - soluble Ag |
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Type IV overview
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Type IV overview:
1. DTH, cell-mediated 2. time: 24-72 hr 3. examples: + TB skin tests, contact dermatitis, poison ivy reaction |
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Type IV mechanism overview
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Type IV mechanism overview:
- memory Th1 cells release cytokines that recruit and activate macs and CTLs - Ag: Tb test, cosmetics, jewelry, poison ivy |
