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82 Cards in this Set
- Front
- Back
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is a heightened state of immune responsiveness that may cause damage to the host.
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Hypersensitivity
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Commonly called an allergy
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type 1 hypersensitivity
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Also known as immediate hypersensitivity due to a rapid onset
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type 1 hypersensitivity
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Directed against soluble Antigen
Secondary response; Mediated by IgE |
Type 1 hypersensitivity
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Type 1 HS involes release of inflammatory mediators by ___ and ___
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mast cells and basophils
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IgE levels depend on an interaction of genetic and environmental factors
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Type 1 HS
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are antigens that trigger the formation of IgE antibodies
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atopic antigens
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Atopic antigens are also referred to as
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allergens
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is the inherited tendency to respond to naturally occurring inhaled and ingested allergens with continued production of IgE
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atopy
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The normal immune response to possible allergens is the responsibility of
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Th1 cells
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People with allergies tend to respond with
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Th2 cells
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Response with TH2 cells results in a different group of mediators which bring about the
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overproduction of IgE
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The IgE produced against allergens is bound to the surface receptors on
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basophils and mast cells
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Binding to cell surface receptors increases the half-life of IgE to at least
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10 days
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As many as _____ receptors may be found on a single cell.
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500,000
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Once bound, IgE serves as an
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antigen receptor
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When atopic antigens bind and cross-link the antibody molecules, the cells
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degranulate and release mediators
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A vasoactive amine
Effects seen 30 – 60 seconds after release |
histamine
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contraction of smooth muscle in bronchioles, blood vessels, & intestines with increased mucous secretion in upper respiratory tract
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H1 receptors
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– increased gastric acid secretion, airway mucous production, & vascular permeability
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H2 receptors
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found only in neural tissue; limited effects.
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H3 receptors
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Histamine in the skin causes
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erythema and wheal & flare formation
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Airflow obstruction caused by smooth muscle contraction and increased mucous production in the bronchioles
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Histamine in the lungs
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Histamine in the vascular system causes
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Hypotension or shock caused by increased vascular permeability
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Eosinophil granules contain
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histaminase and phospholipase D
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Enzymes histaminase and phosphlipase D degrade what?
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histamine and platelet activating factor. (PAF)
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eosinophils act as an internal ____ mechanism
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negative control
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Allergy symptoms are dependent on factors such as
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Route of exposure
Dosage Frequency of exposure |
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Most severe type of allergic response
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anaphylaxsis
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An acute reaction
Involves multiple organs simultaneously Can be fatal if not treated quickly |
anaphylaxsis
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Typical anaphylaxis inducers
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Venom from bee-stings
Drugs such as penicillin Foods such as shellfish, peanuts, & dairy Latex |
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Symptoms begin within minutes of exposure
Severity typically depends on the number of previous exposures Caused by massive release of reactants (especially histamine) from mast cells & basophils |
anaphylaxis
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anaphylaxis symptoms may include
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Bronchospasm
Laryngeal edema Vascular congestion Urticaria (hives) Angioedema Diarrhea & vomiting Intractable shock |
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Death caused by anaphylaxis may result from
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Asphyxiation due to airway edema & congestion
Irreversible shock |
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Antihistamines can be used for localized reactions such as
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hay fever and hives
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Antihistamines, bronchodilators, and sometimes corticosteroids are used to treat
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asthma
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___ is used for quick reversal of systemic symptoms of anaphylaxis
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Epinephrine
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____ may be used as a preventive treatment
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hyposensitization
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Very small quantities of sensitizing antigen are injected into the patient over time.
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hypsensitization
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The purpose of hypsensitization is
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build up IgG antibodies to the antigen.
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IgG antibodies will block the antigen by combining with it before it has a chance to reach the IgE coated cells
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hyposensitization
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Hyposensitization is most effective against antigens that enter the circulation such as
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bee venom
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is used to test for total IgE.
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Radioimmunosorbent test (RIST
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is used to test for antigen-specific IgE.
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Radioallergosorbent test (RAST)
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In vitro testing may be used to test for ___ or for levels of
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Total IgE, antigen specific IgE
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Uses radiolabeled IgE to compete with patient IgE for binding to solid-phase anti-IgE
Radioactivity is indirectly proportional to amount of patient IgE Expensive to perform |
Competitive RIST
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Patient antibody is reacted directly with solid-phase anti-IgE.
Procedure has been modified for the use of enzyme labels. Enzyme-labeled anti-IgE is added forming a sandwich of solid-phase anti-IgE, patient IgE, and labeled anti-IgE. After washing, substrate is added. Color development is directly proportional to amount of patient IgE. |
Noncompetitive RIST
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Noncompetitive test
Especially useful in detecting allergies to common allergens Solid-phase is coated with a specific allergen Patient serum is added & allowed to react After washing, enzyme-labeled anti-IgE is added After washing, substrate is added Color development is directly proportional to the amount of specific patient IgE |
RAST
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Cytotoxic hypersensitivity
Mediated by IgG & IgM |
Type 2 Hypersensitivity
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Directed at Antigen on cell membranes or intracellular matrix
Antigen may be found there naturally or deposited there |
Type 2 Hypersensitivity
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Involves the activation of complement via the classical pathway
Involves opsonization via FcR and CR on phagocytic cells Involves NK cells because they have FcRs |
Type 2 Hypersensitiviity
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Cellular destruction results from antibodies combining with transfused alloantigens
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Transfusion RXN
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Cellular destruction resulting from a mother’s IgG antibodies crossing the placenta & attacking the baby’s cells
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HDN
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Cellular destruction results from autoantibodies to self RBC antigens
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Autoimmune Hemolytic Anemia
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Platelet destruction results from antibodies coated to the platelets
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Autoimmune Thrombocytic Purpura
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Involves the activation of complement via the classical pathway
Involves opsonization via FcR and CR on phagocytic cells Involves NK cells because they have FcRs |
Type 2 Hypersensitiviity
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Cellular destruction results from antibodies combining with transfused alloantigens
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Transfusion RXN
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Cellular destruction resulting from a mother’s IgG antibodies crossing the placenta & attacking the baby’s cells
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HDN
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Cellular destruction results from autoantibodies to self RBC antigens
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Autoimmune Hemolytic Anemia
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Platelet destruction results from antibodies coated to the platelets
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Autoimmune Thrombocytic Purpura
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Autoantibodies directed against epitopes that are part of the basement membranes in the lungs and kidneys
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Goodpastures's Syndrome
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Generation of neoantigens by binding of reactive molecules to erythrocyte surfaces
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Drug induced Hemolytic Anemia
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Immune Complex Disease (ICD)
Involves soluble antigen; may be distributed locally or systemically |
Type 3 Hypersensitivity
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Mediated by IgG, IgM
Requires high titers of both Ag and Ab Involves the activation of complement via the classical pathway, and the actions of phagocytic cells and neutrophils |
Type 3 Hypersensitivity
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Predisposing condition of type 3 hs reactions
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Repeated injection, ingestion, inhalation
Persistent infections Autoimmunity Cancer Temperature sensitive cryoglobulins |
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Damaged Inflicted by type 3 HS reactions
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Blockage of circulation, leading to necrosis
Enzymatic and phagocytic damage initiated by complement fixation Vasodilation and edema (if systemic, can lead to shock) Inflammation |
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Systemic; deposition most evident in joints
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Rheumatoid Arthritis
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Systemic; kidney, skin, vasculature, joints
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Systemic lupus erythematosus
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Cryoglobulins; temperature-dependent
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Reynaud’s syndrome
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Injection of foreign proteins
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Serum sickness
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characterized by inflamed extremities (ears, fingers) after exposure to cold.
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Reynauds Syndrome
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Mediated by autoimmune antibodies (IgM) against antigen on red blood cells.
Relevant epitopes become well exposed on RBC surface only at 30oC or lower. Agglutination by IgM blocks capillaries & leads to inflammation and necrosis. |
Reynauds Syndrome
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Cell mediated; No antibody involved
Delayed type hypersensitivity |
Type 4 hypersensitivity
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directed against molecules that can penetrate into the cell and thus end up being processed and presented on class I molecules
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cytotoxic t cells
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Contact Sensitivity and lung injury and tubercle formation are example of
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Type 4 HS
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Generation of neoantigens by binding of reactive chemicals to cells (often in the skin
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contact sensitivity
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Much of the lung injury suffered in tuberculosis results from DTH, not from the infectious agent
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lung injury and tubercle formation
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TB skin test is a classic example of a
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Delayed HS RXN
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soluble antigens from Mycobacterium tuberculosis induce a reaction in people who have or have had exposure to tuberculosis
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TB skin test
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The antigen used in TB skind test is a purified filtrate from the organism’s cell wall called
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purified protein derivative (PPD).
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Skin testing done same as the tuberculin skin test may be used for
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Candida albicans
Diphtheria toxoid Tetanus toxoid Other fungal antigens |
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testing can be done to determine the cause of persistent dermatitis
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Patch
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