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45 Cards in this Set
- Front
- Back
Type I hypersensitivity is _____________ hypersensitivity.
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Immediate
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Type I hypersensitivity is _____________ mediated.
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IgE
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IgE activating mast cells for rapid release of inflammatory mediators.
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Type I
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IgG, IgM activating complement or ADCC to kill cells
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Type II
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Immune complex deposition in blood vessels leads to inflammation
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Type III
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Cell mediated responses, usually delayed by 2 days or more, where activated lymphocytes and/or macrophages cause tissue damage.
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Type IV
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Allergic rhinitis, anaphylaxis and allergic asthma are examples of type ___ hypersensitivity.
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I
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Autoimmune diseases of the skin and hemolytic anemia are examples of type __ hypersensitivity
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II
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Persistent infections (viral hepatitis) and autoimmune diseases such as SLE are examples of type __ hypersensitivity.
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III
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Poison ivy, granuloma formation in tuberculosis are examples of type __ hypersensitivity
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IV
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_____________ cells are the primary effector for antigen dependent cell mediated cytotoxicity.
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Natural Killer
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IgE antibodies in Type ___ hypersensitivity cause rapid degranulation of _____________ and subsequent release of _____________mediators.
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I, mast cells, inflammatory
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Excessive immune response (often to innocuous antigens) that causes damage.
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Hypersensitivity
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A disease or reaction caused by an immune response to one or more environmental antigens, resulting in tissue inflammation and organ dysfunction.
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Allergy
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An antigen that causes allergy.
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Allergen
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A genetically determined state of hypersensitivity to common environmental allergens, mediated by IgE antibodies.
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Atopy
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In a type I reaction, the allergen is absorbed by an _____________ cell, which then presented to antigen-specific _____________ cells. This leads to the production of _____________ and binding of this antibody to _____________, which degranulate to release _____________.
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Antigen presenting, T, IgE, Mast cells, histamine
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In allergic skin testing, _____________ and _____________ will develop around a positive prick around 20 minutes post inoculation.
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Wheal, flare
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_____________ is a systemic mast cell activation, leading to hypotension, urticaria, angioedema and laryngeal/bronchial obstruction.
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Anaphylaxis
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In type II hypersensitivity, _____________ and _____________ antibodies cause injury by activating _____________.
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IgG, IgM, complement
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These cells bind to target antigen on cells using the antibody as the bridge between them.
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Effector cells
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Examples of effector cells include:
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Macrophages, neutrophils, eosinophils, NK cells
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IN _____________ syndrome, antibodies attack the lungs and kidneys, causing bleeding from the lungs and kidney failure (GBM antigen)
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Goodpasture's
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_____________ is a blistering skin and mucous membrane disease that forms antibodies against desmoglein, which forms the 'glue' that attaches adjacent epidermal cells. The blisters slough off into sores.
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Pemphigus
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Auto reactive antibody is created to acetylcholine receptor on post-synaptic neuromuscular junctions, resulting in muscle weakness.
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Myasthenia gravis
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Incompatible blood transfusions are an example of _____________ hypersensitivity.
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Type II
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Lattice or complex formed by the binding of antibody to soluble antigens that occurs naturally and constantly in the healthy body.
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Immune complex
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Immune complexes are normally taken up by _____________ and eliminated in the _____________ and the _____________.
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RBCs, liver, spleen
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Immune complexes are formed in excess during a type __ hypersensitivity reaction, and they deposit themselves in the _____________, triggering the inflammatory response.
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III, blood vessel walls
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Immune complexes activate _____________ in type III hypersensitivity reactions, which causes inflammation via _____________ receptor mediated ADCC
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Complement, FC
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Persistent infection with malaria or leprosy, autoimmune disorders such as SLE or dermatomyositis and inhaled antigens such as Farmer's Lung, Bronchopulmonary aspergillosis are examples of type __ hypersensitivity.
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III
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A substance, usually very small in molecular size, that alone is not immunogenic but after conjugation to a carrier protein or cells becomes immunogenic and induces antibody production.
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Hapten
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Skin inflammation, including pruritic papules and vesicles on an erythematous base are indicative of _____________
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Alergic contact dermatitis
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Sensitization of allergic contact dermatitis typically takes __ to __ days.
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10-14
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The most common causes of allergic contact dermatitis include:
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Poison ivy, nickel, preservatives/dyes/fragrances, and chemicals in rubber gloves.
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Inflammation of the skin (erythema, edema, hyperkeratosis or vesiculation) that is NONSPECIFIC response to direct chemical damage.
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Irritant contact dermatitis
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Unlike allergic contact dermatitis, irritant contact dermatitis will resolve with the _____________.
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Removal of the irritant
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Sensitization is required/not required for irritant contact dermatitis.
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Not required
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In allergic contact dermatitis, the allergen contacts the skin of a susceptible person. The _____________ cells in the epidermis contact the _____________ carrier complex, then migrate into the regional _____________, where they sensitize a _____________ cell.
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Langerhans, hapten, lymph node, T cell
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In allergic contact dermatitis, _____________ cells are activated by _____________, and then release inflammatory _____________ to act on _____________, _____________ and other cells to produce skin lesions.
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Helper T cells, memory T cells, cytokines, endothelial cells, keratinocytes
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PPD stands for
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Tuberculin purified protein derivative
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In a PPD test, _____________ that have been sensitized to _____________ release cytokines to increase vascular permeability.
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Memory T cells, mycobacterium tuberculosis.
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A positive PPD test will reveal an induration __ to __ hours later measuring _ to __ mm in diameter.
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48-72, 5-15mm
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_____________ form in diseases with a persistent antigen, often an infectious agent such as tuberculosis, leprosy and leishmaniasis.
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Granulomas
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Granulomas contain multinucleated _____________ cells.
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Giant
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