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45 Cards in this Set

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