(Test Bank-Midterm II) Chapter 9: Alterations in Immunity and Inflammation LATEST EDITION 2024/25 ALL 100% CORRECT ANSWERS GUARANTEED GRADE A+

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1. How is hypersensitivity best defined? a. A disturbance in the immunologic tolerance of self-antigens b. An immunologic reaction of one person to the tissue of another person c. An altered immu... nologic response to an antigen that results in disease d. An undetectable immune response in the presence of antigens ANS: C Hypersensitivity is an altered immunologic response to an antigen that results in disease or damage to the host. Autoimmunity is a disturbance in the immunologic tolerance of self-antigens. Alloimmunity is the immunologic reaction of one person to the tissue of another person. An immune deficiency of some type would cause undetectable immune response in the presence of antigens. 2. What is a hypersensitivity reaction that produces an allergic response called? a. Hemolytic shock b. Anaphylaxis c. Necrotizing vasculitis d. Systemic erythematosus ANS: B Examples of systemic anaphylaxis are allergic reactions to beestings, peanuts, and fish. Hemolytic shock would be a state in which erythrocytes are destroyed by complement-mediated lysis to the point of causing a state of shock. Necrotizing vasculitis is inflammation of blood vessel walls that limits perfusion. Systemic lupus erythematosus (SLE) is a chronic, multisystem, inflammatory disease and is one of the most common, complex, and serious of the autoimmune disorders. 3. The common hay fever allergy is expressed through a reaction that is mediated by which class of immunoglobulins? a. IgE b. IgG c. IgM d. T cells ANS: A Type I reactions are mediated by antigen-specific IgE and the products of tissue mast cells. The most common allergies (e.g., pollen allergies) are type I reactions. In addition, most type I reactions occur against environmental antigens and are therefore allergic. Hay fever allergy is not mediated by IgG, IgM, or T cells. 4. What are blood transfusion reactions an example of? a. Autoimmunity b. Alloimmunity c. Homoimmunity d. Hypersensitivity ANS: B Alloimmunity (also termed isoimmunity) occurs when the immune system of one individual produces an immunologic reaction against tissues of another individual. Autoimmunity is a disturbance in the immunologic tolerance of self-antigens. Homoimmunity refers to the resistance of a lysogenic bacterium that is carrying a phage to an infection by the same type of phage. Hypersensitivity is an altered immunologic response to an antigen that results in disease or damage to the host. 5. During an IgE-mediated hypersensitivity reaction, which leukocyte is activated? a. Neutrophils b. Monocytes c. Eosinophils d. T lymphocytes ANS: C Of the options provided, only eosinophils are activated during IgE-mediated hypersensitivity reactions. 6. During an IgE-mediated hypersensitivity reaction, what causes bronchospasm? a. Bronchial edema caused by the chemotactic factor of anaphylaxis b. Bronchial edema caused by binding of the cytotropic antibody c. Smooth muscle contraction caused by histamine bound to H1 receptors d. Smooth muscle contraction caused by histamine bound to H2 receptors ANS: C During an IgE-mediated hypersensitivity reaction, smooth muscle contraction caused by histamine bound to H1 receptors results in bronchospasms. The bronchospasm is not caused by edema or by histamine binding to H2 receptors. 7. A patient is having an IgE-mediated hypersensitivity reaction. What action by the healthcare professional is best? a. Give the patient an antihistamine. b. Prepare to give the patient a blood transfusion. c. Ask the patient is he/she is having pain at the site. d. Apply warm, moist heat to the affected area. ANS: A Histamine is the most potent mediator in an IgE-mediated hypersensitivity reaction (Type 1). Histamine bound to H2 results in the degranulation of mast cells with the release of histamine. Blocking histamine receptors with antihistamines can control some type I responses. The healthcare professional would not need to give the patient blood; warm; moist heat; or ask about pain. 8. What characteristic do atopic individuals have that make them genetically predisposed to develop allergies? a. Greater quantities of histamine b. More histamine receptors c. Greater quantities of IgE d. A deficiency in epinephrine ANS: C Atopic individuals tend to produce higher quantities of IgE and to have more crystalline fragment (Fc) receptors for IgE on their mast cells. Greater quantities of histamine, more histamine receptors, and a deficiency in epinephrine do not lead to a genetic predisposition to allergies. What is the mechanism that results in type II hypersensitivity reactions? a. Antibodies coat mast cells by binding to receptors that signal its degranulation, followed by a discharge of preformed mediators. b. Antibodies bind to soluble antigens that were released into body fluids, and the immune complexes are then deposited in the tissues. c. Cytotoxic T lymphocytes or lymphokine-producing helper T 1 cells directly attack and destroy cellular targets. d. Antibodies bind to the antigens on the cell surface. ANS: D The mechanism that results in a type II hypersensitivity reaction begins with antibody binding to tissue-specific antigens or antigens that have attached to particular tissues. The cell can be destroyed by antibody IgG or IgM and activation of the complement cascade through the classical pathway. 10. When mismatched blood is administered causing an ABO incompatibility, how are the erythrocytes destroyed? a. Complement-mediated cell lysis b. Phagocytosis by macrophages c. Phagocytosis in the spleen d. Natural killer cells ANS: A Erythrocytes are destroyed by complement-mediated lysis in individuals with autoimmune hemolytic anemia or as a result of an alloimmune reaction to ABO-mismatched transfused blood cells. Erythrocytes are not destroyed by phagocytosis or natural killer cells. 11. When antibodies are formed against red blood cell antigens of the Rh system, how are the blood cells destroyed? a. Complement-mediated cell lysis b. Phagocytosis by macrophages c. Phagocytosis in the spleen d. Neutrophil granules and toxic oxygen products ANS: C Antibodies against platelet-specific antigens or against red blood cell antigens of the Rh system coat those cells at low density, resulting in their preferential removal by phagocytosis in the spleen, rather than by complement-mediated lysis. These blood cells are not destroyed by complement-mediated cell lysis, phagocytosis by macrophages, neutrophil granules, or toxic oxygen products. 12. When soluble antigens from infectious agents enter circulation, what is tissue damage a result of? a. Complement-mediated cell lysis b. Phagocytosis by macrophages c. Phagocytosis in the spleen d. Neutrophil granules and toxic oxygen products ANS: D Of the options available, only the components of neutrophil granules as well as the several toxic oxygen products produced by these cells, damage the tissue. 13. How are target cells destroyed in a type II hypersensitivity reaction? a. Complement-mediated cell lysis b. Phagocytosis by macrophages c. Neutrophil granules and toxic oxygen products d. Natural killer cells ANS: D The mechanism that results in a type II hypersensitivity reaction involves a subpopulation of cytotoxic cells that are not antigen specific (natural killer [NK] cells). Antibody on the target cell is recognized by Fc receptors on the NK cells, which releases toxic substances that destroy the target cell. The other options do not cause the destruction of target cells related to a type II hypersensitivity reaction. 14. Graves disease (hyperthyroidism) is an example of which type II hypersensitivity reaction? a. Modulation b. Antibody-dependent cell-mediated cytotoxicity c. Neutrophil-mediated damage d. Complement-mediated lysis ANS: A The antibody reacts with the receptors on the target cell surface and modulates the function of the receptor by preventing interactions with their normal ligands, replacing the ligand and inappropriately stimulating the receptor or destroying the receptor. For example, in the hyperthyroidism (excessive thyroid activity) of Graves disease, autoantibody binds to and activates receptors for thyroid-stimulating hormone (TSH) (a pituitary hormone that controls the production of the hormone thyroxine by the thyroid). Graves disease is not a result of cell-mediated cytotoxicity, neutrophil-mediated damage, or complement-mediated lysis. 15. Type III hypersensitivity reactions are a result of which of these? a. Antibodies coating mast cells by binding to receptors that signal its degranulation, followed by the discharge of preformed mediators b. Antibodies binding to soluble antigens that were released into body fluids and the immune complexes being deposited in the tissues c. Tc cells or lymphokine-producing Th1 cells directly attacking and destroying cellular targets d. Antibodies binding to the antigen on the cell surface ANS: B Antigen-antibody (immune) complexes that are formed in the circulation and then deposited later in vessel walls or extravascular tissues cause most type III hypersensitivity diseases. Type III hypersensitivity reactions are not the result of antibodies coating mast cells to signal their degranulation, immune cells directly attacking and destroying targets, or antibodies binding to the antigen on the cell surface. 16. A type IV hypersensitivity reaction causes which result? a. Antibodies coating mast cells by binding to receptors that signal its degranulation, followed by the discharge of preformed mediators b. Antibodies binding to soluble antigens that were released into body fluids and the immune complexes being deposited in the tissues c. Lymphokine-producing Th1 cells directly attacking and destroying cellular targets d. Antibodies binding to the antigen on the cell surface ANS: C Type I, II, and III hypersensitivity reactions are mediated by antibody, type IV reactions are mediated by T lymphocytes and do not involve antibody. Type IV mechanisms occur through either Tc cells or lymphokine-producing Th1 cells. Tc cells directly attack and destroy cellular targets. 17. In a type III hypersensitivity reaction, the harmful effects after the immune complexes that are deposited in tissues are a result of what? a. Cytotoxic T cells b. Natural killer cells c. Complement activation d. Degranulation of mast cells ANS: C Complement activation, particularly through the generation of chemotactic factors for neutrophils, causes the harmful effects of immune complex deposition. The neutrophils bind to antibody and C3b contained in the complexes and attempt to ingest the immune complexes. Type III hypersensitivity reactions as described are not the result of cytotoxic T cells, natural killer cells, or degranulation of mast cells. Raynaud phenomenon is classified as a type III hypersensitivity reaction and is due to: a. Immune complexes that are deposited in capillary beds, blocking circulation b. Mast cells that are bound to specific endothelial receptors, causing them to degranulate and creating a localized inflammatory reaction that occludes capillary circulation c. Cytotoxic T cells that attack and destroy the capillaries so that they are unable to perfuse local tissues d. Antibodies that detect the capillaries as foreign protein and destroy them using lysosomal enzymes and toxic oxygen species ANS: A Raynaud phenomenon is a condition caused by the temperature-dependent deposition of immune complexes in the capillary beds of the peripheral circulation. None of the other options are involved in causing this condition. 19. Deficiencies in which element can produce depression of both B- and T-cell function? a. Iron b. Zinc c. Iodine d. Magnesium ANS: B Of the options available, only deficient zinc intake can profoundly depress T- and B-cell function. not in our edition [Show More]

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