Print 19 BMD 430 lecture 19 flashcards

19 BMD 430 lecture 19

front 1 Which statement best defines hypersensitivity? A. A normal immune response that clears infection without damage B. A genetic defect in immune cell development C. An exaggerated or inappropriate immune response that causes tissue damage D. A response limited only to autoimmune diseases	back 1 C. An exaggerated or inappropriate immune response that causes tissue damage
front 2 Which type of immunity primarily functions against parasitic infections? A. Type 1 B. Type 2 C. Type 3 D. Type 4	back 2 B. Type 2
front 3 Which of the following is not a characteristic of parasites? A. Large multicellular organisms B. Easily phagocytosed C. Complex eukaryotic structure D. Evasive immune strategies	back 3 B. Easily phagocytosed
front 4 What is the body’s general immune strategy for eliminating parasites? A. Type 1 immunity involving neutrophils and IFN-γ B. Type 2 immunity using IgE, mast cells, and eosinophils to promote expulsion via mucus, coughing, and peristalsis C. Type 3 immunity using complement activation only D. Cytotoxic T-cell–mediated killing through perforin and granzyme	back 4 B. Type 2 immunity using IgE, mast cells, and eosinophils to promote expulsion via mucus, coughing, and peristalsis

front 5 Which cytokines are key mediators of Type 2 immunity? A. IL-2, IFN-γ, TNF B. IL-4, IL-5, IL-13 C. IL-6, IL-8, IL-12 D. IL-10, IL-17, IL-23	back 5 B. IL-4, IL-5, IL-13
front 6 Why is switching from IgE to IgG important during allergic responses? A. IgG4 enhances mast cell activation and increases histamine release B. IgG4 blocks allergens from binding IgE, reducing mast cell activation and chronic inflammation C. IgG4 increases eosinophil degranulation, worsening allergic symptoms D. IgG4 promotes complement activation to intensify inflammation	back 6 B. IgG4 blocks allergens from binding IgE, reducing mast cell activation and chronic inflammation
front 7 Which antibody binds most tightly to FcεRI receptors on mast cells? A. IgA B. IgE C. IgG4 D. IgM	back 7 B. IgE
front 8 What is Ozalimumab, and how does it work? A. A monoclonal antibody that blocks IL-5 to prevent eosinophil activation B. A monoclonal antibody that binds free IgE, reducing mast-cell activation and slightly increasing infection risk C. A drug that destroys mast cells directly to reduce allergic reactions D. A vaccine that induces tolerance to food allergens	back 8 B. A monoclonal antibody that binds free IgE, reducing mast-cell activation and slightly increasing infection risk

front 9 Which of the following cells release major basic protein to kill parasites? A. Mast cells B. Basophils C. Eosinophils D. Dendritic cells	back 9 C. Eosinophils
front 10 How do mast cells contribute to defense against parasites? A. They phagocytose parasites directly and digest them with lysosomal enzymes B. They produce IgM to neutralize parasites in the bloodstream C. They reside in tissues and, when IgE is cross-linked, degranulate to release histamine and proteases that drive inflammation and parasite expulsion D. They activate complement to kill parasites intracellularly	back 10 C. They reside in tissues and, when IgE is cross-linked, degranulate to release histamine and proteases that drive inflammation and parasite expulsion
front 11 Which histamine receptor is primarily responsible for inflammation and smooth muscle contraction? A. H1 B. H2 C. H3 D. H4	back 11 A. H1
front 12 What are secondary mediators, and how does aspirin affect them? A. Protein cytokines released before degranulation; aspirin increases their production B. Lipid mediators such as prostaglandins and leukotrienes made after degranulation; aspirin blocks COX enzymes to reduce prostaglandin synthesis C. Antibodies produced by plasma cells; aspirin prevents class switching D. Histamine molecules stored in granules; aspirin neutralizes them directly	back 12 B. Lipid mediators such as prostaglandins and leukotrienes made after degranulation; aspirin blocks COX enzymes to reduce prostaglandin synthesis

front 13 What type of molecule is most likely to act as an allergen? A. Large insoluble protein B. Small soluble protein structurally similar to parasite antigen C. Nucleic acid fragment D. Lipid antigen	back 13 B. Small soluble protein structurally similar to parasite antigen
front 14 Which best describes the process of sensitization in allergic responses? A. Immediate mast cell degranulation upon first allergen exposure B. Initial exposure to allergen leads to Th2 differentiation, B-cell class switching to IgE, and IgE binding to mast cells, priming them for future exposures C. IgG production that blocks allergen binding to mast cells D. Activation of cytotoxic T cells that directly kill allergen-expressing cells	back 14 B. Initial exposure to allergen leads to Th2 differentiation, B-cell class switching to IgE, and IgE binding to mast cells, priming them for future exposures
front 15 Which environmental factor decreases allergy risk? A. Antibiotic use B. Excessive hygiene C. Early parasite exposure D. Urban pollution	back 15 C. Early parasite exposure
front 16 Which of the following genes or proteins, when altered, can affect allergy susceptibility? A. IL-4R, STAT6, Filaggrin B. HLA, FCER1A, IL-4R C. STAT6, FCER1A, Filaggrin D. All of the above	back 16 D. All of the above

front 17 The “wheal and flare” reaction in skin testing is caused by: A. Complement activation B. Mast cell degranulation C. Cytotoxic T cells D. Neutrophil infiltration	back 17 B. Mast cell degranulation
front 18 Which best differentiates the early and late phases of an allergic response? A. Early phase occurs hours later via cytokines; Late phase occurs within minutes via histamine B. Early phase = histamine release within minutes; Late phase = cytokine-mediated inflammation hours later C. Both early and late phases are mediated only by IgG D. Early phase involves antibody production; Late phase involves mast cell degranulation	back 18 B. Early phase = histamine release within minutes; Late phase = cytokine-mediated inflammation hours later
front 19 A patient eats peanuts and experiences hypotension, airway constriction, and swelling. What type of hypersensitivity is this? A. Type II B. Type I C. Type III D. Type IV	back 19 B. Type I treated with epinephrine
front 20 Which of the following is not a symptom of allergic asthma? A. Airway constriction B. Mucus production C. IL-13 activity D. Complement deposition	back 20 D. Complement deposition

front 21 How does desensitization (allergen immunotherapy) work? A. Gradual allergen exposure increases IgE and mast cell activation B. Rapid allergen exposure triggers immediate tolerance via T-cell deletion C. Gradual allergen exposure increases IgG4 and reduces IgE, promoting immune tolerance D. Allergen exposure only stimulates innate immunity without affecting antibodies	back 21 C. Gradual allergen exposure increases IgG4 and reduces IgE, promoting immune tolerance
front 22 Type II hypersensitivity is primarily mediated by: A. T cells B. IgE C. IgG or IgM D. Immune complexes	back 22 C. IgG or IgM
front 23 A newborn develops anemia due to maternal antibodies crossing the placenta. What is this condition? A. Hemophilia B. Erythroblastosis fetalis C. Thalassemia D. Sickle cell anemia	back 23 B. Erythroblastosis fetalis, TYPE II
front 24 Which mechanism mediates Type III hypersensitivity? A. Antibody-dependent cellular cytotoxicity B. Immune complex deposition C. Mast cell degranulation D. Delayed T cell response	back 24 B. Immune complex deposition

front 25 What is serum sickness? A. A Type I hypersensitivity reaction to food allergens B. A Type II reaction causing hemolysis C. A Type III hypersensitivity reaction caused by immune complex deposition after exposure to foreign serum D. A Type IV T-cell–mediated delayed reaction	back 25 C. A Type III hypersensitivity reaction caused by immune complex deposition after exposure to foreign serum
front 26 Which of the following are common symptoms of serum sickness? A. Vasculitis, arthritis, and nephritis B. Anaphylaxis, hypotension, and airway constriction C. Fever only D. Skin rash without systemic involvement	back 26 A. Vasculitis, arthritis, and nephritis
front 27 Which of the following is not associated with Type IV hypersensitivity? A. Tuberculin skin test B. Contact dermatitis C. Serum sickness D. Poison ivy rash	back 27 C. Serum sickness
front 28 Which best describes the difference between the sensitization and effector phases of delayed-type hypersensitivity (DTH)? A. Sensitization = immediate mast cell degranulation; Effector = antibody production B. Sensitization = memory Th1 cells form; Effector = re-exposure triggers cytokine release and macrophage recruitment C. Sensitization = IgE production; Effector = eosinophil-mediated cytotoxicity D. Sensitization and effector phases are identical	back 28 B. Sensitization = memory Th1 cells form; Effector = re-exposure triggers cytokine release and macrophage recruitment

front 29

Which statement best defines chronic inflammation and explains why it is problematic?

A. Short-term immune response that eliminates pathogens without tissue damage
B. Persistent immune activation causing tissue damage, fibrosis, and potential organ failure
C. Inflammation limited to the skin and mucosa only
D. A beneficial process that always improves tissue repair

back 29

B. Persistent immune activation causing tissue damage, fibrosis, and potential organ failure

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19 BMD 430 lecture 19