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19 BMD 430 lecture 19

front 1 Define hypersensitivity.	back 1 An exaggerated or inappropriate immune response to an antigen that causes tissue damage; classified into Types I–IV
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 strategy to eliminate a parasite?	back 4 Type 2 immunity involving IgE, mast cells, and eosinophils that promote parasite expulsion through mucus, coughing, or 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?	back 6 IgG4 blocks allergens from binding IgE, preventing 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?	back 8 A monoclonal antibody that binds free IgE to prevent mast cell activation; slightly increases infection risk due to lower parasite exposure.

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 Describe how mast cells contribute to defense against parasites.	back 10 Tissue-resident cells with granules of histamine and proteases; when IgE is cross-linked, they degranulate and trigger inflammation and expulsion responses.
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?	back 12 Lipid mediators like prostaglandins and leukotrienes produced after degranulation; aspirin blocks COX enzymes, reducing 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 Explain the process of sensitization.	back 14 Initial exposure to allergen → Th2 differentiation → B cell class switching to IgE → IgE binds mast cells, priming them for re-exposure
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 Name three genes or proteins that, when altered, can affect allergy susceptibility.	back 16 IL-4R, STAT6, Filaggrin, HLA, or FCER1A

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 Differentiate between the early and late phases of an allergic response.	back 18 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? What treatment should be given?	back 19 Type I hypersensitivity (anaphylaxis); treated with epinephrine, which constricts vessels and relaxes airways.
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 Describe how desensitization immunotherapy works	back 21 Gradual allergen exposure increases IgG4 and reduces IgE, leading to 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? What type of hypersensitivity is it?	back 23 Erythroblastosis fetalis; Type II hypersensitivity.
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, and what causes it?	back 25 A Type III reaction caused by immune complex deposition after exposure to foreign serum; symptoms include vasculitis, arthritis, and nephritis
front 26 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 26 C. Serum sickness
front 27 Explain the difference between the sensitization and effector phases of DTH.	back 27 Sensitization = memory Th1 cells form; Effector = re-exposure causes cytokine release and macrophage recruitment.
front 28 Define chronic inflammation and explain why it is problematic.	back 28 Persistent immune activation causes tissue damage, fibrosis, and potential organ failure.