NR-283 Pathophysiology Week 3 Quiz 2026/2027 |ACTUAL EXAM | Verified Q&A with Rationales | Chamberlain | Pass Guaranteed - A+ Graded

Pass your NR-283 Pathophysiology Week 3 Quiz at Chamberlain University with this comprehensive resource featuring verified questions, answers, and detailed rationales – all 100% correct and A+ graded for the 2026/2027 curriculum. This A+ Graded resource for the NR-283 Pathophysiology Week 3 Quiz (2026/2027 | Chamberlain University) contains verified questions, answers, and rationales covering all essential topics related to immunity and immune system disorders. Comprehensive Content Coverage Includes: Innate (Natural) Immunity: First and second lines of defense – physical barriers (skin, mucous membranes), chemical barriers (lysozyme, gastric acid, defensins), phagocytic cells (neutrophils, macrophages, dendritic cells), natural killer (NK) cells, complement system (classical, alternative, lectin pathways – opsonization, chemotaxis, membrane attack complex), inflammatory response (review from Week 1 with immune-specific mediators – interferons, interleukins, TNF-α). Adaptive (Acquired) Immunity: Third line of defense – specificity, memory, self-tolerance. Humoral immunity (B lymphocytes – plasma cells produce antibodies (immunoglobulins: IgG, IgA, IgM, IgE, IgD); memory B cells). Cell-mediated immunity (T lymphocytes – helper T cells CD4+ (Th1, Th2, Th17, Treg), cytotoxic T cells CD8+, memory T cells). Antigen presentation (MHC class I on all nucleated cells for CD8+; MHC class II on antigen-presenting cells – dendritic cells, macrophages, B cells for CD4+). Clonal selection and expansion. Hypersensitivity Reactions (Types I-IV): Type I (Immediate, IgE-mediated): Allergies, anaphylaxis. Mechanism – first exposure (sensitization) produces IgE bound to mast cells/basophils; re-exposure causes cross-linking, degranulation, release of histamine, leukotrienes, prostaglandins. Clinical examples – allergic rhinitis, asthma, anaphylactic shock, food allergies. Treatment – epinephrine, antihistamines, corticosteroids. Type II (Cytotoxic, antibody-mediated): IgG/IgM against cell surface or extracellular matrix antigens. Mechanism – complement activation, opsonization, ADCC. Clinical examples – autoimmune hemolytic anemia, immune thrombocytopenic purpura (ITP), Goodpasture syndrome, Graves' disease (stimulatory), myasthenia gravis (blocking), transfusion reactions, hemolytic disease of the newborn (Rh incompatibility). Type III (Immune complex-mediated): Antigen-antibody complexes deposit in tissues (vessels, kidneys, joints). Mechanism – complement activation, neutrophil recruitment, tissue damage. Clinical examples – systemic lupus erythematosus (SLE), rheumatoid arthritis, serum sickness, post-streptococcal glomerulonephritis, Arthus reaction. Type IV (Delayed, cell-mediated): No antibody involvement – T cell mediated. Mechanism – sensitized T lymphocytes release cytokines, recruit macrophages (24-72 hours). Clinical examples – tuberculin skin test (PPD), contact dermatitis (poison ivy, nickel), graft rejection, Hashimoto's thyroiditis, type 1 diabetes. Autoimmune Disorders: Loss of self-tolerance. Mechanisms – molecular mimicry, release of sequestered antigens, genetic predisposition (HLA associations), environmental triggers. Examples – systemic lupus erythematosus (SLE – autoantibodies against DNA, nuclear proteins – malar rash, arthritis, nephritis, serositis), rheumatoid arthritis (autoantibodies – rheumatoid factor, anti-CCP – synovitis, pannus formation, joint destruction), multiple sclerosis (autoimmune attack on myelin – relapsing-remitting neurologic deficits), type 1 diabetes (autoimmune destruction of pancreatic beta cells – insulin deficiency), Hashimoto's thyroiditis (autoantibodies against thyroid peroxidase, thyroglobulin – hypothyroidism), Graves' disease (autoantibodies stimulating TSH receptor – hyperthyroidism), Sjögren's syndrome (autoimmune destruction of exocrine glands – dry eyes, dry mouth), scleroderma, inflammatory bowel disease (Crohn's, ulcerative colitis). Immunodeficiency Disorders: Primary (congenital): Genetic defects. B-cell deficiencies (Bruton's agammaglobulinemia – recurrent bacterial infections, no B cells), T-cell deficiencies (DiGeorge syndrome – thymic aplasia, hypocalcemia, recurrent viral/fungal infections), combined deficiencies (Severe Combined Immunodeficiency SCID – absence of T and B cells, very susceptible to infections), phagocyte disorders (chronic granulomatous disease – defective respiratory burst, recurrent catalase-positive bacterial/fungal infections), complement deficiencies (increased susceptibility to Neisseria infections, autoimmune disorders). Secondary (acquired): More common. Causes – HIV/AIDS (depletion of CD4+ T cells, opportunistic infections, malignancies), chemotherapy, radiation, malnutrition, splenectomy (encapsulated organisms – Streptococcus pneumoniae, Neisseria meningitidis, Haemophilus influenzae), immunosuppressive drugs (transplant recipients, autoimmune disease treatment), aging (immunosenescence), burns, diabetes. Transplant Rejection and Graft-versus-Host Disease: Major histocompatibility complex (MHC – HLA in humans). Allograft rejection – hyperacute (minutes to hours, preformed antibodies, thrombosis), acute (days to months, T cell mediated, treatable with immunosuppression), chronic (months to years, fibrosis, vascular damage, resistant to treatment). Graft-versus-host disease (GVHD) – donor T cells attack recipient tissues (skin, liver, GI tract) after bone marrow/stem cell transplant. Prevention and treatment – immunosuppressive drugs (calcineurin inhibitors – cyclosporine, tacrolimus; corticosteroids; mycophenolate mofetil; mTOR inhibitors – sirolimus). Each question includes a detailed rationale explaining the immunologic mechanism, clinical correlation, and correct answer reasoning – ensuring you understand the "why" behind every correct choice. With fully verified Q&A plus rationales and our Pass Guarantee, this is the definitive tool to ace your Week 3 Quiz on the first attempt. 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