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Exam (elaborations)

NR 507 Advanced Pathophysiology – Chamberlain University – Midterm Exam Practice Questions – Immunology, Hypersensitivity & Immunodeficiency

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NR 507 Advanced Pathophysiology – Chamberlain University – Midterm Exam Practice Questions – Immunology, Hypersensitivity & Immunodeficiency Covers immunology, hypersensitivity reactions, and immunodeficiency concepts for NR 507 Advanced Pathophysiology at Chamberlain University. Includes 100 exam-style practice questions with highlighted answers and detailed rationales to support midterm preparation and review.

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NR 507
MIDTERM EXAM
Advanced Pathophysiology
Chamberlain University



100 Exam-Style Practice Questions
Immunology, Hypersensitivity & Immunodeficiency
With Highlighted Answers & Detailed Rationales


✔ Correct answers are highlighted in green
📖 Rationales are highlighted in yellow

,1. Which of the following is the underlying pathology for hay fever?
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A. Formation of autoantibodies.
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B. Activation of complement.
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C. Destruction by T-cells.
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D. Mast cell degranulation.
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✔ Answer: D. Mast cell degranulation.
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📖 Rationale: Hay fever (allergic rhinitis) is a Type I (IgE-
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mediated) hypersensitivity reaction. Allergens cross-
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link IgE antibodies on mast cells, triggering degranulation and release of histamine and other mediators, causi
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ng the classic symptoms of sneezing, itching, and nasal congestion.
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2. Which of the following assessment findings would be expected in a patient who presents with u
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rticaria?
A. Eosinophilia.
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B. Decreased thyroid-stimulation hormone level.
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C. Thrombocytopenia.
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D. Leukopenia.
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✔ Answer: A. Eosinophilia.
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📖 Rationale: Urticaria (hives) is an allergic reaction involving IgE-
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mediated mast cell degranulation. Eosinophils are recruited to sites of allergic inflammation and are elevated i
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n the blood (eosinophilia) during allergic reactions. Eosinophils help modulate the immune response by releasi
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ng enzymes that inactivate mast cell mediators.
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3. The diagnosis for an individual who presents to the office with sudden swollen lips and eyes, s
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hortness of breath, and throat tightness after a bee sting is:
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A. Anaphylaxis. tz



B. Asthma. tz



C. Angioedema. tz



D. Reactive airway disease. tz tz tz




✔ Answer: A. Anaphylaxis.
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📖 Rationale: Anaphylaxis is a severe, life-
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threatening systemic Type I hypersensitivity reaction triggered by allergens such as bee venom. It involves ma
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ssive IgE- tz



mediated mast cell degranulation causing angioedema, bronchospasm (throat tightness/shortness of breath),
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and potentially circulatory collapse. Immediate epinephrine is the treatment of choice.
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4. Damage occurs with ABO incompatibility because:
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A. Mast cell degranulation. tz tz tz



B. Autoantibodies specific for thyroid tissue impair the receptors for TSH.
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C. Antigen/Antibody complexes attack the RBC.
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D. Complement damages RBC membrane causing cell lysis.
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Page 2 of 31 tz tz tz

,✔ Answer: D. Complement damages RBC membrane causing cell lysis.
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📖 Rationale: ABO incompatibility is a Type II (cytotoxic) hypersensitivity reaction. Preformed IgM antibodies
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against incompatible ABO antigens activate the complement cascade, which damages and lyses the red bloo
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d cell membrane, leading to intravascular hemolysis, hemoglobinuria, and potentially acute renal failure.
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5. Which of the following statements is true about a primary immunodeficiency?
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A. It is the result of a single gene defect.
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B. It appears primarily in older adults.
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C. It is usually inherited.
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D. It is the result of multiple gene defects.
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✔ Answer: C. It is usually inherited.
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📖 Rationale: Primary immunodeficiencies are disorders caused by intrinsic defects in the immune system,
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most often due to genetic mutations inherited from one or both parents. They typically manifest in infancy or ea
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rly childhood and may involve defects in B cells, T cells, complement, or phagocytes. While some are single-
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gene defects, the defining feature is that they are usually inherited.
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6. ________________ is a predominant cause of secondary immune deficiencies worldwide.
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A. Malnutrition. tz



B. HIV infection. tz tz



C. Chemotherapy. tz



D. Autoimmune disease. tz tz




✔ Answer: A. Malnutrition.
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📖 Rationale: Malnutrition is the most common cause of secondary (acquired) immunodeficiency worldwide,
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particularly in developing countries. Protein- tz tz tz tz



energy malnutrition impairs production of lymphocytes, immunoglobulins, and complement proteins, leaving in
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dividuals vulnerable to opportunistic and common infections.
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7. An example of a secondary immunodeficiency is:
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A. Job Syndrome. tz tz



B. Common Variable Immunodeficiency.
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C. Familial Mediterranean Fever.
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D. Pneumocystis Carinii pneumonia (PCP).
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✔ Answer: D. Pneumocystis Carinii pneumonia (PCP).
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📖 Rationale: Pneumocystis carinii (now jirovecii) pneumonia is an opportunistic infection that arises in indivi
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duals with secondary (acquired) immunodeficiency, most notably AIDS (HIV infection). It is not a primary immu
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nodeficiency itself but serves as an indicator disease of profound immune suppression. Job Syndrome and Co
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mmon Variable Immunodeficiency are examples of primary immunodeficiencies.
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8. An example of a primary immunodeficiency is:
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A. Sinopulmonary infections due to HIV.
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B. Severe Combined Immunodeficiency (SCID).
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Page 3 of 31 tz tz tz

, C. Immunosuppression from corticosteroids.
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D. Lymphopenia secondary to chemotherapy.
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✔ Answer: B. Severe Combined Immunodeficiency (SCID).
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📖 Rationale: Severe Combined Immunodeficiency (SCID) is a primary immunodeficiency caused by inherite
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d genetic defects affecting both T and B lymphocyte development and function. It results in virtually absent ad
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aptive immunity. Affected infants present with recurrent, severe infections early in life. SCID is sometimes call
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ed 'bubble boy disease' because patients must be kept in sterile environments.
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9. Which type of hypersensitivity reaction is responsible for contact dermatitis caused by poison i
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vy?
A. Type I - IgE-mediated tz tz tz tz



B. Type II - Cytotoxic tz tz tz tz



C. Type III - Immune complex-mediated
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D. Type IV - Delayed (cell-mediated)
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✔ Answer: D. Type IV - Delayed (cell-mediated)
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📖 Rationale: Contact dermatitis from poison ivy is a classic Type IV hypersensitivity reaction. Sensitized T ly
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mphocytes recognize the hapten (urushiol) bound to skin proteins. On re-
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exposure, T cells release cytokines causing local inflammation 24–
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72 hours after contact. No antibodies or complement are involved.
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10. A patient is diagnosed with systemic lupus erythematosus (SLE). Which type of hypersensitiv
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ity reaction underlies the tissue damage in SLE?
tz tz tz tz tz tz tz




A. Type I tz tz



B. Type II tz tz



C. Type IIItz tz



D. Type IV tz tz




✔ Answer: C. Type III
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📖 Rationale: SLE is a Type III (immune complex-mediated) hypersensitivity reaction. Antigen-
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antibody complexes (anti- tz tz



dsDNA and other autoantibodies) deposit in tissues such as the glomeruli, blood vessels, and joints. These co
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mplexes activate complement, causing inflammation and tissue injury characteristic of the disease.
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11. Which immunoglobulin is primarily responsible for mediating Type I hypersensitivity reaction
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s?
A. IgA tz



B. IgG tz



C. IgM tz



D. IgE tz




✔ Answer: D. IgE
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📖 Rationale: IgE is the primary antibody mediating Type I (immediate) hypersensitivity reactions. IgE binds t
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o high-affinity Fc receptors on mast cells and basophils. When antigen cross-
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links adjacent IgE molecules, it triggers degranulation and release of histamine, prostaglandins, and leukotrien
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es, causing immediate allergic symptoms.
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Page 4 of 31 tz tz tz

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September 22, 2026
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