NR507 Week 4 Midterm Exams Due 1st February 2026
Complete Actual Exam Question 1- 100 Screenshots NR 507
Advanced Pathophysiology NR 507 Midterms and Finals
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This comprehensive resource is designed to help you master the key
concepts tested on the NR507 Week 4 Midterm Exam. The questions
cover immunology, hematology, cardiology, pulmonology,
endocrinology, neurology, genetics, and renal pathophysiology, and
reflect the most current (2025/2026) nursing curriculum.
SECTION 1 – IMMUNOLOGY & HYPERSENSITIVITY (Questions 1–20)
Q1. Which cells are considered the “first responders” of the innate
immune system?
A) Basophils
B) Eosinophils
C) Neutrophils
D) Lymphocytes
Answer: C – Neutrophils
Rationale: Neutrophils are the first leukocytes to arrive at a site of
infection or injury, phagocytosing pathogens and releasing
inflammatory mediators. They dominate the early inflammatory
response.
Q2. Urticaria (hives) is an example of which type of hypersensitivity
reaction?
A) Type I
B) Type II
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C) Type III
D) Type IV
Answer: A – Type I
Rationale: Type I hypersensitivity is IgE-mediated and involves mast-cell
degranulation with release of histamine, leading to urticaria,
angioedema, and anaphylaxis. Examples include allergic rhinitis,
asthma, and anaphylaxis.
Q3. Allergic contact dermatitis (e.g., poison ivy) is caused by which type
of hypersensitivity?
A) Type I
B) Type II
C) Type III
D) Type IV
Answer: D – Type IV
Rationale: Type IV (delayed-type) hypersensitivity is T-cell mediated,
not antibody-mediated. Symptoms appear 24–72 hours after exposure,
as seen in poison ivy, tuberculin skin tests, and graft rejection.
Q4. Anaphylaxis is a __________ hypersensitivity reaction.
A) Type I
B) Type II
C) Type III
D) Type IV
Answer: A – Type I
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Rationale: Anaphylaxis is a severe, systemic Type I reaction caused by
the massive release of histamine and other mediators from mast cells.
It requires immediate treatment with epinephrine.
Q5. Type II (cytotoxic) hypersensitivity reactions are mediated by:
A) IgA or IgE
B) IgM or IgA
C) IgG or IgM
D) IgE or IgG
Answer: C – IgG or IgM
Rationale: In Type II hypersensitivity, antibodies (IgG or IgM) bind to
antigens on cell surfaces, leading to complement activation, cell lysis, or
opsonization. Examples include autoimmune hemolytic anemia and
transfusion reactions.
Q6. Type III hypersensitivity reactions are characterised by:
A) IgE binding to mast cells
B) Formation and deposition of immune complexes
C) T-cell mediated cytotoxicity
D) Direct antibody binding to cell surfaces
Answer: B – Formation and deposition of immune complexes
Rationale: In Type III reactions, soluble antigen-antibody (IgG/IgM)
complexes are deposited in tissues (e.g., joints, kidneys, blood vessels),
activating complement and causing inflammation. Examples include
systemic lupus erythematosus (SLE) and serum sickness.
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Q7. Which immunoglobulin (Ig) is associated with Type I
hypersensitivity?
A) IgE
B) IgG
C) IgM
D) IgA
Answer: A – IgE
Rationale: IgE is the primary antibody involved in Type I reactions. It
binds to high-affinity receptors on mast cells and basophils, sensitising
them to an allergen.
Q8. Hemolytic disease of the newborn (HDN) can occur if the mother:
A) Is Rh-negative and the fetus is Rh-positive
B) Is Rh-positive and the fetus is Rh-negative
C) Has blood type O and the fetus has type AB
D) Has blood type A and the fetus has type B
Answer: A – Is Rh-negative and the fetus is Rh-positive
Rationale: HDN (erythroblastosis fetalis) occurs when an Rh-negative
mother produces anti-Rh antibodies after exposure to Rh-positive fetal
blood. In subsequent pregnancies, these IgG antibodies cross the
placenta and destroy fetal red blood cells.
Q9. Hypersensitivity is best defined as:
A) An overactive immune system that attacks self-antigens
B) An altered immunologic response to an antigen that results in
disease
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C) The normal immune response to a pathogen
D) A genetic defect in antibody production
Answer: B – An altered immunologic response to an antigen that
results in disease
Rationale: Hypersensitivity refers to excessive or inappropriate immune
responses that cause tissue damage. It encompasses the four classical
Gell and Coombs types.
Q10. The primary treatment for a severe anaphylactic reaction is:
A) Diphenhydramine
B) Epinephrine
C) Corticosteroids
D) Albuterol
Answer: B – Epinephrine
Rationale: Epinephrine is the first-line treatment for anaphylaxis. It
reverses hypotension, bronchospasm, and laryngeal oedema.
Antihistamines and corticosteroids are adjunctive.
Q11. Which cytokines initiate the production of corticotropin-releasing
hormone (CRH)?
A) TNF-α and IFN-γ
B) IL-1 and IL-6
C) IL-2 and IL-4
D) TGF-β and IL-10
Answer: B – IL-1 and IL-6
Rationale: Inflammatory cytokines (IL-1, IL-6, TNF-α) stimulate the
hypothalamus to release CRH, activating the
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hypothalamic-pituitary-adrenal (HPA) axis during stress or
inflammation.
Q12. Perceived stress elicits an emotional, anticipatory response that
begins in which part of the brain?
A) Thalamus
B) Limbic system
C) Brainstem
D) Cerebellum
Answer: B – Limbic system
Rationale: The limbic system (amygdala, hippocampus, hypothalamus)
processes emotional responses and triggers the HPA axis and
sympathetic nervous system during stress.
Q13. A positive tuberculin skin test is an example of:
A) Type I hypersensitivity
B) Type II hypersensitivity
C) Type III hypersensitivity
D) Type IV hypersensitivity
Answer: D – Type IV hypersensitivity
Rationale: The tuberculin skin test relies on a delayed T-cell response
(Type IV) to purified protein derivative (PPD). Induration that appears
48–72 hours after injection indicates prior sensitisation
to Mycobacterium tuberculosis.
Q14. Graves’ disease is an example of:
A) Type I hypersensitivity
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