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NSG 5003 Advanced Pathophysiology Week 2 Knowledge Checks | South University Savannah | 2026/2027 Edition (PDF)

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NSG 5003 Advanced Pathophysiology Week 2 Knowledge Checks | South University Savannah | 2026/2027 Edition (PDF) resource featuring complete quiz bank Q&A, NGN‑style case studies, SATA formats, and 100% correct answers. Comprehensive coverage includes cellular adaptation, oxidative stress, immune mechanisms, inflammatory pathways, genetic mutations, endocrine regulation, cardiovascular and respiratory pathophysiology, renal disorders, and neurological dysfunctions. Designed for guaranteed Grade A performance and full alignment with South University MSN curriculum, this study guide is perfect for students searching NSG 5003 Quiz Bank PDF, Advanced Pathophysiology Study Guide, NSG 5003 Test Bank, NSG 5003 Verified Answers, NSG 5003 Exam Prep 2026/2027, ATI Style Nursing Practice, NSG 5003 Nursing Quiz PDF, NSG 5003 Study Guide Review, and NSG 5003 Comprehensive Solution.

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,NSG5003/NSG 5003 Advanced Pathophysiology Week 2
Knowledge Checks | South University Savannah | 26/27
1. A 42-year-old woman presents with a rash that appeared 48 hours after starting a new medication.
Biopsy reveals T-lymphocyte infiltration with no antibody deposition. Which type of hypersensitivity
reaction does this represent?

A) Type I

B) Type II

C) Type III

D) Type IV



Correct Answer: Type IV



Rationale: Type IV hypersensitivity is cell-mediated and involves T-lymphocytes with a delayed onset
of 24 to 72 hours, typically presenting as contact dermatitis or drug reactions. Type I is IgE-mediated
and immediate, Type II involves IgG or IgM antibodies against tissue antigens, and Type III is caused by
antigen-antibody immune complex deposition. The delayed onset and T-cell infiltration confirm Type
IV.



2. A patient with systemic lupus erythematosus develops renal failure. Which mechanism best
explains the tissue damage in this autoimmune condition?

A) IgE-mediated mast cell degranulation

B) Cytotoxic T-cell direct killing

C) Immune complex deposition activating complement

D) Delayed-type hypersensitivity



Correct Answer: Immune complex deposition activating complement



Rationale: Systemic lupus erythematosus involves Type III hypersensitivity, where circulating antigen-
antibody complexes deposit in tissues such as the glomerulus, activating complement and recruiting
neutrophils that cause tissue damage. IgE-mediated reactions cause allergy, cytotoxic T-cells kill
directly in graft rejection, and delayed hypersensitivity involves T-cell mediated responses.
Recognizing immune complex disease is essential for understanding autoimmune pathophysiology.

,3. Which immunoglobulin is primarily responsible for mediating Type I hypersensitivity reactions?

A) IgA

B) IgG

C) IgM

D) IgE



Correct Answer: IgE



Rationale: IgE binds to mast cells and basophils via its Fc receptor, and cross-linking by antigen triggers
degranulation and release of histamine and other mediators. IgA protects mucosal surfaces, IgG is
involved in Type II and III reactions, and IgM is the first antibody produced in primary immune
responses. Identifying IgE as the mediator of immediate hypersensitivity is fundamental.



4. A 28-year-old man develops hives and wheezing within minutes of eating peanuts. Which mediator
is primarily responsible for the bronchoconstriction observed in this reaction?

A) Histamine

B) Bradykinin

C) Leukotrienes

D) Prostaglandins



Correct Answer: Leukotrienes



Rationale: Leukotrienes are potent bronchoconstrictors released during Type I hypersensitivity and
are primarily responsible for the respiratory symptoms of anaphylaxis. Histamine causes vasodilation
and increased vascular permeability, bradykinin mediates pain and vasodilation, and prostaglandins
contribute to inflammation and fever. Recognizing the specific actions of each mediator guides
targeted treatment.



5. Which component of the immune system provides the first line of defense against pathogens and is
present at birth?

A) Adaptive immunity

, B) Innate immunity

C) Humoral immunity

D) Cell-mediated immunity



Correct Answer: Innate immunity



Rationale: Innate immunity is present at birth and provides immediate, non-specific defense through
physical barriers, phagocytic cells, and inflammatory responses. Adaptive, humoral, and cell-mediated
immunity develop after exposure to specific antigens and provide long-term, targeted protection.
Understanding the distinction between innate and adaptive immunity is foundational.



6. How do surfactant proteins A through D provide innate resistance?

A) They promote phagocytosis by acting as opsonins

B) They directly kill bacteria through membrane disruption

C) They trigger complement activation

D) They neutralize viral particles



Correct Answer: They promote phagocytosis by acting as opsonins



Rationale: Surfactant proteins A through D collect pathogens and enhance their uptake by alveolar
macrophages through opsonization. They do not directly kill bacteria, activate complement, or
neutralize viruses. Recognizing the role of surfactant proteins in pulmonary innate immunity is
essential for understanding respiratory defense mechanisms.



7. Which secretion provides a first line of defense against pathogen invasion through antibacterial and
antifungal fatty acids?

A) Saliva

B) Sebaceous gland sebum

C) Tears

D) Gastric acid

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