This NSG 5003 Week 2 2026/2027 Exam Questions and Answers document provides an extensive 42-page advanced pathophysiology review centered on hypersensitivity reactions, innate and adaptive immunity, inflammation, immunodeficiency, autoimmune disease, transplantation, infectious disease, HIV/AIDS, wound healing, and the physiological stress response. The material is presented primarily through exam-style questions and answers, including single-answer and select-all-that-apply items, giving graduate nursing students substantial practice with immune and inflammatory mechanisms and their clinical implications.
A major section examines Types I–IV hypersensitivity reactions and altered immune responses. The questions address IgE-mediated Type I hypersensitivity, anaphylaxis, urticaria, atopy, Type II antibody-mediated reactions, Type III immune-complex disease, and Type IV cell-mediated hypersensitivity. Clinical examples include Graves disease, systemic lupus erythematosus, Raynaud phenomenon, tuberculin skin testing, poison ivy and nickel exposure. The material also reviews ABO incompatibility, Rh antibodies, alloimmunity, complement-mediated cell lysis, and immune responses associated with organ transplantation and acute rejection.
The document provides detailed coverage of innate immunity and acute inflammation, including first-line defenses, sebaceous secretions, surfactant proteins, complement, coagulation, fibrinolysis, histamine, platelet-activating factor, nitric oxide, prostaglandins, bradykinin, chemotaxis and increased capillary permeability. Students review the mechanisms responsible for redness, heat, edema and pain, as well as leukocyte activity involving neutrophils, monocytes, macrophages, eosinophils and natural killer cells. The sequence of phagocytosis—recognition/opsonization, engulfment, fusion and destruction—is also repeatedly tested.
Another substantial component focuses on tissue repair and wound healing. Questions address fibroblast activity, collagen synthesis, epithelialization, scar formation, resolution, keloid formation and appropriate wound cleansing. Age-related and neonatal differences in inflammatory responses are also considered, including impaired healing associated with chronic illness in older adults and deficiencies in complement and chemotaxis among neonates.
The adaptive-immunity section reviews B and T lymphocytes, macrophages, plasma cells, antigen recognition, epitopes, clonal diversity, clonal selection, MHC molecules, CD4 and CD8 cells, Th1 and Th2 responses, regulatory T cells, cytokines, and humoral versus cell-mediated immunity. Immunoglobulins receive particular attention, including IgA, IgE, IgG and IgM, primary and secondary antibody responses, active-acquired and passive-acquired immunity, maternal antibodies, vaccination, and immune changes associated with aging.
The infectious-disease material examines the progression from colonization to invasion, multiplication and spread, together with infectivity, virulence, pathogenicity and toxigenicity. Students review bacterial exotoxins and endotoxins, viral infection, fungal disease, rickettsial infection and organisms capable of surviving within macrophages. Specific examples appearing in the questions include Clostridium difficile, Mycobacterium tuberculosis, Mycobacterium leprae, Salmonella typhi, Treponema pallidum, Candida, Aspergillus and Rocky Mountain spotted fever.
A dedicated section addresses HIV/AIDS pathophysiology, including HIV as a retrovirus, reverse transcriptase, CD4+ T-helper cells, macrophages, natural killer cells, antibody development, seronegativity, the central nervous system as a reservoir, progressive immune dysfunction and routes of transmission identified in the document. AIDS-related complications reviewed include Kaposi sarcoma, cytomegalovirus retinitis and herpes simplex infection.
The final portion explores stress physiology and psychoneuroimmunology, particularly the General Adaptation Syndrome (GAS), hypothalamus, limbic system, adrenal response, cortisol, epinephrine, norepinephrine, CRH, cytokines and stress-associated immune suppression. The questions examine hyperglycemia, gluconeogenesis, peripheral vasoconstriction, altered T-cell and NK-cell activity, chronic stress, coping, sex-hormone effects on immunity, anxiety and the relationship between prolonged stress and immune function.
Relevant Students: NSG 5003 students, MSN students, graduate nursing students, Family Nurse Practitioner students, Adult-Gerontology Nurse Practitioner students, DNP students, advanced practice nursing students, RN-to-MSN students, and students preparing for advanced pathophysiology examinations covering immunology, inflammation, hypersensitivity, infection, HIV/AIDS, wound healing, and physiological stress responses.
Keywords: NSG 5003 Week 2, NSG 5003 Week 2 2026, NSG 5003 Week 2 2027, NSG 5003 questions and answers, NSG 5003 exam questions, NSG 5003 study guide, advanced pathophysiology Week 2, hypersensitivity questions and answers, Type I hypersensitivity, Type II hypersensitivity, Type III hypersensitivity, Type IV hypersensitivity, IgE hypersensitivity, anaphylaxis pathophysiology, autoimmune disease questions, Graves disease immunology, systemic lupus erythematosus, innate immunity, adaptive immunity, inflammation pathophysiology, inflammatory mediators, complement cascade, histamine inflammation, phagocytosis steps, neutrophils macrophages eosinophils, natural killer cells, wound healing pathophysiology, B lymphocytes, T lymphocytes, immunoglobulins IgA IgE IgG IgM, MHC class I and II, CD4 CD8 cells, clonal selection, active acquired immunity, passive acquired immunity, infectious disease pathophysiology, infectivity virulence pathogenicity, bacterial exotoxins endotoxins, HIV pathophysiology, AIDS questions and answers, reverse transcriptase HIV, General Adaptation Syndrome, stress response pathophysiology, cortisol stress response, epinephrine norepinephrine, psychoneuroimmunology, graduate nursing exam prep
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NSG5003 Week 2 2026/2027
Exam Questions and Answers |
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Hypersensitivity is best defined as a(an) - ANSWER ✔✔c.
Altered immunologic response to an antigen that results in disease
A hypersensitivity reaction that produces an allergic response is called: -
ANSWER ✔✔Anaphylaxis
The common hay fever allergy is expressed through a reaction that is
mediated by which class of immunoglobulins? - ANSWER ✔✔IgE
Which type of antibody is involved in type I hypersensitivity reaction? -
ANSWER ✔✔IgE
,Blood transfusion reactions are an example of: - ANSWER
✔✔Alloimmunity
During an IgE-mediated hypersensitivity reaction, which leukocyte is
activated? - ANSWER ✔✔c.
Eosinophils
During an IgE-mediated hypersensitivity reaction, the degranulation of
mast cells is a result of which receptor action? - ANSWER
✔✔Histamine bound to H2
What characteristic do atopic individuals have that make them
genetically predisposed to develop allergies? - ANSWER ✔✔c.
Greater quantities of IgE
What is the mechanism that results in type II hypersensitivity reactions? -
ANSWER ✔✔d.
Antibodies bind to the antigens on the cell surface.
When mismatched blood is administered causing an ABO incompatibility,
the erythrocytes are destroyed by - ANSWER ✔✔a.
Complement-mediated cell lysis
,When antibodies are formed against red blood cell antigens of the Rh
system, the blood cells are destroyed by: - ANSWER
✔✔Phagocytosis in the spleen
When soluble antigens from infectious agents enter circulation, tissue
damage is a result of: - ANSWER ✔✔d.
Neutrophil granules and toxic oxygen products
How are target cells destroyed in a type II hypersensitivity reaction? -
ANSWER ✔✔d.
Natural killer cells
Graves disease (hyperthyroidism) is an example of which type II
hypersensitivity reaction? - ANSWER ✔✔Modulation
Type III hypersensitivity reactions are a result of which of the following? -
ANSWER ✔✔b.
Antibodies binding to soluble antigens that were released into body
fluids and the immune complexes being deposited in the tissues
A type IV hypersensitivity reaction causes which result? - ANSWER
✔✔.
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, Lymphokine-producing Th1 cells directly attacking and destroying
cellular targets
In a type III hypersensitivity reaction, the harmful effects after the
immune complexes that are deposited in tissues are a result of: -
ANSWER ✔✔Complement activation
Raynaud phenomenon is classified as a type III hypersensitivity reaction
and is due to: - ANSWER ✔✔a.
Immune complexes that are deposited in capillary beds, blocking
circulation
Deficiencies in which element can produce depression of both B- and T-
cell function? - ANSWER ✔✔Zinc
When the maternal immune system becomes sensitized against
antigens expressed by the fetus, what reaction occurs? - ANSWER
✔✔Alloimmunity
Tissue damage caused by the deposition of circulating immune
complexes containing an antibody against the host DNA is the cause of
which disease? - ANSWER ✔✔Systemic lupus erythematosus
Why does tissue damage occurs in acute rejection after organ
transplantation? - ANSWER ✔✔a.