NR 603 CEA – Allergy Overview and
Management Strategies, Questions with Answers
and Rationales
SECTION I: FOUNDATIONS AND PATHOPHYSIOLOGY (Questions 1–
20)
1. A patient presents with symptoms of sneezing, rhinorrhea, and nasal
congestion after exposure to dust mites. Which type of hypersensitivity
reaction is primarily responsible for these symptoms?
A. Type I (anaphylactic) hypersensitivity
B. Type II (cytotoxic) hypersensitivity
C. Type III (immune complex) hypersensitivity
D. Type IV (delayed-type) hypersensitivity
Rationale: Allergic rhinitis is mediated by Type I hypersensitivity, which involves
IgE-mediated mast cell degranulation and release of histamine and other
inflammatory mediators. Type II involves antibody-mediated cell destruction,
Type III involves immune complex deposition, and Type IV is T-cell mediated.
2. Which immunoglobulin is primarily responsible for mediating immediate
hypersensitivity reactions in allergy?
A. IgG
B. IgE
C. IgM
D. IgA
Rationale: IgE is the immunoglobulin responsible for Type I hypersensitivity
reactions. It binds to high-affinity receptors on mast cells and basophils, leading to
degranulation and release of inflammatory mediators upon allergen exposure.
3. A patient experiences wheezing, urticaria, and hypotension within minutes
of receiving intravenous contrast media. This reaction is best classified as:
,A. Type II hypersensitivity
B. Type I hypersensitivity
C. Type III hypersensitivity
D. Type IV hypersensitivity
Rationale: The rapid onset of symptoms following exposure to a trigger
characterizes Type I (immediate) hypersensitivity, which is IgE-mediated. The
clinical presentation of wheezing, urticaria, and hypotension is consistent with
anaphylaxis.
4. Mast cell degranulation releases which of the following preformed
mediators?
A. Leukotrienes
B. Histamine
C. Prostaglandins
D. Cytokines
Rationale: Histamine is a preformed mediator stored in mast cell granules and
released immediately upon degranulation. Leukotrienes and prostaglandins are
newly synthesized mediators, while cytokines are released later in the
inflammatory response.
5. A patient with a history of allergic rhinitis is prescribed a medication that
blocks the H1 receptor. This medication is classified as:
A. Leukotriene receptor antagonist
B. Antihistamine
C. Corticosteroid
D. Mast cell stabilizer
Rationale: Antihistamines work by blocking H1 receptors, thereby inhibiting the
effects of histamine released during allergic reactions. This reduces symptoms such
as sneezing, itching, and rhinorrhea.
6. Which of the following best describes the pathophysiology of allergic
rhinitis?
,A. T-cell mediated destruction of nasal epithelium
B. IgE-mediated mast cell degranulation in response to airborne allergens
C. Autoimmune attack on nasal mucosa
D. Direct irritation of nasal passages by pollutants
Rationale: Allergic rhinitis is an IgE-mediated inflammatory condition of the
nasal mucosa triggered by airborne allergens such as pollen, dust mites, or animal
dander. Mast cell degranulation releases histamine and other mediators that cause
sneezing, rhinorrhea, and nasal congestion.
7. A patient with allergic rhinitis has symptoms that occur year-round. This is
classified as:
A. Seasonal allergic rhinitis
B. Perennial allergic rhinitis
C. Episodic allergic rhinitis
D. Occupational allergic rhinitis
Rationale: Perennial allergic rhinitis occurs year-round and is typically triggered
by indoor allergens such as dust mites, mold, or pet dander. Seasonal allergic
rhinitis occurs during specific pollen seasons.
8. Which cell type is the primary effector cell in the late-phase response of
allergic reactions?
A. Mast cells
B. Basophils
C. Eosinophils
D. Neutrophils
Rationale: Eosinophils are the primary effector cells in the late-phase allergic
response, recruited by chemokines and cytokines released during the early-phase
response. They contribute to chronic inflammation and tissue damage.
9. A patient with allergic asthma experiences bronchoconstriction after
exposure to cat dander. This reaction is mediated by:
, A. Direct stimulation of smooth muscle
B. Complement activation
C. IgE-mediated mast cell degranulation
D. Neutrophil infiltration
Rationale: Allergic asthma is an IgE-mediated Type I hypersensitivity reaction.
Mast cell degranulation releases mediators such as histamine and leukotrienes that
cause bronchoconstriction, mucus production, and airway inflammation.
10. Which of the following is a newly synthesized mediator released during
mast cell activation?
A. Histamine
B. Tryptase
C. Leukotriene C4
D. Heparin
Rationale: Leukotriene C4 is a newly synthesized mediator produced from
arachidonic acid via the lipoxygenase pathway. Histamine, tryptase, and heparin
are preformed mediators stored in mast cell granules.
11. A patient with a known latex allergy develops urticaria and dyspnea after
a dental procedure. This is an example of:
A. Type II hypersensitivity
B. Type I hypersensitivity
C. Type III hypersensitivity
D. Type IV hypersensitivity
Rationale: Latex allergy presenting with urticaria and dyspnea is an IgE-mediated
Type I hypersensitivity reaction. The rapid onset of symptoms following latex
exposure is characteristic of an immediate hypersensitivity response.
12. The process by which mast cells release mediators upon re-exposure to an
allergen is called:
Management Strategies, Questions with Answers
and Rationales
SECTION I: FOUNDATIONS AND PATHOPHYSIOLOGY (Questions 1–
20)
1. A patient presents with symptoms of sneezing, rhinorrhea, and nasal
congestion after exposure to dust mites. Which type of hypersensitivity
reaction is primarily responsible for these symptoms?
A. Type I (anaphylactic) hypersensitivity
B. Type II (cytotoxic) hypersensitivity
C. Type III (immune complex) hypersensitivity
D. Type IV (delayed-type) hypersensitivity
Rationale: Allergic rhinitis is mediated by Type I hypersensitivity, which involves
IgE-mediated mast cell degranulation and release of histamine and other
inflammatory mediators. Type II involves antibody-mediated cell destruction,
Type III involves immune complex deposition, and Type IV is T-cell mediated.
2. Which immunoglobulin is primarily responsible for mediating immediate
hypersensitivity reactions in allergy?
A. IgG
B. IgE
C. IgM
D. IgA
Rationale: IgE is the immunoglobulin responsible for Type I hypersensitivity
reactions. It binds to high-affinity receptors on mast cells and basophils, leading to
degranulation and release of inflammatory mediators upon allergen exposure.
3. A patient experiences wheezing, urticaria, and hypotension within minutes
of receiving intravenous contrast media. This reaction is best classified as:
,A. Type II hypersensitivity
B. Type I hypersensitivity
C. Type III hypersensitivity
D. Type IV hypersensitivity
Rationale: The rapid onset of symptoms following exposure to a trigger
characterizes Type I (immediate) hypersensitivity, which is IgE-mediated. The
clinical presentation of wheezing, urticaria, and hypotension is consistent with
anaphylaxis.
4. Mast cell degranulation releases which of the following preformed
mediators?
A. Leukotrienes
B. Histamine
C. Prostaglandins
D. Cytokines
Rationale: Histamine is a preformed mediator stored in mast cell granules and
released immediately upon degranulation. Leukotrienes and prostaglandins are
newly synthesized mediators, while cytokines are released later in the
inflammatory response.
5. A patient with a history of allergic rhinitis is prescribed a medication that
blocks the H1 receptor. This medication is classified as:
A. Leukotriene receptor antagonist
B. Antihistamine
C. Corticosteroid
D. Mast cell stabilizer
Rationale: Antihistamines work by blocking H1 receptors, thereby inhibiting the
effects of histamine released during allergic reactions. This reduces symptoms such
as sneezing, itching, and rhinorrhea.
6. Which of the following best describes the pathophysiology of allergic
rhinitis?
,A. T-cell mediated destruction of nasal epithelium
B. IgE-mediated mast cell degranulation in response to airborne allergens
C. Autoimmune attack on nasal mucosa
D. Direct irritation of nasal passages by pollutants
Rationale: Allergic rhinitis is an IgE-mediated inflammatory condition of the
nasal mucosa triggered by airborne allergens such as pollen, dust mites, or animal
dander. Mast cell degranulation releases histamine and other mediators that cause
sneezing, rhinorrhea, and nasal congestion.
7. A patient with allergic rhinitis has symptoms that occur year-round. This is
classified as:
A. Seasonal allergic rhinitis
B. Perennial allergic rhinitis
C. Episodic allergic rhinitis
D. Occupational allergic rhinitis
Rationale: Perennial allergic rhinitis occurs year-round and is typically triggered
by indoor allergens such as dust mites, mold, or pet dander. Seasonal allergic
rhinitis occurs during specific pollen seasons.
8. Which cell type is the primary effector cell in the late-phase response of
allergic reactions?
A. Mast cells
B. Basophils
C. Eosinophils
D. Neutrophils
Rationale: Eosinophils are the primary effector cells in the late-phase allergic
response, recruited by chemokines and cytokines released during the early-phase
response. They contribute to chronic inflammation and tissue damage.
9. A patient with allergic asthma experiences bronchoconstriction after
exposure to cat dander. This reaction is mediated by:
, A. Direct stimulation of smooth muscle
B. Complement activation
C. IgE-mediated mast cell degranulation
D. Neutrophil infiltration
Rationale: Allergic asthma is an IgE-mediated Type I hypersensitivity reaction.
Mast cell degranulation releases mediators such as histamine and leukotrienes that
cause bronchoconstriction, mucus production, and airway inflammation.
10. Which of the following is a newly synthesized mediator released during
mast cell activation?
A. Histamine
B. Tryptase
C. Leukotriene C4
D. Heparin
Rationale: Leukotriene C4 is a newly synthesized mediator produced from
arachidonic acid via the lipoxygenase pathway. Histamine, tryptase, and heparin
are preformed mediators stored in mast cell granules.
11. A patient with a known latex allergy develops urticaria and dyspnea after
a dental procedure. This is an example of:
A. Type II hypersensitivity
B. Type I hypersensitivity
C. Type III hypersensitivity
D. Type IV hypersensitivity
Rationale: Latex allergy presenting with urticaria and dyspnea is an IgE-mediated
Type I hypersensitivity reaction. The rapid onset of symptoms following latex
exposure is characteristic of an immediate hypersensitivity response.
12. The process by which mast cells release mediators upon re-exposure to an
allergen is called:
