NR 507 ADVANCED PATHO – MIDTERM EXAM PREP
NEWEST 2025/2026 ACTUAL EXAM COMPLETE
QUESTIONS AND CORRECT DETAILED ANSWERS
(VERIFIED ANSWERS) WITH DETAILED
RATIONALES/ALREADY GRADED A+ || BRAND NEW
VERSION!!
Q1. A 22-year-old develops wheezing, hypotension, and urticaria immediately
after eating peanuts. Which mechanism is responsible for this reaction?
a) IgG-mediated cytotoxicity
b) Immune complex deposition
c) IgE-mediated mast cell degranulation
d) T-cell mediated inflammation
Answer: c) IgE-mediated mast cell degranulation
Rationale: This is a Type I hypersensitivity reaction (anaphylaxis). IgE antibodies
bind to mast cells → degranulation → release of histamine, leukotrienes,
prostaglandins → bronchoconstriction, vasodilation, hypotension.
Q2. A patient develops hemolysis after receiving the wrong blood type transfusion.
What type of hypersensitivity is this?
a) Type I
b) Type II
c) Type III
d) Type IV
Answer: b) Type II
Rationale: Type II hypersensitivity is cytotoxic and tissue-specific. IgG/IgM
antibodies bind to RBCs → complement activation → cell lysis → hemolytic
transfusion reaction.
Q3. A patient with systemic lupus erythematosus presents with kidney damage due
to immune complex deposition. What type of hypersensitivity is this?
a) Type II
b) Type I
,c) Type IV
d) Type III
Answer: d) Type III
Rationale: Type III reactions involve antigen-antibody complexes circulating and
depositing in tissues (kidneys, joints), leading to inflammation and organ damage.
Q4. A nurse notes a rash localized only to the area where a patient touched poison
ivy 3 days ago. What type of reaction is this?
a) Type I
b) Type II
c) Type III
d) Type IV
Answer: d) Type IV
Rationale: Type IV hypersensitivity is delayed and T-cell mediated. Contact
dermatitis appears days after exposure and remains localized.
Q5. Which treatment is most appropriate for a life-threatening Type I
hypersensitivity reaction?
a) Antihistamines
b) Corticosteroids
c) Epinephrine
d) Antibiotics
Answer: c) Epinephrine
Rationale: Epinephrine reverses bronchoconstriction and hypotension in
anaphylaxis. Antihistamines are supportive but not first-line in emergencies.
Q6. A patient with Graves’ disease has antibodies stimulating thyroid receptors.
What type of hypersensitivity is this?
a) Type III
b) Type II
c) Type IV
d) Type I
Answer: b) Type II
Rationale: Type II can alter function (not just destroy tissue). In Graves,
antibodies stimulate TSH receptors → hyperthyroidism.
,Q7. A patient presents with a malar rash, photosensitivity, and positive ANA.
Which condition is most likely?
a) Rheumatoid arthritis
b) Multiple sclerosis
c) Systemic lupus erythematosus
d) Sjogren’s syndrome
Answer: c) Systemic lupus erythematosus
Rationale: Classic SLE findings include malar rash, photosensitivity, ANA
positivity, and multi-organ involvement due to immune complex deposition.
Q8. A patient with contact dermatitis asks why antihistamines are not effective.
What is the best explanation?
a) No mast cells are involved
b) It is antibody mediated
c) It involves complement activation
d) It is caused by infection
Answer: a) No mast cells are involved
Rationale: Type IV reactions are T-cell mediated, not histamine-driven →
antihistamines are ineffective.
Q9. A child is diagnosed with a genetic immune disorder affecting B cells. This is
classified as:
a) Secondary immunodeficiency
b) Primary immunodeficiency
c) Autoimmune disorder
d) Alloimmunity
Answer: b) Primary immunodeficiency
Rationale: Primary immunodeficiencies are genetic defects affecting immune
components like B or T cells.
Q10. A patient with HIV develops Pneumocystis jirovecii pneumonia. This is an
example of:
a) Primary immunodeficiency
b) Autoimmune disorder
c) Secondary immunodeficiency
d) Hypersensitivity
, Answer: c) Secondary immunodeficiency
*Rationale: HIV destroys CD4+ T cells → acquired (secondary)
immunodeficiency, leading to opportunistic infections.*
Q11. Which cytokine is primarily responsible for inducing fever during
inflammation?
a) Interleukin-2 (IL-2)
b) Interleukin-1 (IL-1)
c) Interleukin-4 (IL-4)
d) Interferon-gamma (IFN-γ)
Answer: b) Interleukin-1 (IL-1)
*Rationale: IL-1, IL-6, and TNF-α are pyrogenic cytokines that act on the
hypothalamus to raise body temperature.*
Q12. A patient with rheumatoid arthritis has chronic joint inflammation. Which
cell type is most responsible for joint destruction?
a) B lymphocytes
b) CD8+ T cells
c) Macrophages
d) Eosinophils
Answer: c) Macrophages
*Rationale: Activated macrophages produce TNF-α, IL-1, and matrix
metalloproteinases that erode cartilage and bone.*
Q13. A child born with recurrent bacterial infections and absent T cells is found to
have a thymic shadow absent on chest X-ray. The most likely diagnosis is:
a) Common variable immunodeficiency
b) DiGeorge syndrome
c) Severe combined immunodeficiency (SCID)
d) IgA deficiency
Answer: b) DiGeorge syndrome
*Rationale: DiGeorge syndrome (22q11.2 deletion) causes thymic hypoplasia →
T-cell deficiency. SCID also presents with severe infections but typically both B
and T defects.*
Q14. Which immunoglobulin is the first to be produced during a primary immune
response?
NEWEST 2025/2026 ACTUAL EXAM COMPLETE
QUESTIONS AND CORRECT DETAILED ANSWERS
(VERIFIED ANSWERS) WITH DETAILED
RATIONALES/ALREADY GRADED A+ || BRAND NEW
VERSION!!
Q1. A 22-year-old develops wheezing, hypotension, and urticaria immediately
after eating peanuts. Which mechanism is responsible for this reaction?
a) IgG-mediated cytotoxicity
b) Immune complex deposition
c) IgE-mediated mast cell degranulation
d) T-cell mediated inflammation
Answer: c) IgE-mediated mast cell degranulation
Rationale: This is a Type I hypersensitivity reaction (anaphylaxis). IgE antibodies
bind to mast cells → degranulation → release of histamine, leukotrienes,
prostaglandins → bronchoconstriction, vasodilation, hypotension.
Q2. A patient develops hemolysis after receiving the wrong blood type transfusion.
What type of hypersensitivity is this?
a) Type I
b) Type II
c) Type III
d) Type IV
Answer: b) Type II
Rationale: Type II hypersensitivity is cytotoxic and tissue-specific. IgG/IgM
antibodies bind to RBCs → complement activation → cell lysis → hemolytic
transfusion reaction.
Q3. A patient with systemic lupus erythematosus presents with kidney damage due
to immune complex deposition. What type of hypersensitivity is this?
a) Type II
b) Type I
,c) Type IV
d) Type III
Answer: d) Type III
Rationale: Type III reactions involve antigen-antibody complexes circulating and
depositing in tissues (kidneys, joints), leading to inflammation and organ damage.
Q4. A nurse notes a rash localized only to the area where a patient touched poison
ivy 3 days ago. What type of reaction is this?
a) Type I
b) Type II
c) Type III
d) Type IV
Answer: d) Type IV
Rationale: Type IV hypersensitivity is delayed and T-cell mediated. Contact
dermatitis appears days after exposure and remains localized.
Q5. Which treatment is most appropriate for a life-threatening Type I
hypersensitivity reaction?
a) Antihistamines
b) Corticosteroids
c) Epinephrine
d) Antibiotics
Answer: c) Epinephrine
Rationale: Epinephrine reverses bronchoconstriction and hypotension in
anaphylaxis. Antihistamines are supportive but not first-line in emergencies.
Q6. A patient with Graves’ disease has antibodies stimulating thyroid receptors.
What type of hypersensitivity is this?
a) Type III
b) Type II
c) Type IV
d) Type I
Answer: b) Type II
Rationale: Type II can alter function (not just destroy tissue). In Graves,
antibodies stimulate TSH receptors → hyperthyroidism.
,Q7. A patient presents with a malar rash, photosensitivity, and positive ANA.
Which condition is most likely?
a) Rheumatoid arthritis
b) Multiple sclerosis
c) Systemic lupus erythematosus
d) Sjogren’s syndrome
Answer: c) Systemic lupus erythematosus
Rationale: Classic SLE findings include malar rash, photosensitivity, ANA
positivity, and multi-organ involvement due to immune complex deposition.
Q8. A patient with contact dermatitis asks why antihistamines are not effective.
What is the best explanation?
a) No mast cells are involved
b) It is antibody mediated
c) It involves complement activation
d) It is caused by infection
Answer: a) No mast cells are involved
Rationale: Type IV reactions are T-cell mediated, not histamine-driven →
antihistamines are ineffective.
Q9. A child is diagnosed with a genetic immune disorder affecting B cells. This is
classified as:
a) Secondary immunodeficiency
b) Primary immunodeficiency
c) Autoimmune disorder
d) Alloimmunity
Answer: b) Primary immunodeficiency
Rationale: Primary immunodeficiencies are genetic defects affecting immune
components like B or T cells.
Q10. A patient with HIV develops Pneumocystis jirovecii pneumonia. This is an
example of:
a) Primary immunodeficiency
b) Autoimmune disorder
c) Secondary immunodeficiency
d) Hypersensitivity
, Answer: c) Secondary immunodeficiency
*Rationale: HIV destroys CD4+ T cells → acquired (secondary)
immunodeficiency, leading to opportunistic infections.*
Q11. Which cytokine is primarily responsible for inducing fever during
inflammation?
a) Interleukin-2 (IL-2)
b) Interleukin-1 (IL-1)
c) Interleukin-4 (IL-4)
d) Interferon-gamma (IFN-γ)
Answer: b) Interleukin-1 (IL-1)
*Rationale: IL-1, IL-6, and TNF-α are pyrogenic cytokines that act on the
hypothalamus to raise body temperature.*
Q12. A patient with rheumatoid arthritis has chronic joint inflammation. Which
cell type is most responsible for joint destruction?
a) B lymphocytes
b) CD8+ T cells
c) Macrophages
d) Eosinophils
Answer: c) Macrophages
*Rationale: Activated macrophages produce TNF-α, IL-1, and matrix
metalloproteinases that erode cartilage and bone.*
Q13. A child born with recurrent bacterial infections and absent T cells is found to
have a thymic shadow absent on chest X-ray. The most likely diagnosis is:
a) Common variable immunodeficiency
b) DiGeorge syndrome
c) Severe combined immunodeficiency (SCID)
d) IgA deficiency
Answer: b) DiGeorge syndrome
*Rationale: DiGeorge syndrome (22q11.2 deletion) causes thymic hypoplasia →
T-cell deficiency. SCID also presents with severe infections but typically both B
and T defects.*
Q14. Which immunoglobulin is the first to be produced during a primary immune
response?
