NUR 634 Final Exam Actual Exam QUESTIONS
AND ANSWERS 2026 | Advanced
Pathophysiology | Complete Q&A Graded A+ |
Pass Guaranteed - A+ Graded
Question 1
A 58-year-old male smoker presents with a persistent cough. A lung biopsy reveals replacement
of normal ciliated columnar epithelium with stratified squamous epithelium. This cellular
adaptation is best described as:
A. Dysplasia
B. Metaplasia [CORRECT]
C. Hyperplasia
D. Anaplasia
Correct Answer: B
Rationale: Metaplasia is a reversible change in which one mature, differentiated cell type is
replaced by another mature cell type, typically in response to chronic irritation or stress. In this
case, chronic smoking irritation causes bronchial epithelium to undergo squamous metaplasia,
replacing delicate columnar cells with tougher squamous cells better able to withstand irritation.
This is a protective adaptation but increases cancer risk.
Option A (Dysplasia): Incorrect—dysplasia involves disordered, defective development with
abnormal cellular features (enlarged nuclei, hyperchromasia, loss of polarity), representing a pre-
neoplastic change rather than a reversible adaptation.
Option C (Hyperplasia): Incorrect—hyperplasia is an increase in cell number, not a change in
cell type. The biopsy shows a different cell type, not simply more cells.
Option D (Anaplasia): Incorrect—anaplasia represents loss of cellular differentiation with
bizarre, pleomorphic cells characteristic of malignancy, not a reversible adaptation to irritation.
Question 2
A patient with prolonged hypotension develops acute tubular necrosis. The primary mechanism
of cellular injury is:
,A. Chemical injury
B. Hypoxic injury [CORRECT]
C. Infectious injury
D. Immunologic injury
Correct Answer: B
Rationale: Prolonged hypotension leads to decreased renal perfusion, causing ischemic/hypoxic
injury to the renal tubules. Without adequate oxygen, cells switch to anaerobic glycolysis, ATP
production fails (decreased from 36 ATP to 2 ATP per glucose), the Na⁺/K⁺-ATPase pump fails,
leading to cellular swelling, calcium influx, and ultimately cell death. The proximal tubule (S3
segment) and thick ascending limb are most vulnerable due to high metabolic demand.
Option A (Chemical injury): Incorrect—while toxins can cause ATN, the clinical scenario
describes ischemic ATN from hypotension, not nephrotoxic injury.
Option C (Infectious injury): Incorrect—sepsis can cause ATN through inflammatory
mechanisms, but the primary mechanism described here is hypoperfusion, not direct infection.
Option D (Immunologic injury): Incorrect—immunologic injury would present as
glomerulonephritis or interstitial nephritis, not ATN from hypotension.
Question 3
Which type of necrosis is characterized by preservation of tissue architecture for several days
after cell death due to denaturation of structural proteins and enzymes?
A. Liquefactive necrosis
B. Coagulative necrosis [CORRECT]
C. Caseous necrosis
D. Fat necrosis
Correct Answer: B
Rationale: Coagulative necrosis, typically from ischemia in solid organs (heart, kidney, spleen),
preserves tissue architecture because the denaturation of structural proteins prevents enzymatic
digestion. The "ghost" outlines of cells remain visible microscopically. This results from protein
denaturation occurring faster than enzymatic digestion.
Option A (Liquefactive necrosis): Incorrect—occurs in brain (ischemic or bacterial abscess)
where enzymatic digestion predominates, resulting in liquid transformation without architecture
preservation.
,Option C (Caseous necrosis): Incorrect—characteristic of tuberculosis, appears as amorphous,
granular, "cheese-like" debris without preserved architecture, representing a combination of
coagulative and liquefactive necrosis.
Option D (Fat necrosis): Incorrect—occurs in adipose tissue (pancreatitis, trauma) where lipases
break down fat into fatty acids that combine with calcium (saponification), forming white chalky
deposits without architecture preservation.
Question 4
A 45-year-old woman with rheumatoid arthritis has autoantibodies directed against which
specific self-antigen?
A. Acetylcholine receptors at the neuromuscular junction
B. The Fc portion of IgG (rheumatoid factor) and citrullinated peptides [CORRECT]
C. Thyroid peroxidase and thyroglobulin
D. Pancreatic beta-cell antigens (GAD65, IA-2)
Correct Answer: B
Rationale: Rheumatoid arthritis is characterized by autoantibodies against: (1) the Fc portion of
IgG (rheumatoid factor, RF), and (2) citrullinated proteins/peptides (anti-CCP antibodies),
formed by post-translational modification of arginine to citrulline by peptidylarginine deiminase
(PAD) in the presence of inflammation and smoking. These antibodies form immune complexes
that deposit in joints, activating complement and causing synovitis.
Option A (Acetylcholine receptors): Incorrect—targeted in myasthenia gravis, causing
postsynaptic neuromuscular transmission failure.
Option C (Thyroid peroxidase/thyroglobulin): Incorrect—targeted in Hashimoto's thyroiditis,
causing hypothyroidism through lymphocytic infiltration and destruction.
Option D (Pancreatic beta-cell antigens): Incorrect—targeted in type 1 diabetes mellitus, causing
autoimmune destruction of insulin-producing cells.
Question 5
A patient experiences anaphylaxis within minutes of receiving penicillin. Which hypersensitivity
reaction type and immunological mechanism are responsible?
A. Type I (IgE-mediated immediate hypersensitivity) [CORRECT]
B. Type II (Antibody-mediated cytotoxic hypersensitivity)
C. Type III (Immune complex-mediated hypersensitivity)
, D. Type IV (T-cell-mediated delayed-type hypersensitivity)
Correct Answer: A
Rationale: Anaphylaxis is a Type I hypersensitivity reaction. Penicillin (hapten) binds to carrier
proteins, triggering IgE production by plasma cells sensitized to Th2 cytokines (IL-4, IL-13).
Upon re-exposure, IgE cross-links on mast cells and basophils, triggering degranulation and
release of histamine, leukotrienes (C4, D4, E4), prostaglandins, and platelet-activating factor
(PAF), causing vasodilation, increased vascular permeability, bronchoconstriction, and
cardiovascular collapse.
Option B (Type II): Incorrect—involves IgG/IgM against cell-surface or matrix antigens causing
cytotoxicity (e.g., hemolytic anemia, Goodpasture's syndrome).
Option C (Type III): Incorrect—involves immune complex deposition causing complement
activation and inflammation (e.g., serum sickness, SLE, post-streptococcal glomerulonephritis).
Option D (Type IV): Incorrect—T-cell mediated, delayed 24-72 hours (e.g., contact dermatitis,
TB skin test, granuloma formation).
Question 6
Granulomatous inflammation with caseous necrosis is the characteristic pathological finding in
which condition?
A. Acute bacterial appendicitis
B. Mycobacterium tuberculosis infection [CORRECT]
C. Viral hepatitis
D. Acute pyogenic pneumonia
Correct Answer: B
Rationale: Tuberculosis produces well-formed granulomas with central caseous necrosis
(amorphous, eosinophilic, "cheese-like" debris), surrounded by epithelioid macrophages
(activated macrophages with abundant eosinophilic cytoplasm), Langhans giant cells
(multinucleated with horseshoe arrangement), and a peripheral rim of lymphocytes. This Th1-
mediated response attempts to contain the intracellular mycobacteria.
Option A (Acute appendicitis): Incorrect—characterized by acute suppurative inflammation with
neutrophilic infiltrate, not granulomas.
Option C (Viral hepatitis): Incorrect—characterized by hepatocyte necrosis (apoptotic bodies,
Councilman bodies) and lymphocytic infiltrate, not granulomatous inflammation.
AND ANSWERS 2026 | Advanced
Pathophysiology | Complete Q&A Graded A+ |
Pass Guaranteed - A+ Graded
Question 1
A 58-year-old male smoker presents with a persistent cough. A lung biopsy reveals replacement
of normal ciliated columnar epithelium with stratified squamous epithelium. This cellular
adaptation is best described as:
A. Dysplasia
B. Metaplasia [CORRECT]
C. Hyperplasia
D. Anaplasia
Correct Answer: B
Rationale: Metaplasia is a reversible change in which one mature, differentiated cell type is
replaced by another mature cell type, typically in response to chronic irritation or stress. In this
case, chronic smoking irritation causes bronchial epithelium to undergo squamous metaplasia,
replacing delicate columnar cells with tougher squamous cells better able to withstand irritation.
This is a protective adaptation but increases cancer risk.
Option A (Dysplasia): Incorrect—dysplasia involves disordered, defective development with
abnormal cellular features (enlarged nuclei, hyperchromasia, loss of polarity), representing a pre-
neoplastic change rather than a reversible adaptation.
Option C (Hyperplasia): Incorrect—hyperplasia is an increase in cell number, not a change in
cell type. The biopsy shows a different cell type, not simply more cells.
Option D (Anaplasia): Incorrect—anaplasia represents loss of cellular differentiation with
bizarre, pleomorphic cells characteristic of malignancy, not a reversible adaptation to irritation.
Question 2
A patient with prolonged hypotension develops acute tubular necrosis. The primary mechanism
of cellular injury is:
,A. Chemical injury
B. Hypoxic injury [CORRECT]
C. Infectious injury
D. Immunologic injury
Correct Answer: B
Rationale: Prolonged hypotension leads to decreased renal perfusion, causing ischemic/hypoxic
injury to the renal tubules. Without adequate oxygen, cells switch to anaerobic glycolysis, ATP
production fails (decreased from 36 ATP to 2 ATP per glucose), the Na⁺/K⁺-ATPase pump fails,
leading to cellular swelling, calcium influx, and ultimately cell death. The proximal tubule (S3
segment) and thick ascending limb are most vulnerable due to high metabolic demand.
Option A (Chemical injury): Incorrect—while toxins can cause ATN, the clinical scenario
describes ischemic ATN from hypotension, not nephrotoxic injury.
Option C (Infectious injury): Incorrect—sepsis can cause ATN through inflammatory
mechanisms, but the primary mechanism described here is hypoperfusion, not direct infection.
Option D (Immunologic injury): Incorrect—immunologic injury would present as
glomerulonephritis or interstitial nephritis, not ATN from hypotension.
Question 3
Which type of necrosis is characterized by preservation of tissue architecture for several days
after cell death due to denaturation of structural proteins and enzymes?
A. Liquefactive necrosis
B. Coagulative necrosis [CORRECT]
C. Caseous necrosis
D. Fat necrosis
Correct Answer: B
Rationale: Coagulative necrosis, typically from ischemia in solid organs (heart, kidney, spleen),
preserves tissue architecture because the denaturation of structural proteins prevents enzymatic
digestion. The "ghost" outlines of cells remain visible microscopically. This results from protein
denaturation occurring faster than enzymatic digestion.
Option A (Liquefactive necrosis): Incorrect—occurs in brain (ischemic or bacterial abscess)
where enzymatic digestion predominates, resulting in liquid transformation without architecture
preservation.
,Option C (Caseous necrosis): Incorrect—characteristic of tuberculosis, appears as amorphous,
granular, "cheese-like" debris without preserved architecture, representing a combination of
coagulative and liquefactive necrosis.
Option D (Fat necrosis): Incorrect—occurs in adipose tissue (pancreatitis, trauma) where lipases
break down fat into fatty acids that combine with calcium (saponification), forming white chalky
deposits without architecture preservation.
Question 4
A 45-year-old woman with rheumatoid arthritis has autoantibodies directed against which
specific self-antigen?
A. Acetylcholine receptors at the neuromuscular junction
B. The Fc portion of IgG (rheumatoid factor) and citrullinated peptides [CORRECT]
C. Thyroid peroxidase and thyroglobulin
D. Pancreatic beta-cell antigens (GAD65, IA-2)
Correct Answer: B
Rationale: Rheumatoid arthritis is characterized by autoantibodies against: (1) the Fc portion of
IgG (rheumatoid factor, RF), and (2) citrullinated proteins/peptides (anti-CCP antibodies),
formed by post-translational modification of arginine to citrulline by peptidylarginine deiminase
(PAD) in the presence of inflammation and smoking. These antibodies form immune complexes
that deposit in joints, activating complement and causing synovitis.
Option A (Acetylcholine receptors): Incorrect—targeted in myasthenia gravis, causing
postsynaptic neuromuscular transmission failure.
Option C (Thyroid peroxidase/thyroglobulin): Incorrect—targeted in Hashimoto's thyroiditis,
causing hypothyroidism through lymphocytic infiltration and destruction.
Option D (Pancreatic beta-cell antigens): Incorrect—targeted in type 1 diabetes mellitus, causing
autoimmune destruction of insulin-producing cells.
Question 5
A patient experiences anaphylaxis within minutes of receiving penicillin. Which hypersensitivity
reaction type and immunological mechanism are responsible?
A. Type I (IgE-mediated immediate hypersensitivity) [CORRECT]
B. Type II (Antibody-mediated cytotoxic hypersensitivity)
C. Type III (Immune complex-mediated hypersensitivity)
, D. Type IV (T-cell-mediated delayed-type hypersensitivity)
Correct Answer: A
Rationale: Anaphylaxis is a Type I hypersensitivity reaction. Penicillin (hapten) binds to carrier
proteins, triggering IgE production by plasma cells sensitized to Th2 cytokines (IL-4, IL-13).
Upon re-exposure, IgE cross-links on mast cells and basophils, triggering degranulation and
release of histamine, leukotrienes (C4, D4, E4), prostaglandins, and platelet-activating factor
(PAF), causing vasodilation, increased vascular permeability, bronchoconstriction, and
cardiovascular collapse.
Option B (Type II): Incorrect—involves IgG/IgM against cell-surface or matrix antigens causing
cytotoxicity (e.g., hemolytic anemia, Goodpasture's syndrome).
Option C (Type III): Incorrect—involves immune complex deposition causing complement
activation and inflammation (e.g., serum sickness, SLE, post-streptococcal glomerulonephritis).
Option D (Type IV): Incorrect—T-cell mediated, delayed 24-72 hours (e.g., contact dermatitis,
TB skin test, granuloma formation).
Question 6
Granulomatous inflammation with caseous necrosis is the characteristic pathological finding in
which condition?
A. Acute bacterial appendicitis
B. Mycobacterium tuberculosis infection [CORRECT]
C. Viral hepatitis
D. Acute pyogenic pneumonia
Correct Answer: B
Rationale: Tuberculosis produces well-formed granulomas with central caseous necrosis
(amorphous, eosinophilic, "cheese-like" debris), surrounded by epithelioid macrophages
(activated macrophages with abundant eosinophilic cytoplasm), Langhans giant cells
(multinucleated with horseshoe arrangement), and a peripheral rim of lymphocytes. This Th1-
mediated response attempts to contain the intracellular mycobacteria.
Option A (Acute appendicitis): Incorrect—characterized by acute suppurative inflammation with
neutrophilic infiltrate, not granulomas.
Option C (Viral hepatitis): Incorrect—characterized by hepatocyte necrosis (apoptotic bodies,
Councilman bodies) and lymphocytic infiltrate, not granulomatous inflammation.
