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NR 507 Advanced Pathophysiology Midterm LATEST VERIFIED QUESTION

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LATEST NR 507 Advanced Pathophysiology Midterm Exam 2025/2026 – 200 Practice Questions with Rationales

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NR 507 Advanced Pathophysiology
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NR 507 Advanced Pathophysiology

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NR 507 ADVANCED PATHOPHYSIOLOGY




NR 507 Advanced Pathophysiology Midterm
Exam 2025/2026 – 200 Practice Questions with
Rationales




Table of Contents
1. Topic 1: Cellular Adaptation & Injury – Questions 1–20
2. Topic 2: Genetics & Neoplasia – Questions 21–33
3. Topic 3: Inflammation & Immunity – Questions 34–45
4. Topic 4: Fluid, Electrolyte & Acid-Base Balance – Questions 46–60
5. Topic 5: Cardiovascular Pathophysiology – Questions 61–70
6. Topic 6: Respiratory Pathophysiology – Questions 71–80
7. Topic 7: Renal & Urinary Pathophysiology – Questions 81–90
8. Topic 8: Endocrine Pathophysiology – Questions 91–100
9. Topic 9: Neurologic & Musculoskeletal Pathophysiology – Questions
101–110
10. Topic 10: Hematologic Pathophysiology – Questions 111–120
11. Topic 11: Gastrointestinal & Hepatobiliary Pathophysiology –
Questions 121–130
12. Topic 12: Renal & Urinary Pathophysiology (Continued) – Questions
131–140
13. Topic 13: Endocrine Pathophysiology (Continued) – Questions 141–
150
14. Topic 14: Multisystem & Infectious Disease – Questions 151–160
15. Topic 15: General Pathophysiology & Miscellaneous Concepts –
Questions 161–200




Topic 1: Cellular Adaptation & Injury



1. A patient with a history of chronic hepatitis B develops liver fibrosis and
a shrunken, nodular liver tissue. This irreversible cellular change is best
described as:

, NR 507 ADVANCED PATHOPHYSIOLOGY

A. Hyperplasia
B. Metaplasia
C. Dysplasia
D. Cirrhosis

Answer: D. Cirrhosis
Rationale: Cirrhosis is the end-stage result of chronic liver injury, characterized
by irreversible fibrosis and the formation of regenerative nodules. It is not a
cellular adaptation like the other options.




2. Which cellular adaptation is most likely to occur in the bladder
epithelium of a chronic smoker in response to chronic irritation?
A. Squamous metaplasia
B. Columnar metaplasia
C. Glandular hyperplasia
D. Transitional to squamous metaplasia

Answer: D. Transitional to squamous metaplasia
Rationale: Chronic irritation, such as from smoking, can cause the normal
transitional epithelium of the bladder to undergo metaplasia, converting into a
more resilient stratified squamous epithelium. This change can increase the risk
for cancer.




3. Reperfusion injury, which can occur after blood flow is restored to an
area of myocardial infarction, is primarily mediated by:
A. ATP depletion
B. Reactive oxygen species (ROS)
C. Lactic acidosis
D. Apoptosis inhibition

Answer: B. Reactive oxygen species (ROS)
Rationale: Upon reoxygenation, a burst of reactive oxygen species (like
superoxide and peroxynitrite) is generated. These molecules cause extensive
damage to cellular lipids, proteins, and DNA, leading to further injury beyond
the initial ischemic event.




4. Caseous necrosis is a pathognomonic finding for which condition?
A. Ischemic stroke
B. Tuberculosis

, NR 507 ADVANCED PATHOPHYSIOLOGY

C. Acute pancreatitis
D. Gangrene

Answer: B. Tuberculosis
Rationale: Caseous necrosis is a distinctive form of cell death where tissue takes
on a soft, cheese-like, granular appearance. It is characteristic of tuberculosis
(TB) infections. Other forms of necrosis are seen in different conditions (e.g.,
liquefactive in the brain).




5. A patient with long-standing, uncontrolled hypertension develops heart
failure and bilateral lower extremity edema. This cardiac change is best
classified as:
A. Atrophic failure
B. Pathologic hypertrophy
C. Physiologic hyperplasia
D. Dystrophic calcification

Answer: B. Pathologic hypertrophy
Rationale: The chronic pressure overload from hypertension forces the heart to
work harder, causing an increase in the size of individual cardiac muscle cells
(hypertrophy). Over time, this adaptive change becomes maladaptive
(pathologic), leading to impaired contractility and, eventually, heart failure and
edema.




6. The hallmark of irreversible cell injury, visible on electron microscopy, is:
A. Ribosome detachment
B. Flocculent densities in mitochondria
C. Chromatin clumping
D. Plasma membrane blebbing

Answer: B. Flocculent densities in mitochondria
Rationale: The presence of flocculent densities within the mitochondria
indicates catastrophic and irreversible mitochondrial damage. While other
changes like membrane blebbing and chromatin clumping can be seen in
reversible injury, these mitochondrial densities are a sign point of no return.




7. Which of the following findings indicates that cell injury is still
reversible?
A. Rupture of lysosomes

, NR 507 ADVANCED PATHOPHYSIOLOGY

B. Mitochondrial cristae disruption with swelling
C. Nuclear chromatin clumping
D. Cell membrane blebbing that resolves

Answer: D. Cell membrane blebbing that resolves
Rationale: Reversible cell injury is characterized by cellular swelling, blebbing of
the cell membrane, and mild mitochondrial changes. If the injurious stimulus is
removed, these changes can resolve, and the cell can return to normal.
Irreversible injury is marked by lysosomal rupture and severe nuclear changes.




8. In the kidneys, the earliest ultrastructural change seen in ischemic acute
tubular necrosis (ATN) is:
A. Karyorrhexis (nuclear fragmentation)
B. Loss of brush border microvilli
C. Coagulative necrosis
D. Pyknosis (nuclear shrinkage)

Answer: B. Loss of brush border microvilli
Rationale: The proximal tubular cells are highly sensitive to ischemia. The
earliest change is the loss of the brush border microvilli and loss of cell polarity.
These changes are initially reversible if blood flow is restored quickly. Pyknosis
and karyorrhexis are signs of irreversible injury and cell death.




9. Apoptotic bodies are removed from a tissue by which process, without
causing inflammation?
A. Inflammation by neutrophils
B. Phagocytosis by macrophages without inflammation
C. Complement-mediated lysis
D. Degranulation of mast cells

Answer: B. Phagocytosis by macrophages without inflammation
Rationale: Apoptosis, or programmed cell death, is a clean and controlled
process. Cells shrink and break into membrane-bound apoptotic bodies, which
are rapidly recognized and phagocytized by macrophages or neighboring cells.
Crucially, this process does not trigger an inflammatory response, preserving the
integrity of the surrounding tissue.




10. A patient has a lung biopsy. The pathologist's report describes cells
that are enlarged, have hyperchromatic (dark-staining) nuclei, show

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