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NU 208 Pathophysiology Final Exam 2025 (With Solns

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NU 208 Pathophysiology Final Exam 2025 (With SolnsNU 208 Pathophysiology Final Exam 2025 (With SolnsNU 208 Pathophysiology Final Exam 2025 (With SolnsNU 208 Pathophysiology Final Exam 2025 (With Solns












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April 30, 2025
Number of pages
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NU 208 Pathophysiology

Complete Final Exam (Qns & Ans)

2025

1. Scenario: A patient suffering an acute myocardial infarction
undergoes reperfusion therapy. Shortly afterward, additional
myocardial damage is noted. Which mechanism most likely
underlies the reperfusion injury observed in this patient?
Options:
A) Reperfusion leads to excessive calcium deposition within the
myocardium.
B) A sudden influx of oxygen results in the generation of
reactive oxygen species (ROS).
C) The reestablished flow “washes out” vital nutrients.
D) Reperfusion triggers an autoimmune response targeting
cardiac cells.
ANS: B) A sudden influx of oxygen results in the generation
of reactive oxygen species (ROS).

©2025

, Rationale: Reperfusion injury is largely mediated by oxygen-
derived free radicals that cause oxidative damage to cellular
membranes, proteins, and DNA. This mechanism is critical
following restoration of blood flow.


2. Scenario: A septic patient develops multi-organ dysfunction.
In this context, which cellular event is most responsible for
disseminated tissue injury?
Options:
A) A cytokine storm that increases vascular permeability and
leads to tissue edema.
B) Direct bacterial invasion of organ tissues.
C) Overproduction of growth factors that cause uncontrolled
cell proliferation.
D) Enhanced activity of anti-inflammatory mediators.
ANS: A) A cytokine storm that increases vascular
permeability and leads to tissue edema.
Rationale: In sepsis, an overwhelming inflammatory response
(“cytokine storm”) disrupts vascular integrity and causes
widespread tissue injury and organ dysfunction.


3. Scenario: A diabetic patient with years of poor glycemic
control develops microvascular complications. Which
pathophysiologic mechanism is most implicated in these
complications?

©2025

, Options:
A) Oxidative DNA damage without glycation of proteins.
B) Non-enzymatic glycation leading to the formation of
advanced glycation end products (AGEs).
C) Increased apoptotic activity in endothelial cells alone.
D) Enhanced insulin sensitivity causing stimulus overload.
ANS: B) Non-enzymatic glycation leading to the formation
of advanced glycation end products (AGEs).
Rationale: Chronic hyperglycemia results in non-enzymatic
glycation of proteins and lipids, forming AGEs that alter vessel
structure and function, thereby causing microvascular damage.


4. Scenario: A cancer patient undergoing chemotherapy shows
evidence of programmed cell death in non-target tissues. Which
intracellular pathway is most likely activated in this process?
Options:
A) The extrinsic (death receptor-mediated) pathway of
apoptosis.
B) The intrinsic (mitochondrial) pathway of apoptosis.
C) Unregulated cell necrosis due to sudden ATP depletion.
D) Autophagy leading exclusively to cell survival.
ANS: B) The intrinsic (mitochondrial) pathway of apoptosis.


©2025

, Rationale: Many chemotherapeutic agents trigger the
mitochondrial pathway of apoptosis by inducing mitochondrial
membrane permeabilization, release of cytochrome c, and
subsequent caspase activation, even in off-target tissues.


5. Scenario: A newborn suffering from perinatal asphyxia
shows cellular swelling and eventual rupture of the plasma
membrane. What type of cell death is most consistent with this
presentation?
Options:
A) Apoptosis
B) Necrosis
C) Autophagy
D) Necroptosis
ANS: B) Necrosis
Rationale: Necrosis is characterized by cell swelling, plasma
membrane rupture, and typically triggers an inflammatory
response. In contrast, apoptosis is a controlled process with
minimal inflammation.


6. Scenario: In a patient with chronic liver injury, repeated
bouts of cell injury lead to excessive deposition of extracellular
matrix proteins. Which cytokine is most closely linked to the
fibrotic process in this context?
Options:
©2025

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