ANSWERS | VERIFIED ANSWERS PLUS RATIONALES | EXAM
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1. Which of the following is the primary mechanism of cell injury in hypoxia?
A. Oxidative stress
B. ATP depletion
C. Lysosomal rupture
D. Membrane hyperpolarization
Answer: B – ATP depletion is the primary mechanism of cell injury in hypoxia because
lack of oxygen prevents oxidative phosphorylation, leading to decreased energy supply.
2. A patient presents with jaundice and elevated liver enzymes. Which type of cell death is
most likely occurring in hepatocytes?
A. Necrosis
B. Apoptosis
C. Autophagy
D. Pyroptosis
Answer: A – Necrosis is characterized by cell swelling, membrane rupture, and
inflammation, which commonly occurs in liver injury.
3. Which intracellular signaling molecule is most associated with apoptosis via the intrinsic
pathway?
A. Caspase-8
B. Cytochrome c
C. TNF-α
D. Fas ligand
Answer: B – Cytochrome c is released from mitochondria and triggers the intrinsic
apoptotic pathway.
4. Chronic inflammation is most likely to lead to:
A. Necrosis
B. Fibrosis
C. Apoptosis
D. Cellular regeneration
Answer: B – Chronic inflammation often stimulates fibroblasts, leading to collagen
deposition and fibrosis.
5. A patient with myocardial ischemia develops cell swelling and membrane blebbing. This
is an example of:
A. Apoptosis
B. Necrosis
C. Autophagy
D. Oncosis
Answer: D – Oncosis refers to cell swelling due to injury, often preceding necrosis.
6. Oxidative stress primarily causes cell injury by:
A. Activating caspases
B. Damaging DNA, proteins, and lipids
, C. Increasing ATP production
D. Enhancing cellular repair
Answer: B – Reactive oxygen species damage cellular components, leading to
dysfunction and death.
7. Which cytokine is most associated with systemic inflammation in sepsis?
A. IL-1
B. IL-10
C. TGF-β
D. IL-4
Answer: A – IL-1 is a pro-inflammatory cytokine that mediates fever and systemic
inflammatory responses.
8. In which type of necrosis is the tissue architecture preserved for a period, often seen in
infarcts of solid organs?
A. Liquefactive
B. Coagulative
C. Caseous
D. Fat
Answer: B – Coagulative necrosis maintains the tissue structure temporarily, typical of
ischemic infarcts.
9. Which electrolyte abnormality is most likely to exacerbate cardiac cell injury?
A. Hypokalemia
B. Hypercalcemia
C. Hypomagnesemia
D. Hyponatremia
Answer: B – Hypercalcemia activates degradative enzymes in cells, worsening injury.
10. Free radical injury is most commonly counteracted by:
A. Lipase
B. Antioxidants
C. ATP synthase
D. Cyclooxygenase
Answer: B – Antioxidants neutralize free radicals, preventing oxidative damage.
11. Which type of cellular adaptation occurs in response to increased workload on skeletal
muscle?
A. Atrophy
B. Hypertrophy
C. Hyperplasia
D. Metaplasia
Answer: B – Hypertrophy is an increase in cell size due to increased workload.
12. Barrett’s esophagus is an example of which cellular adaptation?
A. Hypertrophy
B. Atrophy
C. Metaplasia
D. Dysplasia
Answer: C – Metaplasia is the reversible replacement of one cell type with another, often
due to chronic irritation.
,13. Dysplasia is characterized by:
A. Reversible cell injury
B. Disordered growth with abnormal cellular morphology
C. Increased cell size without proliferation
D. Programmed cell death
Answer: B – Dysplasia shows abnormal size, shape, and organization of cells, often
precancerous.
14. Which of the following is a common cause of reversible cell injury?
A. Severe hypoxia
B. Ischemia for 1–2 minutes
C. Mild oxidative stress
D. Toxin exposure at sub-lethal dose
Answer: D – Sub-lethal toxin exposure can cause reversible injury, such as cellular
swelling.
15. Lipid accumulation in hepatocytes is termed:
A. Steatosis
B. Glycogenosis
C. Fibrosis
D. Necrosis
Answer: A – Steatosis refers to fatty change in cells, commonly in the liver.
16. The primary mediator of acute inflammation that causes vasodilation is:
A. Histamine
B. Interleukin-10
C. Platelet-derived growth factor
D. Prostaglandin E2
Answer: A – Histamine, released by mast cells, causes vasodilation and increased
vascular permeability.
17. Which cell type is first to arrive at a site of acute inflammation?
A. Lymphocytes
B. Neutrophils
C. Macrophages
D. Eosinophils
Answer: B – Neutrophils are the predominant early responders in acute inflammation.
18. Chronic inflammation is often driven by:
A. Neutrophils
B. Lymphocytes and macrophages
C. Platelets
D. Eosinophils
Answer: B – Macrophages and lymphocytes sustain long-term inflammation.
19. Amyloidosis results from:
A. Fat accumulation
B. Protein misfolding and deposition
C. Glycogen storage
D. Cellular necrosis
Answer: B – Amyloidosis is due to extracellular deposition of misfolded proteins.
, 20. Which type of necrosis is classically associated with tuberculosis?
A. Coagulative
B. Liquefactive
C. Caseous
D. Fat
Answer: C – Caseous necrosis has a cheese-like appearance and is typical in TB
granulomas.
21. A patient has ischemic injury to the brain. The predominant type of necrosis seen is:
A. Coagulative
B. Liquefactive
C. Caseous
D. Fat
Answer: B – Brain infarcts usually undergo liquefactive necrosis due to high lipid
content.
22. Cellular swelling in early hypoxic injury is caused by:
A. Sodium and water influx
B. Calcium efflux
C. ATP overproduction
D. Lipid accumulation
Answer: A – Sodium accumulates inside cells due to ATP-dependent pump failure,
bringing water in.
23. Which type of cell death elicits an inflammatory response?
A. Apoptosis
B. Necrosis
C. Autophagy
D. Senescence
Answer: B – Necrosis causes cell rupture and releases contents that trigger
inflammation.
24. Which intracellular organelle is most sensitive to hypoxic injury?
A. Nucleus
B. Mitochondria
C. Lysosome
D. Golgi apparatus
Answer: B – Mitochondria are highly sensitive to oxygen deprivation, affecting ATP
synthesis.
25. Reactive oxygen species in reperfusion injury primarily damage cells through:
A. Membrane lipid peroxidation
B. DNA replication
C. Protein glycosylation
D. Cytokine inactivation
Answer: A – ROS attack membrane lipids, leading to cell lysis.
26. Cellular senescence is best described as:
A. Reversible cell injury
B. Permanent cell cycle arrest
C. Apoptotic death