Apoptosis vs Necrosis MCQ — NEET PG Practice Question | NEETPGAI
Apoptosis vs Necrosis
medium
microscope Pathology
A 38-year-old woman from Bangalore undergoes chemotherapy with doxorubicin for breast cancer. One week after the first cycle, a bone marrow biopsy is performed to assess hematologic toxicity. Microscopy reveals scattered individual lymphocytes with condensed, fragmented nuclei surrounded by intact cell membranes, with no inflammatory cell infiltration. Electron microscopy shows intact mitochondria and organized rough endoplasmic reticulum within these cells. Which type of cell death is being demonstrated?
A. Apoptosis with preservation of cellular organelles and membrane integrity
B. Necroptosis with mixed features of apoptosis and necrosis
C. Liquefactive necrosis with enzymatic degradation of cell contents
D. Coagulative necrosis with denaturation of structural proteins
Explanation
Apoptosis in Chemotherapy-Induced Cell Death
The clinical vignette describes chemotherapy-induced cell death in bone marrow lymphocytes. The morphologic and ultrastructural findings are diagnostic of apoptosis, the primary mechanism by which cytotoxic chemotherapy eliminates rapidly dividing cells.
Morphologic and Ultrastructural Hallmarks of Apoptosis
Table
Feature
Apoptosis
Necrosis
Nuclear condensation (pyknosis)
Early, prominent
Late
Nuclear fragmentation (karyorrhexis)
Organized into apoptotic bodies
Random, chaotic
Cell membrane
Intact, blebs form
Ruptured early
Mitochondria
Intact, organized
Swollen, disrupted
Rough ER
Organized, preserved
Disrupted, swollen
Inflammation
Absent or minimal
Dense, acute
Energy requirement
ATP-dependent
ATP-independent
Key Point
Apoptosis is an energy-dependent, programmed cell death that requires intact ATP production. Doxorubicin induces apoptosis by intercalating into DNA and triggering p53-mediated caspase activation. The intact mitochondria and ER indicate the cell retained metabolic capacity during the death process.
High-YieldNEET PG
The absence of inflammatory infiltration is a critical distinguishing feature. Apoptosis is immunologically silent because the cell membrane remains intact, preventing release of damage-associated molecular patterns (DAMPs) that would recruit neutrophils. Necrosis, by contrast, ruptures the membrane and triggers acute inflammation.
Mnemonic
APOP = Active Protein synthesis, Organelles Preserved. Apoptosis is an orderly, energy-dependent process.
Mechanism of Chemotherapy-Induced Apoptosis
1.
Doxorubicin intercalates into DNA → DNA damage
2.
p53 activation → upregulation of pro-apoptotic genes (BAX, PUMA, NOXA)
3.
Mitochondrial outer membrane permeabilization (MOMP) → cytochrome c release
4.
Caspase-9 and caspase-3 activation → nuclear fragmentation and membrane blebbing
5.
Phagocytosis of apoptotic bodies by macrophages (no inflammation)
Clinical Pearl
Bone marrow is a rapidly proliferating tissue, making it exquisitely sensitive to chemotherapy-induced apoptosis. This is why hematologic toxicity is a common side effect of cytotoxic agents.
Robbins 10e Ch 1
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