Apoptosis
Results from severe cell injury and is irreversible, unlike apoptosis.
Apoptosis
- Extrinsic: death receptor-mediated (e.g., FAS ligand)
- Intrinsic (mitochondrial): regulated by BCL2 family
- Both converge → caspase cascade → cell destruction
- BCL2 family — the critical balance:
- BH3-only proteins tilt balance toward pro-apoptotic molecules → apoptosis proceeds
Read this in Hallmarks of Cancer: Molecular Basis, Cell Cycle & Oncogenes
What our notes say
- Results from severe cell injury and is irreversible, unlike apoptosis. (General Pathology I)
- Both apoptosis and necrosis are methods of achieving cell death (Medical MCQs: Chemical Pathology & Haematology Exam Review)
- The donor lymphocytes engraft and attack host tissues, including epidermal keratinocytes, causing apoptosis. (Immunopathology complete mcqs — Past Paper Questions & Answers)
- Vacuolating cytotoxin A (VacA): Induces vacuolation in host cells, disrupts tight junctions, and can cause apoptosis. (Gi sem2 patho — Past Paper Questions & Answers)
- E6 protein binds to and promotes degradation of the p53 tumor suppressor protein → loss of cell cycle control and apoptosis. (Female rep y3 — Past Paper Questions & Answers)
- | Mitochondrion | Forms ATP for energy; induces apoptosis; supports cellular proliferation; heme and steroid synthesis | (Medical Physiology Assorted SAQs — With Answers (Past Paper Study Guide))
Study material on Apoptosis
- Molecular Basis of Cancer: Cell Cycle, Apoptosis & Angiogenesis
- ONCOPATHOLOGY - MCQs WITH EXPLANATIONS
- General Pathology MCQs: Cancer, Tumors & Molecular Path Review
- ONCOPATHOLOGY - 30 KEY SHORT ANSWER QUESTIONS Hallmarks 1,2 & 3
- Medical MCQs: Chemical Pathology & Haematology Exam Review
- Hallmarks of Cancer: Molecular Basis, Cell Cycle & Oncogenes
- general Pathology Q&A
- Dr. Irungu Notes
- General Pathology Revision: Cell Injury, Inflammation & Adaptation (MBPA 3500 Paper 1)
- Pathology CAT 1: Cell Injury, Metaplasia & Hypoxia Q&A
- Pathology MCQs: Cell Injury, Cell Death, and Adaptations
- 50 Multiple Choice Questions
- Cell Injury, Adaptation & Death.
- Cell Injury & Adaptation
- PATHOLOGY MCQs: CELL INJURY, DEATH, AND ADAPTATIONS
- TUMOR SUPPRESSOR GENES & CELL CYCLE CONTROL MCQs
Images
Practice questions on Apoptosis
Which feature would BEST distinguish apoptosis from necrosis in tissue sections?
- Presence of eosinophilic cytoplasm
- Lack of adjacent inflammatory response
- Evidence of DNA fragmentation
- Cell membrane disruption
Answer: B. While both may show DNA fragmentation and eosinophilia, the ABSENCE of inflammation is the most reliable distinguishing feature of apoptosis in routine sections. Apoptotic cells maintain membrane integrity and are rapidly phagocytosed without eliciting inflammation, whereas necrosis causes membrane rupture and inflammation. ---
In the intrinsic pathway of apoptosis, which protein family member DIRECTLY creates channels in the mitochondrial membrane?
- BCL-2 and BCL-XL
- BID and BIM
- BAX and BAK
- Cytochrome c and Smac/DIABLO
Answer: C. BAX and BAK oligomerize and insert into the outer mitochondrial membrane to form channels, allowing cytochrome c release. BCL-2/BCL-XL are anti-apoptotic and prevent this. BID and BIM are BH3-only proteins that activate BAX/BAK. Cytochrome c is released THROUGH the channels, not forming them. ---
Fas-mediated apoptosis can be inhibited by viral protein FLIP, which works by:
- Blocking cytochrome c release from mitochondria
- Preventing caspase-8 activation at the DISC
- Upregulating BCL-2 expression
- Degrading Fas ligand before receptor binding
Answer: B. FLIP (FLICE-inhibitory protein) binds to procaspase-8, blocking its activation at the death-inducing signaling complex (DISC). It doesn't affect mitochondria, BCL-2, or Fas ligand. Some viruses produce FLIP to protect infected cells from immune-mediated apoptosis—a viral escape mechanism. ---
Which statement about caspases in apoptosis is MOST accurate?
- Caspase-3 is an initiator caspase in both pathways
- Caspase-9 is activated by the apoptosome
- Caspase-8 requires mitochondrial cytochrome c for activation
- All caspases have serine in their active site
Answer: B. Caspase-9 is activated when cytochrome c binds APAF-1 to form the apoptosome. Caspase-3 is an EXECUTIONER, not initiator. Caspase-8 is activated by death receptors, independent of mitochondria. Caspases have CYSTEINE (not serine) in their active sites—hence the name "caspase." ---
A patient receiving chemotherapy develops tumor lysis syndrome. Massive apoptosis of tumor cells would be expected to release all of the following EXCEPT:
- Potassium
- Lactate dehydrogenase
- Interleukin-1
- Phosphate
Answer: C. Apoptotic cells maintain membrane integrity and are phagocytosed without releasing contents or causing inflammation. IL-1 is a pro-inflammatory cytokine NOT released during apoptosis. K+, LDH, and phosphate are released during NECROSIS (which can follow massive apoptosis if clearance is overwhelmed), but the question asks about apoptosis itself. ---
Programmed cell death during embryonic development differs from pathologic apoptosis in that:
- It does not involve caspase activation
- It occurs in response to lack of survival signals
- It happens at precise, genetically determined times
- It triggers a local inflammatory response
Answer: C. Developmental programmed cell death occurs at precise times controlled by developmental genes (e.g., digit formation, neural tube closure). Both developmental and pathologic apoptosis use caspases, lack inflammation, and may involve loss of survival signals, but the TIMING precision distinguishes developmental programmed cell death. ---