Apoptosis and Cell Death — MCQs
Type of necrosis seen in case of burn:
The following gene mutation protects tumor cells from apoptosis:
Which of the following is an example of programmed cell death?
Which of the following is not a feature of apoptosis?
Fibrinoid necrosis with neutrophilic infiltration is seen in ?
Which of the following is known as a caspase-independent programmed cell death?
Which of the following statements is false about apoptosis?
Which of the following is an example of an antiapoptotic gene?
Apoptosis is characterized by all of the following except which of the following?
Which of the following induces apoptosis in a cell?
Apoptosis and Cell Death Indian Medical PG Practice Questions and MCQs
Question 1: Type of necrosis seen in case of burn:
- A. Coagulative necrosis. (Correct Answer)
- B. Liquefactive necrosis.
- C. Caseous necrosis.
- D. Both coagulative and liquefactive.
Explanation: ***Coagulative necrosis.*** [1] - Burn injuries cause **protein denaturation** due to heat, leading to **cell death** where the cellular architecture is preserved for some time [1]. - This is the **primary and characteristic** type of necrosis directly resulting from thermal injury [1]. - The coagulation of intracellular proteins results in an **infarcted area** that appears firm and opaque [1]. *Both coagulative and liquefactive.* - While coagulative necrosis is the primary type, liquefactive necrosis may occur **secondarily** if there is superimposed infection or tissue breakdown. - However, the question asks for the type of necrosis **seen in case of burn**, which refers to the **primary pathological process** caused by thermal injury itself. - The characteristic and predominant pattern is **coagulative**, not both simultaneously. *Liquefactive necrosis.* - **Liquefactive necrosis** is characterized by the dissolution of dead cells into a viscous liquid mass due to enzymatic digestion. - Typically seen in **bacterial abscesses**, **brain infarcts**, and **hypoxic death of CNS tissue**. - This is not the primary type of necrosis directly caused by thermal injury of a burn. *Caseous necrosis.* - **Caseous necrosis** is a distinct form of cell death associated with specific granulomatous diseases, most notably **tuberculosis**. - Results in cheese-like, friable dead tissue with loss of cellular architecture. - Not characteristic of burn injuries. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, pp. 51-55.
Question 2: The following gene mutation protects tumor cells from apoptosis:
- A. BRCA
- B. RB
- C. TGFβ
- D. Bcl-2 (Correct Answer)
Explanation: ***bcl-2*** - The **bcl-2 gene** produces a protein that inhibits apoptosis, thereby allowing tumor cells to evade programmed cell death [1][2]. - Overexpression of **bcl-2** is associated with various cancers, making it pivotal in cancer biology [1]. *RB* - The **RB gene** is primarily a tumor suppressor, regulating the cell cycle, and does not directly prevent apoptosis. - Loss of RB function leads to unregulated cell division rather than inhibition of cell death. *TGFβ* - **TGFβ** acts as a tumor suppressor and can induce apoptosis in certain contexts, particularly in oncogenic processes. - Its primary role involves regulating cell growth and differentiation, not directly protecting against apoptosis. *BRCA* - **BRCA genes** (BRCA1 and BRCA2) are involved in DNA repair mechanisms; mutations increase cancer susceptibility but do not prevent apoptosis directly. - Dysfunction in BRCA proteins primarily impacts the repair of DNA damage, leading to genomic instability rather than apoptosis resistance. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 310-311. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, p. 310.
Question 3: Which of the following is an example of programmed cell death?
- A. Apoptosis (Correct Answer)
- B. Cytolysis
- C. Necrosis
- D. Autophagy
Explanation: ***Apoptosis*** - Apoptosis is a form of **programmed cell death** [1], essential for normal cellular turnover and development. - It is characterized by cellular shrinkage, chromatin condensation, and membrane blebbing, without provoking an inflammatory response [4]. *Cytolysis* - Cytolysis refers to the **destruction of cells by external agents**, such as toxins or pathogens, leading to membrane rupture. - It typically results in **inflammation** and is not a programmed or controlled process like apoptosis. *Necrosis* - Necrosis is an **uncontrolled form of cell death** resulting from acute cellular injury, leading to inflammation and damage to surrounding tissues. - Unlike apoptosis, necrosis involves rapid cell swelling and bursting of cell membranes, causing inflammation. However, some forms of necrosis can be programmed, such as necroptosis [2][3]. *Proptosis* - Proptosis refers to **eye bulging** (exophthalmos), often due to thyroid disease or certain tumors, and is not related to cell death. - It does not involve a process of cell death but rather anatomical displacement of the eyeball. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, pp. 63-64. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, p. 71. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, pp. 69-71. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, pp. 67-69.
Question 4: Which of the following is not a feature of apoptosis?
- A. Membrane blebbing
- B. Inflammation (Correct Answer)
- C. DNA fragmentation
- D. Cell shrinkage
Explanation: ***Inflammation*** - **Apoptosis** is a programmed cell death process that does not typically induce an inflammatory response because the cellular contents are neatly packaged and cleared by phagocytes without spilling into the surrounding tissue [1]. - Unlike **necrosis**, apoptosis is considered a "clean" form of cell death that avoids triggering immune reactions [1]. *Membrane blebbing* - **Membrane blebbing** is a characteristic morphological change observed during apoptosis, where the cell membrane forms irregular buds or protrusions. - This process helps in the formation of **apoptotic bodies**, which are then readily phagocytosed [1]. *DNA fragmentation* - **DNA fragmentation** into nucleosome-sized units (180-200 base pairs) is a hallmark of apoptosis, mediated by **caspase-activated DNases** [2]. - This ensures the orderly breakdown of the genetic material as part of the cell's self-destruction program. *Cell shrinkage* - **Cell shrinkage** and condensation of the cytoplasm and nucleus are early and prominent features of apoptosis. - This reduction in cell volume occurs as water and ions are extruded from the cell, contributing to the formation of condensed apoptotic bodies. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, pp. 67-69. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, pp. 64-65.
Question 5: Fibrinoid necrosis with neutrophilic infiltration is seen in ?
- A. Polyarteritis Nodosa (PAN) (Correct Answer)
- B. Giant Cell Arteritis
- C. Takayasu Arteritis
- D. Wegener's Granulomatosis
Explanation: ***PAN*** - **Fibrinoid necrosis** with **neutrophilic infiltration** is characteristic of Polyarteritis Nodosa (PAN), which primarily affects medium-sized arteries [1]. - The necrosis is often seen in the context of **systemic vasculitis**, where it leads to damage and inflammation of vessel walls [3]. *Takayasu arteritis* - Primarily affects **large vessels** like the aorta and its major branches, typically presenting with **pulselessness** or **claudication**. - It shows **granulomatous inflammation** rather than fibrinoid necrosis with neutrophilic infiltration. *Giant cell arteritis* - Predominantly affects large and medium arteries, especially the **temporal artery**, often leading to headaches and visual disturbances. - It is associated with **giant cells** and lymphocytic infiltration rather than fibrinoid necrosis. *Wegener's granulomatosis* - Characterized by **granulomatous inflammation** and vasculitis affecting small to medium vessels, particularly in the lungs and kidneys. - It does not typically present with **fibrinoid necrosis**; instead, it shows necrotizing granulomas [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 517-518. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 518-519. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Osteoarticular And Connective Tissue Disease, pp. 687-688.
Question 6: Which of the following is known as a caspase-independent programmed cell death?
- A. Necroptosis (Correct Answer)
- B. Apoptosis
- C. Pyroptosis
- D. None of the options
Explanation: ***Necroptosis*** - A form of programmed cell death that is **caspase-independent**, often occurring when apoptosis is inhibited [1][2]. - It is triggered by specific signals and is associated with **inflammation and membrane rupture**, distinguishing it from traditional apoptosis [1]. *Pyroptosis* - Involves caspase-1 activation and is typically associated with **inflammatory responses** and pathogens like **bacteria** [1]. - It leads to cell swelling and lysis, but is not classified as caspase-independent. *All of the above* - Implies that all mentioned processes are caspase-independent, which is incorrect as only necroptosis fits this category. - Includes options that are specifically associated with caspase-dependent pathways, like apoptosis and pyroptosis. *Apoptosis* - A **caspase-dependent** process characterized by cell shrinkage, chromatin condensation, and formation of apoptotic bodies [3][4]. - It is a key mechanism of programmed cell death, contrasting sharply with necroptosis, which does not rely on caspases [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, p. 71. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, pp. 69-71. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, pp. 64-65. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, p. 67.
Question 7: Which of the following statements is false about apoptosis?
- A. Swelling of organelles (Correct Answer)
- B. No inflammation
- C. Affected by dedicated genes
- D. Intact plasma membrane
Explanation: ***Swelling of organelles*** - **Swelling of organelles** is a characteristic feature of **necrosis**, not apoptosis, which involves cellular shrinkage [1]. - In apoptosis, the cell undergoes controlled **shrinkage** and fragmentation into apoptotic bodies, maintaining organelle integrity until later stages. *No inflammation* - Apoptosis is a programmed cell death process that does not induce an **inflammatory response** because the cellular contents are neatly packaged and cleared by phagocytes [4]. - This lack of inflammation distinguishes apoptosis from necrosis, where cell lysis releases intracellular components that trigger inflammation [4]. *Affected by dedicated genes* - Apoptosis is a highly regulated process controlled by a complex network of **genes** and proteins, including the Bcl-2 family and caspases [2]. - Genes like **p53** can also initiate apoptosis in response to DNA damage, ensuring proper cellular function and preventing uncontrolled cell growth [3]. *Intact plasma membrane* - During apoptosis, the **plasma membrane** generally remains intact, although with altered permeability and surface changes that facilitate recognition by phagocytes [4]. - This maintains the cell's internal environment and prevents the leakage of cellular contents, thereby *avoiding local inflammation* [4]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, pp. 69-71. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, pp. 64-65. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, p. 310. [4] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, pp. 67-69.
Question 8: Which of the following is an example of an antiapoptotic gene?
- A. FLIP (Correct Answer)
- B. P53
- C. BAX
- D. BIM
Explanation: ***FLIP*** - **FLIP** is an **antiapoptotic gene** that inhibits the activation of caspase-8, thereby blocking the extrinsic apoptotic pathway. - It acts as an **FLICE-inhibitory protein**, preventing the formation of the death-inducing signaling complex (DISC) or its downstream activation. *P53* - **P53** is a **tumor suppressor gene** that promotes apoptosis in response to DNA damage or cellular stress. - It is a **pro-apoptotic gene**, orchestrating cell cycle arrest and apoptosis to prevent the propagation of damaged cells. *BAX* - **BAX** is a **pro-apoptotic gene** belonging to the Bcl-2 family, which promotes the release of cytochrome c from mitochondria. - This release initiates the **intrinsic apoptotic pathway**, leading to caspase activation and cell death. *BIM* - **BIM** is a **pro-apoptotic gene** of the Bcl-2 family, acting as a sensitizer for apoptosis by binding to and inhibiting anti-apoptotic Bcl-2 family proteins. - Its activation leads to the **neutralization of survival factors**, thereby promoting mitochondrial outer membrane permeabilization and apoptosis.
Question 9: Apoptosis is characterized by all of the following except which of the following?
- A. Chromatin condensation
- B. Cell shrinkage
- C. DNA fragmentation
- D. Cell proliferation (Correct Answer)
Explanation: ***Inflammation*** - Apoptosis is a programmed cell death process that **does not induce inflammation**, contrasting with necrosis, which does [1]. - It is characterized by its **clean uptake** by surrounding cells without eliciting an immune response [1]. *DNA fragmentation* - A hallmark of apoptosis, where **DNA is cleaved** into smaller fragments as part of the intrinsic cell death pathway [2]. - This fragmentation can be detected via techniques such as **agarose gel electrophoresis**. *Cell shrinkage* - In apoptosis, cells exhibit **shrinkage**, also known as **pyknosis**, as they lose their volume and adopt a condensed morphology. - This shrinkage is due to changes in the cytoskeleton and loss of intracellular water. *Chromatin condensation* - One of the early features of apoptosis is **chromatin condensation**, which leads to the formation of dense nuclear material [3]. - This process is part of the typical morphology seen during programmed cell death. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, pp. 67-69. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Cellular Responses to Stress and Toxic Insults: Adaptation, Injury, and Death, pp. 64-65. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 80-81.
Question 10: Which of the following induces apoptosis in a cell?
- A. Glucocorticoids (Correct Answer)
- B. Isoprenoids
- C. Myristic acid
- D. Oleic acid
Explanation: ***Glucocorticoids*** - **Glucocorticoids** are known to induce apoptosis in various cell types, particularly lymphocytes, making them useful in **lymphoid malignancies**. - They activate a complex signaling pathway that leads to the activation of pro-apoptotic proteins and the suppression of anti-apoptotic proteins, ultimately resulting in **programmed cell death**. *Isoprenoids* - **Isoprenoids** are a large class of organic compounds derived from isoprene, involved in various metabolic processes like cholesterol synthesis and protein prenylation, but do not directly induce apoptosis. - While some isoprenoid precursors or inhibitors of isoprenoid synthesis can affect cell proliferation or survival, isoprenoids themselves are not primary apoptosis inducers. *Myristic acid* - **Myristic acid** is a saturated fatty acid primarily involved in protein myristoylation, a post-translational modification essential for various cellular functions. - It is not known to be a direct inducer of apoptosis but can influence signaling pathways that may indirectly impact cell survival or death. *Oleic acid* - **Oleic acid** is a monounsaturated fatty acid that is a major component of cell membranes and is involved in energy storage and signaling. - It is generally considered cytoprotective and can even inhibit apoptosis in some contexts, rather than inducing it.
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