NEET-PG 2015 — Pathology
89 Previous Year Questions with Answers & Explanations
Gastric carcinoma is associated with all of the following EXCEPT:
Hyaline degeneration is found in -
Which molecule is primarily responsible for nuclear fragmentation during apoptosis?
During cell death, myelin figures are derived from which of the following?
What is the definition of lipofuscin?
Which of the following is not an apoptotic gene?
What is the primary process involved in Wallerian degeneration?
What is the characteristic feature of neuropraxia?
What is the first cellular response observed after a sharp nerve cut?
Which of the following statements about peripheral nerve injury is false?
NEET-PG 2015 - Pathology NEET-PG Practice Questions and MCQs
Question 1: Gastric carcinoma is associated with all of the following EXCEPT:
- A. Over expression of C-met
- B. Inactivation of p53
- C. Over expression of C-erb
- D. Activation of RAS (Correct Answer)
Explanation: ***Activation of RAS*** - **RAS mutations** are relatively uncommon in gastric carcinoma compared to other gastrointestinal malignancies. While KRAS mutations can occur in approximately 10-15% of gastric cancers (particularly intestinal type), they are **far less frequent** than in **pancreatic adenocarcinoma** (~90%) or **colorectal carcinoma** (~40%). - In the context of gastric carcinoma, RAS pathway alterations are **not considered a major oncogenic driver** compared to the other molecular changes listed, making this the **LEAST characteristically associated** alteration. *Inactivation of p53* - **Inactivation of the p53 tumor suppressor gene** is one of the most frequent molecular events in gastric carcinoma, occurring in approximately **50-60% of cases**. - Loss of p53 function leads to genomic instability, uncontrolled cell proliferation, and resistance to apoptosis, contributing significantly to **tumorigenesis** and **poor prognosis**. *Over expression of C-met* - **Overexpression of C-MET**, a receptor tyrosine kinase for hepatocyte growth factor (HGF), is commonly observed in gastric carcinoma (30-40% of cases) and is strongly linked to **tumor growth**, **invasion**, and **metastasis**. - C-MET amplification and overexpression promote cell proliferation, survival, migration, and angiogenesis, making it an important **therapeutic target** in advanced gastric cancer. *Over expression of C-erb* - **Overexpression of C-erbB-2 (HER2/neu)** is found in approximately **10-20% of gastric adenocarcinomas**, particularly the intestinal type. - HER2 amplification or overexpression is a significant **prognostic and predictive biomarker**, and is specifically targeted by **trastuzumab** (Herceptin) therapy in HER2-positive advanced gastric cancer, improving survival outcomes.
Question 2: Hyaline degeneration is found in -
- A. Alzheimer's disease
- B. Alcoholic liver disease (Correct Answer)
- C. Acute myocardial infarction
- D. Acute appendicitis
Explanation: ***Alcoholic liver disease*** - **Mallory bodies**, a form of hyaline degeneration, are characteristic histologic findings in hepatocytes in alcoholic liver disease. - They represent aggregates of **intermediate filaments** and other proteins, indicating severe hepatocellular damage. *Acute myocardial infarction* - Characterized by **coagulative necrosis** of cardiac myocytes due to ischemia, not hyaline degeneration. - Inflammation and subsequent repair with **fibrosis** are key features. *Alzheimer's disease* - Defined by the presence of **senile plaques** (amyloid-beta deposits) and **neurofibrillary tangles** (hyperphosphorylated tau protein). - These are specific protein aggregates, distinct from hyaline degeneration of cellular components. *Acute appendicitis* - Involves acute inflammation of the appendix, leading to **neutrophilic infiltration** and often **fibrinopurulent exudate**. - There is no characteristic hyaline degeneration associated with this inflammatory process.
Question 3: Which molecule is primarily responsible for nuclear fragmentation during apoptosis?
- A. Caspases (Correct Answer)
- B. Apaf - 1
- C. Oxygen free radicals
- D. Endonuclease G
Explanation: ***Caspases*** - **Caspases** are a family of proteases that play a central role in the execution phase of apoptosis, including the **cleavage of nuclear proteins** and DNA fragmentation [1]. - Specifically, **executioner caspases** (e.g., caspase-3, -6, -7) activate **CAD (caspase-activated DNase)** by cleaving its inhibitor ICAD, leading to **nuclear fragmentation** and DNA laddering [1]. - This is the **primary mechanism** of nuclear breakdown in apoptosis. *Apaf-1* - **Apaf-1 (apoptotic protease activating factor 1)** is an adaptor protein that, upon activation by cytochrome c, forms the **apoptosome** [1]. - While essential for **caspase activation** (specifically caspase-9), Apaf-1 does not directly cleave nuclear components or cause fragmentation itself [1]. *Oxygen free radicals* - **Oxygen free radicals** (reactive oxygen species) can induce cellular damage and stress, and in high concentrations, can trigger apoptosis [2]. - However, they are generally upstream initiators of apoptosis pathways and do not directly mediate nuclear fragmentation; this process is carried out by **caspases**. *Endonuclease G* - **Endonuclease G** is a mitochondrial nuclease released during apoptosis that can contribute to DNA degradation. - However, it plays a **secondary role** and acts in a caspase-independent manner, whereas **caspases** remain the primary executors of nuclear fragmentation in apoptosis. **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. 64-67. [2] 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. 100-101.
Question 4: During cell death, myelin figures are derived from which of the following?
- A. Cell membrane (lipid bilayer) (Correct Answer)
- B. Cytoplasmic components
- C. Mitochondrial structures
- D. Nuclear membrane
Explanation: ***Cell membrane (lipid bilayer)*** - **Myelin figures** are whorled phospholipid masses formed during cell injury and death from the breakdown of **cellular membranes**, particularly the plasma membrane and **endoplasmic reticulum**. - These structures represent damaged membrane lipids (phospholipids) that undergo structural rearrangement into concentric lamellar (layered) configurations resembling myelin. - The term "cell membrane" encompasses both the plasma membrane and lipid-rich intracellular membranes, making this the most accurate answer among the options provided. - They are a characteristic morphologic feature of **irreversible cell injury** and can be seen with electron microscopy. *Cytoplasmic components* - While cytoplasmic proteins and organelles do degrade during cell death, they do not form the organized **phospholipid structures** characteristic of myelin figures. - Cytoplasmic breakdown produces different morphologic changes such as cytoplasmic eosinophilia and loss of ribosomes. *Mitochondrial structures* - Mitochondria have their own membranes that are damaged during cell death (leading to release of cytochrome c and other apoptotic factors). - However, mitochondrial membranes are not the primary source of **myelin figures**, which predominantly arise from ER and plasma membranes. *Nuclear membrane* - The nuclear envelope does fragment during cell death, contributing to nuclear changes like **karyopyknosis, karyorrhexis, and karyolysis**. - While technically a membrane structure, the nuclear envelope is not the primary source of myelin figures, which are mainly derived from the more abundant plasma and ER membranes.
Question 5: What is the definition of lipofuscin?
- A. Wear and tear pigment (Correct Answer)
- B. Fat deposits
- C. Blood pigment
- D. Form of calcification
Explanation: ***Wear and tear pigment*** - Lipofuscin is known as **wear and tear pigment** that accumulates in cells over time, especially in aging cells [1]. - It is a byproduct of **cellular lipid peroxidation** and protein degradation, indicative of oxidative stress [1]. *Form of calcification* - Not to be confused with calcification, lipofuscin is a **pigment** and not related to calcium deposition [1]. - Calcification usually occurs in response to tissue injury or necrosis, which differs fundamentally from lipofuscin accumulation. *Fat deposits* - Lipofuscin is made up of **an insoluble complex** and is not classified simply as fat or fat deposits [1]. - It is the result of the **degradation of cellular components**, rather than the accumulation of unutilized fats [1]. *Blood pigment* - Lipofuscin is not derived from **hemoglobin** or any blood components, distinguishing it from true blood pigments like **bilirubin**. - It is associated with **cellular aging** rather than with any specific blood function or metabolism [1]. **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. 75-77.
Question 6: Which of the following is not an apoptotic gene?
- A. Mcl-1
- B. Bax
- C. P53
- D. n-myc (oncogene) (Correct Answer)
Explanation: ***n-myc*** - **n-myc** is primarily known for its role in **cell proliferation and differentiation**, not specifically associated with apoptosis [2]. - It is an **oncogene** that can contribute to tumorigenesis, but does not directly regulate apoptotic pathways [3]. *P53* - **P53** is a well-known **tumor suppressor gene** that plays a crucial role in inducing apoptosis in response to DNA damage [1]. - Activation of P53 leads to the transcription of genes that promote cell death, thus it is definitely an apoptotic gene [1]. *Bax* - **Bax** is a pro-apoptotic member of the **Bcl-2 family**, promoting apoptosis by facilitating mitochondrial outer membrane permeabilization [4,5]. - It plays a direct role in the apoptotic pathway, making it an important apoptotic gene [5]. *Mcl-1* - **Mcl-1** is an anti-apoptotic member of the **Bcl-2 family**, which helps prevent apoptosis by inhibiting pro-apoptotic factors [2,3]. - Its function is to **promote cell survival**, not apoptosis, but it is still classified as part of the apoptotic regulatory network [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 303-304. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, p. 310. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 310-311. [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. 65-67. [5] 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 7: What is the primary process involved in Wallerian degeneration?
- A. Nerve degeneration (Correct Answer)
- B. Muscle degeneration
- C. Nerve regeneration
- D. Muscle regeneration
Explanation: ***Nerve degeneration*** - **Wallerian degeneration** specifically refers to the process of **axon degeneration** that occurs distal to the site of injury when a nerve fiber is severed [2]. - This process involves the breakdown of the **axon** and its myelin sheath, leading to loss of function [1]. *Muscle degeneration* - While prolonged nerve degeneration can lead to muscle **atrophy** due to denervation, **muscle degeneration itself** is not the primary process of Wallerian degeneration. - Wallerian degeneration focuses on the **nerve itself**, not the target tissue. *Nerve regeneration* - **Nerve regeneration** is the process where damaged nerves attempt to regrow and re-establish connections [2]. - This is a subsequent, and not always successful, event that can occur *after* Wallerian degeneration has cleared the debris [1]. *Muscle regeneration* - **Muscle regeneration** refers to the repair and regrowth of damaged muscle tissue, typically involving satellite cells. - It is unrelated to Wallerian degeneration, which is a process affecting the **nerve**. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 697-698. [2] 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. 109-110.
Question 8: What is the characteristic feature of neuropraxia?
- A. Damage to the endoneurium
- B. Damage to the epineurium
- C. No structural damage to the nerve (Correct Answer)
- D. Damage to the axon
Explanation: ***No structural damage to the nerve*** - **Neuropraxia** is the mildest form of nerve injury, characterized by a **temporary block in nerve conduction** without structural damage to the axon or surrounding connective tissues. - This typically results in **temporary sensory and/or motor deficits** that fully resolve within weeks to months. *Damage to the endoneurium* - Damage to the **endoneurium** would indicate a more severe injury, such as **axonotmesis**, where the axon is damaged but the connective tissue sheaths are preserved. - This level of injury suggests that wallerian degeneration would occur distal to the lesion, leading to **slower and incomplete recovery**. *Damage to the epineurium* - Damage to the **epineurium**, along with the endoneurium and perineurium, signifies **neurotmesis**, the most severe nerve injury. - This involves a **complete transection of the nerve**, requiring surgical intervention for any chance of functional recovery. *Damage to the axon* - Damage to the **axon** itself, often alongside preserved connective tissues, is characteristic of **axonotmesis**. - While recovery is possible through axonal regeneration, it is **slower and less complete** than in neuropraxia.
Question 9: What is the first cellular response observed after a sharp nerve cut?
- A. Chromatolysis (Correct Answer)
- B. Polymorphic arrangement
- C. Increased protein synthesis
- D. Macrophage activation
Explanation: ***Chromatolysis*** - **Chromatolysis** is the dissolution of the Nissl bodies (rough endoplasmic reticulum) in the neuron cell body following axonal injury, which is the **first observable cellular response** [1]. - This process is a preparatory step for neuronal regeneration, indicating the cell's attempt to repair the damaged axon [1]. *Polymorphic arrangement* - This term is not typically used to describe an immediate cellular response to a nerve cut; it might refer to diverse cell shapes or arrangements in different contexts but is not a recognized initial post-injury event. - The neuron's immediate response involves changes within the cell body, not a re-arrangement of its cellular structure with other cells. *Increased protein synthesis* - While increased protein synthesis does occur during neuronal repair and regeneration, it is a consequence of chromatolysis and part of a later, more sustained response, not the very first visible cellular change [1]. - **Chromatolysis precedes** and facilitates the subsequent increase in protein synthesis necessary for axonal regrowth [1]. *Macrophage activation* - **Macrophage activation** is a crucial part of the inflammatory response and debris clearance following nerve injury, but it is not the *first cellular response* of the neuron itself [2]. - Macrophages migrate to the site of injury hours to days after the initial insult, whereas chromatolysis begins within the neuron's cell body much earlier [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1254-1256. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 697-698.
Question 10: Which of the following statements about peripheral nerve injury is false?
- A. Wallerian degeneration starts in axonotmesis
- B. Neuropraxia is irreversible (Correct Answer)
- C. Neurotmesis is the most severe form of injury
- D. Epineurium is intact in axonotmesis
Explanation: This question asks which statement is **FALSE** about peripheral nerve injury. ***Neuropraxia is irreversible*** - This statement is **FALSE** (making it the correct answer to this question). - Neuropraxia represents the **mildest form** of peripheral nerve injury, characterized by local **demyelination** or temporary conduction block without axonal damage [2]. - Recovery from neuropraxia is typically **complete and rapid**, usually within **weeks to months**, as axonal continuity is preserved. - **No Wallerian degeneration** occurs because the axon remains intact. *Epineurium is intact in axonotmesis* - This statement is **TRUE**. In **axonotmesis**, there is disruption of the axon and myelin sheath, but the **connective tissue sheaths** (epineurium, perineurium, and endoneurium) remain intact. - The intact connective tissue provides a guide for **axonal regeneration**, which makes recovery possible, although often incomplete [1]. - Recovery occurs at approximately **1 mm/day** or **1 inch/month**. *Neurotmesis is the most severe form of injury* - This statement is **TRUE**. **Neurotmesis** involves complete severance of the nerve fiber, including the axon, myelin, and **all supporting connective tissue structures** (epineurium, perineurium, and endoneurium). - This type of injury has the **poorest prognosis** for recovery and usually requires **surgical intervention** to attempt repair [1]. *Wallerian degeneration starts in axonotmesis* - This statement is **TRUE**. **Wallerian degeneration** is a process that occurs when a nerve fiber is severed or severely injured, affecting the segment **distal to the injury** [1]. - In **axonotmesis**, the axon is disrupted, leading to degeneration of the distal axonal segment and its myelin sheath, which is characteristic of Wallerian degeneration. - Wallerian degeneration also occurs in **neurotmesis** but NOT in **neuropraxia**. **References:** [1] 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. 109-110. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, p. 1232.