General Pathology — MCQs
On this page
What is the primary function of CD-95?
Which of the following statements is true regarding metastatic calcification?
Who is credited with the introduction of electron microscopy?
Michaelis-Gutmann bodies are seen in:
In toxicological studies, necrosis of the appendix has been reported with exposure to all of the following substances except:
What is the special stain that is most diagnostic for amyloidosis?
In which of the following locations can fat necrosis occur?
Coagulative necrosis is due to which of the following?
Caseous necrosis is typically associated with which of the following conditions?
Barr bodies are seen in which of the following conditions?
General Pathology Indian Medical PG Practice Questions and MCQs
Question 1431: What is the primary function of CD-95?
- A. Promoting cell survival
- B. Facilitating protein degradation
- C. Stimulating immune response
- D. Inducing apoptosis (Correct Answer)
Explanation: ***Apoptosis*** - CD-95, also known as **Fas receptor**, is a key mediator in the **apoptotic** pathway [1], triggering programmed cell death. - Its activation leads to a cascade of events that culminate in **cellular dismantling** and removal without inflammation [2]. *Cell necrosis* - Necrosis is associated with **uncontrolled cell death** resulting from conditions like **ischemia** or **toxins**, not regulated mechanisms like apoptosis. - It leads to a **pro-inflammatory response** due to cell rupture, contrasting with the clean process of apoptosis mediated by CD-95. *Proteolysis* - Proteolysis refers to the breakdown of **proteins** into smaller peptides or amino acids, which is unrelated to CD-95's function. - This process is primarily involved in **protein turnover** and degradation, not in inducing **apoptotic** signaling. *Interferon activation* - Interferons are molecules that play a role in **viral defense** and **immune modulation**, not directly associated with the apoptosis signaling pathway of CD-95. - Their functions include **antiviral activities** and stimulating immune responses, whereas CD-95 primarily signals for programmed cell death [3]. **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. 67. [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.
Question 1432: Which of the following statements is true regarding metastatic calcification?
- A. Occurs primarily in damaged or necrotic tissues.
- B. Occurs in viable tissues, often due to systemic hypercalcemia. (Correct Answer)
- C. Calcification is associated with systemic hypercalcemia.
- D. Serum calcium levels are typically low or normal.
Explanation: ***Calcification starts in mitochondria*** - Metastatic calcification primarily occurs in **living tissues** and is initiated in the **mitochondria**, reflecting cellular damage. - It is characterized by the deposition of calcium salts due to **increased calcium levels** in the serum, particularly in certain organs [1][3]. *Serum ca level is normal* - Metastatic calcification is associated with **elevated serum calcium levels**, indicating abnormal calcium homeostasis [1][2]. - A normal serum calcium level suggests **other forms of calcification**, such as dystrophic, rather than metastatic [1]. *Occurs in dead/dying tissue* - This describes **dystrophic calcification**, which occurs in necrotic tissues rather than **metastatic calcification**, which can occur in viable tissues [1]. - Metastatic calcification is linked to **hypercalcemia** rather than tissue death [1][2]. *Occurs in damaged heart valves* - Damaged heart valves undergo **dystrophic calcification**, typically due to aging or injury, not metastatic calcification. - Metastatic calcification is a consequence of **abnormal calcium levels** affecting various tissues rather than localized injury [1][3]. **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. 134-135. [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. 127-128. [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. 76-77.
Question 1433: Who is credited with the introduction of electron microscopy?
- A. Leeuwenhoek
- B. Robert Koch
- C. Ruska (Correct Answer)
- D. Paul Ehrlich
Explanation: ***Ruska*** - **Ernst Ruska** was a German electrical engineer and Nobel laureate who, along with Max Knoll, is credited with the invention of the **electron microscope** in 1931. - His work was pivotal in developing a microscope that uses a beam of electrons to illuminate a specimen and create a magnified image, allowing for much higher resolution than light microscopes. *Leeuwenhoek* - **Antonie van Leeuwenhoek** is known for his pioneering work in microscopy and for significantly improving the simple microscope in the 17th century. - He is often referred to as the "Father of Microbiology" for his observations of microorganisms, but he did not invent the electron microscope. *Robert Koch* - **Robert Koch** was a German physician and microbiologist who is largely recognized for his role in identifying the specific causative agents of infectious diseases. - He developed Koch's postulates and made significant discoveries related to anthrax, tuberculosis, and cholera, but he was not involved in the development of electron microscopy. *Paul Ehrlich* - **Paul Ehrlich** was a German physician and scientist who worked in the fields of hematology, immunology, and chemotherapy. - He is known for his contributions to immunology, his discovery of the first effective treatment for syphilis, and coining the term "chemotherapy," but not for electron microscopy.
Question 1434: Michaelis-Gutmann bodies are seen in:
- A. Malakoplakia (Correct Answer)
- B. Melioidosis
- C. Brucellosis
- D. Tularemia
Explanation: ***Malakoplakia*** - **Michaelis-Gutmann bodies** are pathognomonic histological features of **malakoplakia**, a chronic inflammatory condition. - These bodies are characteristic laminated, intracellular, and extracellular calcium-containing concretions found within **macrophages** (Von Hansemann cells). *Melioidosis* - **Melioidosis** is caused by the bacterium *Burkholderia pseudomallei* and is characterized by abscess formation, not Michaelis-Gutmann bodies. - It can present with diverse clinical manifestations ranging from localized infection to severe sepsis. *Brucellosis* - **Brucellosis** is a zoonotic infection caused by *Brucella* species, typically presenting with fever, sweats, and arthralgia, and is not associated with Michaelis-Gutmann bodies. - Histologically, it often involves granulomatous inflammation. *Tularemia* - **Tularemia**, caused by *Francisella tularensis*, is characterized by ulceroglandular disease, pneumonia, or typhoidal forms, and does not involve Michaelis-Gutmann bodies. - Histopathology typically reveals suppurative granulomas.
Question 1435: In toxicological studies, necrosis of the appendix has been reported with exposure to all of the following substances except:
- A. Cadmium
- B. Arsenic (Correct Answer)
- C. Mercury
- D. Lysol
Explanation: ***Arsenic*** - While arsenic is a highly toxic substance known to cause various systemic effects, **necrosis of the appendix** is **not a commonly reported toxicological finding** specifically linked to arsenic exposure in the scientific literature [1]. - Arsenic toxicity typically manifests as **gastrointestinal symptoms**, skin lesions, cardiovascular issues, and neurological damage, but not specific appendiceal necrosis [1]. *Cadmium* - **Cadmium** is a heavy metal that has been implicated in **gastrointestinal toxicity**, including necrosis, through various mechanisms such as oxidative stress and cellular damage. - Studies have shown that cadmium exposure can lead to **tissue damage** in the digestive tract. *Lysol* - **Lysol**, a common household disinfectant, contains **phenolic compounds** that are highly corrosive and toxic if ingested. - Ingestion can lead to severe **chemical burns and necrosis** in any part of the gastrointestinal tract, including the appendix. *Mercury* - **Mercury**, particularly its inorganic salts, is known to be **nephrotoxic** and can cause significant **gastrointestinal damage**, including necrosis, especially after acute exposure. - It interferes with cellular enzymes and structural proteins, leading to **tissue destruction**. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 420-421.
Question 1436: What is the special stain that is most diagnostic for amyloidosis?
- A. Lugol’s Iodine
- B. Sudan black
- C. Congo red with birefringence under polarized light (Correct Answer)
- D. Congo red without birefringence under polarized light
Explanation: ***Congo red polarized light*** [1] - This special stain shows **apple-green birefringence** under polarized light [1], which is highly specific for amyloid deposits. - Its ability to bind preferentially to amyloid fibrils makes it the **most diagnostic stain** in confirming the presence of amyloidosis [1]. *Congo red in Illumination* - While Congo red assists in the identification of amyloid, **non-polarized illumination** does not reveal the characteristic birefringence necessary for diagnosis. - It is less definitive as it does not emphasize the **structural features** of amyloid compared to polarized light. *Lugol's Iodine* - Primarily a stain for **glycogen** and other polysaccharides, Lugol's Iodine is not specific to amyloid detection. - It lacks diagnostic utility for amyloidosis, as it does not react with amyloid fibrils in tissue samples. *Sudan black* - Sudan black is used to stain **lipids** and does not interact with amyloid deposits, thus making it unsuitable for amyloid diagnosis. - The stain is effective for identifying **lipid accumulation**, not protein misfolding as seen in amyloidosis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 268-269.
Question 1437: In which of the following locations can fat necrosis occur?
- A. All of the options (Correct Answer)
- B. Omental fat
- C. Breast tissue
- D. Retroperitoneal fat
Explanation: ***All of the above*** - Fat necrosis can occur in various conditions involving fat tissue, including **omentum**, **retroperitoneal fat**, and **breast tissue**. - It typically arises due to **trauma**, **infarction**, or **inflammation** leading to necrosis of adipocytes in these areas [1]. *Omentum* - While fat necrosis can occur in the **omentum**, it does not account for the complete picture as it can occur in other sites as well. - Conditions like abdominal trauma can lead to omental necrosis, but **other areas also commonly exhibit fat necrosis**. *Retroperitoneal fat* - Fat necrosis can indeed be associated with **retroperitoneal fat**, particularly after trauma or surgery. - However, it is limited to this specific area and not an exhaustive answer, as fat necrosis is also recognized in the **breast and omentum**. *Breast* - Fat necrosis is **common in the breast**, often following surgery or **radiation** therapy; however, it is not exclusive to this area. - Given that fat necrosis occurs in multiple sites, stating only the breast does not encapsulate **all conditions** where fat necrosis is common. **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. 55.
Question 1438: Coagulative necrosis is due to which of the following?
- A. Denaturation of protein (Correct Answer)
- B. Enzymatic digestion
- C. Infection
- D. Increased enzymatic activity
Explanation: ***Denaturation of protein*** - Coagulative necrosis primarily results from the **denaturation of proteins** within cells, which leads to cell membrane stability loss [1]. - Commonly associated with **ischemia** or **hypoxia**, causing localized tissue damage while preserving the basic structure of the necrotic tissue [1]. *Infection* - Infection can lead to **other forms of necrosis** such as liquefactive necrosis, but **not coagulative necrosis** directly. - Typically involves microbial agents that induce inflammation, instead of mere protein denaturation. *Enzymatic digestion* - Enzymatic digestion is characteristic of **liquefactive necrosis** where **enzymes degrade cellular structures**, leading to a liquid mass. - This process is not relevant to coagulative necrosis, which is marked by solid tissue with preserved outlines. *None* - The statement "None" doesn't accurately reflect the mechanism of coagulative necrosis, which **specifically involves protein denaturation**. - This oes not acknowledge the pathogenic factors involved in coagulative necrosis. **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. 53-55.
Question 1439: Caseous necrosis is typically associated with which of the following conditions?
- A. Tuberculosis (Correct Answer)
- B. Lymphogranuloma venereum
- C. Cytomegalovirus infection
- D. Granulomatosis with polyangiitis
Explanation: ***Tuberculosis*** - **Caseous necrosis** is the hallmark of **tuberculosis**, often described as having a "cottage cheese-like" appearance [1]. - This type of necrosis is characteristic of the **granulomas** formed in bacterial infections, especially by *Mycobacterium tuberculosis* [1]. *Lymphogranuloma venereum* - This sexually transmitted infection, caused by *Chlamydia trachomatis* serovars L1, L2, or L3, leads to **suppurative necrosis** in lymph nodes, characterized by stellate abscesses. - The necrosis seen is typically **liquefactive** and purulent, not caseous. *Cytomegalovirus infection* - CMV infection can cause various histological changes, including **cytomegalic inclusions** and necrosis, but it is not typically associated with caseous necrosis. - The cellular changes and inflammation are distinct from those seen in granulomatous diseases with caseation. *Granulomatosis with polyangiitis* - This autoimmune vasculitis is characterized by **necrotizing granulomas** and **vasculitis**, primarily affecting the respiratory tract and kidneys. - While it involves necrosis within granulomas, it is described as **fibrinoid necrosis** of vessels and surrounding tissue, not the classic caseous necrosis of tuberculosis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 383-384.
Question 1440: Barr bodies are seen in which of the following conditions?
- A. 46 XY
- B. Klinefelter's syndrome (Correct Answer)
- C. Testicular feminization syndrome
- D. Turner's syndrome
Explanation: ***Klinefelter's syndrome*** - Individuals with **Klinefelter's syndrome** have a **47, XXY karyotype**, meaning they have two X chromosomes. - One of these X chromosomes undergoes **X-inactivation** to form a Barr body, which is a condensed, inactive X chromosome [1]. *Turners syndrome* - Individuals with **Turner's syndrome** typically have a **45, XO karyotype**, meaning they have only one X chromosome [1]. - Since they lack a second X chromosome, they do not form a **Barr body**. *Testicular feminization syndrome* - Individuals with **testicular feminization syndrome** (now known as **Androgen Insensitivity Syndrome**) have a **46, XY karyotype**. - As they have only one X chromosome, they do not form a **Barr body**. *46 XY* - A **46, XY karyotype** represents a typical male, meaning they have one X and one Y chromosome. - Since they have only one X chromosome, they do not form a **Barr body**. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 173-174.
Practice by Chapter
Cell Injury and Cell Death
Practice Questions
Adaptations of Cellular Growth
Practice Questions
Accumulations and Deposits
Practice Questions
Acute and Chronic Inflammation
Practice Questions
Tissue Repair and Wound Healing
Practice Questions
Hemodynamic Disorders
Practice Questions
Genetic Disorders
Practice Questions
Environmental Pathology
Practice Questions
Nutritional Diseases
Practice Questions
Molecular Basis of Disease
Practice Questions
Want unlimited practice?
Get full access to all questions, explanations, and performance tracking.
Start For Free