Which of the following is derived from fibroblast cells?
Post-streptococcal glomerulonephritis (PSGN) is an example of which type of hypersensitivity?
What is the number of antigens typically evaluated in comprehensive HLA matching for organ transplantation?
What is the most common type of graft rejection?
Caseating necrosis most commonly occurs in
Which genetic condition is considered the most lethal due to monosomy?
Which of the following is a chromosomal instability syndrome?
Structure of chromosomes is studied by?
Reversible change from one cell type to another is known as -
What is the characteristic feature of neuropraxia?
NEET-PG 2015 - Pathology NEET-PG Practice Questions and MCQs
Question 11: Which of the following is derived from fibroblast cells?
- A. MMP2
- B. Collagen (Correct Answer)
- C. Angiopoietin
- D. TGF-β
Explanation: ***Collagen*** - Collagen is a structural protein that is predominantly produced by **fibroblast cells** in the extracellular matrix [1][2]. - It provides tensile strength and structural support to various tissues, playing a crucial role in wound healing and tissue repair [2]. *TGF-13* - Transforming Growth Factor-beta 1 (TGF-β1) is primarily produced by **immune cells** and is involved in cell growth and differentiation, not primarily by fibroblasts. - It plays a role in **fibrosis** and inflammation, but is not directly synthesized by fibroblast cells themselves. *MMP2* - Matrix Metalloproteinase-2 (MMP-2) is produced by various cell types, including **endothelial and epithelial cells**, but not predominantly by fibroblasts. - It is involved in the degradation of **extracellular matrix** components rather than being a product of fibroblast synthesis. *Angiopoietin* - Angiopoietin is primarily secreted by **endothelial cells** and plays a significant role in blood vessel formation and maturation. - It is not derived from fibroblast cells and is unrelated to their primary function of producing the extracellular matrix. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. With Illustrations By, pp. 31-32. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. With Illustrations By, pp. 34-35.
Question 12: Post-streptococcal glomerulonephritis (PSGN) is an example of which type of hypersensitivity?
- A. Type -1 hypersensitivity
- B. Type -2 hypersensitivity
- C. Type -3 hypersensitivity (Correct Answer)
- D. Type -4 hypersensitivity
Explanation: ***Type -3 hypersensitivity*** - Post-streptococcal glomerulonephritis (PSGN) is caused by **immune complex deposition**, a hallmark of type III hypersensitivity reactions [1][2][3]. - It involves the formation of **antigen-antibody complexes** following a streptococcal infection, leading to inflammation in the kidneys [1][2]. *Type -1 hypersensitivity* - Characterized by **IgE-mediated** reactions, such as allergies and anaphylaxis, which do not apply to PSGN. - It typically involves **mast cells** and histamine release, notably absent in PSGN cases. *Type -4 hypersensitivity* - Involves **T-cell mediated** responses and is related to delayed-type reactions, not applicable to PSGN. - Common examples include **contact dermatitis** and graft-versus-host disease, differing fundamentally from PSGN's mechanism. *Type -2 hypersensitivity* - Characterized by **antibody-mediated cytotoxicity**, such as in hemolytic anemia, unrelated to immune complexes in PSGN. - Typically involves direct damage to cells, contrasting with the immune complex mechanism observed in PSGN [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 214-215. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 910-915. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 215-216.
Question 13: What is the number of antigens typically evaluated in comprehensive HLA matching for organ transplantation?
- A. 10 (Correct Answer)
- B. 4
- C. 16
- D. 22
Explanation: ***10*** - The **number of criteria for HLA matching** in organ transplantation is typically 10, consisting of 6 class I and 4 class II antigens. - Proper HLA matching is critical for minimizing the risk of **graft rejection** and ensuring **recipient compatibility** [1]. *16* - While there are various HLA antigens, a total of **16** criteria is not a standard number used for matching purposes. - This number may include other factors but does not represent the core criteria for **HLA matching**. *4* - HLA matching involves more than **4 criteria**, inadequate for reliable transplantation outcomes. - This number does not encompass the essential **class I and class II antigens** that are necessary for effective matching. *22* - A total of **22 criteria** exceeds the conventional standard for HLA matching, which is not practical or necessary. - This figure may relate to overall HLA typing but is not applicable for the matching process itself. **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. 179-180.
Question 14: What is the most common type of graft rejection?
- A. Hyperacute
- B. Acute (Correct Answer)
- C. Chronic
- D. Acute on chronic
Explanation: ***Acute*** - **Acute rejection** is the most common type of graft rejection, occurring in **10-40% of transplant recipients**. [1] - It typically occurs **days to weeks to months** after transplantation (most commonly within the first 6 months). [1] - Mediated primarily by **T-lymphocytes** (cellular rejection) or **antibodies** (antibody-mediated rejection) reacting against donor antigens. [1] - Usually **responsive to immunosuppressive therapy** when detected early. *Hyperacute* - **Hyperacute rejection** is rare (occurs in <1% of cases) due to routine **pre-transplant cross-matching**. - Occurs within **minutes to hours** after transplantation due to **pre-existing circulating antibodies** against donor antigens. [1] - Results in immediate thrombosis and graft necrosis, requiring **immediate graft removal**. [1] *Chronic* - **Chronic rejection** (chronic allograft dysfunction) develops **months to years** after transplantation. - It is the **most common cause of late graft failure**, but not the most common type of rejection episode. - Characterized by **gradual, progressive loss of graft function** with vascular and fibrotic changes. - **Largely irreversible** and poorly responsive to treatment. *Acute on chronic* - This is **not a primary category** of graft rejection but represents an **acute rejection episode superimposed** on a graft already undergoing chronic changes. - Reflects exacerbation in a chronically rejecting graft. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 239-242.
Question 15: Caseating necrosis most commonly occurs in
- A. Brain
- B. Liver
- C. Kidney
- D. Lung (Correct Answer)
Explanation: ***lung*** - **Caseating necrosis** is classically associated with **tuberculosis**, which primarily affects the lungs [1]. - It is characterized by the presence of **granulomatous inflammation**, often leading to the formation of cavities in pulmonary tissue. *Brain* - While certain infections can lead to necrosis in the brain, they typically do not present as **caseating necrosis**, which is specific to certain conditions like tuberculosis. - The brain may show **liquefactive necrosis** or other types of necrosis, rather than **caseation**. *liver* - The liver usually shows **macrovesicular steatosis** or **apoptosis** in conditions like hepatitis, not caseating necrosis. - **Granulomatous hepatitis** can occur, but it does not typically result in **caseating** type necrosis associated with lung pathology. *kidney* - The kidneys can experience necrosis from various causes, but caseating necrosis is not typical; they are more often involved in **focal segmental glomerulosclerosis** or **acute tubular necrosis**. - Chronic kidney conditions may involve granulomas, but they usually are not characterized by **caseation** similar to that seen in pulmonary tissue. **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 16: Which genetic condition is considered the most lethal due to monosomy?
- A. Autosomal monosomy (Correct Answer)
- B. Chromosomal monosomy
- C. Autosomal trisomy
- D. Chromosomal trisomy
Explanation: ***Autosomal monosomy*** - **Autosomal monosomy** is the most lethal form of monosomy because it involves the loss of an entire autosome, leading to a severe imbalance in gene dosage. [1] - The human body cannot typically survive with the loss of a whole autosome, resulting in early embryonic or fetal demise. [1] *Chromosomal monosomy* - This is a broader term that includes both **autosomal monosomy** and **sex chromosome monosomy**. - While many forms of chromosomal monosomy are lethal, **sex chromosome monosomy (e.g., Turner syndrome)** is survivable, making the general term "chromosomal monosomy" less specific for the *most lethal* condition. [1] *Autosomal trisomy* - **Autosomal trisomy** involves an extra copy of an autosome (e.g., Trisomy 21 for Down syndrome), which, while causing significant health issues, is generally less lethal than the complete loss of an autosome. [1] - Many individuals with autosomal trisomies can survive to birth and beyond, unlike most cases of autosomal monosomy. [1] *Chromosomal trisomy* - This refers to having an extra copy of any chromosome, including **autosomes** and **sex chromosomes**. - While conditions like **Trisomy 13 (Patau syndrome)** and **Trisomy 18 (Edwards syndrome)** are highly lethal, the presence of *extra* genetic material is typically less universally lethal than the *absence* of an entire autosome. [1] **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 168-169.
Question 17: Which of the following is a chromosomal instability syndrome?
- A. Bloom syndrome (Correct Answer)
- B. Fanconi anemia
- C. Ataxia-telangiectasia
- D. None of the options
Explanation: ***Bloom syndrome*** - Bloom syndrome is the **classic chromosomal instability syndrome** characterized by **spontaneous chromosomal breaks, gaps, and markedly increased sister chromatid exchanges (SCEs)**. - It is an **autosomal recessive disorder** caused by mutations in the BLM gene (RecQ helicase family), leading to impaired DNA repair and replication [1]. - Patients exhibit **growth deficiency, photosensitive facial erythema, immunodeficiency**, and a dramatically **increased risk of cancers** at an early age. - The **hallmark laboratory finding** is a 10-fold increase in sister chromatid exchanges, making it the **prototypical chromosomal instability disorder**. *Fanconi anemia* - Fanconi anemia is **also a chromosomal instability syndrome**, characterized by **chromosomal breakage** when lymphocytes are exposed to DNA crosslinking agents (DEB/MMC test) [1]. - However, it presents primarily with **progressive bone marrow failure, congenital anomalies** (thumb/radial ray, café-au-lait spots, short stature), and increased cancer risk (particularly AML and squamous cell carcinomas). - While chromosomal instability is present, the **clinical presentation is dominated by bone marrow failure**, distinguishing it from Bloom syndrome. *Ataxia-telangiectasia* - Ataxia-telangiectasia is **also a chromosomal instability syndrome** with chromosomal breaks and translocations (especially involving chromosomes 7 and 14) [1]. - Caused by **ATM gene mutations**, leading to defective DNA double-strand break repair and cell cycle checkpoint control. - However, it is **clinically characterized primarily by progressive cerebellar ataxia, oculocutaneous telangiectasias, immunodeficiency**, and elevated AFP levels. - The **neurological manifestations predominate** the clinical picture, distinguishing it from Bloom syndrome. *None of the options* - This option is incorrect because Bloom syndrome is the **classic and prototypical chromosomal instability syndrome**, characterized predominantly by chromosomal instability features rather than other system involvement. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 322-323.
Question 18: Structure of chromosomes is studied by?
- A. C-banding
- B. Q-banding
- C. BrdU staining
- D. G-banding (Correct Answer)
Explanation: ***G-banding*** - G-banding is the most commonly used method for the **detailed examination of chromosomes**, allowing visualization of banding patterns [1][2]. - It facilitates the identification of **chromosomal abnormalities** and is essential in **cytogenetic studies** [1][2]. *Q-banding* - Q-banding reveals a different pattern that is primarily used for **detection of specific chromosome markers** but is less common than G-banding. - It is more useful for cases requiring **fluorescent bright bands** but not for overall structural analysis. *C-banding* - C-banding specifically highlights the **centromeric regions** of chromosomes, not the overall structure. - It is limited in scope compared to G-banding since it doesn't provide a complete picture of chromosome morphology. *Brd V-staining* - Brd V-staining focuses on specific **DNA regions** and is related to the **visualization of viral DNA** in infected cells rather than chromosome structure. - It does not offer insights into the **general structural characteristics** of chromosomes like G-banding does. **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. 54-55. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 167-168.
Question 19: Reversible change from one cell type to another is known as -
- A. Hypertrophy
- B. Dysplasia
- C. Hyperplasia
- D. Metaplasia (Correct Answer)
Explanation: ***Metaplesia*** - Refers to the **reversible change** from one cell type to another in response to chronic irritation or damage [1][2]. - It often occurs as an adaptive response in **epithelial tissues**, such as in the respiratory tract in smokers [1][2]. *Hypertrophy* - Represents an **increase in cell size** rather than a change in cell type [2]. - It is often a response to increased functional demand, as seen in **cardiac muscle** in athletes. *Hyperplesia* - Refers to an **increase in cell number** within a tissue or organ, not a change in cell type [2]. - Common in conditions such as **benign prostatic hyperplasia** but does not involve differentiation into other cell types. *Dysplasia* - Indicates an **abnormal growth or development** of cells, leading to disordered morphology rather than a transformation into another cell type. - It is often a precursor to cancer but does not signify the reversible nature of metaplasia. **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. 49. [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. 85-92.
Question 20: 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.