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?
What is the initial event in serum sickness?
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 -
Which of the following is an oncogene?
NEET-PG 2015 - Pathology NEET-PG Practice Questions and MCQs
Question 21: 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 22: 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 23: 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 24: 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 25: What is the initial event in serum sickness?
- A. It is associated with hypocomplementemia.
- B. It is a type III hypersensitivity reaction.
- C. It occurs due to exposure to heterologous antigens. (Correct Answer)
- D. It can lead to leukocytoclastic vasculitis.
Explanation: ***Can lead to leukocytoclastic vasculitis*** - Serum sickness is characterized by the formation of **immune complexes**, which can trigger **leukocytoclastic vasculitis** affecting the blood vessels [1][2]. - Symptoms can include **rash, fever, and arthralgia**, typically occurring 1-3 weeks after exposure to the offending antigen [2]. *Can occur due to homologous antigen* - Serum sickness is usually a reaction to **heterologous** antigens, such as those from animal serum, not **homologous** ones. - Homologous antigens do not typically elicit the immune response seen in serum sickness; hence, this statement is incorrect. *Type 2 hypersensitivity* - Serum sickness is classified as a **Type III hypersensitivity** reaction due to the immune complex formation, not Type II [1]. - Type II is characterized by antibody-mediated destruction of **target cells**, which does not apply here. *Hypercomplementemia* - Serum sickness is associated with **hypocomplementemia** due to complement consumption from immune complex formation, not hypercomplementemia. - This can lead to **decreased complement levels** during the response, making this statement incorrect. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 214-216. [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. 172-173.
Question 26: 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 27: 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 28: 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 29: 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 30: Which of the following is an oncogene?
- A. WT-1
- B. Rb
- C. p53
- D. RAS (Correct Answer)
Explanation: ***RAS*** - RAS is an **oncogene**, not a tumor suppressor gene; it promotes cell proliferation and survival [1]. - Mutations in RAS lead to uncontrolled cell division, contributing to various cancers. *p53* - p53 is a crucial **tumor suppressor gene** responsible for regulating the cell cycle and preventing tumor formation [1,2]. - It functions by inducing apoptosis in cells with damaged DNA, preventing their proliferation [2]. *WT-1* - WT-1 is a **tumor suppressor gene** associated with Wilms' tumor and regulates kidney and gonadal development. - It plays a role in cell growth and differentiation, preventing tumorigenesis when functioning correctly. *Rb* - The Rb gene encodes the **retinoblastoma protein**, a key tumor suppressor that regulates the cell cycle by inhibiting cell division [1,2]. - Loss of Rb function is primarily associated with retinoblastoma and other cancers, indicating its critical role in tumor suppression [1,2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 297-301. [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. 227-228.