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?
Carcinoma originating from glands is called?
Which protein is defective in dilated cardiomyopathy?
Lines of Zahn are LEAST likely to be seen in -
Which of the following is a type of small vessel vasculitis?
Which type of white blood cell plays a primary role in cardiac remodeling and chronic inflammation in heart failure?
Parasitosis of extraocular eye muscles is seen in?
NEET-PG 2015 - Pathology NEET-PG Practice Questions and MCQs
Question 51: 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 52: 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 53: 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 54: 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.
Question 55: Carcinoma originating from glands is called?
- A. Basal cell carcinoma
- B. Squamous cell carcinoma
- C. Adenocarcinoma (Correct Answer)
- D. Fibrosarcoma
Explanation: ***Adenocarcinoma*** - Carcinoma that arises from **glandular epithelium** is specifically classified as adenocarcinoma [1]. - It often presents in organs like the **breast**, **prostate**, and **gastrointestinal tract** [4,5]. *Fibrosarcoma* - This is a **malignant tumor** derived from **fibrous connective tissue**, not glands. - Typically occurs in **soft tissues**, and is distinct from epithelial tumors like adenocarcinoma. *Squamous cell carcinoma* - Originates from **squamous epithelial cells** and primarily affects areas such as the **skin** and **mucous membranes** [2]. - It is not associated with glandular structures, differing markedly from adenocarcinoma. *Basal cell carcinoma* - Arises from **basal cells** in the **epidermis** (skin), not from glandular tissue. - It is the most common type of skin cancer and is largely not relevant to glandular origin. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 335-336. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 336-337. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 777-778. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Alimentary System Disease, pp. 348-349.
Question 56: Which protein is defective in dilated cardiomyopathy?
- A. Tropomyosin
- B. Myosin
- C. Troponin
- D. Dystrophin (Correct Answer)
Explanation: ***Dystrophin*** - **Dystrophin** is a crucial protein in the **muscle cell membrane** that anchors the cytoskeleton to the extracellular matrix. - Defects in dystrophin lead to sarcolemmal fragility, causing muscle damage and can result in **dilated cardiomyopathy**, especially in conditions like **Duchenne muscular dystrophy** [1]. *Myosin* - **Myosin** is a fundamental **motor protein** involved in muscle contraction, forming the thick filaments. - While mutations in myosin can cause various cardiac conditions, like hypertrophic cardiomyopathy, direct primary defects in myosin are not typically identified as the cause of dilated cardiomyopathy [2]. *Troponin* - **Troponin** is a protein complex that regulates muscle contraction by controlling the interaction between actin and myosin, particularly in response to calcium. - Although troponins are vital for cardiac function and are released during myocardial injury, their primary defect is not typically implicated in the etiology of dilated cardiomyopathy [2]. *Tropomyosin* - **Tropomyosin** is a protein that winds around actin filaments and, along with troponin, regulates the binding of myosin to actin. - While essential for muscle contraction, direct defects in tropomyosin are not a common genetic cause of dilated cardiomyopathy. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Peripheral Nerves and Skeletal Muscles, pp. 1244-1245. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 574.
Question 57: Lines of Zahn are LEAST likely to be seen in -
- A. Liver
- B. Kidney
- C. Heart
- D. Lung (Correct Answer)
Explanation: ***Lung*** - **Lines of Zahn are LEAST likely in the lungs** because most pulmonary thrombi are actually **emboli that formed elsewhere** (typically in deep leg veins) and then **lodged in pulmonary vessels**. - These pre-formed thrombi developed in **low-flow venous environments** and therefore **lack the characteristic layered appearance** of Lines of Zahn. - Even when thrombi form in situ in pulmonary vessels, the vascular bed characteristics make Lines of Zahn formation less common compared to other sites. *Heart* - **Mural thrombi** in heart chambers (especially post-MI in left ventricle or in atrial fibrillation) commonly show **Lines of Zahn**. - The **high-flow, turbulent environment** with continuous cardiac contractions creates ideal conditions for alternating platelet-fibrin and RBC layer deposition. - These are classic examples of antemortem thrombi with visible Lines of Zahn. *Liver* - **Portal vein thrombosis** and **hepatic vein thrombosis** (Budd-Chiari syndrome) can exhibit **Lines of Zahn**. - Despite being venous, these vessels have **sufficient flow velocity and turbulence** to allow layered thrombus formation. - Lines of Zahn indicate the thrombus formed during life with flowing blood. *Kidney* - **Renal artery thrombosis** and **renal vein thrombosis** frequently show **Lines of Zahn**. - Both arterial and venous renal circulation have adequate flow dynamics for layered thrombus formation. - These represent antemortem thrombi formed in vessels with active blood flow.
Question 58: Which of the following is a type of small vessel vasculitis?
- A. Classical PAN
- B. Giant cell arteritis
- C. Granulomatosis with polyangiitis (GPA) (Correct Answer)
- D. None of the options
Explanation: ***Granulomatosis with polyangiitis (GPA)*** - GPA is a prototypic **ANCA-associated small vessel vasculitis** characterized by necrotizing granulomas and vasculitis [1], [2]. - It commonly involves the **upper and lower respiratory tracts** and the **kidneys** with necrotizing granulomatous inflammation [1], [2]. - Classified as small vessel vasculitis according to the **Chapel Hill Consensus Conference** classification. *Classical PAN* - This refers to **Polyarteritis Nodosa (PAN)**, which is a **medium-sized vessel vasculitis**. - PAN is characterized by multifocal inflammatory and necrotizing lesions of medium-sized muscular arteries, **not small vessels**. *Giant cell arteritis* - **Giant cell arteritis (GCA)** is a **large vessel vasculitis** that primarily affects the aorta and its major branches, particularly the temporal artery [3]. - Symptoms include headache, jaw claudication, and visual disturbances, reflecting the involvement of larger blood vessels [3]. *None of the options* - This option is incorrect because Granulomatosis with polyangiitis (GPA) is a clear example of a small vessel vasculitis. - There is a correct answer among the provided choices. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 519-520. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 536-537. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 515-516.
Question 59: Which type of white blood cell plays a primary role in cardiac remodeling and chronic inflammation in heart failure?
- A. Eosinophils
- B. Macrophages (Correct Answer)
- C. T cells
- D. B cells
Explanation: ***Macrophages*** - **Macrophages** are increasingly recognized for their critical role in the pathogenesis and progression of **heart failure**, contributing to **cardiac remodeling**, chronic inflammation, and fibrosis - They infiltrate failing myocardium and play dual roles: promoting both **inflammation** and **tissue repair** - Their activation state (M1 vs M2 phenotypes) can significantly influence cardiac function and prognosis in heart failure patients - They secrete **cytokines**, **growth factors**, and **matrix metalloproteinases** that contribute to ventricular remodeling *Eosinophils* - **Eosinophils** are primarily involved in **allergic reactions** and defense against **parasitic infections** - While they can contribute to inflammation in specific cardiac conditions (e.g., **eosinophilic myocarditis**, **Loeffler endocarditis**), they are not primarily associated with the general pathophysiology of chronic heart failure *T cells* - **T cells** are central to **adaptive immunity**, including cell-mediated responses and modulation of immune reactions - Though T cells play a role in inflammatory processes in certain forms of heart disease, particularly **viral myocarditis**, they are not the predominant immune cell driving chronic cardiac remodeling in heart failure *B cells* - **B cells** are responsible for producing **antibodies** and are key players in humoral immunity - While B cells can contribute to autoimmune forms of heart disease and certain inflammatory processes, they are not typically the primary immune cell associated with the progression of chronic heart failure
Question 60: Parasitosis of extraocular eye muscles is seen in?
- A. Trichinella infection (Correct Answer)
- B. Cysticercus infection
- C. Amoebic infection
- D. Ascariasis infection
Explanation: ***Trichinella infection*** - **Trichinellosis** (caused by *Trichinella spiralis*) commonly involves the **extraocular muscles** during the muscle encystment phase [1]. - Ocular symptoms like **periorbital edema**, eosinophilic myositis of extraocular muscles, and subconjunctival hemorrhage are characteristic [1]. *Cysticercus infection* - **Cysticercosis**, caused by *Taenia solium* larvae, can affect the eye, predominantly forming **subretinal** or **vitreous cysts** [2]. - While it can involve orbital muscles, involvement of extraocular muscles is less typical and less specific than in trichinellosis [2]. *Amoebic infection* - **Amoebic infections** primarily cause **keratitis** (e.g., *Acanthamoeba*) [3] or can lead to granulomatous encephalitis in immunocompromised individuals. - They do not typically cause direct parasitosis of the extraocular muscles. *Ascariasis infection* - **Ascariasis**, caused by *Ascaris lumbricoides*, is an intestinal nematode and is not known to infect the extraocular muscles. - Ocular manifestations are rare and usually involve migration of adult worms to the orbit or eyelid, not muscle encystment. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 404-405. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 403-404. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Manifestations Of Central And Peripheral Nervous System Disease, pp. 735-736.