The MOST COMMON cause of concentric hypertrophy of left ventricle is?
Fibrinoid necrosis with neutrophilic infiltration is seen in ?
All of the following are true regarding fibromuscular dysplasia EXCEPT:
What is the sequence of events in acute inflammation?
Macrophages are converted to epithelioid cells by which cytokine?
Which of the following is not a germ cell tumor?
Which of the following statements is true regarding light microscopy findings in minimal change disease?
Hurthle cell carcinoma is a variant of which type of carcinoma?
Flexner-Wintersteiner rosette is seen in-
Gastric carcinoma is associated with all of the following EXCEPT:
NEET-PG 2013 - Pathology NEET-PG Practice Questions and MCQs
Question 41: The MOST COMMON cause of concentric hypertrophy of left ventricle is?
- A. Hypertension (Correct Answer)
- B. Aortic stenosis
- C. Mitral stenosis
- D. Aortic regurgitation
Explanation: ***Hypertension*** - Chronic **hypertension** is the most common cause of **pressure overload** on the left ventricle, leading to concentric hypertrophy [1]. - In response to the increased afterload, the ventricular wall thickens uniformly inward, reducing the chamber size while maintaining normal wall stress [2]. - Due to its high prevalence (30-40% of adults), hypertension is epidemiologically the most frequent cause of concentric LVH [1]. *Aortic stenosis* - While **aortic stenosis** is the classic pathological cause of **pressure overload** and concentric hypertrophy [2], **hypertension** is more prevalent in the population. - Aortic stenosis causes fixed outflow obstruction, leading to significant pressure work for the left ventricle. - This is the second most common cause but occurs in only 2-5% of elderly patients. *Mitral stenosis* - **Mitral stenosis** primarily causes pressure overload on the **left atrium** and **pulmonary circulation**, not the left ventricle. - It doesn't typically lead to **left ventricular hypertrophy** directly; instead, it causes left atrial enlargement and right ventricular hypertrophy. *Aortic regurgitation* - **Aortic regurgitation** results in **volume overload** of the left ventricle due to blood flowing back into the chamber during diastole. - This typically leads to **eccentric hypertrophy**, where the chamber dilates and the wall thickens proportionally, rather than concentric hypertrophy [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, pp. 560-562. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Heart, p. 536.
Question 42: Fibrinoid necrosis with neutrophilic infiltration is seen in ?
- A. Polyarteritis Nodosa (PAN) (Correct Answer)
- B. Giant Cell Arteritis
- C. Takayasu Arteritis
- D. Wegener's Granulomatosis
Explanation: ***PAN*** - **Fibrinoid necrosis** with **neutrophilic infiltration** is characteristic of Polyarteritis Nodosa (PAN), which primarily affects medium-sized arteries [1]. - The necrosis is often seen in the context of **systemic vasculitis**, where it leads to damage and inflammation of vessel walls [3]. *Takayasu arteritis* - Primarily affects **large vessels** like the aorta and its major branches, typically presenting with **pulselessness** or **claudication**. - It shows **granulomatous inflammation** rather than fibrinoid necrosis with neutrophilic infiltration. *Giant cell arteritis* - Predominantly affects large and medium arteries, especially the **temporal artery**, often leading to headaches and visual disturbances. - It is associated with **giant cells** and lymphocytic infiltration rather than fibrinoid necrosis. *Wegener's granulomatosis* - Characterized by **granulomatous inflammation** and vasculitis affecting small to medium vessels, particularly in the lungs and kidneys. - It does not typically present with **fibrinoid necrosis**; instead, it shows necrotizing granulomas [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 517-518. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 518-519. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Osteoarticular And Connective Tissue Disease, pp. 687-688.
Question 43: All of the following are true regarding fibromuscular dysplasia EXCEPT:
- A. Medium size vessels are affected
- B. Aneurysm may occur
- C. Irregular hyperplasia
- D. OCPs predispose (Correct Answer)
Explanation: ***OCPs predispose*** - **Oral contraceptive pills (OCPs)** are not identified as a predisposing factor for fibromuscular dysplasia (FMD). FMD is largely considered a sporadic condition with some genetic predisposition, but not linked to OCP use [1]. - While hormonal influences are suspected given its higher prevalence in women, direct causation or exacerbation by OCPs has not been established [1]. *Medium size vessels are affected* - Fibromuscular dysplasia (FMD) predominantly affects **medium-sized arteries**, most commonly the renal and carotid arteries [1]. - This involvement leads to characteristic stenoses, aneurysms, or dissections in those vessels. *Aneurysm may occur* - The abnormal arterial wall architecture in FMD, characterized by alternating areas of stenosis and dilation, can lead to the formation of **aneurysms**. - These aneurysms are usually **intracranial** or within the affected renal and carotid arteries, and represent a significant risk of rupture or dissection. *Irregular hyperplasia* - FMD involves **irregular fibrous or fibromuscular hyperplasia** of the arterial wall layers (intima, media, or adventitia). - This abnormal cellular proliferation and connective tissue deposition result in the characteristic "string of beads" appearance on angiography. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 493-494.
Question 44: What is the sequence of events in acute inflammation?
- A. Transient vasoconstriction - Stasis - Vasodilatation - Increased permeability
- B. Transient vasoconstriction - Vasodilatation - Increased permeability - Stasis (Correct Answer)
- C. Transient vasoconstriction - Vasodilatation - Stasis - Increased permeability
- D. Vasodilatation - Stasis - Transient vasoconstriction - Increased permeability
Explanation: ***Transient vasoconstriction → Vasodilatation → Increased permeability → Stasis*** - This sequence accurately reflects the **initial phase** of acute inflammation where **vasoconstriction** briefly occurs for tissue protection, followed by **vasodilatation** that enhances blood flow [3]. - **Increased permeability** allows plasma proteins to exit the bloodstream, crucial for inflammatory responses [1], while **stasis** occurs as blood flow slows, facilitating leukocyte adhesion [2]. *Transient vasoconstriction → Stasis → Vasodilatation → Increased permeability* - This option incorrectly places **stasis** before **vasodilatation**, as stasis occurs only after blood flow has increased. - **Vasodilatation** is essential for increased blood flow, which precedes stasis, making this sequence incorrect. *Transient vasoconstriction → Vasodilatation → Stasis → Increased permeability* - Although it includes **vasodilatation** and **transient vasoconstriction**, it incorrectly suggests that **stasis** occurs before the increase in vascular permeability. - **Increased permeability** is a critical event after vasodilatation [1], thus this order is not accurate. *Vasodilatation → Stasis → Transient vasoconstriction → Increased permeability* - This sequence is incorrect as it starts with **vasodilatation**, neglecting the initial protective phase of **transient vasoconstriction**. - **Transient vasoconstriction** is the first event, making this option inaccurate as it misrepresents the order of events in acute inflammation. **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. 187-188. [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. 186-187. [3] 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. 185-186.
Question 45: Macrophages are converted to epithelioid cells by which cytokine?
- A. TNF-α
- B. TGF-β
- C. IFN-γ (Correct Answer)
- D. IL-4
Explanation: ***IFN-γ: A cytokine involved in classical macrophage activation*** - **Interferon-gamma (IFN-γ)** is a key cytokine produced by activated T cells and NK cells that plays a crucial role in activating macrophages and converting them into **epithelioid cells** [1]. - This conversion is essential for the formation of **granulomas**, a hallmark of chronic inflammatory responses, particularly in infections like tuberculosis [1]. *TNF-α: A cytokine involved in granuloma maintenance* - **Tumor Necrosis Factor-alpha (TNF-α)** is vital for the **formation and maintenance** of granulomas, but it is not directly responsible for the initial conversion of macrophages to epithelioid cells. - While TNF-α helps to **organize and contain** the infection within the granuloma, IFN-γ drives the phenotypic change of macrophages. *TGF-β: A cytokine involved in tissue remodeling* - **Transforming Growth Factor-beta (TGF-β)** is predominantly involved in **tissue repair, fibrosis, and immune regulation**, promoting extracellular matrix production. - It does not primarily induce the differentiation of macrophages into epithelioid cells; rather, it often plays a role in the later stages of granuloma development, contributing to **fibrotic encapsulation** [1]. *IL-4: A cytokine involved in alternative macrophage activation* - **Interleukin-4 (IL-4)** is a characteristic cytokine that drives **alternative macrophage activation (M2 pathway)**, leading to roles in allergic responses and tissue repair [1]. - The M2 phenotype is distinct from the classically activated (M1) phenotype associated with epithelioid cell formation, which is driven by IFN-γ. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, p. 109.
Question 46: Which of the following is not a germ cell tumor?
- A. Embryonal carcinoma
- B. Endodermal sinus
- C. Seminoma
- D. Leydig cell tumor (Correct Answer)
Explanation: ***Leydig cell tumor*** - Leydig cell tumors are classified as **sex-cord stromal tumors**, not germ cell tumors [1]. - These tumors are derived from **Leydig cells** which produce androgens, affecting the endocrine function rather than germ cell lineage [1]. *Endodermal sinus* - Endodermal sinus tumors, or **yolk sac tumors**, are indeed germ cell tumors characterized by **alpha-fetoprotein (AFP)** production [2]. - They typically arise in the testis or ovaries and are known for rapid growth and aggressiveness. *Embryonal carcinoma* - Embryonal carcinoma is a type of **germ cell tumor** commonly associated with elevated levels of **beta-hCG** [2]. - It primarily affects the testes in males and can occur in the ovaries, and it is known for its aggressive behavior. *Seminoma* - Seminomas are classic examples of **germ cell tumors**, noted for their sensitivity to radiation and chemotherapy [3]. - They usually present with **increased beta-hCG** levels and can coexist with non-seminomatous germ cell tumors [3]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 510-514. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lower Urinary Tract and Male Genital System, pp. 979-980. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Lower Urinary Tract and Male Genital System, pp. 980-982.
Question 47: Which of the following statements is true regarding light microscopy findings in minimal change disease?
- A. Foot process effacement is observed under electron microscopy, not light microscopy.
- B. Anti-GBM antibodies are associated with Goodpasture syndrome, not minimal change disease.
- C. No significant changes are seen under light microscopy. (Correct Answer)
- D. IgA deposits are characteristic of IgA nephropathy, not minimal change disease.
Explanation: ***No change seen*** - In minimal change disease, **light microscopy** typically shows no significant changes, which is a key characteristic of the condition [1]. - The disease primarily affects the **podocytes** leading to **nephrotic syndrome**, while light microscopy does not reveal any abnormalities [1]. *Loss of foot process seen* - Loss of foot processes is actually observed under **electron microscopy**, not light microscopy. - Light microscopy remains normal, differentiating minimal change disease from other glomerular diseases. *IgA deposits seen* - IgA deposits are associated with **IgA nephropathy**, which is a different condition characterized by mesangial deposition. - Minimal change disease does not have **immunofluorescence** findings, and thus shows no such deposits on light microscopy [1]. *Anti GBM Abs seen* - Anti-GBM antibodies are characteristic of **Goodpasture syndrome**, which presents with significant changes in glomerular structure. - In minimal change disease, there are no **anti-GBM antibodies** or major changes visible under light microscopy. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 927-928.
Question 48: Hurthle cell carcinoma is a variant of which type of carcinoma?
- A. Medullary carcinoma
- B. Papillary carcinoma
- C. Follicular carcinoma (Correct Answer)
- D. Anaplastic carcinoma
Explanation: **Follicular carcinoma** - **Hürthle cell carcinoma**, also known as **oxyphilic follicular carcinoma**, is a specific variant of **follicular carcinoma of the thyroid**. - It is characterized by the presence of large polygonal cells with abundant eosinophilic, granular cytoplasm known as **Hürthle cells** (or oxyphil cells) within the neoplastic growth. *Medullary carcinoma* - **Medullary carcinoma** originates from the **parafollicular C cells** of the thyroid, which produce calcitonin. - It is histologically distinct, featuring nests or cords of cells often associated with **amyloid deposits**, and is not related to Hürthle cell morphology. *Papillary carcinoma* - **Papillary carcinoma** is the most common type of thyroid cancer, characterized by distinctive **nuclear features** such as **Orphan Annie eye nuclei**, nuclear grooves, and intranuclear cytoplasmic inclusions. - Its histological origin and morphological appearance are different from Hürthle cell neoplasms, which are follicular in origin. *Anaplastic carcinoma* - **Anaplastic carcinoma** is a highly aggressive and undifferentiated thyroid malignancy with a very poor prognosis. - It is characterized by pleomorphic, giant, and spindle cells and lacks the specific differentiation seen in follicular or Hürthle cell tumors.
Question 49: Flexner-Wintersteiner rosette is seen in-
- A. Retinoblastoma (Correct Answer)
- B. Hepatoblastoma
- C. Nephroblastoma
- D. Neuroblastoma
Explanation: ***Retinoblastoma*** - Flexner-Wintersteiner rosettes are **characteristic histological features** seen in retinoblastoma, indicating retinal differentiation [1]. - These rosettes reflect the **presence of photoreceptor-like structures**, which are specific to this type of tumor [1]. *Hepatoblastoma* - Histologically, hepatoblastoma shows **primitive epithelial cells** and **mixed patterns**, not Flexner-Wintersteiner rosettes. - It is primarily associated with **liver** and does not present with retinal differentiation. *Nephroblastoma* - Nephroblastoma, or Wilms tumor, typically exhibits **triphasic histology** (epithelial, stromal, and blastemal components) without rosette formation. - It primarily affects the **kidney** and does not involve the retina. *Neuroblastoma* - Neuroblastoma is characterized by **small round blue cells** and **neuroid differentiation** but lacks Flexner-Wintersteiner rosettes. - This tumor usually arises in the **adrenal glands** or sympathetic nervous system, not in retinal tissue. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Eye, p. 1342.
Question 50: 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.