Which of the following is not a germ cell tumor?
Flexner-Wintersteiner rosette is seen in-
Which of the following statements is true regarding light microscopy findings in minimal change disease?
Which of the following are examples of trinucleotide repeat mutations?
Amyloidosis is associated with all of the following conditions except?
Which of the following is a sign of reversible injury in alcoholic liver disease?
Caseous necrosis is seen in -
Dystrophic calcification is seen in
Which of the following cell types is classified as a labile cell?
Which of the following changes is NOT seen in atherosclerotic plaque at the time of rupture?
NEET-PG 2013 - Pathology NEET-PG Practice Questions and MCQs
Question 21: 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 22: 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 23: 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 24: Which of the following are examples of trinucleotide repeat mutations?
- A. Friedreich ataxia
- B. Fragile X syndrome
- C. Huntington's chorea
- D. All of the options (Correct Answer)
Explanation: ***All of the options*** - **Fragile X syndrome**, **Friedreich ataxia**, and **Huntington's chorea** are all well-known examples of genetic disorders caused by trinucleotide repeat expansions [1]. - The mutations involve an abnormal increase in the number of repetitions of a specific three-nucleotide sequence in the DNA [1]. *Fragile X syndrome* - This condition is caused by an expansion of the **CGG repeat** in the **FMR1 gene** on the X chromosome [1]. - The expansion leads to hypermethylation and silencing of the gene, impairing the production of fragile X mental retardation protein [1]. *Friedreich ataxia* - This is an autosomal recessive neurodegenerative disorder caused by an expansion of the **GAA repeat** in an intron of the **frataxin gene (FXN)**. - The repeat expansion interferes with transcription, leading to reduced frataxin protein levels. *Huntington's chorea* - This is an autosomal dominant neurodegenerative disorder caused by an expansion of the **CAG repeat** in the **huntingtin gene (HTT)**. - The expanded polyglutamine tract in the huntingtin protein leads to protein misfolding and neuronal damage, particularly in the striatum [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Genetic Disorders, pp. 177-181.
Question 25: Amyloidosis is associated with all of the following conditions except?
- A. Chronic bronchitis (Correct Answer)
- B. Osteomyelitis
- C. Bronchiectasis
- D. Tuberculosis
Explanation: ***Chronic bronchitis*** - Chronic bronchitis is primarily characterized by **inflammation of the airways** and **excess mucus production**, not typically associated with amyloidosis [1]. - Amyloidosis more commonly relates to chronic inflammatory states but does not directly result from the long-term exposure seen in chronic bronchitis [1]. *Tuberculosis* - Tuberculosis can lead to chronic inflammation, which may precipitate **secondary amyloidosis** due to persistent infection [1]. - It often causes systemic effects, including weight loss and fever, which can result in **amyloid deposition** [1]. *Osteomyelitis* - Osteomyelitis, as a chronic bone infection, can trigger an inflammatory response leading to **secondary amyloidosis** [1]. - The ongoing inflammation can result in the accumulation of amyloid proteins in the bone and surrounding tissues [1]. *Bronchiectasis* - Bronchiectasis often results from persistent lung infections leading to chronic inflammation, which can cause **amyloid deposition** [1,3]. - It is associated with recurrent lung infections and can lead to systemic complications, including amyloidosis [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. 135-136. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of the Immune System, pp. 269-270.
Question 26: Which of the following is a sign of reversible injury in alcoholic liver disease?
- A. Cytoplasmic vacuole (Correct Answer)
- B. Pyknosis (nuclear shrinkage)
- C. Loss of cell membrane integrity
- D. Nuclear karyolysis (nuclear dissolution)
Explanation: ***Cytoplasmic vacuole*** - The presence of **cytoplasmic vacuoles** in liver cells indicates fatty change, which is a **reversible injury** in alcoholic liver disease [1][2]. - This injury allows the liver to recover if **alcohol consumption** is ceased, highlighting its reversible nature [1]. *Nuclear karyolysis* - **Nuclear karyolysis** signifies severe cellular damage and necrosis, indicating an irreversible process [2]. - This feature involves the dissolution of the nucleus, which does not align with reversible injury. *Loss of cell membrane* - Loss of the **cell membrane** indicates irreversible damage, leading to cell death rather than a reversible condition [2]. - This change is associated with significant cellular impairment, contrary to the concept of recovery. *Pyknosis* - **Pyknosis**, the condensation of chromatin in the nucleus, suggests irreversible cellular injury and impending necrosis [2]. - It is often a precursor to cell death and is not indicative of reversible damage in liver pathology. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, pp. 848-850. [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. 51-53.
Question 27: Caseous necrosis is seen in -
- A. Tuberculosis (Correct Answer)
- B. CMV infection
- C. Treponemal infection
- D. Staphylococcal infection
Explanation: ***Tuberculosis*** - **Caseous necrosis** is the **pathognomonic** and **most characteristic** form of necrosis seen in **tuberculosis (TB)** caused by *Mycobacterium tuberculosis* [1]. - It appears as a **cheesy, friable, granular material** in the center of **tuberculous granulomas** (tubercles) [1], [2]. - The unique **lipid-rich cell wall** of *M. tuberculosis* combined with the host's **type IV hypersensitivity reaction** results in this distinctive pattern of tissue destruction [2]. - This is a **classic histopathological hallmark** of TB and is essential for diagnosis [2]. *Treponemal infection* - **Syphilis**, caused by *Treponema pallidum*, causes **gummatous necrosis**, NOT caseous necrosis [3]. - Gummas have a **rubbery consistency** and different histological appearance compared to the cheesy, friable caseous necrosis. - While syphilis produces granulomatous inflammation, the necrosis pattern is distinctly different from TB [3]. *CMV infection* - **Cytomegalovirus (CMV)** infection typically causes **coagulative necrosis** with **cytopathic effects** (enlarged cells with intranuclear and intracytoplasmic inclusions - "owl's eye" appearance) [3]. - Does NOT produce caseous necrosis. *Staphylococcal infection* - **Staphylococcal infections** (e.g., *Staphylococcus aureus*) cause **liquefactive necrosis** leading to **abscess formation** [3]. - Dead cells are enzymatically digested into **liquid pus**, completely different from the solid, cheesy appearance of caseous 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, p. 55. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 383-384. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, p. 360.
Question 28: Dystrophic calcification is seen in
- A. Vitamin A intoxication
- B. Atheromatous plaque (Correct Answer)
- C. Milk alkali syndrome
- D. Hyperparathyroidism
Explanation: ***Atheromatous plaque*** - Dystrophic calcification occurs in **local areas of tissue injury**, like atheromatous plaques, where necrotic debris provides a nidus for calcification [1]. - It's commonly observed in chronic **atherosclerosis**, leading to the deposition of calcium in the damaged arterial walls [1]. *Hyperparathyroidism* - Typically associated with **metastatic calcification** due to elevated calcium levels, not dystrophic calcification [2][3]. - It results in renal, pulmonary, or vascular calcifications rather than calcifications in previously damaged tissues [3]. *Milk alkali syndrome* - Involves **hypercalcemia** and can lead to calcifications, but they are primarily **metastatic** rather than dystrophic [2][3]. - The syndrome results from excess calcium intake and is associated with renal injury rather than tissue necrosis. *Vitamin A intoxication* - Can cause **hyperostosis** and **calcifications**, but these are diffuse and not primarily dystrophic in nature. - The calcifications in this condition do not stem from necrotic tissue but rather are due to toxicity effects on bone metabolism. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of Infancy and Childhood, pp. 506-507. [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. 134-135. [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 29: Which of the following cell types is classified as a labile cell?
- A. Liver parenchymal cells
- B. Vascular smooth muscle cells
- C. Surface epithelium (Correct Answer)
- D. Neurons
Explanation: ***Surface epithelium*** - Surface epithelium is classified as **labile tissue**, meaning it undergoes constant regeneration due to its high turnover rate [1]. - Cells in this tissue are typically found in areas that experience frequent damage or abrasion, such as the skin and lining of the intestines. *Cardiac cell* - Cardiac cells are considered **permanent cells**, as they do not undergo significant regeneration after injury or damage. - Damage to cardiac cells typically leads to **fibrosis** rather than repair of the original tissue. *Liver parenchymal cell* - Liver parenchymal cells are categorized as **stable cells**, which can regenerate but do so under specific circumstances, such as injury. - They have a slower turnover rate compared to labile cells and do not constantly renew under normal conditions. *Vascular endothelial cells* - Vascular endothelial cells are considered **stable cells** as well, typically maintaining a stable population but capable of regeneration following injury. - They do not have the same rapid turnover and regeneration capability as labile cells do, especially under normal physiological conditions. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Inflammation and Repair, pp. 113-115.
Question 30: Which of the following changes is NOT seen in atherosclerotic plaque at the time of rupture?
- A. Inflammatory cell infiltration
- B. Thick fibrous cap (Correct Answer)
- C. Cell debris
- D. Smooth muscle cell atrophy
Explanation: ***Smooth muscle cell hypertrophy*** - **Smooth muscle cell hypertrophy** is generally associated with stable plaques and does not typically occur in ruptured atherosclerotic plaques [2]. - At rupture, there is **loss of smooth muscle cells** and thinning of the fibrous cap, leading to plaque instability [2]. *Thin fibrosis cap* - A **thin fibrous cap** is a critical feature of vulnerable plaques, making them prone to rupture [2]. - It indicates a **weakened structure** that can no longer withstand the pressure of the underlying lipid core [2]. *Cell debris* - **Cell debris** is often found at the site of rupture, resulting from the necrosis of foam cells and smooth muscle cells. - This indicates **plaque instability** and contributes to the thrombus formation at the rupture site. *Multiple foam cap* - The presence of **multiple foam cells** reflectsing lipid accumulation in the plaque but does not contribute to the phenomenon of plaque rupture directly. - While foam cells are associated with rupture, a **foam cap** is not a recognized pathological finding at the time of rupture. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Cardiovascular Disease, pp. 271-272. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Cardiovascular Disease, pp. 268-270.