Which mediators are involved in the resolution of inflammation?
Caseous necrosis is seen in -
Linitis plastica is a type of ?
Centrilobular necrosis of the liver may be seen with?
What are Councilman bodies and in which condition are they typically observed?
Peliosis hepatis is caused by all except?
Hurthle cell carcinoma is a variant of which type of carcinoma?
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?
NEET-PG 2013 - Pathology NEET-PG Practice Questions and MCQs
Question 41: Which mediators are involved in the resolution of inflammation?
- A. TNF Alfa, IL-1, and CRP
- B. IL-10, IL-1 receptor antagonist, and TGF-β
- C. Interferon-gamma and IL-12
- D. Resolvins, protectins, and lipoxins (Correct Answer)
Explanation: ***Resolvins, protectins, and lipoxins*** - These are **specialized pro-resolving mediators (SPMs)** derived from omega-3 and omega-6 polyunsaturated fatty acids that actively promote the resolution phase of inflammation. - **Lipoxins** (from arachidonic acid) inhibit neutrophil chemotaxis and promote macrophage-mediated clearance of apoptotic cells. - **Resolvins** (from EPA and DHA) actively terminate inflammatory signals, reduce neutrophil infiltration, and enhance bacterial clearance. - **Protectins** promote resolution by limiting neutrophil recruitment and enhancing clearance of inflammatory debris. - These mediators represent the **endogenous "stop signals"** that actively resolve inflammation rather than simply suppressing it. *IL-10, IL-1 receptor antagonist, and TGF-β* - While these have **anti-inflammatory** effects, they are not classified as primary resolution mediators. - **IL-10** inhibits pro-inflammatory cytokine synthesis and suppresses immune responses (immunosuppressive rather than pro-resolving). - **IL-1 receptor antagonist (IL-1Ra)** blocks IL-1 signaling, preventing inflammation amplification. - **TGF-β** promotes tissue repair and has immunosuppressive functions. - These are **anti-inflammatory mediators** that prevent or dampen inflammation, distinct from specialized pro-resolving mediators that actively orchestrate the resolution process. *TNF-alpha, IL-1, and CRP* - **TNF-alpha** and **IL-1** are classic **pro-inflammatory cytokines** that initiate and amplify inflammation. - **CRP (C-reactive protein)** is an acute-phase reactant and biomarker of inflammation, not a mediator of resolution. *Interferon-gamma and IL-12* - **IFN-γ** and **IL-12** promote **Th1 immune responses** and cellular immunity. - These are pro-inflammatory mediators involved in host defense against intracellular pathogens, not resolution of inflammation.
Question 42: 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 43: Linitis plastica is a type of ?
- A. Benign ulcer
- B. GIST
- C. Manifestation of gastric cancer (Correct Answer)
- D. Plastic-like appearance of stomach lining
Explanation: ***Diffuse carcinoma of stomach*** - Linitis plastica is a specific type of **gastric cancer** characterized by **thickening of the stomach wall**, leading to a rigid, non-distensible abdomen [1]. - It often presents with **significant weight loss** and **early satiety**, distinguishing it from other stomach conditions. *Benign ulcer* - Benign ulcers do not cause the **extensive wall thickening** or **desmoplastic response** seen in linitis plastica [1]. - They typically heal with treatment and are associated with typical ulcer symptoms, unlike the progressive nature of linitis plastica. *Plastic like lining of stomach* - While linitis plastica describes a **plastic-like appearance**, it is not classified as a mere lining change but rather a sign of underlying **malignancy** [1]. - This option misrepresents it as a benign condition rather than a serious **stomach adenocarcinoma**. *GIST* - Gastrointestinal stromal tumors (GIST) are **soft tissue tumors** of mesenchymal origin, differing fundamentally from the **invasive** characteristics of linitis plastica [2]. - GISTs typically present with **mass lesions** in the GI tract, not the diffuse rigidity seen in linitis plastica [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, pp. 779-780. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Gastrointestinal Tract, p. 779.
Question 44: Centrilobular necrosis of the liver may be seen with?
- A. Arsenic
- B. Ethanol
- C. CCl4 (Correct Answer)
- D. Phosphorus
Explanation: ***CCl4*** - **Carbon tetrachloride (CCl4)** is the **classic and prototypical** hepatotoxin that causes **centrilobular (zone 3) necrosis**. - The **centrilobular zone (zone 3)** is particularly vulnerable due to its high concentration of **cytochrome P450 enzymes**, which metabolize CCl4 into **toxic free radicals (trichloromethyl radicals)**. - This is the **most characteristic** cause of centrilobular necrosis in toxicology and is the preferred answer for exam purposes. *Ethanol* - **Ethanol** can also cause **centrilobular necrosis** in **alcoholic hepatitis**, as zone 3 is most susceptible to hypoxic injury and oxidative stress. - However, alcoholic liver disease presents with a **spectrum of changes** including steatosis (earliest), hepatitis with ballooning degeneration and Mallory-Denk bodies, and eventual cirrhosis. - While centrilobular necrosis occurs in alcoholic hepatitis, **CCl4 remains the prototype** for pure centrilobular necrosis in exam contexts. *Phosphorus* - **Elemental phosphorus** toxicity causes **periportal (zone 1) necrosis**, which is the opposite pattern from centrilobular necrosis. - It also causes widespread fatty change and hemorrhagic necrosis within the liver. *Arsenic* - **Arsenic poisoning** causes **diffuse/generalized hepatocellular necrosis** and cholestasis, rather than the specific centrilobular pattern. - Chronic exposure is associated with non-cirrhotic portal fibrosis and portal hypertension.
Question 45: What are Councilman bodies and in which condition are they typically observed?
- A. Wilson's disease
- B. Ballooning degeneration of hepatocytes
- C. Acute viral hepatitis (Correct Answer)
- D. Alcoholic liver disease
Explanation: **Option G*****Acute viral hepatitis*** - Councilman bodies are **characteristic histological findings** in acute viral hepatitis, associated with apoptotic hepatocytes [1]. - They represent **necrosis** of liver cells, which is commonly seen during the acute phase of viral infections affecting the liver [1]. *Alcoholic cirrhosis* - While liver damage is present, Councilman bodies are not typical; they are more associated with acute conditions rather than the chronic nature of cirrhosis. - **Fibrosis** and **bridging necrosis** are evident in alcoholic cirrhosis, distinct from the **acute necrotic changes** seen in viral hepatitis. *Ballooning of cells - Damaged cells show diffuse swelling known as ballooning degeneration.* - Ballooning degeneration indicates **cellular swelling**, often noted in conditions like steatosis or alcoholic liver disease, but does not lead to the formation of Councilman bodies. - These changes are different from the **pyknotic or karyolytic changes** associated with Councilman bodies in acute infections. *Hepatic cell necrosis - The necrosis is usually focal or centirzonal.* - This refers to various types of necrosis in the liver but does not specifically indicate the presence of Councilman bodies, which are linked with apoptotic cells. - While necrosis is common in hepatic pathology, Councilman bodies are particularly associated with **viral hepatitis**. *Wilson's disease* - Although it causes liver damage, it typically results in **copper accumulation** and associated features, not specifically Councilman bodies in its pathology. - The findings in Wilson's disease include **hepatocellular degeneration** without the distinct apoptotic features seen in **acute viral hepatitis**. Option F*Autoimmune hepatitis* - This condition may cause liver cell damage and necrosis but does not typically show Councilman bodies in its histological profile. - It primarily shows **interface hepatitis** and **lymphocytic infiltration**, contrasting with the **apoptotic bodies** seen in acute viral scenarios. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Liver And Biliary System Disease, pp. 386-387.
Question 46: Peliosis hepatis is caused by all except?
- A. OC pills
- B. Danazol
- C. Anabolic steroids
- D. Analgesics (Correct Answer)
Explanation: ***Analgesics*** - While various drugs can cause liver injury, **analgesics** are not typically associated with the development of **peliosis hepatis**. [1] - **Peliosis hepatis** involves blood-filled cysts in the liver and is linked to specific agents, not common pain relievers. *Anabolic steroids* - **Anabolic steroids** are a well-known cause of **peliosis hepatis**, especially with prolonged high-dose use. - They can induce sinusoidal dilation and hemorrhage, leading to **blood-filled cysts** in the liver. *OC pills* - **Oral contraceptive pills** (OCPs) containing estrogen have been implicated in the development of **peliosis hepatis**, though it is rare. - The estrogen component is thought to affect the **vascular endothelium** and sinusoidal integrity of the liver. *Danazol* - **Danazol**, an attenuated androgen, is strongly associated with **peliosis hepatis** and other liver complications. - It can cause severe damage to the **hepatic sinusoids**, leading to the characteristic blood-filled cavities. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, pp. 847-848.
Question 47: 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 48: 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 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: 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.