Which viral proteins are known to act as carcinogens in causing carcinoma cervix?
What is the Rose Waaler test used for?
Indirect Coombs test detects:
Parasitosis of extraocular eye muscles is seen in?
Most common cause of idiopathic interstitial pneumonia is
What is the key pathophysiological difference between acid and alkali injuries in terms of tissue necrosis?
Aetiology of Dressler Syndrome is
Basket weave appearance of glomerular basement membrane on electron microscopy is seen in
Which is a hormone dependent liver tumor?
Which type of anemia is most commonly characterized by marked poikilocytosis and anisocytosis on peripheral blood smear?
NEET-PG 2015 - Pathology NEET-PG Practice Questions and MCQs
Question 61: Which viral proteins are known to act as carcinogens in causing carcinoma cervix?
- A. P 24 - gene
- B. E - gene (Correct Answer)
- C. L - gene
- D. H - gene
Explanation: ***E - gene*** - The **E - gene** in human papillomavirus (HPV) is known to play a crucial role in the **transformation of cervical cells**, leading to cancer development [1]. - Specifically, the **E6 and E7 proteins** encoded by this gene interfere with tumor suppressor functions, contributing to cervical carcinoma [1,2]. *L - gene* - The **L - gene** is associated with the virus's structural proteins, primarily aiding in the formation of the viral capsid. - It does not have a direct role in the oncogenic process leading to cervical cancer. *H - gene* - The **H - gene** is not specifically linked to the oncogenic effects of HPV; it is not recognized for contributing to cancer development. - It is often confused in discussions but doesn't directly influence the carcinogenic pathway like the E gene does. *P 24 - gene* - The **P 24 - gene** is not related to HPV; instead, it is associated with **HIV** and its structural components. - This gene does not play any role in the development of cervical carcinoma or transformation of cervical cells. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Female Genital Tract, pp. 1006-1007. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 334-335.
Question 62: What is the Rose Waaler test used for?
- A. Ring precipitation
- B. Precipitation in gel
- C. Complement fixation test
- D. Passive hemagglutination test (Correct Answer)
Explanation: ***Passive hemagglutination test*** - The **Rose Waaler test** is a historical **rheumatoid factor (RF)** detection method based on **passive hemagglutination**. - It uses sheep red blood cells coated with a subagglutinating dose of rabbit anti-sheep red blood cell antibody to detect RF in patient serum. *Complement fixation test* - This assay detects the presence of **antibody** or **antigen** by observing whether **complement** is consumed in an antigen-antibody reaction. - The Rose Waaler test does not involve the measurement of complement consumption. *Precipitation in gel* - This technique, such as **immunodiffusion**, involves the formation of a visible **precipitate** when soluble antigens and antibodies diffuse through a gel matrix and meet at optimal concentrations. - The Rose Waaler test relies on agglutination of red blood cells, not precipitation in gel. *Ring precipitation* - A **ring precipitation test** involves layering an antigen solution over an antibody solution, creating an antigen-antibody complex visible as a **precipitate ring** at the interface of the two solutions. - This method is distinct from the Rose Waaler test which uses red blood cell agglutination.
Question 63: Indirect Coombs test detects:
- A. Antibodies in the serum (Correct Answer)
- B. Antibodies bound to RBC Surface
- C. Antigens bound to RBC Surface
- D. Antigens in the plasma
Explanation: ***Antibodies in the serum*** - The **indirect Coomb's test** is designed to detect the presence of **antibodies** against red blood cells (RBCs in the serum) before transfusion or during pregnancy [1]. - It is crucial in identifying **hemolytic disease of the newborn** (HDN) and ensuring safe blood transfusions [1]. *Antibodies attached to RBC Surface* - This scenario describes the **direct Coomb's test**, which identifies antibodies that are already bound to **RBCs**. - Direct testing assesses conditions like **autoimmune hemolytic anemia**, not the serum. *Antigens attached to RBC Surface* - This option suggests evaluating **antigens** present on the surface of RBCs, which is not the purpose of the indirect Coomb's test. - Antigens are important in blood typing and compatibility assessments, but this test focuses on antibodies. *Antigens in the serum* - Indirect Coomb's does not detect **antigens** but rather the **antibodies** related to those antigens. - Additionally, serum testing for antigens is not a standard procedure for assessing transfusion compatibility. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 627-628.
Question 64: 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.
Question 65: Most common cause of idiopathic interstitial pneumonia is
- A. Idiopathic pulmonary fibrosis (Correct Answer)
- B. Organizing pneumonia
- C. Sarcoidosis
- D. Lipoid pneumonia
Explanation: ***Idiopathic pulmonary fibrosis (IPF)*** - This is the **most common** form of idiopathic interstitial pneumonia, accounting for approximately **50-60% of all IIP cases** - Represents the **most severe** IIP subtype with poor prognosis - Characterized by progressive **usual interstitial pneumonia (UIP) pattern** with fibroblastic foci and honeycombing - Presents with progressive dyspnea, dry cough, and restrictive lung disease *Organizing pneumonia* - While **Cryptogenic Organizing Pneumonia (COP)** is a form of idiopathic interstitial pneumonia, it is **much less common than IPF** [1] - Characterized by **intra-alveolar granulation tissue (Masson bodies)** [1] - Better prognosis and steroid-responsive compared to IPF [1] *Sarcoidosis* - This is **NOT classified as an idiopathic interstitial pneumonia** - It is a separate **multisystem granulomatous disease** with **non-caseating granulomas** - Has a distinct etiology related to altered immune response - Does not belong to the IIP classification system *Lipoid pneumonia* - This is **NOT an idiopathic interstitial pneumonia** - Results from **aspiration of lipid substances** causing exogenous lipoid pneumonia - Has a **known extrinsic cause**, therefore not "idiopathic" - Not part of the IIP classification **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Respiratory Tract Disease, pp. 330-331.
Question 66: What is the key pathophysiological difference between acid and alkali injuries in terms of tissue necrosis?
- A. Acid injuries cause coagulative necrosis
- B. Alkali injuries lead to deeper tissue damage
- C. Acid injuries are less severe than alkali injuries
- D. Alkali injuries cause liquefactive necrosis (Correct Answer)
Explanation: ***Alkali injuries cause liquefactive necrosis*** - **Alkali burns** result in **liquefaction necrosis**, which involves the dissolution of tissue and cells, leading to a much deeper and progressive injury as the alkali penetrates further into tissues. - This is the **key pathophysiological difference** that distinguishes alkali from acid injuries - the TYPE of necrosis (liquefactive vs coagulative). - This type of necrosis allows the alkali to continue damaging underlying tissues and can lead to more extensive and severe scarring and complications. *Acid injuries cause coagulative necrosis* - While this statement is **medically true**, it only describes what acids do without explicitly stating the **difference** or comparison with alkali injuries. - The question asks for the KEY **difference**, and this option presents only one half of the comparison. - **Acid burns** typically cause **coagulation necrosis**, forming a coagulum or eschar that precipitates proteins and creates a barrier, thereby limiting the depth of penetration. - The correct answer (alkali → liquefactive necrosis) better captures the distinguishing pathophysiological feature. *Alkali injuries lead to deeper tissue damage* - This statement is true but serves as a **consequence** of the underlying **liquefactive necrosis** rather than the primary pathophysiological mechanism itself. - The liquefaction process continuously destroys cells and extracellular matrix, enabling the caustic agent to propagate deeply into the tissue. - This describes the OUTCOME rather than the KEY pathophysiological mechanism. *Acid injuries are less severe than alkali injuries* - This is a **generalization about severity** rather than identifying the specific pathophysiological mechanism of tissue death. - While generally true due to the **coagulation necrosis** limiting the depth of penetration of acids, severity can vary based on concentration, duration of exposure, and other factors. - The formation of a protective eschar in acid burns often prevents further significant tissue destruction, unlike the progressive damage seen in alkali burns.
Question 67: Aetiology of Dressler Syndrome is
- A. Autoimmune (Correct Answer)
- B. Toxin mediated
- C. Viral infection
- D. Idiopathic cause
Explanation: ***Autoimmune*** - Dressler syndrome is a form of **pericarditis** that occurs several days to weeks after myocardial injury (e.g., myocardial infarction, cardiac surgery, trauma). [3] - It is considered an **autoimmune phenomenon** where the body's immune system attacks damaged cardiac tissue. [1] *Viral infection* - While viral infections can cause general pericarditis, Dressler syndrome specifically refers to **post-cardiac injury** inflammation, not direct viral involvement. [2], [3] - Viral pericarditis typically has a more acute presentation without a preceding cardiac event. [2] *Toxin mediated* - There is no evidence to suggest that Dressler syndrome is caused by **toxins** or toxic substances. - The pathogenesis is linked to an immune response to damaged myocardial cells. *Idiopathic cause* - While some forms of pericarditis are idiopathic, Dressler syndrome has a clear **triggering event** (cardiac injury) and a well-understood autoimmune mechanism. [3] - Therefore, it is not classified as idiopathic. **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 Heart, pp. 581-582. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Cardiovascular Disease, pp. 297-298.
Question 68: Basket weave appearance of glomerular basement membrane on electron microscopy is seen in
- A. Alport syndrome (Correct Answer)
- B. Polyarteritis nodosa
- C. Giant cell arteritis
- D. Acute post-streptococcal glomerulonephritis
Explanation: ***Alport syndrome*** - **Alport syndrome** is characterized by a "basket weave" appearance of the **glomerular basement membrane (GBM)** on electron microscopy due to irregular thickening, thinning, and splitting of the lamina densa. - This structural abnormality results from mutations in genes encoding **Type IV collagen**, particularly **COL4A5**, leading to progressive kidney disease, hearing loss, and ocular abnormalities. *Polyarteritis nodosa* - This is a **necrotizing vasculitis** primarily affecting medium-sized arteries, and its renal involvement typically manifests as a focal or diffuse necrotizing glomerulonephritis, often without specific GBM changes. - The electron microscopic findings would generally show inflammatory cell infiltration and fibrinoid necrosis of vessel walls, not a characteristic GBM pattern. *Giant cell arteritis* - **Giant cell arteritis** is a vasculitis affecting large- and medium-sized arteries, typically in the elderly, and often involves the temporal arteries. - Renal involvement is rare, and the characteristic pathological finding is **granulomatous inflammation** within the arterial wall with giant cells, not GBM changes. *Acute post-streptococcal glomerulonephritis* - This condition is characterized by **subepithelial immune deposits ("humps")** on electron microscopy, not a "basket weave" pattern of the GBM. - The GBM itself may show minor changes but does not exhibit the lamellated and split appearance seen in Alport syndrome.
Question 69: Which is a hormone dependent liver tumor?
- A. Adenoma (Correct Answer)
- B. Hemangioma
- C. Hepatocellular carcinoma
- D. Hemangiopericytoma
Explanation: ***Adenoma*** - Hepatic adenomas are **hormone-dependent tumors** commonly associated with conditions like **oral contraceptive use** and are influenced by estrogen [1]. - These tumors can present as **benign liver masses**, but they have a risk of hemorrhage and malignant transformation [1]. *Hepatocellular carcinoma* - This is a **malignant tumor** of the liver primarily associated with cirrhosis and chronic liver disease, not directly hormone-dependent. - Risk factors include **viral hepatitis** and **alcohol exposure**, rather than hormonal influences. *Hemangioma* - Liver hemangiomas are **vascular lesions** that are usually asymptomatic and are **not hormone-dependent**. - They are the most common benign liver tumors, often discovered incidentally during imaging. *Hemangiopericytoma* - A rare tumor, hemangiopericytoma originates from **pericytes** around blood vessels and is not specifically associated with liver tissue or hormones. - It can arise in various organs but lacks the dependency on hormones seen in hepatic adenomas. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Liver and Gallbladder, p. 874.
Question 70: Which type of anemia is most commonly characterized by marked poikilocytosis and anisocytosis on peripheral blood smear?
- A. Megaloblastic anemia
- B. Iron deficiency anemia (Correct Answer)
- C. Nutritional anemia
- D. Thalassemia
Explanation: ***Iron deficiency anaemia*** - Characterized by **poikilocytosis** (abnormal shapes) and **anisocytosis** (variation in red blood cell sizes), which are common findings in iron deficiency [1]. - Typically results in **microcytic hypochromic anemia** [1], distinguishing it from other types of anemia. *Nutritional deficiency anaemia* - May present with various blood cell morphology but does not specifically exhibit **poikilocytosis** and **anisocytosis** characteristic of iron deficiency anemia. - Usually includes deficiencies like **vitamin B12** or **folate**, which result in **macrocytic anemia** instead. *Megaloblastic anaemia* - Primarily caused by deficiency of **vitamin B12** or **folate**, leading to large, immature red blood cells (megaloblasts) rather than varied shapes and sizes. - Associated with **hypersegmented neutrophils** in the blood smear, which differentiates it from iron deficiency anemia. *Thalassemia* - Characterized by **microcytic hypochromic red blood cells** and often involves **target cells** rather than generalized poikilocytosis and anisocytosis. - Typically presents with **hemolytic anemia** but does not show the same variability in cell shapes and sizes as seen in iron deficiency anemia. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 590-591.