MALT lymphoma is positive for which of the following markers?
Localized Langerhans cell histiocytosis affecting head and neck is?
Which is not a feature of paroxysmal nocturnal hemoglobinuria?
In which condition are Pseudo-Pelger-Huët cells typically seen?
Intracorpuscular hemolytic anemia is seen in ?
Which of the following statements is false regarding hereditary spherocytosis?
Which of the following statements about sickle cell anemia is false?
Donath-Landsteiner antibody is seen in?
Gastric carcinoma is associated with all of the following EXCEPT:
Linitis plastica is a type of ?
NEET-PG 2013 - Pathology NEET-PG Practice Questions and MCQs
Question 31: MALT lymphoma is positive for which of the following markers?
- A. CD20 (Correct Answer)
- B. CD19
- C. CD43
- D. CD5
Explanation: ***CD20*** - MALT lymphoma is a type of **B-cell non-Hodgkin lymphoma**, and CD20 is a **pan B-cell marker consistently expressed** in MALT lymphomas. - CD20 positivity is **crucial for diagnosis** and is the **primary therapeutic target** for anti-CD20 monoclonal antibody therapy (Rituximab). - In diagnostic practice, **CD20 is the most important B-cell marker** for identifying MALT lymphoma and guiding treatment decisions. *CD19* - CD19 is also a **pan B-cell marker** and is **typically positive in MALT lymphoma** along with CD20. - However, in the context of this question, **CD20 is the preferred answer** because it is the **standard diagnostic marker emphasized in clinical practice** and the **primary therapeutic target**. - Both markers are positive, but CD20 has greater **clinical and therapeutic significance** in MALT lymphoma management. *CD43* - CD43 is primarily a **T-cell and myeloid marker**, but can show **aberrant expression in 40-50% of MALT lymphomas**. - While it may be positive in some cases, it is **not a defining B-cell lineage marker** and is not used as a primary diagnostic criterion for MALT lymphoma. - Its variable expression makes it **less reliable** than consistent B-cell markers like CD20. *CD5* - CD5 is typically associated with **T-cells** and certain B-cell lymphomas, particularly **chronic lymphocytic leukemia/small lymphocytic lymphoma (CLL/SLL)** and **mantle cell lymphoma**. - **MALT lymphoma is characteristically CD5-negative**, which is an important feature for **differentiating it from CD5+ B-cell lymphomas**.
Question 32: Localized Langerhans cell histiocytosis affecting head and neck is?
- A. Eosinophilic granuloma (Correct Answer)
- B. Letterer-siwe disease
- C. Pulmonary Langerhans cell histiocytosis
- D. Hand-Schuller-Christian disease
Explanation: ***Eosinophilic granuloma*** - This is a localized form of **Langerhans cell histiocytosis** that typically presents in the head and neck region, often affecting areas like the skull and mandible [1]. - Characterized by **bone lesions** and may present with **pain or swelling** in the affected area, making it a prominent form in children and young adults. *Pulmonary langerhans cell histiocytosis* - Primarily affects the **lungs** and is associated with **cough, dyspnea**, and pulmonary nodules, not the head and neck region. - Occurs predominantly in **smokers** and involves interstitial lung disease patterns on imaging studies. *Hand-schuller-christian disease* - This condition is a systemic form of Langerhans cell histiocytosis that affects multiple systems rather than being localized, commonly presenting with **diabetes insipidus** and bone lesions. - It is often associated with **exophthalmos** and may involve lymphadenopathy, affecting older children and adults, not localized head and neck involvement. *Letterer-siwe disease* - This represents the acute, disseminated form of Langerhans cell histiocytosis, affecting infants, and is marked by systemic symptoms like **fever**, **rash**, and **hepatosplenomegaly** [1]. - Typically presents with serious manifestations and not specifically localized in the **head and neck area** as seen in eosinophilic granuloma. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, p. 630.
Question 33: Which is not a feature of paroxysmal nocturnal hemoglobinuria?
- A. Thrombocytopenia
- B. Hemolysis
- C. Increased LAP score (Correct Answer)
- D. Thrombosis
Explanation: ***Increased LAP score*** - In paroxysmal nocturnal hemoglobinuria, the **LAP score** is typically **low** due to ineffective hematopoiesis and not elevated. - The presence of a low LAP score is inconsistent with the features of this condition, making it the correct choice. *Thrombosis* - Paroxysmal nocturnal hemoglobinuria is **associated with a high risk of thrombosis**, particularly in the **venous system** [2]. - This is due to **increased platelet activation** and excessive thrombin generation resulting from hemolysis. *Hemolysis* - **Hemolysis** is a hallmark feature of paroxysmal nocturnal hemoglobinuria, where there is **destruction of red blood cells** [2,3]. - Patients often present with signs of hemolytic anemia including **elevated bilirubin** and **low haptoglobin** levels. *Thrombocytopenia* - **Thrombocytopenia** is a common finding in paroxysmal nocturnal hemoglobinuria due to **expanded consumption** of platelets during episodes of hemolysis. - This can lead to an **increased risk of bleeding** in affected patients. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 601-602. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 650-651.
Question 34: In which condition are Pseudo-Pelger-Huët cells typically seen?
- A. Hairy cell leukemia
- B. Multiple myeloma
- C. Hodgkin's lymphoma
- D. Myelodysplastic syndrome (Correct Answer)
Explanation: ***Mylodysplastic syndrome*** - Pseudo-Pelger-Huet cells are characteristic and often observed in myelodysplastic syndromes, indicating an ineffective hematopoiesis [1]. - These cells appear as **hyposegmented neutrophils** and are associated with dysplastic changes in the bone marrow [1]. *Hairy cell leukemia* - Typically presents with **hairy cells** in peripheral blood and often involves splenomegaly; pseudo-Pelger-Huet cells are not usual in this condition. - Associated with **PANCYTOPENIA** and reticulin fibrosis, differing from myelodysplastic syndrome. *Hodgkin's lymphoma* - Characterized by the presence of **Reed-Sternberg cells** and typically involves lymphadenopathy. - Peripheral blood findings generally do not include pseudo-Pelger-Huet cells; the focus is on lymphatic tissue. *Multiple myeloma* - Commonly presents with **plasma cells** and related symptoms like bone pain and renal failure, not associated with pseudo-Pelger-Huet cells. - It primarily causes an increase in monoclonal proteins rather than dysplastic changes seen in myelodysplastic syndrome. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 613-614.
Question 35: Intracorpuscular hemolytic anemia is seen in ?
- A. Thalassemia (Correct Answer)
- B. Infection
- C. Thrombotic thrombocytopenic purpura (TTP)
- D. Autoimmune hemolytic anemia
Explanation: ***Thalassemia*** - Thalassemia is characterized by **intracorpuscular hemolysis** due to defective hemoglobin synthesis, leading to premature destruction of red blood cells [1][2]. - It manifests as **microcytic anemia** with associated **extramedullary erythropoiesis** in severe cases [1]. *Autoimmune hemolytic anemia* - This condition leads to **extravascular hemolysis**, primarily affecting red blood cells in the spleen, not within the plasma [2]. - It is often associated with **positive direct Coombs test**, indicating reactants on the RBC surface. *TIP* - TIP (Thrombotic Microangiopathy) primarily involves **microangiopathic hemolytic anemia** and is not classified as intracorpuscular [2]. - The hemolysis in TIP occurs due to **microthrombi**, causing damage to red blood cells as they pass through narrowed vessels. *Infection* - Infections can lead to **hemolysis**, but this is typically **extravascular** due to splenic clearance or due to other mechanisms like **malaria** [2]. - The hemolytic mechanism is not intracorpuscular, as seen in conditions like thalassemia. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 601-602. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 596-597.
Question 36: Which of the following statements is false regarding hereditary spherocytosis?
- A. Defect in ankyrin
- B. Reticulocytosis
- C. Decreased MCHC (Correct Answer)
- D. Normal to increased MCV
Explanation: ***Decreased MCHC*** - Hereditary spherocytosis typically presents with an **increased MCHC** due to the spherocytes being more concentrated. - MCHC is a measure of the hemoglobin concentration in red blood cells, and in spherocytosis, this value is often elevated rather than decreased. *Defect in ankyrin* - This is a true statement; hereditary spherocytosis is associated with a defect in **ankyrin**, a protein that helps maintain the cell's membrane structure [2]. - Mutations in ankyrin lead to instability of the red blood cell membrane, resulting in spherocyte formation [2]. *Decreased MCV* - In hereditary spherocytosis, MCV is often **normal or slightly increased**, as it reflects the volume of red blood cells, which can be misinterpreted due to the presence of spherocytes. - Spherocytes are smaller cells, which can mistakenly suggest a falsely decreased MCV if not properly interpreted [1]. *Reticulocytosis* - This condition typically presents with **reticulocytosis** as a response to hemolysis, indicating the bone marrow is producing more red blood cells to compensate [1]. - The presence of reticulocytosis is a common finding in hereditary spherocytosis due to increased destruction of spherocytes. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 597-598. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 640-641.
Question 37: Which of the following statements about sickle cell anemia is false?
- A. Sickle cells are present in sickle cell anemia.
- B. Target cells are commonly seen in sickle cell anemia.
- C. Ringed sideroblasts are associated with sickle cell anemia. (Correct Answer)
- D. Howell Jolly bodies can be found in sickle cell anemia.
Explanation: ***Ringed sideroblast*** - **Ringed sideroblasts** are not typically associated with sickle cell anemia; they are indicative of disorders like **sideroblastic anemia**. - In sickle cell anemia, the primary findings include **hemolysis** and ineffective erythropoiesis, not ringed sideroblasts [3]. *Howell jolly bodies* - These bodies are remnants of nuclear material and can be found in individuals with **spleen dysfunction**, which can occur in sickle cell anemia [1]. - They are actually a common finding due to **hyposplenism** or **asplenia** in patients with sickle cell disease [2]. *Sickle cells* - The presence of **sickle-shaped red blood cells** is a hallmark of sickle cell anemia, caused by the mutation in the **beta-globin chain** [3]. - These sickle cells are responsible for the characteristic complications of the disease, such as **vaso-occlusive crises** [1][3]. *Target cells* - Target cells, or **codocytes**, are often seen in disorders like **thalassemia** and liver disease, and can also be present in sickle cell anemia. - They are formed due to an increase in the **surface area to volume ratio** of red blood cells, often secondary to **membrane abnormalities** seen in sickle cell changes [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 644-646. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 570-571. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 598-599.
Question 38: Donath-Landsteiner antibody is seen in?
- A. PNH
- B. Waldenstrom's macroglobulinemia
- C. Malaria
- D. Paroxysmal cold hemoglobinuria (Correct Answer)
Explanation: ***Paroxysmal cold hemoglobinuria*** - **Donath-Landsteiner antibody** is a **biphasic IgG autoantibody** that binds to red blood cells in the cold and causes **hemolysis** upon warming, characteristic of paroxysmal cold hemoglobinuria. - This antibody has **anti-P specificity**, meaning it targets the P antigen on red blood cells, leading to complement activation and cell lysis. *PNH* - **Paroxysmal nocturnal hemoglobinuria** (PNH) is characterized by a deficiency in **GPI-anchored proteins** on red blood cells, notably **CD55** and **CD59**, making them susceptible to complement-mediated lysis. - It is not associated with the Donath-Landsteiner antibody; rather, it is identified by **flow cytometry** showing absence of CD55/CD59. *Waldenstrom's macroglobulinemia* - This is a **B-cell lymphoma** characterized by the overproduction of **monoclonal IgM antibodies**, leading to hyperviscosity syndrome and other symptoms. - It does not involve Donath-Landsteiner antibodies or cold-induced hemolysis in the same manner as paroxysmal cold hemoglobinuria. *Malaria* - **Malaria** is caused by **Plasmodium parasites** that infect and destroy red blood cells, leading to hemolytic anemia and fever. - While it causes **hemolysis**, it is not mediated by the Donath-Landsteiner antibody; the destruction is primarily due to parasitic replication and immune responses against infected cells.
Question 39: 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.
Question 40: 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.