Hematology — MCQs
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Which of the following statements about paroxysmal nocturnal hemoglobinuria (PNH) is false?
Which of the following conditions is associated with thrombocytopenia?
A 60-year-old man is referred for evaluation of marked erythrocytosis and splenomegaly. Laboratory studies confirm an elevated red blood cell count and additionally demonstrate a moderate increase in circulating granulocytes and platelets. Oxygen saturation studies are normal, and isotopic studies reveal an increase in total red cell mass. Which of the following is characteristic of this disorder?
All are true regarding Anaemia of Chronic Diseases, except?
Fresh Frozen Plasma (FFP) is not indicated in which of the following conditions?
A patient has normal prothrombin time (PT) and platelet count with increased activated partial thromboplastin time (aPTT), factor 8 levels given as 60 IU/ml, and no history of bleeding. What is the diagnosis?
All the following are true in Immune thrombocytopenic Purpura (ITP) EXCEPT?
A 35-year-old female presents with cervical and axillary lymphadenopathy. She has a history of fever and drenching night sweats and is diagnosed with Hodgkin's lymphoma. What is the stage of the disease?
Intracorpuscular hemolytic anemia is seen in which of the following conditions?
What is the best prognostic indicator of multiple myeloma at the time of diagnosis?
Hematology Indian Medical PG Practice Questions and MCQs
Question 661: Which of the following statements about paroxysmal nocturnal hemoglobinuria (PNH) is false?
- A. Thrombosis is the leading cause of death.
- B. Bone marrow is hyperplastic.
- C. The gold standard test is the sucrose lysis test. (Correct Answer)
- D. Hemolysis is precipitated during exercise.
Explanation: Paroxysmal Nocturnal Hemoglobinuria (PNH) is an acquired clonal hematopoietic stem cell disorder caused by a mutation in the PIGA gene, leading to a deficiency of GPI-anchored proteins (CD55 and CD59) on the cell membrane [1]. This makes RBCs highly susceptible to complement-mediated lysis, representing a rare form of acquired intravascular hemolysis [1]. Why Option C is the correct (False) statement: The Sucrose Lysis Test and the Ham Test (Acidified Serum Test) are historical screening tools with low specificity and sensitivity. They have been replaced by Flow Cytometry as the current gold standard. Flow cytometry identifies the absence of GPI-anchored proteins (CD55/CD59) on RBCs and leukocytes (specifically using FLAER—Fluorescent Aerolysin—for white cells). Analysis of other options: * Option A: Thrombosis (often in unusual sites like hepatic veins—Budd-Chiari syndrome) is indeed the most common cause of mortality in PNH patients. * Option B: The bone marrow is typically hyperplastic as it attempts to compensate for chronic hemolysis. However, PNH can also be associated with aplastic anemia (hypoplastic marrow). * Option C: Hemolysis is triggered by factors that activate the complement system, such as infections, stress, and strenuous exercise. High-Yield Clinical Pearls for NEET-PG: * Triad of PNH: Hemolytic anemia, Pancytopenia, and Thrombosis. * Urine Findings: Hemosiderinuria is a classic finding in chronic intravascular hemolysis. * Treatment: Eculizumab (a monoclonal antibody against C5) is the drug of choice to prevent hemolysis. * Association: PNH has a strong link with Aplastic Anemia and may transform into Acute Myeloid Leukemia (AML).
Question 662: Which of the following conditions is associated with thrombocytopenia?
- A. Gray platelet syndrome
- B. Glanzmann thrombasthenia
- C. Bernard-Soulier syndrome (Correct Answer)
- D. Storage pool disease
Explanation: The correct answer is **Bernard-Soulier Syndrome (BSS)**. **1. Why Bernard-Soulier Syndrome is correct:** BSS is a rare autosomal recessive bleeding disorder caused by a deficiency or dysfunction of the **GPIb-IX-V complex**, which serves as the receptor for von Willebrand factor (vWF) [1]. This defect impairs platelet adhesion to the subendothelium. A hallmark diagnostic feature of BSS is **thrombocytopenia** (usually mild to moderate) accompanied by **Giant Platelets** (often as large as red blood cells) [2]. On peripheral smear, these are often referred to as "macrothrombocytopenia." **2. Why the other options are incorrect:** * **Glanzmann Thrombasthenia:** This is caused by a deficiency of **GPIIb/IIIa**, leading to defective platelet aggregation [1]. Crucially, the **platelet count and morphology are normal** in these patients. * **Gray Platelet Syndrome:** This is an alpha-granule deficiency. While it can occasionally present with mild thrombocytopenia, its primary characteristic is the "ghost-like" or gray appearance of platelets due to the lack of granules, rather than a primary quantitative defect. * **Storage Pool Disease:** This involves a deficiency of dense granules (delta-SPD). Like Glanzmann’s, the **platelet count is typically normal**, but the platelets fail to release ADP/serotonin, leading to impaired secondary aggregation. **NEET-PG High-Yield Pearls:** * **BSS vs. Glanzmann:** In BSS, platelets **do not** aggregate with Ristocetin, and the addition of normal plasma does **not** correct it (unlike vWD). In Glanzmann, Ristocetin aggregation is **normal**, but aggregation with ADP, collagen, and epinephrine is defective. * **Giant Platelets Differential:** Think of BSS, May-Hegglin anomaly, and Bernard-Soulier Syndrome. * **Mnemonic:** **B**ernard **S**oulier = **B**ig **S**ize (Giant platelets) and **B**elow count (Thrombocytopenia).
Question 663: A 60-year-old man is referred for evaluation of marked erythrocytosis and splenomegaly. Laboratory studies confirm an elevated red blood cell count and additionally demonstrate a moderate increase in circulating granulocytes and platelets. Oxygen saturation studies are normal, and isotopic studies reveal an increase in total red cell mass. Which of the following is characteristic of this disorder?
- A. Frequent association with thrombosis or hemorrhagic phenomena (Correct Answer)
- B. Increased erythropoietin concentration
- C. Manifestation of Cushing syndrome
- D. Most often secondary to hypoxia
Explanation: ### Explanation **Diagnosis: Polycythemia Vera (PV)** The clinical presentation of a 60-year-old man with **panmyelosis** (elevation of all three cell lines: RBCs, granulocytes, and platelets), **splenomegaly**, and an **increased red cell mass** with normal oxygen saturation is classic for Polycythemia Vera, a chronic myeloproliferative neoplasm [1]. **1. Why Option A is Correct:** In PV, the marked increase in red cell mass leads to **hyperviscosity**, while the increased and often dysfunctional platelets contribute to a prothrombotic state [1]. Paradoxically, very high platelet counts (>1.5 million) can lead to acquired von Willebrand syndrome, causing **hemorrhagic phenomena**. Thrombosis (e.g., Budd-Chiari syndrome, stroke, or MI) is a leading cause of morbidity and mortality in these patients [1]. **2. Why Other Options are Incorrect:** * **Option B:** In PV, erythropoietin (EPO) levels are characteristically **low or suppressed** because the erythropoiesis is autonomous (driven by the *JAK2* mutation) and independent of EPO stimulation. * **Option C:** Cushing syndrome is associated with secondary polycythemia due to cortisol-induced stimulation of the bone marrow, but it does not typically present with splenomegaly or panmyelosis. * **Option D:** Hypoxia causes **secondary polycythemia** [1]. In this patient, the normal oxygen saturation and the presence of thrombocytosis/leukocytosis rule out hypoxia as the primary driver. **Clinical Pearls for NEET-PG:** * **Molecular Marker:** >95% of PV cases are associated with the **JAK2 V617F mutation** [1]. * **Classic Symptom:** **Aquagenic pruritus** (itching after a warm bath) is highly suggestive of PV [1]. * **Treatment:** The goal is to maintain **Hematocrit <45%** through phlebotomy and/or cytoreductive therapy (e.g., Hydroxyurea). * **Complication:** PV can transform into Myelofibrosis or Acute Myeloid Leukemia (AML).
Question 664: All are true regarding Anaemia of Chronic Diseases, except?
- A. Decreased serum iron
- B. Decreased ferritin (Correct Answer)
- C. Decreased total iron-binding capacity
- D. Increased bone marrow iron
Explanation: **Explanation:** Anemia of Chronic Disease (ACD), also known as Anemia of Inflammation, is primarily mediated by **Hepcidin**, an acute-phase reactant produced by the liver in response to inflammatory cytokines (mainly IL-6) [1]. **Why Option B is the Correct Answer (The False Statement):** In ACD, serum **ferritin is increased or normal**, never decreased. Ferritin acts as an acute-phase reactant; inflammation triggers its synthesis and traps iron within the reticuloendothelial system (macrophages). A **decreased ferritin** is the hallmark and most sensitive indicator of **Iron Deficiency Anemia (IDA)**, not ACD [2]. **Analysis of Incorrect Options (True Statements for ACD):** * **A. Decreased serum iron:** Hepcidin degrades ferroportin channels, preventing iron release from macrophages and absorption from the gut [1]. This leads to low circulating iron (hypoferremia). * **C. Decreased TIBC:** In states of chronic inflammation, the body downregulates transferrin production (the protein measured by TIBC) to limit iron availability to potential pathogens. * **D. Increased bone marrow iron:** Because iron is "trapped" inside macrophages and cannot be utilized for erythropoiesis, bone marrow biopsy with Prussian blue staining shows abundant iron stores [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Transferrin Saturation:** Usually low or normal in ACD (but higher than in IDA). * **Soluble Transferrin Receptor (sTfR):** Normal in ACD, but **increased in IDA**. This is a key differentiator [2]. * **Morphology:** Usually Normocytic Normochromic, but can become Microcytic Hypochromic in long-standing cases [1]. * **Treatment:** Treat the underlying inflammatory condition; Erythropoietin (EPO) may be used in specific cases (e.g., CKD or malignancy) [1].
Question 665: Fresh Frozen Plasma (FFP) is not indicated in which of the following conditions?
- A. Thrombotic Thrombocytopenic Purpura (TTP)
- B. Factor XII deficiency (Correct Answer)
- C. Vitamin K deficiency
- D. Antithrombin III deficiency
Explanation: The correct answer is **Factor XII deficiency (Hageman factor deficiency)**. **1. Why Factor XII deficiency is the correct answer:** Factor XII deficiency is a unique hematological condition characterized by a **markedly prolonged Activated Partial Thromboplastin Time (aPTT)** in vitro, but **no clinical bleeding tendency** in vivo [2]. Since patients do not suffer from hemorrhagic complications (and may actually be at a slightly increased risk for thrombosis), there is no clinical indication for the administration of FFP or replacement therapy, even before major surgery. **2. Analysis of Incorrect Options:** * **Thrombotic Thrombocytopenic Purpura (TTP):** FFP is a mainstay of treatment. It is used during **plasmapheresis** (plasma exchange) to replace the deficient **ADAMTS13** enzyme, which is essential for cleaving large von Willebrand factor multimers. * **Vitamin K Deficiency:** FFP is indicated for the **urgent reversal** of coagulopathy (deficiency of Factors II, VII, IX, and X) when there is active bleeding or a need for emergency surgery, as Vitamin K administration takes 6–24 hours to be effective [1]. * **Antithrombin III (AT-III) Deficiency:** FFP contains AT-III. It is indicated in patients with hereditary AT-III deficiency who are undergoing high-risk procedures or are resistant to heparin therapy (since heparin requires AT-III to function). **Clinical Pearls for NEET-PG:** * **FFP Dosage:** Usually 10–15 mL/kg; it raises clotting factor levels by approximately 20-30%. * **Factor XII Paradox:** Prolonged aPTT + No bleeding = Factor XII deficiency [2]. * **Storage:** FFP is stored at -18°C or colder and must be used within 24 hours of thawing to ensure adequate levels of labile factors (V and VIII) [1].
Question 666: A patient has normal prothrombin time (PT) and platelet count with increased activated partial thromboplastin time (aPTT), factor 8 levels given as 60 IU/ml, and no history of bleeding. What is the diagnosis?
- A. Factor IX deficiency (Correct Answer)
- B. Thalassemia
- C. Factor VIII inhibitors
- D. Lupus anticoagulant
Explanation: The clinical presentation of a **normal PT**, **normal platelet count**, and **isolated prolonged aPTT** indicates a defect in the **intrinsic pathway** of the coagulation cascade (Factors XII, XI, IX, or VIII) [1]. 1. **Why Factor IX Deficiency is correct:** Factor IX is a key component of the intrinsic pathway. Its deficiency (Hemophilia B) leads to a prolonged aPTT while PT and bleeding time remain normal [2]. The question specifies **Factor VIII levels are normal (60 IU/ml)**, which effectively rules out Hemophilia A or von Willebrand Disease [3], making Factor IX deficiency the most logical diagnosis among the options. *Note: While severe Hemophilia B usually presents with bleeding, mild cases may be asymptomatic until surgical challenge.* 2. **Why other options are incorrect:** * **Thalassemia:** This is a quantitative hemoglobinopathy leading to microcytic hypochromic anemia; it does not affect the coagulation cascade or aPTT. * **Factor VIII Inhibitors:** These are acquired antibodies against Factor VIII. While they prolong aPTT, the **Factor VIII levels would be significantly low**, not normal (60 IU/ml). * **Lupus Anticoagulant (LA):** While LA prolongs aPTT in vitro and typically presents without bleeding, it is an antiphospholipid antibody associated with **thrombosis**, not a factor deficiency. Given the specific mention of Factor VIII levels, the question directs focus toward the intrinsic factor hierarchy. **High-Yield Clinical Pearls for NEET-PG:** * **Isolated prolonged aPTT:** Think Factors VIII, IX, XI, XII, or Lupus Anticoagulant [1]. * **Isolated prolonged PT:** Think Factor VII deficiency (Extrinsic pathway) [1]. * **Mixing Study:** If aPTT corrects with normal plasma, it’s a **factor deficiency**; if it does not correct, it’s a **factor inhibitor** (like Lupus Anticoagulant) [1]. * **Factor XII Deficiency:** Characterized by a very high aPTT but **no clinical bleeding** tendency.
Question 667: All the following are true in Immune thrombocytopenic Purpura (ITP) EXCEPT?
- A. Chronic ITP commonly occurs in adult women.
- B. Associated with prolonged bleeding time. (Correct Answer)
- C. Prothrombin Time (PT) and Partial Thromboplastin Time (PTT) are normal.
- D. Increased megakaryocytes in bone marrow.
Explanation: ### Explanation **Immune Thrombocytopenic Purpura (ITP)** is an acquired autoimmune disorder characterized by isolated thrombocytopenia due to the production of IgG autoantibodies against platelet surface antigens (like GPIIb/IIIa) [1]. #### Why Option B is the Correct Answer (The "Except" Statement) In the context of standard hematology examinations like NEET-PG, **Bleeding Time (BT)** is a test of platelet function and number. While BT is technically prolonged in severe thrombocytopenia, it is **not** a diagnostic or recommended test for ITP. The diagnosis of ITP is one of exclusion. Furthermore, in ITP, the circulating platelets are often "young" (megathrombocytes) and functionally superior, meaning patients may not bleed as much as their low count suggests [2]. Most importantly, in modern clinical practice, BT is considered unreliable and is rarely used to characterize ITP. #### Analysis of Other Options * **A. Chronic ITP in adult women:** True. While acute ITP is common in children (post-viral), the chronic form predominantly affects adults, with a female-to-male ratio of approximately 3:1. * **C. Normal PT and PTT:** True. ITP is a disorder of primary hemostasis (platelets) [2]. Secondary hemostasis (clotting factors) remains intact; therefore, the Prothrombin Time and Partial Thromboplastin Time are characteristically normal. * **D. Increased megakaryocytes:** True. The bone marrow responds to peripheral platelet destruction by increasing the number of megakaryocytes (compensatory hyperplasia). #### High-Yield Clinical Pearls for NEET-PG * **First-line Treatment:** Corticosteroids (Prednisolone) or IVIG. * **Splenectomy:** Indicated in refractory cases; the spleen is the primary site of both antibody production and platelet destruction. * **Peripheral Smear:** Shows isolated thrombocytopenia with large platelets (megathrombocytes); no schistocytes (unlike TTP/HUS). * **Key Association:** Always rule out secondary causes like HIV, HCV, and SLE [1].
Question 668: A 35-year-old female presents with cervical and axillary lymphadenopathy. She has a history of fever and drenching night sweats and is diagnosed with Hodgkin's lymphoma. What is the stage of the disease?
- A. II-A
- B. II-B (Correct Answer)
- C. IIE-A
- D. IIE-B
Explanation: ### Explanation The staging of Hodgkin’s Lymphoma (HL) is determined using the **Ann Arbor Staging System** (modified by the Cotswolds criteria) [1]. **1. Why Option B (II-B) is correct:** * **Stage II:** The patient has involvement of two or more lymph node regions (cervical and axillary) on the **same side of the diaphragm** (both are above the diaphragm) [1]. * **Modifier "B":** The presence of systemic symptoms—specifically unexplained fever (>38°C), drenching night sweats, or weight loss (>10% body weight in 6 months)—designates the "B" category [1], [2]. Since this patient has fever and night sweats, she is classified as Stage II-B. **2. Why other options are incorrect:** * **Option A (II-A):** The modifier "A" denotes the **absence** of constitutional (B) symptoms [1]. This patient clearly exhibits B symptoms. * **Options C & D (IIE):** The modifier "E" is used for **extranodal** involvement (e.g., localized involvement of an extralymphatic organ like the lung or liver) adjacent to a known nodal site. This patient’s involvement is limited to lymph nodes only. **3. High-Yield Clinical Pearls for NEET-PG:** * **Stage I:** Single lymph node region or single extralymphatic site. * **Stage III:** Lymph node involvement on **both sides** of the diaphragm. * **Stage IV:** Diffuse or disseminated involvement of one or more extralymphatic organs (e.g., bone marrow, liver). * **Bulky Disease:** Defined as a nodal mass >10 cm or >1/3rd of the transthoracic diameter on CXR [1]. * **Most Common Subtype:** Nodular Sclerosis (often presents with mediastinal mass in young females). * **Best Prognosis:** Lymphocyte Predominant. * **Worst Prognosis:** Lymphocyte Depleted.
Question 669: Intracorpuscular hemolytic anemia is seen in which of the following conditions?
- A. Autoimmune hemolytic anemia
- B. Thrombotic thrombocytopenic purpura
- C. Thalassemia (Correct Answer)
- D. Infection
Explanation: Hemolytic anemias are broadly classified based on the site of the defect into **Intracorpuscular (Intrinsic)** and **Extracorpuscular (Extrinsic)** causes. **Why Thalassemia is Correct:** Thalassemia is an **intracorpuscular** hemolytic anemia [1]. The defect lies within the red blood cell (RBC) itself—specifically, a genetic mutation leading to the reduced synthesis of globin chains ($\alpha$ or $\beta$) [1]. This imbalance causes the precipitation of unpaired globin chains, leading to membrane damage, ineffective erythropoiesis, and premature destruction of RBCs by the spleen. Other examples of intracorpuscular defects include membrane defects (Hereditary Spherocytosis) [3], enzyme deficiencies (G6PD deficiency) [1], and hemoglobinopathies (Sickle Cell Anemia) [1]. **Analysis of Incorrect Options:** * **A. Autoimmune Hemolytic Anemia (AIHA):** This is an **extracorpuscular** cause where the RBC is structurally normal, but external factors (antibodies) tag the cell for destruction [2]. * **B. Thrombotic Thrombocytopenic Purpura (TTP):** This is an **extracorpuscular** microangiopathic hemolytic anemia (MAHA). RBCs are fragmented (schistocytes) as they pass through small vessels obstructed by fibrin/platelet thrombi. * **D. Infection:** Infections (e.g., Malaria, Clostridium welchii) cause **extracorpuscular** hemolysis through direct parasite invasion or toxin-mediated damage to the RBC membrane [2]. **NEET-PG High-Yield Pearls:** * **Rule of Thumb:** Almost all intracorpuscular defects are **hereditary** [1], with one notable exception: **Paroxysmal Nocturnal Hemoglobinuria (PNH)**, which is an acquired intracorpuscular defect [2]. * **Extracorpuscular** causes are typically **acquired** (Immune, Mechanical, or Infectious). * **Coombs Test:** Usually positive in immune-mediated extracorpuscular hemolysis (AIHA) and negative in intracorpuscular defects like Thalassemia.
Question 670: What is the best prognostic indicator of multiple myeloma at the time of diagnosis?
- A. Number of myeloma cells in the marrow
- B. Beta 2 microglobulin (Correct Answer)
- C. Alkaline phosphatase level
- D. Hypercalcemia
Explanation: The prognosis of Multiple Myeloma (MM) is currently determined by the **International Staging System (ISS)**, which identifies **Serum Beta-2 Microglobulin (β2M)** as the single most important prognostic marker [1]. 1. **Why Beta-2 Microglobulin is correct:** β2M is a component of the MHC Class I molecule found on the surface of nucleated cells. In MM, its levels reflect the **total tumor burden** and the **severity of renal impairment**. Higher levels correlate with a larger mass of plasma cells and poorer survival outcomes [1]. It is the cornerstone of both the ISS and the Revised-ISS (R-ISS) staging systems. [1] 2. **Why other options are incorrect:** * **Number of myeloma cells (A):** While the percentage of plasma cells in the bone marrow is used for *diagnosis* (e.g., >10% for MM), it does not correlate as accurately with survival or prognosis as biochemical markers like β2M. [1] * **Alkaline Phosphatase (C):** In MM, bone lesions are purely **osteolytic** (mediated by osteoclasts). Because there is no osteoblastic activity, the ALP level is typically **normal**. An elevated ALP in a suspected MM patient should prompt a search for an alternative diagnosis or a fracture. * **Hypercalcemia (D):** While hypercalcemia is a "CRAB" feature indicating end-organ damage, it is a reversible complication and not as reliable a predictor of long-term survival as β2M. **High-Yield Clinical Pearls for NEET-PG:** * **ISS Staging:** Stage I (β2M <3.5 mg/L + Albumin ≥3.5 g/dL); Stage III (β2M ≥5.5 mg/L). [1] * **R-ISS:** Adds **LDH levels** and **High-risk Cytogenetics** [t(4;14), t(14;16), or del(17p)] to the standard ISS for even more precise prognosis. * **Serum Albumin:** Low albumin is also a poor prognostic sign in MM (reflecting IL-6 mediated suppression). [1]
Practice by Chapter
Anemia Evaluation and Management
Practice Questions
Hemoglobinopathies
Practice Questions
Thalassemias
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Platelet Disorders
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Coagulation Disorders
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Thrombotic Disorders
Practice Questions
Leukemias
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Lymphomas
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Multiple Myeloma and Plasma Cell Disorders
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Myeloproliferative Neoplasms
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Transfusion Medicine
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Hematopoietic Stem Cell Transplantation
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