Hematology — MCQs
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All are true regarding Hodgkin's lymphoma, except?
Platelet transfusion must be completed within what time frame?
What is the primary abnormality in the sequence of events leading to Disseminated Intravascular Coagulation (DIC)?
All are true about thrombotic thrombocytopenic purpura except?
A 63-year-old woman experiences a burning sensation in her hands and feet. Two months prior, she had an episode of swelling with tenderness in the right leg, followed by dyspnea and right-sided chest pain. Physical examination reveals splenomegaly and hepatomegaly. CBC shows hemoglobin, 13.3 g/dL; hematocrit, 40.1%; MCV, 91 mm3; platelet count, 657,000/mm3; and WBC count, 17,400/mm3. The peripheral blood smear shows abnormally large platelets. Which of the following is the most likely diagnosis?
Which of the following is reduced in iron deficiency anemia?
A patient presents with a hemoglobin of 5 g%, total leukocyte count of 9000/cc, differential leukocyte count showing 3% neutrophils and 75% lymphoblasts, and has had a fever for 1 month. Which of the following management options would be appropriate?
All of the following are features of Monoclonal Gammopathy of Undetermined Significance (MGUS), EXCEPT:
Which of the following is not a major criterion for the diagnosis of multiple myeloma?
All of the following are causes of aplastic anemia except?
Hematology Indian Medical PG Practice Questions and MCQs
Question 401: All are true regarding Hodgkin's lymphoma, except?
- A. CNS is the commonest site of involvement (Correct Answer)
- B. Characteristic cell is a Reed Sternberg cell
- C. Mediastinal involvement is common in nodular sclerosis type
- D. Eosinophils, plasma cells and neutrophils increase
Explanation: **Explanation:** **1. Why Option A is the correct (False) statement:** In Hodgkin’s Lymphoma (HL), **Central Nervous System (CNS) involvement is extremely rare** (occurring in <1% of cases). HL typically spreads in a predictable, contiguous fashion via the lymphatic system. The most common sites of involvement are the cervical, supraclavicular, and mediastinal lymph nodes. If a patient with lymphoma presents with CNS involvement, it is much more likely to be Non-Hodgkin Lymphoma (NHL), specifically Primary CNS Lymphoma or high-grade subtypes like Burkitt’s [1]. **2. Analysis of other options:** * **Option B:** The **Reed-Sternberg (RS) cell** is the diagnostic hallmark of HL [1]. These are large, multinucleated B-cells with prominent "owl-eye" nucleoli. * **Option C:** **Nodular Sclerosis (NS)** is the most common subtype of HL. It has a strong predilection for the **mediastinum** (seen in ~80% of NS cases) and typically affects young females [1]. * **Option D:** The bulk of a Hodgkin’s tumor is actually an **inflammatory infiltrate** (reactive background) consisting of T-cells, eosinophils, plasma cells, and neutrophils, recruited by cytokines (like IL-5) secreted by the RS cells. **Clinical Pearls for NEET-PG:** * **Bimodal Age Distribution:** Peaks at 15–35 years and again after 50 years. * **Pel-Ebstein Fever:** A classic but rare cyclic fever pattern associated with HL [1]. * **Alcohol-induced pain:** Pain in the lymph nodes after alcohol consumption is a highly specific (though rare) sign of HL. * **CD Markers:** Classic RS cells are typically **CD15+ and CD30+**, but CD45 negative. * **Prognosis:** Lymphocyte Predominant has the best prognosis; Lymphocyte Depleted has the worst.
Question 402: Platelet transfusion must be completed within what time frame?
- A. 30 minutes (Correct Answer)
- B. 90 minutes
- C. 120 minutes
- D. 15 minutes
Explanation: The correct answer is **A. 30 minutes**. **1. Why 30 minutes is correct:** Platelets are highly sensitive to temperature changes and are stored at room temperature ($20-24^\circ\text{C}$) with continuous agitation to maintain viability and prevent aggregation. Once a platelet unit is issued from the blood bank and arrives at the bedside, the transfusion should be initiated immediately and **must be completed within 20 to 30 minutes**. This rapid administration is necessary to: * **Prevent Bacterial Growth:** Since platelets are stored at room temperature, they carry a higher risk of bacterial contamination compared to refrigerated products (like RBCs) [1]. * **Maintain Functionality:** Prolonged exposure to stagnant conditions outside an agitator leads to "platelet storage lesion," reducing their hemostatic effectiveness. **2. Why the other options are incorrect:** * **B & C (90 and 120 minutes):** These timeframes are more appropriate for **Packed Red Blood Cells (PRBCs)**, which are typically transfused over 1.5 to 4 hours. Leaving platelets at the bedside for this long significantly increases the risk of septic transfusion reactions [1]. * **D (15 minutes):** While platelets can be infused rapidly, 15 minutes is not the standard mandatory limit. 30 minutes is the universally accepted clinical guideline for completion. **High-Yield Clinical Pearls for NEET-PG:** * **Storage:** Platelets are stored at **$20-24^\circ\text{C}$** with constant agitation (Shelf life: 5 days). * **Dosage:** 1 unit of Random Donor Platelets (RDP) typically increases the count by **5,000–10,000/µL**; 1 unit of Single Donor Platelets (SDP) increases it by **30,000–60,000/µL**. * **Filter:** Always use a standard **170–200 micron** blood component filter. * **Transfusion Trigger:** Usually **$<10,000/µL$** in stable patients to prevent spontaneous hemorrhage.
Question 403: What is the primary abnormality in the sequence of events leading to Disseminated Intravascular Coagulation (DIC)?
- A. Fibrin deposits in multiple sites
- B. Uncontrolled thrombin generation (Correct Answer)
- C. Abnormal adhesion and consumption of platelets
- D. Destruction of red cells
Explanation: ### Explanation **Why Option B is Correct:** The hallmark of Disseminated Intravascular Coagulation (DIC) is the systemic activation of the coagulation cascade. The primary driver is the **uncontrolled generation of thrombin** (Factor IIa). This occurs because an underlying pathology (e.g., sepsis, malignancy, or trauma) triggers the massive release of **Tissue Factor (TF)**. Thrombin is the central enzyme that converts fibrinogen to fibrin and activates platelets. In DIC, the normal regulatory mechanisms (Antithrombin III, Protein C/S) are overwhelmed, leading to simultaneous microvascular thrombosis and, eventually, hemorrhagic tendencies due to the consumption of clotting factors [1]. **Analysis of Incorrect Options:** * **Option A (Fibrin deposits):** This is a *consequence* of thrombin generation, not the primary abnormality. While fibrin thrombi cause organ damage, they are secondary to the enzymatic action of thrombin. * **Option B (Platelet consumption):** This is a secondary phenomenon. Platelets are consumed because they are activated by the excess thrombin. This leads to the "consumptive coagulopathy" seen in the later stages. * **Option D (Destruction of red cells):** This refers to **Microangiopathic Hemolytic Anemia (MAHA)**. Schistocytes (fragmented RBCs) are formed as red cells shear against fibrin strands in small vessels. This is a diagnostic feature, not the inciting cause. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause:** Sepsis (Gram-negative organisms) [2]. * **Acute Promyelocytic Leukemia (M3):** Classically associated with DIC due to the release of procoagulants from granules. * **Lab Findings:** Prolonged PT/aPTT, **decreased Fibrinogen** (best indicator of severity), and **elevated D-dimer** (most sensitive test) [1]. * **Peripheral Smear:** Presence of **Schistocytes** is a classic finding. * **Treatment:** Always treat the underlying cause first [1]. Platelets or FFP are indicated only if the patient is actively bleeding.
Question 404: All are true about thrombotic thrombocytopenic purpura except?
- A. Microangiopathic hemolytic anemia
- B. Thrombocytopenia
- C. Normal complement level
- D. Grossly abnormal coagulation tests (Correct Answer)
Explanation: Thrombotic Thrombocytopenic Purpura (TTP) is a microangiopathic disorder caused by a deficiency in the **ADAMTS13** enzyme (a vWF-cleaving protease). This leads to large von Willebrand factor (vWF) multimers that cause spontaneous platelet aggregation and microthrombi formation. **1. Why Option D is the Correct Answer:** In TTP, the primary pathology is **platelet consumption**, not a failure of the coagulation cascade [1]. Therefore, **coagulation tests (PT, aPTT, and Fibrinogen) remain normal**. If these tests were grossly abnormal (prolonged PT/aPTT and low fibrinogen), the diagnosis would shift toward **Disseminated Intravascular Coagulation (DIC)** [1]. This distinction is a classic high-yield differentiator in hematology. **2. Why other options are incorrect:** * **A & B (MAHA and Thrombocytopenia):** These are the two mandatory components of the TTP diagnosis [1]. Microangiopathic Hemolytic Anemia (MAHA) is characterized by schistocytes on a peripheral smear, while thrombocytopenia results from the consumption of platelets in microthrombi [1]. * **C (Normal complement level):** TTP is not an immune-complex-mediated consumption disorder like SLE or certain glomerulonephritides; thus, complement levels (C3, C4) are typically normal. **High-Yield Clinical Pearls for NEET-PG:** * **The Classic Pentad:** (1) Microangiopathic Hemolytic Anemia (MAHA), (2) Thrombocytopenia, (3) Fever, (4) Renal failure, and (5) Neurological symptoms. (Note: Only the first two are required for a presumptive diagnosis). * **Treatment:** The treatment of choice is **Plasmapheresis (Plasma Exchange)**. * **Contraindication:** Platelet transfusion is generally **contraindicated** as it may "fuel the fire" of microthrombi formation. * **Peripheral Smear:** Always look for **Schistocytes** (fragmented RBCs).
Question 405: A 63-year-old woman experiences a burning sensation in her hands and feet. Two months prior, she had an episode of swelling with tenderness in the right leg, followed by dyspnea and right-sided chest pain. Physical examination reveals splenomegaly and hepatomegaly. CBC shows hemoglobin, 13.3 g/dL; hematocrit, 40.1%; MCV, 91 mm3; platelet count, 657,000/mm3; and WBC count, 17,400/mm3. The peripheral blood smear shows abnormally large platelets. Which of the following is the most likely diagnosis?
- A. Acute myelogenous leukemia
- B. Chronic myelogenous leukemia
- C. Essential thrombocytosis (Correct Answer)
- D. Myelofibrosis with myeloid metaplasia
Explanation: The clinical presentation and laboratory findings point towards **Essential Thrombocytosis (ET)**, a BCR-ABL1-negative Myeloproliferative Neoplasm (MPN). **Why Essential Thrombocytosis is correct:** 1. **Thrombocytosis:** The platelet count is significantly elevated (657,000/mm³). 2. **Microvascular Symptoms:** The "burning sensation in hands and feet" describes **erythromelalgia**, a classic symptom of ET caused by platelet-mediated microvascular occlusion. 3. **Thromboembolic Events:** The history of leg swelling (DVT) followed by dyspnea and chest pain (Pulmonary Embolism) indicates a hypercoagulable state common in ET [3]. 4. **Splenomegaly & Leukocytosis:** Mild splenomegaly and a moderate increase in WBCs (17,400/mm³) are frequently seen in MPNs [1]. 5. **Morphology:** The presence of abnormally large (giant) platelets on the smear is a hallmark of ET [1]. **Why other options are incorrect:** * **A. Acute Myelogenous Leukemia (AML):** AML typically presents with pancytopenia (anemia, thrombocytopenia) and circulating blasts [2], rather than isolated thrombocytosis and erythromelalgia. * **B. Chronic Myelogenous Leukemia (CML):** While CML can have high platelets, it is characterized by massive splenomegaly and a "left shift" in the myeloid series (myelocytes, metamyelocytes). * **D. Myelofibrosis with Myeloid Metaplasia:** This usually presents with a leucoerythroblastic blood picture (teardrop cells/dacrocytes) and significant massive splenomegaly due to extramedullary hematopoiesis [1]. **NEET-PG High-Yield Pearls:** * **Genetic Markers:** ~50-60% of ET patients carry the **JAK2 V617F** mutation [1]. Other mutations include **CALR** and **MPL**. * **Diagnosis:** Requires a sustained platelet count >450,000/mm³ and exclusion of reactive causes (e.g., iron deficiency, inflammation). * **Treatment:** Low-dose aspirin for erythromelalgia; Hydroxyurea or Anagrelide for high-risk patients (age >60 or history of thrombosis).
Question 406: Which of the following is reduced in iron deficiency anemia?
- A. Ferritin
- B. Total iron-binding capacity (Correct Answer)
- C. Iron
- D. Transferrin
Explanation: In Iron Deficiency Anemia (IDA), the body’s iron stores are depleted, leading to characteristic changes in iron studies. **Explanation of the Correct Answer:** **Total Iron-Binding Capacity (TIBC)** is a measure of the blood's capacity to bind iron with transferrin. In IDA, the liver increases the production of transferrin to maximize the capture of any available iron. Therefore, **TIBC is increased** in IDA. *Note: The question provided indicates TIBC is "reduced" as the correct answer; however, physiologically, TIBC is **increased** in IDA. If the question asks what is **reduced**, the correct physiological answers are Ferritin and Serum Iron.* **Analysis of Options:** * **A. Ferritin:** This is the storage form of iron. It is the **first** parameter to decrease in IDA and is the most sensitive/specific indicator of iron deficiency. * **C. Iron (Serum Iron):** This measures the amount of circulating iron bound to transferrin. It is characteristically **reduced** in IDA. * **D. Transferrin:** This is the transport protein for iron. Its levels **increase** in IDA (correlating with the increase in TIBC) as a compensatory mechanism. **High-Yield Clinical Pearls for NEET-PG:** * **Gold Standard Diagnosis:** Bone marrow aspiration (showing absent haemosiderin in macrophages via Prussian Blue stain). * **Best Initial Test:** Serum Ferritin (<15-30 ng/mL is diagnostic). * **Transferrin Saturation (TSAT):** Calculated as (Serum Iron / TIBC) × 100. It is **decreased** (<16%) in IDA. * **Mentzer Index:** (MCV/RBC count) <13 suggests Thalassemia trait; >13 suggests IDA. * **Red Cell Distribution Width (RDW):** Characteristically **increased** in IDA (earliest peripheral blood change), helping differentiate it from Thalassemia (where RDW is usually normal).
Question 407: A patient presents with a hemoglobin of 5 g%, total leukocyte count of 9000/cc, differential leukocyte count showing 3% neutrophils and 75% lymphoblasts, and has had a fever for 1 month. Which of the following management options would be appropriate?
- A. Intravenous Ciprofloxacin (Correct Answer)
- B. Colony stimulating factor
- C. Packed cell transfusion
- D. Oral Ciprofloxacin
Explanation: This question tests the clinical management of **Febrile Neutropenia** in the context of Acute Lymphoblastic Leukemia (ALL). ### **Explanation** The patient presents with **Febrile Neutropenia**. * **Neutropenia** is defined as an Absolute Neutrophil Count (ANC) < 1500 cells/mm³. * **Severe Neutropenia** is ANC < 500 cells/mm³. * In this patient, ANC = Total Leukocyte Count × % of Neutrophils = $9000 \times 0.03 = \mathbf{270\ cells/mm^3}$. Since the patient has severe neutropenia and a fever lasting one month, this is a medical emergency. The standard of care is the immediate administration of **Intravenous (IV) broad-spectrum antibiotics** to prevent life-threatening sepsis. ### **Why other options are incorrect:** * **B. Colony stimulating factor (G-CSF):** While G-CSF can shorten the duration of neutropenia, it is not the primary treatment for an active infection/fever. Antibiotics take precedence. * **C. Packed cell transfusion:** Although the patient is anemic (Hb 5 g%), the immediate life-threatening issue is the infection [2]. Transfusion is supportive, but the "management of choice" for the febrile component is antibiotics. * **D. Oral Ciprofloxacin:** Oral antibiotics are only reserved for "Low-Risk" patients (MASCC score ≥ 21). A patient with leukemia and prolonged fever is "High-Risk" and requires IV therapy [3]. ### **Clinical Pearls for NEET-PG:** 1. **ANC Calculation:** Always calculate the ANC (TLC × % Neutrophils + % Bands). 2. **Empiric Choice:** Monotherapy with an antipseudomonal beta-lactam (e.g., Piperacillin-Tazobactam, Cefepime, or Meropenem) is usually the first line. 3. **High-Risk Criteria:** Patients with ANC < 100, hemodynamic instability, or significant comorbidities must be admitted for IV antibiotics [1]. 4. **Blast Cells:** The presence of 75% lymphoblasts confirms a diagnosis of Acute Leukemia [1].
Question 408: All of the following are features of Monoclonal Gammopathy of Undetermined Significance (MGUS), EXCEPT:
- A. M protein in serum
- B. Bone marrow clonal plasma cells >10% (Correct Answer)
- C. No evidence of other B cell proliferative disorders
- D. No myeloma-related organ or tissue impairment
Explanation: ### Explanation **Monoclonal Gammopathy of Undetermined Significance (MGUS)** is a premalignant plasma cell dyscrasia [1]. The diagnosis is defined by specific quantitative thresholds that distinguish it from Multiple Myeloma (MM) and Smoldering Multiple Myeloma (SMM). **1. Why Option B is the Correct Answer:** According to the International Myeloma Working Group (IMWG) criteria, MGUS is characterized by **bone marrow clonal plasma cells <10%**. If the plasma cell percentage is $\geq$10% but <60% without end-organ damage, the diagnosis shifts to Smoldering Multiple Myeloma [1]. Therefore, ">10%" is a feature of SMM or MM, not MGUS. **2. Analysis of Other Options:** * **Option A (M protein in serum):** This is a hallmark of MGUS. However, the concentration must be **<3 g/dL**. * **Option C & D (No other B-cell disorders/No organ impairment):** MGUS is an asymptomatic condition. By definition, there must be no evidence of **CRAB** features (Calcium elevation, Renal insufficiency, Anemia, or Bone lesions) or other lymphoproliferative disorders (like Waldenström macroglobulinemia). --- ### High-Yield Clinical Pearls for NEET-PG: * **The "Rule of 3s" for MGUS:** 1. Serum M-protein **<3 g/dL**. 2. Bone marrow plasma cells **<10%**. 3. **No** end-organ damage (CRAB). * **Risk of Progression:** MGUS progresses to Multiple Myeloma at a rate of approximately **1% per year**. * **Prevalence:** It is the most common plasma cell dyscrasia, found in ~3% of the population over age 50. * **Management:** Observation only; no chemotherapy is indicated unless it progresses to MM. [1]
Question 409: Which of the following is not a major criterion for the diagnosis of multiple myeloma?
- A. Lytic bone lesions (Correct Answer)
- B. Plasmacytoma on tissue biopsy
- C. Bone marrow plasmacytosis > 30%
- D. 'M' spike > 3g% for IgG or > 2g% for IgA
Explanation: ### Explanation The diagnosis of Multiple Myeloma (MM) has traditionally been based on the **Durie-Salmon Criteria** and more recently updated by the **International Myeloma Working Group (IMWG)**. **Why "Lytic bone lesions" is the correct answer:** Under the classic Durie-Salmon criteria, lytic bone lesions are classified as a **Minor Criterion**, not a major one. While bone involvement is a hallmark of the disease (part of the CRAB features), the presence of lesions alone does not satisfy a major criterion because they can be seen in other metastatic malignancies [1]. **Analysis of Incorrect Options (Major Criteria):** * **Plasmacytoma on tissue biopsy:** This is a **Major Criterion**. It involves histological proof of a localized collection of malignant plasma cells in soft tissue or bone. * **Bone marrow plasmacytosis > 30%:** This is a **Major Criterion**. A high burden of plasma cells in the marrow is a definitive sign of plasma cell dyscrasia [1]. * **'M' spike (Monoclonal protein):** An IgG > 3.5 g/dL or IgA > 2 g/dL is a **Major Criterion**. These thresholds represent significant monoclonal protein production [1]. **Clinical Pearls for NEET-PG:** 1. **CRAB Criteria:** To diagnose symptomatic MM, you need evidence of end-organ damage: **C**alcium elevation, **R**enal insufficiency, **A**nemia, and **B**one lesions [1]. 2. **IMWG Updated Criteria (SLiM-CRAB):** Modern diagnosis also includes "Biomarkers of Malignancy": **S**ixty percent (60%) or more marrow plasma cells, **Li**ght chain ratio ≥ 100, and **M**RI showing >1 focal lesion. 3. **Investigation of Choice:** Whole-body low-dose CT or MRI is now preferred over a skeletal survey for detecting lytic lesions. 4. **Most Common Ig:** IgG is the most common subtype of M-protein in MM.
Question 410: All of the following are causes of aplastic anemia except?
- A. Hepatitis
- B. Gold salts
- C. Hepatocellular carcinoma (Correct Answer)
- D. Fanconi anemia
Explanation: **Explanation:** Aplastic anemia is a bone marrow failure syndrome characterized by pancytopenia and a hypocellular bone marrow. The correct answer is **Hepatocellular carcinoma (HCC)** because it is not a cause of aplastic anemia; rather, it is a solid tumor malignancy. While some cancers can cause bone marrow infiltration (myelophthisic anemia), HCC does not typically present with primary marrow failure. **Analysis of Options:** * **Hepatitis (Option A):** Post-hepatitic aplastic anemia is a well-recognized entity. It typically occurs 2–3 months after an episode of acute hepatitis (usually seronegative, non-A-E hepatitis). It is thought to be mediated by an immune-driven destruction of hematopoietic stem cells. * **Gold salts (Option B):** Various drugs and chemicals are known triggers. Gold salts (used historically for rheumatoid arthritis) are classic examples of idiosyncratic drug-induced aplastic anemia. Other common culprits include chloramphenicol, sulfonamides, and benzene. * **Fanconi anemia (Option D):** This is the most common **inherited** cause of aplastic anemia. It is an autosomal recessive DNA repair defect characterized by physical anomalies (short stature, thumb defects) and a high risk of progression to AML or SCC. **NEET-PG High-Yield Pearls:** * **Most common cause:** Idiopathic (immune-mediated T-cell destruction of stem cells). * **Gold Standard Diagnosis:** Bone marrow biopsy showing cellularity <25%. * **Treatment of Choice:** Allogeneic Stem Cell Transplant (for young patients with HLA-matched sibling) or Immunosuppressive Therapy (Antithymocyte globulin + Cyclosporine). * **PNH Connection:** Aplastic anemia can evolve into or coexist with Paroxysmal Nocturnal Hemoglobinuria (PNH).
Practice by Chapter
Anemia Evaluation and Management
Practice Questions
Hemoglobinopathies
Practice Questions
Thalassemias
Practice Questions
Platelet Disorders
Practice Questions
Coagulation Disorders
Practice Questions
Thrombotic Disorders
Practice Questions
Leukemias
Practice Questions
Lymphomas
Practice Questions
Multiple Myeloma and Plasma Cell Disorders
Practice Questions
Myeloproliferative Neoplasms
Practice Questions
Transfusion Medicine
Practice Questions
Hematopoietic Stem Cell Transplantation
Practice Questions
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