Hematology — MCQs

A 65-year-old patient presented with weakness, fatigue for 6 months, and mild abdominal discomfort. Examination revealed moderate splenomegaly. Lab findings showed severe normocytic normochromic anemia, neutropenia with monocytopenia, and thrombocytopenia. Bone marrow aspiration resulted in a 'dry' tap. A bone marrow biopsy was performed. Which of the following CD markers can be positive in this condition EXCEPT?

Hematology Indian Medical PG Practice Questions and MCQs

Question 621: Following blood transfusion, non-cardiogenic pulmonary edema may sometimes occur because of?

A. RBC incompatibility
B. Antigen-antibody mechanism involving human leukocyte antigen (Correct Answer)
C. Platelet surface antigen reaction
D. Antibody to IgA in donor plasma

Explanation: ### Explanation The clinical scenario described is **TRALI (Transfusion-Related Acute Lung Injury)**, which is the leading cause of transfusion-related fatalities. It is defined as new-onset non-cardiogenic pulmonary edema occurring within 6 hours of transfusion. **Why Option B is Correct:** The primary mechanism of TRALI involves the **"Two-Hit Hypothesis."** The "second hit" (and most common trigger) is the infusion of **donor antibodies** (usually IgG) directed against the recipient’s **Human Leukocyte Antigens (HLA)** or Neutrophil-Specific Antigens (HNA). These antibodies activate recipient neutrophils sequestered in the pulmonary microvasculature, leading to endothelial damage, capillary leak, and alveolar edema. **Analysis of Incorrect Options:** * **Option A (RBC Incompatibility):** This typically causes Acute Hemolytic Transfusion Reactions (AHTR), characterized by fever, chills, hypotension, and hemoglobinuria, rather than isolated pulmonary edema [1]. * **Option C (Platelet surface antigen reaction):** While platelet-specific antibodies can cause Post-Transfusion Purpura (PTP), they are not the primary drivers of the massive pulmonary inflammatory response seen in TRALI. * **Option D (Antibody to IgA):** This is the mechanism behind **Anaphylactic reactions**. It occurs in IgA-deficient recipients who have pre-formed anti-IgA antibodies. It presents with wheezing and shock, but not typically with non-cardiogenic pulmonary edema. **NEET-PG High-Yield Pearls:** * **Most common source:** Multiparous women (due to sensitization to fetal HLA during pregnancy). This is why many centers prefer male-only plasma. * **Clinical Hallmark:** Sudden respiratory distress, hypoxia, and "white-out" on CXR with **normal PCWP** (distinguishes it from TACO - Transfusion Associated Circulatory Overload). * **Management:** Immediate cessation of transfusion and aggressive **supportive care** (oxygen/ventilation). Diuretics are generally avoided as the patient is often intravascularly depleted [1].

Question 622: A 25-year-old pregnant lady presents with leukocytosis, a platelet count less than 50,000, and fragmented red blood cells on peripheral smear. Which of the following is the least likely differential diagnosis?

A. Disseminated Intravascular Coagulation (DIC)
B. Thrombotic Thrombocytopenic Purpura (TTP)
C. HELLP syndrome
D. Evans' syndrome (Correct Answer)

Explanation: The clinical presentation describes a **Microangiopathic Hemolytic Anemia (MAHA)**, characterized by thrombocytopenia and fragmented RBCs (schistocytes) on a peripheral smear [1]. **1. Why Evans' Syndrome is the least likely (Correct Answer):** Evans' syndrome is defined as the simultaneous or sequential occurrence of **Immune Thrombocytopenic Purpura (ITP)** and **Autoimmune Hemolytic Anemia (AIHA)**. Crucially, AIHA is a warm-antibody mediated process where RBCs are destroyed by splenic macrophages, leading to **spherocytes**, not schistocytes. The absence of mechanical fragmentation (schistocytes) makes Evans' syndrome inconsistent with the peripheral smear findings provided. **2. Analysis of Incorrect Options:** * **HELLP Syndrome:** A pregnancy-specific complication (Hemolysis, Elevated Liver enzymes, Low Platelets) that is a classic cause of MAHA and schistocytes in the third trimester [1]. * **TTP:** Characterized by the pentad of microangiopathic hemolytic anemia, thrombocytopenia, neurological symptoms, fever, and renal failure. It is a major differential for MAHA in pregnancy [1]. * **DIC:** Often triggered by obstetric complications (e.g., abruptio placentae) [2]. It involves systemic activation of coagulation, leading to consumption of platelets and clotting factors, resulting in schistocytes on the smear [2]. **Clinical Pearls for NEET-PG:** * **Schistocytes = MAHA:** Always think of TTP, HUS, DIC, or HELLP [1]. * **Spherocytes = AIHA or Hereditary Spherocytosis:** Think of Evans' syndrome if associated with low platelets. * **TTP vs. DIC:** TTP usually has normal coagulation profiles (PT/aPTT), whereas DIC has prolonged PT/aPTT and low fibrinogen [2]. * **HELLP vs. TTP:** HELLP is typically associated with hypertension and significant transaminitis.

Question 623: What is true about Multiple Myeloma?

A. Bence Jones protein in urine
B. Hypogammaglobulinemia
C. Amyloidosis
D. All of the above (Correct Answer)

Explanation: Multiple Myeloma (MM) is a neoplastic proliferation of a single clone of plasma cells derived from B cells, leading to the overproduction of monoclonal (M) proteins [1]. 1. **Bence Jones Protein (BJP):** In MM, there is often an excess production of monoclonal free light chains (kappa or lambda). These are small enough to be filtered by the glomerulus and appear in the urine as Bence Jones proteins [1]. They are unique because they precipitate at 40–60°C and redissolve at 100°C. 2. **Hypogammaglobulinemia:** While there is a massive increase in one specific monoclonal immunoglobulin (the M-spike), the production of normal, functional polyclonal immunoglobulins is suppressed [1]. This "secondary hypogammaglobulinemia" makes patients highly susceptible to recurrent bacterial infections (the leading cause of death). 3. **Amyloidosis:** In approximately 10–15% of cases, the excess light chains deposit in tissues as insoluble fibrils, leading to **AL (Primary) Amyloidosis**. This can manifest as macroglossia, nephrotic syndrome, or restrictive cardiomyopathy. **Clinical Pearls for NEET-PG:** * **CRAB Criteria:** Remember the hallmark features: **C**alcium elevation, **R**enal insufficiency, **A**nemia, and **B**one lesions (punched-out lytic lesions) [1]. * **Diagnosis:** Bone marrow biopsy showing **>10% clonal plasma cells** is the gold standard [1]. * **Blood Film:** Look for **Rouleaux formation** due to increased ESR [1]. * **Urine Dipstick:** Often **negative** for protein because dipsticks primarily detect albumin, not light chains (BJP). Sulfosalicylic acid (SSA) test is used to detect BJP.

Question 624: To prevent excessive bleeding during surgery, a patient with hemophilia A may be given which of the following?

A. Whole blood
B. Fresh frozen plasma
C. Factor VIII concentrate (Correct Answer)
D. Factor IX concentrate

Explanation: **Explanation:** **Hemophilia A** is an X-linked recessive bleeding disorder caused by a deficiency of **Clotting Factor VIII** [1]. To achieve surgical hemostasis, the goal is to raise Factor VIII levels to 80–100% of normal. **Why Factor VIII concentrate is correct:** Factor VIII concentrate (either plasma-derived or recombinant) is the **treatment of choice** [1]. It provides a highly concentrated dose of the specific missing factor without the risk of volume overload. Recombinant products are preferred in modern practice to eliminate the risk of blood-borne viral transmission (HIV, Hepatitis B/C) [2]. **Why the other options are incorrect:** * **Whole blood:** Contains very low concentrations of clotting factors relative to volume. It is used for massive hemorrhage with shock, not targeted factor replacement. * **Fresh frozen plasma (FFP):** While FFP contains all coagulation factors, the concentration of Factor VIII is low. Achieving therapeutic levels for surgery would require massive volumes, leading to **Transfusion Associated Circulatory Overload (TACO)**. * **Factor IX concentrate:** This is the specific treatment for **Hemophilia B** (Christmas Disease). It has no role in treating Hemophilia A. **High-Yield Clinical Pearls for NEET-PG:** * **Cryoprecipitate:** Contains Factor VIII, Fibrinogen, von Willebrand Factor (vWF), and Factor XIII. It was historically used for Hemophilia A but is now a second-line treatment if concentrates are unavailable. * **Desmopressin (DDAVP):** Useful in **mild** Hemophilia A; it releases endogenous Factor VIII and vWF from endothelial Weibel-Palade bodies [2]. * **Mixing Study:** In Hemophilia, the prolonged aPTT **corrects** upon mixing with normal plasma (distinguishing it from Factor VIII inhibitors/antibodies). * **Emicizumab:** A newer bispecific monoclonal antibody that mimics Factor VIII function by bridging Factors IXa and X.

Question 625: With iron treatment, by how much does hemoglobin increase per week?

A. 2 gm/week
B. 1 gm/week (Correct Answer)
C. 2 gm/month
D. 1 gm/month

Explanation: **Explanation:** In the management of Iron Deficiency Anemia (IDA), the response to iron therapy follows a predictable chronological sequence. After initiating oral or parenteral iron, the first hematological sign of improvement is a **reticulocytosis**, which typically peaks between **7 to 10 days**. This is followed by a steady rise in hemoglobin levels. [1] **1. Why Option B is Correct:** Under optimal conditions (adequate iron absorption and no ongoing blood loss), the expected rate of hemoglobin increase is approximately **0.7 to 1.0 g/dL per week**. Therefore, 1 gm/week is the standard clinical benchmark used to monitor the efficacy of treatment. A significant response is usually defined as a 2 g/dL increase within 3 weeks. **2. Why Other Options are Incorrect:** * **Option A (2 gm/week):** This is physiologically unrealistic. The bone marrow has a finite capacity for erythropoiesis, and a rise of 2 gm/week exceeds the maximum rate of red cell production even under intense stimulation. * **Options C & D (2 gm/month / 1 gm/month):** These rates are too slow. If a patient increases by only 1 gm in a month, the clinician must investigate "non-response," which could be due to poor compliance, malabsorption (e.g., Celiac disease), or ongoing occult blood loss. **High-Yield Clinical Pearls for NEET-PG:** * **First sign of recovery:** Subjective improvement in well-being (within 24–48 hours). * **First hematological sign:** Reticulocytosis (7–10 days). [1] * **Normalization of Hemoglobin:** Usually takes 6–8 weeks. * **Duration of therapy:** Iron should be continued for **3 to 6 months** after hemoglobin normalizes to replenish depleted **iron stores (Ferritin)**. [1] * **Oral Iron Absorption:** Best absorbed on an empty stomach; Vitamin C (Ascorbic acid) enhances absorption, while tea, calcium, and phytates inhibit it.

Question 626: Aplastic anemia can progress to all of the following except?

A. Acute myeloid leukemia (AML)
B. Myelodysplastic syndrome
C. Pure red cell aplasia (Correct Answer)
D. Paroxysmal nocturnal hemoglobinuria (PNH)

Explanation: Aplastic Anemia (AA) is a bone marrow failure syndrome characterized by pancytopenia and a hypocellular marrow. It is considered a "clonal" disorder of hematopoietic stem cells, which predisposes patients to late clonal evolution into other myeloid malignancies. **Why Pure Red Cell Aplasia (PRCA) is the correct answer:** PRCA is a condition characterized by a selective failure of erythropoiesis (only red cell precursors are absent), while white cells and platelets remain normal. It is **not** a complication or a progressive stage of Aplastic Anemia. In fact, the relationship is often the reverse: PRCA is a lineage-specific failure, whereas AA is a global stem cell failure. Progression from a global failure (AA) to a single-lineage failure (PRCA) does not occur. **Analysis of Incorrect Options:** * **Paroxysmal Nocturnal Hemoglobinuria (PNH):** There is a strong clinical link between AA and PNH. Up to 40-50% of AA patients may have a small PNH clone (PIGA mutation) at diagnosis, and many go on to develop clinical PNH. * **Myelodysplastic Syndrome (MDS) & Acute Myeloid Leukemia (AML):** These represent the "clonal evolution" of AA [1]. Approximately 10-15% of patients with AA (especially those treated with immunosuppressive therapy) may eventually develop MDS or AML, often associated with chromosomal abnormalities like Monosomy 7. **Clinical Pearls for NEET-PG:** * **Most common chromosomal abnormality** in clonal evolution of AA: **Monosomy 7**. * **Gold Standard Treatment:** Bone Marrow Transplant (for young patients with a matched sibling donor) or Immunosuppressive Therapy (ATG + Cyclosporine + Eltrombopag). * **PNH Screening:** All patients with Aplastic Anemia must be screened for PNH clones using **Flow Cytometry** (CD55/CD59 deficiency).

Question 627: What is the standard treatment for Central Nervous System (CNS) leukemia?

A. Intrathecal methotrexate (Correct Answer)
B. Vincristine and prednisolone
C. Intrathecal vincristine
D. Intravenous prednisolone

Explanation: **Explanation:** The Blood-Brain Barrier (BBB) prevents most systemic chemotherapeutic agents from reaching therapeutic concentrations within the cerebrospinal fluid (CSF) [3]. Therefore, standard intravenous therapy is often ineffective for treating or preventing CNS involvement in leukemia [1]. **1. Why Intrathecal Methotrexate is Correct:** **Intrathecal (IT) Methotrexate** is the gold standard because it bypasses the BBB, delivering high concentrations of the antimetabolite directly into the subarachnoid space. It is used both as **prophylaxis** (to prevent CNS relapse in ALL) and as **treatment** for active CNS leukemia [1]. It is often used alone or as part of "triple intrathecal therapy" (Methotrexate + Cytarabine + Hydrocortisone). **2. Why the other options are incorrect:** * **Vincristine and Prednisolone (Option B):** While these are backbone drugs for induction therapy in Acute Lymphoblastic Leukemia (ALL) [1], they are administered systemically and do not achieve sufficient CNS penetration to treat active CNS disease. * **Intrathecal Vincristine (Option C):** **CRITICAL CONTRAINDICATION.** Vincristine is highly neurotoxic if given intrathecally. Accidental IT administration leads to progressive ascending paralysis and is almost **universally fatal**. It must only be given intravenously. * **Intravenous Prednisolone (Option D):** While glucocorticoids (like Dexamethasone) have some CNS penetration [2], they are insufficient as monotherapy for CNS leukemia. **Clinical Pearls for NEET-PG:** * **Prophylaxis:** CNS prophylaxis is mandatory in all patients with ALL because the CNS acts as a "pharmacological sanctuary." * **Triple IT Therapy:** Consists of Methotrexate, Cytarabine (Ara-C), and Hydrocortisone. * **Fatal Error:** Always remember: *"Vincristine is for the Vein only."* * **Alternative:** Cranial irradiation is an alternative but is less preferred in children due to long-term neurocognitive sequelae.

Question 628: Multiple punched-out lesions on skull X-ray are found in which of the following conditions?

A. Down syndrome
B. Hyperparathyroidism
C. Multiple myeloma (Correct Answer)
D. All of the above

Explanation: ### Explanation **Correct Answer: C. Multiple Myeloma** **Underlying Medical Concept:** In Multiple Myeloma, malignant plasma cells in the bone marrow [1] secrete **Osteoclast Activating Factors (OAFs)**, such as IL-1 (Osteoclast Activating Factor), TNF-beta, and IL-6. These cytokines stimulate osteoclasts and inhibit osteoblasts, leading to purely **lytic bone destruction** without new bone formation. On a skull X-ray, this manifests as classic **"punched-out" lesions**—sharp, well-circumscribed lytic areas without a sclerotic rim [1][2]. **Analysis of Incorrect Options:** * **A. Down Syndrome:** While Down syndrome is associated with an increased risk of hematological malignancies (specifically ALL and AML/AMKL), it does not characteristically present with lytic bone lesions on X-ray. * **B. Hyperparathyroidism:** Primary hyperparathyroidism typically presents with **"Salt and Pepper" skull** (mottled appearance due to diffuse demineralization) rather than discrete punched-out lesions. It may also show "Brown tumors" (osteitis fibrosa cystica), but these are radiologically distinct from the lesions in myeloma. **High-Yield Clinical Pearls for NEET-PG:** * **CRAB Criteria:** Remember the hallmark features of Multiple Myeloma: **C**alcium elevation, **R**enal insufficiency, **A**nemia, and **B**one lesions [2]. * **Technetium-99m Bone Scan:** This is often **negative** in Multiple Myeloma because it depends on osteoblastic activity, which is absent in these lesions. Skeletal survey (X-ray) or MRI is preferred [2]. * **Bence-Jones Proteins:** These are monoclonal light chains found in urine; they do not show up on a standard dipstick (which detects albumin). * **M-Spike:** Found on Serum Protein Electrophoresis (SPEP), usually representing IgG or IgA [2].

Question 629: Poorest prognosis in Acute Myeloid Leukemia (AML) is seen in which cytogenetic abnormality?

A. Monosomy 7 (Correct Answer)
B. No cytogenetic abnormality
C. t(15;17)
D. inv(16)

Explanation: **Explanation:** In Acute Myeloid Leukemia (AML), cytogenetics is the single most important predictor of treatment response and overall survival [1]. **Why Monosomy 7 is the Correct Answer:** Monosomy 7 (-7) or a deletion of the long arm of chromosome 7 (7q-) is categorized under the **Adverse/Poor Risk group** [1]. It is frequently associated with complex karyotypes, prior exposure to chemotherapy (therapy-related AML), or evolution from Myelodysplastic Syndrome (MDS). These cases are notorious for multi-drug resistance and a very high rate of relapse, often requiring Allogeneic Stem Cell Transplant as the only curative option [1]. **Analysis of Incorrect Options:** * **B. No cytogenetic abnormality:** This represents the **Intermediate Risk group** [1]. While not as favorable as specific translocations, it has a significantly better prognosis than Monosomy 7. * **C. t(15;17):** This is the hallmark of Acute Promyelocytic Leukemia (APL). It carries a **Favorable prognosis** due to its high sensitivity to All-trans Retinoic Acid (ATRA) and Arsenic Trioxide [1]. * **D. inv(16):** Along with t(8;21), this belongs to the Core Binding Factor (CBF) leukemias. It is categorized as a **Favorable prognosis** with high rates of complete remission following high-dose Cytarabine [1]. **High-Yield NEET-PG Pearls:** * **Best Prognosis:** t(15;17) followed by t(8;21) and inv(16) [1]. * **Worst Prognosis:** Monosomy 7, Monosomy 5, 11q23 abnormalities, and complex karyotypes (≥3 abnormalities) [1]. * **FLT3-ITD Mutation:** The most common molecular abnormality associated with a poor prognosis in otherwise normal cytogenetics. * **NPM1 and CEBPA Mutations:** Generally associated with a favorable prognosis in cytogenetically normal AML.

Question 630: A 65-year-old patient presented with weakness, fatigue for 6 months, and mild abdominal discomfort. Examination revealed moderate splenomegaly. Lab findings showed severe normocytic normochromic anemia, neutropenia with monocytopenia, and thrombocytopenia. Bone marrow aspiration resulted in a 'dry' tap. A bone marrow biopsy was performed. Which of the following CD markers can be positive in this condition EXCEPT?

A. CD11c
B. CD103
C. CD117 (Correct Answer)
D. CD25

Explanation: The clinical presentation of an elderly patient with pancytopenia (including characteristic **monocytopenia**), splenomegaly, and a **"dry tap"** on bone marrow aspiration strongly suggests **Hairy Cell Leukemia (HCL)**. HCL is a rare B-cell lymphoproliferative disorder where the bone marrow becomes fibrotic, necessitating a biopsy which typically shows "fried-egg" appearance cells. **Why CD117 is the Correct Answer:** * **CD117 (c-kit)** is a marker for hematopoietic stem cells and myeloid precursors. It is typically positive in **Acute Myeloid Leukemia (AML)** and Mastocytosis. It is **not** expressed in Hairy Cell Leukemia, making it the correct "except" choice. **Analysis of Incorrect Options (Markers positive in HCL):** * **CD11c:** An adhesion molecule (integrin) highly expressed in HCL. * **CD103:** Considered the most specific marker for HCL among the B-cell disorders. * **CD25:** The IL-2 receptor alpha chain, characteristically positive in HCL (unlike most other B-cell lymphomas). * *Note: Other positive markers include CD19, CD20, CD22, and Annexin A1 (most specific).* **Clinical Pearls for NEET-PG:** 1. **TRAP Positive:** Hairy cells show Tartrate-Resistant Acid Phosphatase (TRAP) activity. 2. **BRAF V600E Mutation:** Present in nearly 100% of classic HCL cases. 3. **Monocytopenia:** A high-yield diagnostic clue; HCL is one of the few conditions where pancytopenia specifically includes a lack of monocytes. 4. **Treatment:** Cladribine (2-CdA) is the drug of choice.

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

Want unlimited practice?

Get full access to all questions, explanations, and performance tracking.

Start For Free

Hematology — MCQs

Hematology — MCQs

On this page

Practice by Chapter

Want unlimited practice?