Hematology Practice Questions

Q: 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?

Evans' syndrome. 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.

Q: What is true about Multiple Myeloma?

All of the above. 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.

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

Factor VIII concentrate. **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.

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

1 gm/week. **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.

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

Pure red cell aplasia. 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).

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

Intrathecal methotrexate. **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.

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

Multiple myeloma. ### 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].

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

Monosomy 7. **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.

Q: 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?

CD117. 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.

Question 1

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

Accepted Answer

Antigen-antibody mechanism involving human leukocyte antigen

Answer

RBC incompatibility

Answer

Platelet surface antigen reaction

Answer

Antibody to IgA in donor plasma

Question 2

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?

Accepted Answer

Evans' syndrome

Answer

Disseminated Intravascular Coagulation (DIC)

Answer

Thrombotic Thrombocytopenic Purpura (TTP)

Answer

HELLP syndrome

Question 3

What is true about Multiple Myeloma?

Accepted Answer

All of the above

Answer

Bence Jones protein in urine

Answer

Hypogammaglobulinemia

Answer

Amyloidosis

Question 4

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

Accepted Answer

Factor VIII concentrate

Answer

Whole blood

Answer

Fresh frozen plasma

Answer

Factor IX concentrate

Question 5

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

Accepted Answer

1 gm/week

Answer

2 gm/week

Answer

2 gm/month

Answer

1 gm/month

Question 6

Aplastic anemia can progress to all of the following except?

Accepted Answer

Pure red cell aplasia

Answer

Acute myeloid leukemia (AML)

Answer

Myelodysplastic syndrome

Answer

Paroxysmal nocturnal hemoglobinuria (PNH)

Question 7

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

Accepted Answer

Intrathecal methotrexate

Answer

Vincristine and prednisolone

Answer

Intrathecal vincristine

Answer

Intravenous prednisolone

Question 8

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

Accepted Answer

Multiple myeloma

Answer

Down syndrome

Answer

Hyperparathyroidism

Answer

All of the above

Question 9

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

Accepted Answer

Monosomy 7

Answer

No cytogenetic abnormality

Answer

t(15;17)

Answer

inv(16)

Question 10

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?

Accepted Answer

CD117

Answer

CD11c

Answer

CD103

Answer

CD25

Hematology — MCQs

Hematology — MCQs

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