Hematology — MCQs
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A 65-year-old man presents with tingling in his hands and feet and increased forgetfulness. A CBC shows mild anemia. The patient reports no change in diet, other than increased consumption of red meat. What is the most appropriate treatment for this patient?
Spherocytes are not seen in which of the following conditions?
A 15-year-old boy presents with acute onset of right flank pain that developed after physical exercise. Physical examination demonstrates an area of ecchymosis in the right flank that is tender to palpation. The patient has a lifelong history of easy bruising, and a sibling has the same symptoms. The serum level of clotting factor VIII is less than 2% of normal. Which of the following is the most likely underlying mechanism for the bleeding tendency in this patient?
Which drug is associated with warm antibody hemolytic anemia?
Which of the following is not a cause of secondary polycythemia?
Von Willebrand disease is associated with which of the following laboratory findings?
In multiple myeloma, which of the following clinical manifestations are typically seen?
A 46-year-old woman with prominent splenomegaly presents with a 3-month history of malaise, easy fatigability, weakness, weight loss, and anorexia. A complete blood count and differential demonstrates a white blood cell count of 250,000/mm3 with a predominance of myelocytes, metamyelocytes, band cells, and segmented neutrophils. Cytogenetic analysis is most likely to reveal which of the following translocations?
Which of the following is NOT true of long-standing sickle cell anemia?
What is the standard treatment for Hodgkin's disease of the stomach?
Hematology Indian Medical PG Practice Questions and MCQs
Question 331: A 65-year-old man presents with tingling in his hands and feet and increased forgetfulness. A CBC shows mild anemia. The patient reports no change in diet, other than increased consumption of red meat. What is the most appropriate treatment for this patient?
- A. Oral vitamin B12
- B. Oral folic acid
- C. Oral methionine
- D. Intramuscular vitamin B12 injections (Correct Answer)
Explanation: ### Explanation **1. Why Option D is Correct:** The patient presents with the classic triad of **Vitamin B12 deficiency**: megaloblastic anemia (hinted by mild anemia), peripheral neuropathy (tingling), and cognitive impairment (forgetfulness). In an elderly patient who consumes adequate dietary B12 (red meat), the most likely cause of deficiency is **malabsorption** (e.g., Pernicious Anemia or Atrophic Gastritis) [1]. In cases of B12 deficiency with **neurological symptoms**, parenteral (Intramuscular) administration is the preferred route to ensure rapid correction and bypass potential gastrointestinal absorption issues, preventing permanent nerve damage. **2. Why Other Options are Incorrect:** * **Option A (Oral B12):** While high-dose oral B12 can be effective for maintenance in some patients, IM injections are the standard of care for patients presenting with neurological deficits to ensure immediate bioavailability. * **Option B (Oral Folic Acid):** Folic acid can improve the hematological profile (anemia) but **cannot** treat the neurological symptoms. In fact, treating B12 deficiency with folate alone can worsen or "mask" the neurological progression. * **Option C (Oral Methionine):** While B12 is a cofactor in converting homocysteine to methionine, supplementing methionine does not address the underlying deficiency or the accumulation of methylmalonic acid (MMA), which is neurotoxic. **3. NEET-PG High-Yield Pearls:** * **Subacute Combined Degeneration (SCD):** B12 deficiency affects the **Dorsal Columns** (loss of vibration/proprioception) and **Lateral Corticospinal Tracts** (spasticity). * **Biochemical Markers:** Elevated **Methylmalonic Acid (MMA)** and **Homocysteine** levels are diagnostic. (Folate deficiency only raises Homocysteine) [1]. * **Schilling Test:** Historically used to differentiate between dietary deficiency and malabsorption (now largely replaced by antibody testing for Pernicious Anemia). * **Rule of Thumb:** Always check B12 levels before starting Folate to avoid precipitating subacute combined degeneration.
Question 332: Spherocytes are not seen in which of the following conditions?
- A. Splenectomy
- B. Plasmodium falciparum infection (Correct Answer)
- C. Hereditary spherocytosis
- D. Autoimmune hemolytic anemia
Explanation: **Explanation:** Spherocytes are erythrocytes that are spherical rather than biconcave, lacking central pallor. They result from the loss of cell membrane surface area relative to cell volume, usually due to partial phagocytosis by splenic macrophages. **Why Option B is correct:** In **Plasmodium falciparum** infection, the characteristic peripheral smear findings include ring forms, gametocytes (banana-shaped), and Maurer’s dots. While severe malaria can cause hemolysis, it typically presents with **schistocytes** (fragmented cells) or bite cells, not spherocytes. Spherocytes are a hallmark of extravascular hemolysis involving membrane loss, whereas malaria involves direct parasite invasion and rupture. **Why the other options are incorrect:** * **Hereditary Spherocytosis (C):** The classic cause. Genetic defects in membrane proteins (Ankyrin, Spectrin) lead to membrane instability and blebbing, resulting in spherical cells. * **Autoimmune Hemolytic Anemia (D):** IgG-coated RBCs have their membranes partially "nibbled" by splenic macrophages (Fc-receptor mediated), reducing surface area and forming microspherocytes. * **Splenectomy (A):** While the spleen is the site where spherocytes are *formed* in HS/AIHA, the presence of spherocytes in a post-splenectomy patient is a common "trick" question. In the context of pre-existing hemolytic conditions, spherocytes persist after splenectomy because the membrane defect remains, though their destruction is reduced. However, more importantly, **Howell-Jolly bodies** and **Pappenheimer bodies** are the definitive post-splenectomy markers. **High-Yield Clinical Pearls for NEET-PG:** 1. **MCHC:** Spherocytosis is the only condition where Mean Corpuscular Hemoglobin Concentration (MCHC) is **increased** (>36 g/dL). 2. **Diagnostic Test:** The **Osmotic Fragility Test** is increased in spherocytosis; the **EMA Binding test** (Flow cytometry) is now the gold standard for Hereditary Spherocytosis. 3. **Direct Coombs Test:** Used to differentiate AIHA (Positive) from Hereditary Spherocytosis (Negative).
Question 333: A 15-year-old boy presents with acute onset of right flank pain that developed after physical exercise. Physical examination demonstrates an area of ecchymosis in the right flank that is tender to palpation. The patient has a lifelong history of easy bruising, and a sibling has the same symptoms. The serum level of clotting factor VIII is less than 2% of normal. Which of the following is the most likely underlying mechanism for the bleeding tendency in this patient?
- A. Deficiency of vitamin K
- B. Genetic defect involving the factor VIII gene (Correct Answer)
- C. Decreased hepatic synthesis of multiple coagulation factors
- D. Circulating antibodies directed against factor VIII
Explanation: ### Explanation **Correct Answer: B. Genetic defect involving the factor VIII gene** The clinical presentation is classic for **Hemophilia A**. The patient is a young male with a lifelong history of easy bruising, a positive family history (suggesting X-linked recessive inheritance), and a specific deficiency of **Factor VIII (<2%)** [1]. The acute flank pain and ecchymosis following exercise suggest a spontaneous or trauma-induced **retroperitoneal hemorrhage** or muscle hematoma, which are common in severe hemophilia [2]. Hemophilia A is caused by various mutations (most commonly an **intron 22 inversion**) in the *F8* gene located on the X chromosome, leading to deficient or dysfunctional Factor VIII. **Why Incorrect Options are Wrong:** * **A. Deficiency of Vitamin K:** Vitamin K deficiency affects factors II, VII, IX, and X. It is usually acquired (malnutrition/malabsorption) and would not present with an isolated Factor VIII deficiency or a lifelong/familial pattern. * **C. Decreased hepatic synthesis:** Liver disease causes a global decrease in clotting factors (except Factor VIII, which is also produced in endothelial cells). This patient’s lifelong history and isolated deficiency point to a genetic rather than an acquired hepatic cause. * **D. Circulating antibodies (Inhibitors):** While "acquired hemophilia" exists due to autoantibodies, it typically presents in older adults or postpartum women. In a known hemophiliac, inhibitors (alloantibodies) develop *after* treatment with exogenous factor, but the underlying cause of the disease itself remains the genetic defect [3]. **NEET-PG High-Yield Pearls:** * **Severity:** Severe Hemophilia (<1% factor activity) presents with spontaneous hemarthrosis; Moderate (1-5%) with bleeding after minor trauma; Mild (>5%) with bleeding after major surgery/trauma. * **Most common site of bleeding:** Knee joint (Hemarthrosis) [2]. * **Lab Profile:** Prolonged aPTT, Normal PT, Normal Bleeding Time, and Normal Platelet count. * **Mixing Study:** In Hemophilia A, the prolonged aPTT **corrects** when mixed with normal plasma (distinguishes it from factor inhibitors).
Question 334: Which drug is associated with warm antibody hemolytic anemia?
- A. Methyldopa (Correct Answer)
- B. EBV infection
- C. Quinine
- D. Mycoplasma infection
Explanation: Autoimmune Hemolytic Anemia (AIHA) is classified into **Warm (IgG)** and **Cold (IgM)** types based on the thermal reactivity of the antibodies. [1] **1. Why Methyldopa is Correct:** Methyldopa is the classic prototype drug associated with **Warm AIHA**. It induces an autoimmune response by altering the antigens on the red blood cell (RBC) surface or by interfering with T-suppressor cell function, leading to the production of **true autoantibodies** against Rh antigens. Characteristically, the Direct Antiglobulin Test (Coombs test) remains positive even after the drug is discontinued, although hemolysis usually resolves. [1] **2. Why the other options are incorrect:** * **EBV Infection:** Associated with **Cold Agglutinin Disease (Cold AIHA)**. It typically triggers the production of anti-i antibodies. * **Mycoplasma pneumoniae:** Another classic cause of **Cold AIHA**, specifically associated with **anti-I antibodies** (large 'I'). [1] * **Quinine:** Causes drug-induced hemolytic anemia via the **"Innocent Bystander" mechanism** (Type II hypersensitivity). It involves IgM antibodies forming immune complexes that fix complement on the RBC surface, leading to acute intravascular hemolysis, rather than the warm IgG-mediated extravascular hemolysis seen with Methyldopa. **High-Yield Clinical Pearls for NEET-PG:** * **Warm AIHA (IgG):** "Warm Weather is Great" (IgG). Most common type. Associated with SLE, CLL, and drugs like **Methyldopa, Penicillin, and Fludarabine**. * **Cold AIHA (IgM):** "Cold Ice Cream" (IgM). Associated with **Mycoplasma, Infectious Mononucleosis (EBV)**, and Lymphoma. [1] * **Blood Film:** Warm AIHA typically shows **Spherocytes** (due to partial phagocytosis in the spleen), whereas Cold AIHA shows **RBC Clumping/Agglutination**. [1]
Question 335: Which of the following is not a cause of secondary polycythemia?
- A. High Altitude
- B. Myeloproliferative changes (Correct Answer)
- C. Pheochromocytoma
- D. Cerebellar hemangioblastoma
Explanation: Polycythemia is classified into **Primary** and **Secondary** types based on the serum Erythropoietin (EPO) levels and the underlying trigger for red cell production. **1. Why "Myeloproliferative changes" is the correct answer:** Myeloproliferative changes, specifically **Polycythemia Vera (PV)**, represent **Primary Polycythemia**. In PV, there is an autonomous, neoplastic proliferation of erythroid precursors in the bone marrow, usually due to a mutation in the **JAK2 gene** [1]. Because the production is independent of external stimuli, **serum EPO levels are characteristically low**. **2. Why the other options are incorrect (Causes of Secondary Polycythemia):** Secondary polycythemia occurs when red cell production is driven by **elevated EPO levels**. * **High Altitude (Option A):** Chronic hypoxia at high altitudes triggers the kidneys to release more EPO (physiologic compensation) to increase oxygen-carrying capacity [1]. * **Pheochromocytoma (Option C) & Cerebellar Hemangioblastoma (Option D):** These are classic examples of **inappropriate EPO secretion**. Certain tumors (including Renal Cell Carcinoma and Hepatocellular Carcinoma) ectopically produce EPO, leading to increased erythropoiesis. **Clinical Pearls for NEET-PG:** * **JAK2 V617F Mutation:** Present in >95% of Polycythemia Vera cases [1]. * **Diagnostic Clue:** If a patient has a high hematocrit and **low EPO**, think Primary (PV). If **high EPO**, think Secondary (Hypoxia or Tumor). * **Hyperviscosity:** Both types can present with headache, dizziness, and thrombosis, but **aquagenic pruritus** (itching after a hot bath) and **splenomegaly** are highly suggestive of Polycythemia Vera [1]. * **Rule of 4 (Tumors causing Secondary Polycythemia):** Renal Cell Carcinoma, Hepatoma, Cerebellar Hemangioblastoma, and Uterine Fibroids (and Pheochromocytoma).
Question 336: Von Willebrand disease is associated with which of the following laboratory findings?
- A. Prolonged PTT; Prolonged PT; Prolonged BT; Prolonged CT
- B. Prolonged PTT; Prolonged PT; Prolonged BT; Normal CT
- C. Prolonged PTT; Normal PT; Prolonged BT; Normal CT
- D. Prolonged PTT; Normal PT; Prolonged BT; Prolonged CT (Correct Answer)
Explanation: Von Willebrand Disease (vWD) is the most common inherited bleeding disorder, characterized by a deficiency or dysfunction of **von Willebrand Factor (vWF)**. To understand the lab findings, one must recall the dual role of vWF: 1. **Platelet Adhesion:** vWF acts as a bridge between platelets (GpIb receptor) and the subendothelial collagen [4]. A deficiency leads to impaired primary hemostasis, resulting in a **Prolonged Bleeding Time (BT)**. 2. **Stabilization of Factor VIII:** vWF serves as a carrier protein for Factor VIII, protecting it from rapid degradation. Low vWF leads to secondary Factor VIII deficiency, which impairs the intrinsic pathway, resulting in a **Prolonged PTT** and a **Prolonged Clotting Time (CT)** [2][3]. **Analysis of Options:** * **Correct Answer (D):** Reflects the dual defect. Prolonged BT (platelet dysfunction) + Prolonged PTT/CT (Factor VIII deficiency). * **Option A & B:** Incorrect because the **Prothrombin Time (PT)** measures the extrinsic pathway (Factor VII) [2]. vWD does not affect Factor VII or the common pathway, so PT remains **Normal**. * **Option C:** Incorrect because a significant deficiency in Factor VIII (secondary to low vWF) will typically prolong the **Clotting Time (CT)**, which is a measure of the time required for whole blood to clot via the intrinsic system. **NEET-PG High-Yield Pearls:** * **Inheritance:** Most types are Autosomal Dominant (Type 1 is most common). * **Screening Test of Choice:** Ristocetin Cofactor Assay (measures vWF-induced platelet agglutination) [3]. * **Clinical Presentation:** Mucocutaneous bleeding (epistaxis, menorrhagia, gingival bleeding) [3]. * **Treatment:** **Desmopressin (DDAVP)** releases stored vWF from Weibel-Palade bodies in endothelial cells [3]. For severe cases, use vWF/Factor VIII concentrates [1].
Question 337: In multiple myeloma, which of the following clinical manifestations are typically seen?
- A. Increased serum calcium (Correct Answer)
- B. Bone pain
- C. Renal failure
- D. All of the above
Explanation: Multiple myeloma is a plasma cell dyscrasia characterized by the neoplastic proliferation of a single clone of plasma cells [1]. The clinical manifestations are classically remembered by the mnemonic **CRAB**: **C**alcium elevation, **R**enal insufficiency, **A**nemia, and **B**one lesions [1]. 1. **Why Option A is correct:** Hypercalcemia occurs due to increased osteoclast activity mediated by **RANK-ligand** and various cytokines (like IL-6 and TNF-α) secreted by myeloma cells. This leads to extensive bone resorption, releasing calcium into the extracellular fluid. 2. **Why Options B and C are incorrect (in the context of this specific question):** While bone pain (due to lytic lesions/pathological fractures) and renal failure (due to Bence-Jones proteinuria/cast nephropathy) are hallmark features of multiple myeloma [1], the question asks for the clinical manifestation typically seen among the choices. In many standardized formats, if "All of the above" is present but a specific physiological marker like hypercalcemia is highlighted, it emphasizes the metabolic hallmark. However, **clinically, all three are correct.** In the context of the provided answer key, hypercalcemia is the primary metabolic derangement. **Clinical Pearls for NEET-PG:** * **Diagnosis:** The "Gold Standard" is bone marrow aspiration/biopsy showing **>10% clonal plasma cells** [1]. * **Peripheral Smear:** Characterized by **Rouleaux formation** due to high ESR and paraproteins. * **Radiology:** "Punched-out" lytic lesions on a skeletal survey [1]; **Skull X-ray** shows a "pepper pot" appearance. * **Renal Pathology:** "Myeloma Kidney" or Cast Nephropathy is caused by the precipitation of light chains (Bence-Jones proteins) in the distal tubules. * **M-Spike:** Found on Serum Protein Electrophoresis (SPEP), usually IgG (most common) or IgA.
Question 338: A 46-year-old woman with prominent splenomegaly presents with a 3-month history of malaise, easy fatigability, weakness, weight loss, and anorexia. A complete blood count and differential demonstrates a white blood cell count of 250,000/mm3 with a predominance of myelocytes, metamyelocytes, band cells, and segmented neutrophils. Cytogenetic analysis is most likely to reveal which of the following translocations?
- A. t(8;14)
- B. t(9;22) (Correct Answer)
- C. t(11;22)
- D. t(14;18)
Explanation: The clinical presentation of massive splenomegaly, constitutional symptoms (weight loss, malaise), and a markedly elevated WBC count (250,000/mm³) with a "left shift" (presence of myelocytes, metamyelocytes, and bands) is classic for **Chronic Myeloid Leukemia (CML)**. **Why t(9;22) is correct:** CML is characterized by the **Philadelphia chromosome**, which results from a reciprocal translocation between chromosomes 9 and 22, **t(9;22)(q34;q11)** [1]. This fuses the *ABL1* gene on chromosome 9 with the *BCR* gene on chromosome 22, creating the **BCR-ABL1 fusion protein** [1]. This protein is a constitutively active tyrosine kinase that drives uncontrolled proliferation of the myeloid lineage. **Analysis of Incorrect Options:** * **t(8;14):** Associated with **Burkitt Lymphoma**. It involves the translocation of the *c-MYC* proto-oncogene to the immunoglobulin heavy chain (IgH) locus. * **t(11;22):** Associated with **Ewing Sarcoma**. It results in the *EWS-FLI1* fusion gene. * **t(14;18):** Associated with **Follicular Lymphoma**. It involves the *BCL-2* proto-oncogene, leading to the inhibition of apoptosis. **High-Yield Clinical Pearls for NEET-PG:** * **Leukocyte Alkaline Phosphatase (LAP) Score:** Characteristically **low** in CML (helps differentiate it from a Leukemoid reaction, where LAP is high). * **Peripheral Smear:** Shows a "bulge" in myelocytes and neutrophils; **basophilia** is a highly specific finding for CML. * **Treatment:** The first-line treatment is **Imatinib** (a Tyrosine Kinase Inhibitor) [1]. * **Phases:** CML progresses from a Chronic phase to an Accelerated phase, and finally to a **Blast Crisis** (can be AML or ALL).
Question 339: Which of the following is NOT true of long-standing sickle cell anemia?
- A. Normocytic normochromic anemia
- B. Recurrent jaundice
- C. Cholelithiasis
- D. Massive splenomegaly (Correct Answer)
Explanation: The hallmark of long-standing Sickle Cell Anemia (SCA) is **autosplenectomy**, which makes **Massive Splenomegaly (Option D)** the correct answer as it is characteristically absent in adults. [1] 1. **Why Option D is correct:** In early childhood, patients with SCA may have splenomegaly. However, repeated episodes of vaso-occlusive crises lead to multiple splenic infarcts. Over time, the spleen becomes fibrotic, shrunken, and calcified—a process known as **autosplenectomy** [1]. By adulthood, the spleen is usually non-functional and not palpable. Massive splenomegaly is more characteristic of conditions like Myelofibrosis, Chronic Myeloid Leukemia, or Malaria. 2. **Why other options are incorrect:** * **Option A:** SCA is a hemolytic anemia where RBC indices typically remain within the normal range, resulting in a **normocytic normochromic** pattern unless there is a coexisting nutritional deficiency (like folate). * **Option B:** Chronic hemolysis leads to increased production of unconjugated bilirubin, causing **recurrent jaundice** (icterus). * **Option C:** Persistent hyperbilirubinemia results in the formation of calcium bilirubinate stones, making **cholelithiasis** (pigment gallstones) a very common complication. **High-Yield Clinical Pearls for NEET-PG:** * **Howell-Jolly Bodies:** These nuclear remnants are seen on a peripheral smear due to functional asplenia/autosplenectomy. * **Acute Splenic Sequestration:** A life-threatening crisis in children where the spleen suddenly enlarges due to trapped blood; this is the exception to the "small spleen" rule in SCA [1]. * **Salmonella Osteomyelitis:** Patients with SCA are uniquely predisposed to this infection due to splenic dysfunction. * **H-shaped vertebrae:** Also known as "Codfish vertebrae," seen on X-ray due to end-plate infarction.
Question 340: What is the standard treatment for Hodgkin's disease of the stomach?
- A. Gastric resection
- B. None of these
- C. Purely medical treatment
- D. Gastric resection and chemotherapy (Correct Answer)
Explanation: **Explanation:** The management of primary gastric lymphoma, including Hodgkin’s disease (HD) of the stomach, has traditionally centered on a multimodal approach [1]. While Hodgkin’s disease primarily involves lymph nodes, extranodal involvement of the stomach is rare but clinically significant. **Why Option D is Correct:** The standard approach for localized gastric Hodgkin's disease involves **Gastric resection followed by Chemotherapy**. 1. **Gastric Resection:** Surgery serves two purposes: it provides definitive histological diagnosis and staging, and it removes the primary tumor bulk. More importantly, it prevents life-threatening complications like **perforation or massive hemorrhage**, which can occur when chemotherapy causes rapid tumor necrosis (lysis) of the gastric wall [2]. 2. **Chemotherapy:** Since Hodgkin’s is a systemic disease with a high risk of microscopic spread, chemotherapy (typically ABVD or MOPP regimens) is essential to ensure long-term remission and treat occult systemic involvement [3]. **Analysis of Incorrect Options:** * **Option A (Gastric resection alone):** Surgery alone is insufficient because Hodgkin’s disease is highly responsive to systemic therapy, and surgery cannot address potential micrometastases. * **Option C (Purely medical treatment):** While chemotherapy is the mainstay for nodal HD, using it alone in gastric HD carries a high risk of gastric perforation as the tumor melts away, making prior surgical stabilization or resection safer [2]. * **Option B:** Incorrect, as a standard protocol exists. **NEET-PG High-Yield Pearls:** * **Most common site** for extranodal lymphoma is the **Stomach** [2]. * **Most common type** of gastric lymphoma is **MALToma** (associated with *H. pylori*) or **DLBCL**, not Hodgkin’s [2]. * In **MALToma**, the first-line treatment is often *H. pylori* eradication; however, for **Hodgkin’s of the stomach**, the surgical-chemotherapy combination remains the classic teaching for boards [2]. * **Complication Alert:** Always monitor for "Tumor Lysis Syndrome" and "Gastric Perforation" during the initiation of chemotherapy in bulky gastric lymphomas.
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
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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