Hematology — MCQs
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A 56-year-old male presents with low back pain, weight loss, fatigue, and recurrent sinus infections. He has no history of trauma. Examination reveals focal tenderness at the T10 level. Laboratory investigations show Hb of 9 g/dl and deranged renal function tests. A skull X-ray was performed. Bone marrow biopsy and serum protein electrophoresis are planned. What is the characteristic abnormality expected on the peripheral blood film?
Schilling's test may be used to establish a diagnosis of:
Which of the following is a nutritional deficiency anemia?
Which of the following is the most common cause of transfusion-associated hepatitis?
The MOST severe complication of idiopathic hyper-eosinophilic syndrome is:
A 47-year-old man presents with a 6-week history of increasing fatigue and dark-colored stools. Complete blood count shows hemoglobin of 8.6 g/dL and microcytic, hypochromic RBCs. Upper gastrointestinal endoscopy reveals a peptic ulcer along the lesser curvature of the stomach. This patient's anemia is most likely caused by deficiency of which of the following?
A 62-year-old man reports early satiety, fatigue, and generally feeling unwell. The symptoms started gradually and are getting worse. He notes no chest discomfort, respiratory symptoms, or abdominal pain. On physical examination, he appears pale, the vital signs are normal, and the pertinent findings are a large spleen, absence of lymph nodes, and normal heart and lungs. His blood count is abnormal; the WBC is 50,000/mL with increased mature granulocytes, hemoglobin is 9.5 g/dL, and platelets are 450,000/mL. Which of the following cytogenetic changes is most characteristic of his condition?
All of the following are inherited platelet function disorders except?
Which of the following statements regarding hematological malignancies is true?
What is the intermediate form of Non-Hodgkin's lymphoma?
Hematology Indian Medical PG Practice Questions and MCQs
Question 711: A 56-year-old male presents with low back pain, weight loss, fatigue, and recurrent sinus infections. He has no history of trauma. Examination reveals focal tenderness at the T10 level. Laboratory investigations show Hb of 9 g/dl and deranged renal function tests. A skull X-ray was performed. Bone marrow biopsy and serum protein electrophoresis are planned. What is the characteristic abnormality expected on the peripheral blood film?
- A. Anemia
- B. Pelger-Huet anomaly
- C. Rouleaux formation (Correct Answer)
- D. Neutrophilia
Explanation: The clinical presentation of bone pain (low back pain), constitutional symptoms (weight loss, fatigue), recurrent infections, and renal impairment in an elderly male is highly suggestive of **Multiple Myeloma (MM)** [1]. The "CRAB" features (Calcium elevation, Renal insufficiency, Anemia, and Bone lesions) are classic indicators [1]. **1. Why Rouleaux formation is correct:** In Multiple Myeloma, there is a monoclonal proliferation of plasma cells leading to the overproduction of monoclonal (M) proteins (immunoglobulins) [1]. These high levels of paraproteins reduce the zeta potential (negative charge) on the surface of Red Blood Cells (RBCs). This allows RBCs to stack together like a "pile of coins," a phenomenon known as **Rouleaux formation** [2]. This is the characteristic peripheral smear finding in MM and is also responsible for the characteristically high ESR seen in these patients [1]. **2. Analysis of Incorrect Options:** * **Anemia (A):** While the patient has anemia (Hb 9 g/dl), it is a *finding*, not a *characteristic morphological abnormality* on the film. * **Pelger-Huet anomaly (B):** This refers to hyposegmented neutrophils, typically seen in Myelodysplastic Syndromes (MDS) or congenital conditions, not MM. * **Neutrophilia (D):** Patients with MM are often neutropenic due to marrow infiltration or have normal counts; neutrophilia is not a characteristic feature. **Clinical Pearls for NEET-PG:** * **Skull X-ray:** Look for "punched-out" lytic lesions [1]. * **Diagnosis:** Gold standard is Bone Marrow Biopsy (>10% clonal plasma cells) [1]. * **Bence-Jones Proteins:** These are free light chains found in urine; they do not show up on standard dipsticks [1]. * **M-Spike:** Seen on Serum Protein Electrophoresis (SPEP), usually in the Gamma globulin region [1].
Question 712: Schilling's test may be used to establish a diagnosis of:
- A. Intrinsic factor deficiency (Correct Answer)
- B. Pancreatic endocrine dysfunction
- C. Megaloblastic anemia from folic acid deficiency
- D. All of the above
Explanation: The **Schilling test** is a classic diagnostic tool used to determine the cause of Vitamin B12 (cobalamin) malabsorption. It is performed in stages to pinpoint the specific anatomical or physiological defect. **1. Why Option A is Correct:** Intrinsic Factor (IF) deficiency is the hallmark of **Pernicious Anemia** [1]. In the Schilling test, Stage I involves giving oral radiolabeled B12. If excretion in the urine is low, Stage II is performed by co-administering oral B12 with **exogenous Intrinsic Factor**. If the B12 absorption normalizes (increased urinary excretion) during Stage II, it confirms that the primary pathology was a lack of IF, thereby establishing the diagnosis. **2. Why Other Options are Incorrect:** * **Option B:** While pancreatic **exocrine** insufficiency (lack of proteases to cleave R-binder from B12) can cause malabsorption, the option specifies **endocrine** dysfunction (e.g., Diabetes), which does not affect B12 absorption. * **Option C:** Folic acid deficiency is a cause of megaloblastic anemia, but its absorption is independent of Intrinsic Factor and the B12-specific pathways tested by the Schilling test [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Stage III** of the Schilling test uses antibiotics to check for **Small Intestinal Bacterial Overgrowth (SIBO)**. * **Stage IV** uses pancreatic enzymes to check for **Chronic Pancreatitis**. * **Prerequisite:** Before starting the test, a
Question 713: Which of the following is a nutritional deficiency anemia?
- A. Aplastic anemia
- B. Sickle cell anemia
- C. Megaloblastic anemia (Correct Answer)
- D. Hemolytic anemia
Explanation: **Explanation:** **Megaloblastic anemia** is the correct answer because it is primarily caused by a deficiency of essential nutrients—specifically **Vitamin B12 (Cobalamin)** and **Vitamin B9 (Folic Acid)** [1]. These nutrients are critical cofactors for DNA synthesis. When they are deficient, there is a "nuclear-cytoplasmic asynchrony" where the cell's nucleus matures slower than the cytoplasm, leading to the formation of large, immature red blood cell precursors (megaloblasts) in the bone marrow and macrocytic cells in the peripheral blood [1]. **Analysis of Incorrect Options:** * **Aplastic Anemia:** This is a bone marrow failure syndrome characterized by pancytopenia and a hypocellular marrow. It is usually caused by autoimmune destruction of stem cells, toxins, or drugs, rather than a lack of dietary nutrients. * **Sickle Cell Anemia:** This is a genetic (hereditary) hemoglobinopathy caused by a point mutation in the ̢-globin gene (Glu → Val at the 6th position), leading to the production of abnormal Hemoglobin S. * **Hemolytic Anemia:** This refers to a group of disorders where red blood cells are destroyed prematurely. Causes can be intrinsic (e.g., G6PD deficiency, Spherocytosis) or extrinsic (e.g., Autoimmune hemolytic anemia), but it is not fundamentally a nutritional deficiency. **High-Yield Clinical Pearls for NEET-PG:** * **Peripheral Smear:** Look for **macro-ovalocytes** and **hypersegmented neutrophils** (≥ 5 lobes in > 5% of neutrophils or a single neutrophil with ≥ 6 lobes). * **Neurological Symptoms:** Only Vitamin B12 deficiency causes Subacute Combined Degeneration (SCD) of the spinal cord (dorsal columns and lateral corticospinal tracts). Pure Folate deficiency does **not** cause neurological deficits [1]. * **Schilling Test:** Historically used to differentiate causes of B12 malabsorption (e.g., Pernicious anemia vs. dietary deficiency).
Question 714: Which of the following is the most common cause of transfusion-associated hepatitis?
- A. Hepatitis A
- B. Hepatitis B (Correct Answer)
- C. Hepatitis C
- D. Hepatitis D
Explanation: The correct answer is **Hepatitis B (HBV)**. While Hepatitis C was historically the most common cause of post-transfusion hepatitis before the discovery of the virus and the implementation of rigorous screening, modern nucleic acid testing (NAT) has significantly reduced the risk for both HBV and HCV. However, **Hepatitis B remains the most common** transfusion-transmitted viral infection (TTI) globally and in India. This is primarily due to the "occult" HBV infection (HBsAg negative but DNA positive) and the longer window period compared to other viruses, which allows it to occasionally bypass standard screening protocols. **Analysis of Incorrect Options:** * **Hepatitis A:** It is primarily transmitted via the fecal-oral route [1]. While transient viremia occurs, it is an extremely rare cause of transfusion-associated hepatitis because it does not have a chronic carrier state. * **Hepatitis C:** Formerly the leading cause of "Non-A, Non-B" post-transfusion hepatitis. Since the introduction of highly sensitive NAT, the risk has plummeted to less than 1 in 2 million units in developed regions, making it less common than HBV. * **Hepatitis D:** This is a defective virus that requires the presence of HBsAg to replicate. It is only transmitted alongside HBV and is not considered an independent primary cause of transfusion-associated hepatitis. **High-Yield Pearls for NEET-PG:** * **Most common TTI overall:** Hepatitis B. * **Most common cause of post-transfusion purpura:** Antibodies against HPA-1a. * **Most common cause of transfusion-related mortality:** TRALI (Transfusion-Related Acute Lung Injury). * **Window Period:** HBV has a longer window period (~30-60 days) compared to HIV (~7-10 days) or HCV (~3-5 days) when using NAT. [2]
Question 715: The MOST severe complication of idiopathic hyper-eosinophilic syndrome is:
- A. Endocardial fibrosis (Correct Answer)
- B. Eosinophilic gastroenteritis
- C. Interstitial pneumonia
- D. Bone marrow failure
Explanation: **Explanation:** **Idiopathic Hypereosinophilic Syndrome (HES)** is characterized by a persistent absolute eosinophil count >1500/µL for more than 6 months, leading to multi-organ damage. **Why Endocardial Fibrosis is Correct:** The most severe and life-threatening complication of HES is cardiac involvement, specifically **Loeffler’s Endocarditis**. Eosinophils release toxic granules (Major Basic Protein and Eosinophil Peroxidase) that cause direct endomyocardial damage. This progresses through three stages: 1. **Acute Necrotic Stage:** Myocardial damage. 2. **Thrombotic Stage:** Formation of mural thrombi. 3. **Fibrotic Stage:** Development of **Endocardial Fibrosis**, leading to restrictive cardiomyopathy and congestive heart failure. This is the primary cause of morbidity and mortality in these patients. **Why Other Options are Incorrect:** * **B. Eosinophilic gastroenteritis:** While the GI tract is frequently involved (causing diarrhea or pain), it is rarely fatal compared to cardiac failure. * **C. Interstitial pneumonia:** Pulmonary involvement (Loeffler’s syndrome/infiltrates) is common but usually responds well to steroids and is less severe than permanent cardiac remodeling. * **D. Bone marrow failure:** HES is a proliferative disorder, not an aplastic one. While it can evolve into myeloid leukemia, marrow failure is not a characteristic complication. **NEET-PG High-Yield Pearls:** * **Target Organ Damage:** Heart > Lungs > Skin > CNS. * **Cardiac Hallmark:** Restrictive cardiomyopathy with apical obliteration on Echo. * **Treatment:** Corticosteroids are the first-line treatment; Imatinib is used in cases with the *FIP1L1-PDGFRA* fusion gene.
Question 716: A 47-year-old man presents with a 6-week history of increasing fatigue and dark-colored stools. Complete blood count shows hemoglobin of 8.6 g/dL and microcytic, hypochromic RBCs. Upper gastrointestinal endoscopy reveals a peptic ulcer along the lesser curvature of the stomach. This patient's anemia is most likely caused by deficiency of which of the following?
- A. Folic acid
- B. Iron (Correct Answer)
- C. Thiamine
- D. Vitamin B12
Explanation: **Explanation:** The patient presents with classic features of **Iron Deficiency Anemia (IDA)** secondary to chronic gastrointestinal blood loss [1]. **1. Why Iron is correct:** The clinical triad of **fatigue** (anemic symptom), **dark-colored stools** (melena indicating upper GI bleed), and a confirmed **peptic ulcer** points toward chronic blood loss [3]. In adults, the most common cause of iron deficiency is occult GI bleeding [1]. Laboratory findings of **microcytic, hypochromic RBCs** (low MCV, low MCHC) are the hallmark of IDA [2], as iron is a critical component of heme synthesis. Without iron, hemoglobin production is impaired, leading to smaller, paler red cells [1]. **2. Why the other options are incorrect:** * **Folic acid & Vitamin B12:** Deficiency of these vitamins leads to **Megaloblastic Anemia**, characterized by **macrocytic** (high MCV) RBCs and hypersegmented neutrophils, not microcytic cells [4]. * **Thiamine (Vitamin B1):** Thiamine deficiency typically presents as Beriberi (cardiovascular or neurological symptoms) or Wernicke-Korsakoff syndrome; it does not cause microcytic anemia. **Clinical Pearls for NEET-PG:** * **Rule of Thumb:** In any adult male or post-menopausal female with iron deficiency anemia, **GI malignancy** or **peptic ulcer disease** must be ruled out via endoscopy/colonoscopy [1]. * **Mentzer Index:** (MCV/RBC count) < 13 suggests Thalassemia trait, while **> 13** suggests Iron Deficiency Anemia. * **Earliest Marker:** A decrease in **Serum Ferritin** is the earliest laboratory sign of iron deficiency. * **Pica and Koilonychia** (spoon-shaped nails) are specific physical exam findings associated with chronic IDA.
Question 717: A 62-year-old man reports early satiety, fatigue, and generally feeling unwell. The symptoms started gradually and are getting worse. He notes no chest discomfort, respiratory symptoms, or abdominal pain. On physical examination, he appears pale, the vital signs are normal, and the pertinent findings are a large spleen, absence of lymph nodes, and normal heart and lungs. His blood count is abnormal; the WBC is 50,000/mL with increased mature granulocytes, hemoglobin is 9.5 g/dL, and platelets are 450,000/mL. Which of the following cytogenetic changes is most characteristic of his condition?
- A. Deletion of chromosome 14
- B. Reciprocal translocation of 9 and 22 (Philadelphia chromosome) (Correct Answer)
- C. Translocation of the renal artery stenosis (RAS) oncogene
- D. Trisomy 21
Explanation: The clinical presentation of massive splenomegaly, constitutional symptoms (fatigue, early satiety), and a markedly elevated WBC count with a "left shift" (increased mature granulocytes) is classic for **Chronic Myeloid Leukemia (CML)**. **Why Option B is Correct:** The hallmark of CML is the **Philadelphia chromosome (Ph)**, which results from a **reciprocal translocation between chromosomes 9 and 22 [t(9;22)(q34;q11)]**. This translocation fuses the *ABL1* gene on chromosome 9 with the *BCR* gene on chromosome 22, creating the **BCR-ABL1 fusion oncogene**. This gene encodes a constitutively active tyrosine kinase that drives uncontrolled proliferation of the myeloid lineage. **Why Incorrect Options are Wrong:** * **Option A:** Deletions of chromosome 14 are not characteristic of CML; they are more commonly associated with certain T-cell lymphomas or multiple myeloma. * **Option C:** RAS mutations are common in various solid tumors and some leukemias (like CMML), but they are not defined by a specific translocation of the renal artery. * **Option D:** Trisomy 21 (Down Syndrome) is associated with a significantly increased risk of **Acute Megakaryoblastic Leukemia (AMKL/M7)** and Transient Myeloproliferative Disorder, but not specifically CML [2]. **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 "full spectrum" of myeloid cells (myelocytes, metamyelocytes, bands, and neutrophils) with a characteristic **basophilia**. * **Treatment:** The first-line treatment is **Imatinib**, a selective Tyrosine Kinase Inhibitor (TKI) [1]. * **Natural History:** If untreated, CML progresses from a Chronic Phase to an Accelerated Phase and finally a **Blast Crisis** (can be AML or ALL) [2].
Question 718: All of the following are inherited platelet function disorders except?
- A. Bernard-Soulier syndrome
- B. Glanzmann thrombasthenia
- C. Wiskott-Aldrich syndrome
- D. Weber-Christian disease (Correct Answer)
Explanation: The question asks to identify the condition that is **not** an inherited platelet function disorder. **Weber-Christian disease** (Relapsing febrile non-suppurative panniculitis) is the correct answer because it is an inflammatory condition characterized by recurrent nodules of the subcutaneous fat (panniculitis), often accompanied by systemic symptoms like fever. It is **not** a hematological disorder of platelet function. **Analysis of Incorrect Options:** * **Bernard-Soulier Syndrome:** An autosomal recessive disorder caused by a deficiency of the **GpIb-IX-V complex** (the receptor for von Willebrand factor) [1]. It is characterized by giant platelets and failure of platelets to aggregate with Ristocetin. * **Glanzmann Thrombasthenia:** An autosomal recessive disorder caused by a deficiency or dysfunction of **GpIIb/IIIa** (the receptor for fibrinogen) [1]. Platelets fail to aggregate with all agonists (ADP, collagen, epinephrine) except Ristocetin. * **Wiskott-Aldrich Syndrome:** An X-linked recessive disorder characterized by the triad of **thrombocytopenia (with small platelets)**, eczema, and immunodeficiency. It involves a defect in the WASP protein, affecting the platelet cytoskeleton. **NEET-PG High-Yield Pearls:** * **Adhesion Defect:** Bernard-Soulier Syndrome (GpIb deficiency) [1]. * **Aggregation Defect:** Glanzmann Thrombasthenia (GpIIb/IIIa deficiency) [1]. * **Platelet Size:** Giant platelets are seen in Bernard-Soulier; **Small platelets** are a hallmark of Wiskott-Aldrich Syndrome. * **Ristocetin Test:** In Bernard-Soulier, the Ristocetin cofactor assay is abnormal and **does not** correct with the addition of normal plasma (unlike von Willebrand Disease).
Question 719: Which of the following statements regarding hematological malignancies is true?
- A. Chronic myeloid leukemia characteristically occurs in individuals over 50 years of age.
- B. Hairy cell leukemia in individuals less than 50 years of age generally has a good prognosis.
- C. Acute lymphoid leukemia in infants less than 1 year of age has a poor prognosis. (Correct Answer)
- D. Chronic lymphocytic leukemia characteristically occurs in individuals less than 50 years of age.
Explanation: **Explanation:** The prognosis of **Acute Lymphoblastic Leukemia (ALL)** is heavily influenced by age and cytogenetics [1]. In infants (less than 1 year of age), ALL is associated with a very poor prognosis. This is primarily due to the high frequency of the **t(4;11) translocation**, which involves the **MLL (KMT2A) gene** rearrangement [1]. These patients often present with high white blood cell counts, central nervous system involvement, and a poor response to standard chemotherapy. **Analysis of Incorrect Options:** * **Option A:** While Chronic Myeloid Leukemia (CML) can occur at any age, the peak incidence is typically between **40–60 years**. However, it is not "characteristically" restricted to those over 50 in the same way that CLL is associated with the elderly. * **Option B:** Hairy Cell Leukemia (HCL) is a disease of middle-aged to elderly men (median age ~50–55). While it has a good prognosis due to its excellent response to **Cladribine**, it is rare in individuals under 50. * **Option D:** Chronic Lymphocytic Leukemia (CLL) is the most common leukemia in the West and is a disease of the **elderly**. The median age at diagnosis is **70 years**; it is very rare in individuals under 40–50 years of age. **High-Yield Clinical Pearls for NEET-PG:** * **Best Prognosis in ALL:** Age 1–9 years, low WBC count, and **t(12;21)** (ETV6-RUNX1). * **Worst Prognosis in ALL:** Age <1 year or >10 years, high WBC count, and **t(9;22)** (Philadelphia chromosome) or **t(4;11)** [1]. * **CLL Marker:** Characterized by the presence of **Smudge cells** on peripheral smear and **CD5+ B-cells**. * **HCL Marker:** Characterized by **TRAP positivity** and "fried egg" appearance on bone marrow biopsy.
Question 720: What is the intermediate form of Non-Hodgkin's lymphoma?
- A. Small noncleaved cell
- B. Diffuse, small cleaved cell (Correct Answer)
- C. Lymphoblastic
- D. Large cell immunoblastic
Explanation: This question refers to the **Working Formulation for Clinical Usage**, a classification system that categorizes Non-Hodgkin’s Lymphomas (NHL) into three prognostic groups: Low Grade, Intermediate Grade, and High Grade. ### **Explanation of the Correct Answer** **B. Diffuse, small cleaved cell:** Under the Working Formulation, lymphomas are categorized based on their architectural pattern (follicular vs. diffuse) and cell morphology. While follicular lymphomas are generally low-grade, **diffuse** patterns often shift the prognosis toward the **Intermediate Grade**. Specifically, Diffuse small cleaved cell, Diffuse mixed (small and large cell), and Diffuse large cell lymphomas constitute the Intermediate Grade category. ### **Analysis of Incorrect Options** * **A. Small noncleaved cell (Burkitt’s):** This is categorized as a **High Grade** lymphoma. It is characterized by a very high proliferation index and a "starry-sky" appearance on histology. * **C. Lymphoblastic:** This is a **High Grade** lymphoma, typically seen in children and young adults, often presenting with a mediastinal mass (T-cell origin). It is highly aggressive and requires intensive chemotherapy. * **D. Large cell immunoblastic:** This is also a **High Grade** lymphoma. It is an aggressive subtype of diffuse large B-cell lymphoma with distinct prominent nucleoli. ### **High-Yield NEET-PG Pearls** * **Low Grade:** Includes Small Lymphocytic (SLL) and Follicular (predominantly small cleaved). * **Intermediate Grade:** Includes Diffuse small cleaved, Diffuse mixed, and Diffuse large cell. * **High Grade:** Includes Large cell immunoblastic, Lymphoblastic, and Small noncleaved (Burkitt’s). * **Clinical Rule:** Low-grade lymphomas are generally indolent but incurable; High-grade lymphomas are aggressive but have a higher potential for complete cure with intensive treatment. * **Most Common NHL:** Diffuse Large B-Cell Lymphoma (DLBCL), which falls under the Intermediate/High category depending on the specific classification used.
Practice by Chapter
Anemia Evaluation and Management
Practice Questions
Hemoglobinopathies
Practice Questions
Thalassemias
Practice Questions
Platelet Disorders
Practice Questions
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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