Hematology — MCQs
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A 48-year-old woman presented with a two-month history of weakness. On examination, cervical lymph nodes were enlarged, and the spleen was palpable 2 cm below the costal margin. Her hemoglobin was 10.5 g/dL, platelet count was 237 x 10^9/L, and total leukocyte count was 40 x 10^9/L, which included 80% mature lymphoid cells with coarse clumped chromatin. Bone marrow revealed a nodular lymphoid infiltrate. The peripheral blood lymphoid cells were positive for CD19, CD5, CD20, and CD23 and were negative for CD79b and FMC-7. What is the most likely diagnosis?
Which of the following is NOT typically seen in hemolytic anemia?
Which of the following conditions has the least 5-year survival rate following allogeneic bone marrow transplantation?
A 78-year-old man presents with anorexia, fatigue, and generally feeling unwell. On examination, he has a large spleen, appears pale, and the rest of the examination is normal. His blood count is abnormal; the WBC is 46000/ml with increased mature granulocytes, hemoglobin 9.0 g/dL, and platelets 450,000/mL. Further investigations reveal BCR-ABL transcripts. T315I mutation is also seen. What is the drug of choice for this condition?
In sickle cell anemia, which of the following is true?
MCV > 100 fL in all of the following except?
What is a characteristic feature of sickle cell trait?
All are true regarding fetal RBCs, EXCEPT:
Gum hypertrophy is a clinical feature of which of the following conditions?
What is the preservation solution used for storing blood for transfusion?
Hematology Indian Medical PG Practice Questions and MCQs
Question 141: A 48-year-old woman presented with a two-month history of weakness. On examination, cervical lymph nodes were enlarged, and the spleen was palpable 2 cm below the costal margin. Her hemoglobin was 10.5 g/dL, platelet count was 237 x 10^9/L, and total leukocyte count was 40 x 10^9/L, which included 80% mature lymphoid cells with coarse clumped chromatin. Bone marrow revealed a nodular lymphoid infiltrate. The peripheral blood lymphoid cells were positive for CD19, CD5, CD20, and CD23 and were negative for CD79b and FMC-7. What is the most likely diagnosis?
- A. T-cell rich B-cell lymphoma with leukemic spillover into the blood.
- B. Chronic lymphocytic leukemia. (Correct Answer)
- C. Mantle cell lymphoma.
- D. A definitive diagnosis cannot be made in this patient without a lymph node biopsy.
Explanation: This case presents a classic clinical and immunophenotypic profile of **Chronic Lymphocytic Leukemia (CLL)**. [1] ### **Why Option B is Correct** The diagnosis is established through a combination of clinical, morphological, and immunophenotypic findings: 1. **Morphology:** The presence of absolute lymphocytosis (>5 x 10⁹/L) with "mature lymphoid cells" showing "coarse clumped chromatin" (soccer-ball appearance) is characteristic of CLL. 2. **Immunophenotype (The Gold Standard):** CLL cells characteristically express B-cell markers (**CD19, CD20**) along with the T-cell marker **CD5** and the activation marker **CD23**. Crucially, CLL is typically **negative for FMC-7 and CD79b** (or expresses them very weakly), which distinguishes it from other B-cell malignancies. [1] 3. **Clinical Presentation:** Generalized lymphadenopathy and splenomegaly in an elderly patient are typical. ### **Why Other Options are Incorrect** * **Option A:** T-cell rich B-cell lymphoma would not typically present with this specific CD5+/CD23+ B-cell immunophenotype or such a high count of mature-appearing lymphocytes in the blood. * **Option B:** **Mantle Cell Lymphoma (MCL)** is the primary differential for CD5+ B-cell malignancies. However, MCL is characteristically **CD23 negative** and **FMC-7/CD79b positive**. [2] * **Option D:** While a biopsy helps in many lymphomas, the **Matutes Scoring System** allows for a definitive diagnosis of CLL based solely on peripheral blood morphology and flow cytometry. ### **High-Yield NEET-PG Pearls** * **Matutes Score:** Points are given for CD5+, CD23+, weak sIg, weak/absent CD79b, and absent FMC-7. A score of 4 or 5 is highly diagnostic of CLL. * **Smudge Cells:** Often seen on peripheral smears due to the fragility of CLL cells. * **Richter Transformation:** The sudden transformation of CLL into an aggressive Diffuse Large B-cell Lymphoma (DLBCL), marked by rapidly enlarging nodes and systemic symptoms. * **ZAP-70 and CD38:** Expression of these markers indicates a poorer prognosis.
Question 142: Which of the following is NOT typically seen in hemolytic anemia?
- A. Yellowing of eyes and sclera
- B. Increased LDH
- C. Decreased haptoglobin
- D. Low reticulocyte count (Correct Answer)
Explanation: In hemolytic anemia, the hallmark is the **premature destruction of red blood cells (RBCs)**. To compensate for this loss, the bone marrow becomes hyperactive, increasing the production and release of immature RBCs into the circulation. Therefore, a **high reticulocyte count** (reticulocytosis) is a characteristic finding, reflecting an appropriate marrow response. A low reticulocyte count suggests a production failure (e.g., aplastic anemia or nutritional deficiencies) rather than hemolysis. **Explanation of Incorrect Options:** * **A. Yellowing of eyes and sclera:** Hemolysis releases hemoglobin, which is metabolized into unconjugated bilirubin. When levels exceed the liver's conjugating capacity, **unconjugated hyperbilirubinemia** occurs, leading to clinical jaundice (icterus). * **B. Increased LDH:** Lactate Dehydrogenase is an enzyme found in high concentrations inside RBCs. When these cells rupture, LDH is released into the serum, making it a sensitive (though non-specific) marker of hemolysis. * **C. Decreased haptoglobin:** Haptoglobin is a plasma protein that binds free hemoglobin. In intravascular hemolysis, haptoglobin levels drop significantly as it is consumed while clearing the released hemoglobin from the circulation [1]. **NEET-PG High-Yield Pearls:** * **Markers of Hemolysis:** ↑ Indirect Bilirubin, ↑ LDH, ↑ Reticulocytes, and ↓ Haptoglobin [1]. * **Aplastic Crisis:** If a patient with chronic hemolysis (like Spherocytosis or Sickle Cell) suddenly presents with a **low reticulocyte count**, suspect **Parvovirus B19 infection**. * **Urinalysis:** Look for hemosiderinuria and hemoglobinuria in cases of intravascular hemolysis [1].
Question 143: Which of the following conditions has the least 5-year survival rate following allogeneic bone marrow transplantation?
- A. Severe Combined Immunodeficiency state
- B. Aplastic Anemia
- C. Blast crisis in Chronic Myeloid Leukemia (Correct Answer)
- D. Chronic lymphocytic leukemia
Explanation: **Explanation:** The success of allogeneic bone marrow transplantation (BMT) depends primarily on the underlying disease state, the patient’s age, and the degree of HLA matching. **Why C is Correct:** **Blast crisis in Chronic Myeloid Leukemia (CML)** represents the terminal phase of the disease, characterized by a high burden of immature blasts and complex genetic mutations. Even with aggressive conditioning and BMT, the risk of **relapse** is extremely high, and the 5-year survival rate is generally the lowest among the options (often **less than 10-20%**) [1]. In contrast, BMT performed during the chronic phase of CML yields much higher survival rates (70-80%). **Why the other options are incorrect:** * **A. Severe Combined Immunodeficiency (SCID):** These patients have the best outcomes (often >80-90% survival) because they are naturally "immunosuppressed," reducing the risk of graft rejection, and the transplant is curative for their genetic defect. * **B. Aplastic Anemia:** In young patients with a matched sibling donor, the 5-year survival rate for BMT is excellent, typically ranging from **70% to 90%**. * **D. Chronic Lymphocytic Leukemia (CLL):** While CLL is usually managed with targeted therapies, BMT is reserved for high-risk cases. However, because CLL is a more indolent (slow-growing) disease compared to CML blast crisis, the survival outcomes are significantly better [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Best prognosis for BMT:** Non-malignant conditions like SCID and Aplastic Anemia. * **CML Timing:** The single most important prognostic factor for BMT in CML is the **stage of disease** at the time of transplant (Chronic phase > Accelerated phase > Blast crisis). * **Graft-versus-Leukemia (GVL) effect:** This is beneficial in CML, but in blast crisis, the disease progression often outpaces the immune system's ability to clear the malignant cells.
Question 144: A 78-year-old man presents with anorexia, fatigue, and generally feeling unwell. On examination, he has a large spleen, appears pale, and the rest of the examination is normal. His blood count is abnormal; the WBC is 46000/ml with increased mature granulocytes, hemoglobin 9.0 g/dL, and platelets 450,000/mL. Further investigations reveal BCR-ABL transcripts. T315I mutation is also seen. What is the drug of choice for this condition?
- A. Bosutinib
- B. Ponatinib (Correct Answer)
- C. Bortezomib
- D. Chlorambucil
Explanation: The clinical presentation of a 78-year-old man with massive splenomegaly, leukocytosis (46,000/mL) with mature granulocytes, and the presence of **BCR-ABL transcripts** (Philadelphia chromosome) confirms the diagnosis of **Chronic Myeloid Leukemia (CML)** [1]. The critical finding in this case is the presence of the **T315I mutation** (often called the "gatekeeper mutation"). This specific mutation involves a threonine-to-isoleucine substitution at position 315, which creates steric hindrance that prevents first-generation (Imatinib) and second-generation (Dasatinib, Nilotinib, Bosutinib) Tyrosine Kinase Inhibitors (TKIs) from binding to the ATP-binding pocket of the BCR-ABL protein [1]. **Why Ponatinib is correct:** **Ponatinib** is a third-generation TKI specifically designed with a carbon-carbon triple bond that bypasses the steric hindrance caused by the T315I mutation. It is currently the only approved TKI effective against CML harboring this specific mutation. **Why other options are incorrect:** * **Bosutinib:** A second-generation TKI. While effective against many mutations, it is ineffective against the T315I mutation [1]. * **Bortezomib:** A proteasome inhibitor used primarily in Multiple Myeloma, not CML. * **Chlorambucil:** An alkylating agent used in Chronic Lymphocytic Leukemia (CLL), not indicated for BCR-ABL positive CML [2]. **Clinical Pearls for NEET-PG:** * **T315I Mutation:** The most common cause of resistance to 1st and 2nd generation TKIs in CML. * **Drug of Choice for CML (General):** Imatinib (1st gen) or Nilotinib/Dasatinib (2nd gen) [1]. * **Drug of Choice for T315I Mutation:** Ponatinib. * **Side Effect Note:** Ponatinib is associated with a high risk of arterial thrombotic events (prothrombotic state). * **Asciminib:** A newer "STAMP" inhibitor (Specifically Targeting the ABL Myristoyl Pocket) is also used for T315I mutations in patients resistant to other therapies.
Question 145: In sickle cell anemia, which of the following is true?
- A. Autosplenectomy due to thrombosis and infarction (Correct Answer)
- B. Microcytosis
- C. Microcardia
- D. Splenomegaly
Explanation: ### Explanation **Correct Option: A. Autosplenectomy due to thrombosis and infarction** In Sickle Cell Anemia (SCA), deoxygenation causes HbS to polymerize, leading to the formation of sickle-shaped erythrocytes [2]. These rigid cells cause **vaso-occlusion** in the microvasculature. The spleen is particularly vulnerable due to its slow circulation and low oxygen tension. Repeated episodes of micro-infarctions and thrombosis lead to progressive fibrosis and shrinkage of the splenic tissue [1]. By adulthood, the spleen becomes a small, fibrous remnant—a process known as **autosplenectomy** [1]. **Why the other options are incorrect:** * **B. Microcytosis:** SCA is typically a **normocytic, normochromic anemia**. Microcytosis is characteristic of Iron Deficiency Anemia or Thalassemia. If a sickle cell patient has microcytosis, it usually suggests a co-existing α or β-thalassemia trait. * **C. Microcardia:** Patients with chronic severe anemia like SCA develop a hyperdynamic circulation to compensate for low oxygen-carrying capacity. This leads to **cardiomegaly** (enlarged heart) and potentially high-output heart failure, not microcardia [1]. * **D. Splenomegaly:** While splenomegaly can occur in children during the early stages of SCA (or in Sickle-Thalassemia/HbSC disease), it is not the definitive long-term fate in classic SCA [1]. Eventually, the spleen undergoes atrophy (autosplenectomy). **High-Yield Clinical Pearls for NEET-PG:** * **Howell-Jolly Bodies:** Their presence on a peripheral smear is a hallmark of functional asplenia/autosplenectomy. * **Infection Risk:** Autosplenectomy increases susceptibility to **encapsulated organisms** (*S. pneumoniae, H. influenzae, N. meningitidis*). * **Splenic Sequestration Crisis:** A life-threatening complication in children where blood is trapped in the spleen, leading to sudden splenomegaly and hypovolemic shock [1]. * **Salmonella Osteomyelitis:** SCA patients have a unique predisposition to *Salmonella* bone infections.
Question 146: MCV > 100 fL in all of the following except?
- A. Alcoholic liver disease
- B. Folate deficiency
- C. Reticulocytosis
- D. Lead poisoning (Correct Answer)
Explanation: **Explanation:** The Mean Corpuscular Volume (MCV) measures the average size of red blood cells (RBCs). An MCV > 100 fL indicates **macrocytosis**, while an MCV < 80 fL indicates **microcytosis** [2]. **Why Lead Poisoning is the Correct Answer:** Lead poisoning is a classic cause of **microcytic hypochromic anemia** (MCV < 80 fL). Lead inhibits key enzymes in the heme synthesis pathway, specifically **delta-aminolevulinate dehydratase (ALAD)** and **ferrochelatase**. This inhibition prevents the incorporation of iron into protoporphyrin, resulting in smaller, pale RBCs. Therefore, it does not cause macrocytosis. **Analysis of Incorrect Options:** * **Alcoholic Liver Disease:** Chronic alcohol consumption is a common cause of non-megaloblastic macrocytosis. It occurs due to the direct toxic effect of ethanol on the bone marrow and alterations in the RBC lipid membrane. * **Folate Deficiency:** This leads to **megaloblastic anemia** [3]. Lack of folate impairs DNA synthesis (specifically thymidine production), resulting in nuclear-cytoplasmic dyssynchrony where the cell grows but cannot divide its nucleus properly, leading to very high MCV (>110 fL) [3]. * **Reticulocytosis:** Reticulocytes (immature RBCs) are physically larger than mature erythrocytes. In conditions with high RBC turnover (like hemolysis), a high reticulocyte count will falsely elevate the average MCV. **NEET-PG High-Yield Pearls:** 1. **Basophilic Stippling:** A hallmark of lead poisoning (due to inhibition of pyrimidine 5'-nucleotidase), though also seen in thalassemia [1]. 2. **Burton’s Line:** Bluish-purple line on the gums associated with chronic lead poisoning [4]. 3. **Megaloblastic vs. Non-megaloblastic:** Folate/B12 deficiency shows hypersegmented neutrophils; Alcohol/Hypothyroidism/Liver disease typically do not. 4. **Drug-induced Macrocytosis:** Common culprits include Hydroxyurea, Methotrexate, and Zidovudine.
Question 147: What is a characteristic feature of sickle cell trait?
- A. Anemia
- B. Bony pain
- C. Dactylitis
- D. Isosthenuria (Correct Answer)
Explanation: **Explanation:** **Sickle Cell Trait (HbAS)** occurs when an individual inherits one normal hemoglobin gene (HbA) and one sickle gene (HbS). Unlike Sickle Cell Disease (HbSS), the trait is generally a benign, asymptomatic carrier state. **Why Isosthenuria is the Correct Answer:** The most common clinical manifestation of sickle cell trait is **isosthenuria** (the inability to concentrate or dilute urine, resulting in a fixed specific gravity). This occurs because the renal medulla is a hypoxic and hypertonic environment, which triggers localized sickling in the vasa recta. This leads to subclinical micro-infarctions (renal papillary necrosis), impairing the countercurrent exchange mechanism. Another common finding in trait patients is **painless hematuria**. **Why the Other Options are Incorrect:** * **A. Anemia:** Patients with sickle cell trait have normal hemoglobin levels, normal RBC indices, and a normal peripheral smear [1]. Significant anemia suggests HbSS or another hemoglobinopathy. * **B. Bony pain & C. Dactylitis:** These are hallmarks of **Vaso-occlusive Crises (VOC)**. In HbAS, the concentration of HbS is typically <40%, which is insufficient to cause spontaneous sickling or systemic VOC under physiological conditions [2]. These symptoms only occur in HbAS under extreme circumstances (e.g., severe hypoxia at high altitudes or extreme physical exertion). **High-Yield Clinical Pearls for NEET-PG:** * **Screening Test:** Solubility test (Sodium dithionite test) is positive in both trait and disease. * **Confirmatory Test:** Hb Electrophoresis (HbAS shows HbA > HbS; HbSS shows no HbA). * **Renal Association:** Sickle cell trait is a recognized risk factor for **Renal Medullary Carcinoma**, a highly aggressive malignancy. * **Protection:** HbAS provides a survival advantage against severe *Plasmodium falciparum* malaria.
Question 148: All are true regarding fetal RBCs, EXCEPT:
- A. Elevated 2,3-DPG (Correct Answer)
- B. Decreased carbonic anhydrase activity
- C. Decreased life span
- D. High RBC volume
Explanation: The correct answer is **A. Elevated 2,3-DPG**. This is false because fetal RBCs actually have a **decreased affinity for 2,3-DPG**. [1], [2] **1. Why Option A is the Correct Answer (The False Statement):** Fetal hemoglobin (HbF) consists of two alpha and two gamma chains ($\alpha_2\gamma_2$). The gamma chains lack certain binding sites for 2,3-Bisphosphoglycerate (2,3-DPG) compared to the beta chains in adult hemoglobin (HbA). Because HbF binds 2,3-DPG poorly, the hemoglobin remains in a "relaxed" state with a **higher affinity for oxygen**. This creates a partial pressure gradient that allows the fetus to effectively "pull" oxygen from maternal blood across the placenta. [1], [2] **2. Analysis of Other Options:** * **B. Decreased carbonic anhydrase activity:** This is a **true** characteristic. Fetal RBCs have significantly lower levels of carbonic anhydrase compared to adult cells, which results in a slower conversion of $CO_2$ to bicarbonate. * **C. Decreased life span:** This is **true**. Fetal RBCs have a shorter survival time (approximately **60–90 days**) compared to the 120-day lifespan of adult RBCs. This contributes to the physiological jaundice often seen in neonates. * **D. High RBC volume:** This is **true**. Fetal RBCs are **macrocytic** (Mean Corpuscular Volume is typically >110 fL at birth). [2] The hematocrit and hemoglobin levels are also physiologically higher at birth to compensate for the relatively hypoxic intrauterine environment. [1] **Clinical Pearls for NEET-PG:** * **P50 Value:** The P50 (partial pressure of $O_2$ at which Hb is 50% saturated) is **lower** in fetuses (~19 mmHg) than in adults (~27 mmHg), representing a **left shift** in the oxygen dissociation curve. [1] * **Apt Test:** Used to differentiate maternal blood from fetal blood (HbF is resistant to alkali denaturation, whereas HbA is not). * **Kleihauer-Betke Test:** Used to quantify fetal-maternal hemorrhage by identifying HbF-containing cells in maternal circulation.
Question 149: Gum hypertrophy is a clinical feature of which of the following conditions?
- A. Acute Myeloid Leukemia (AML) (Correct Answer)
- B. Mitral Stenosis (MS)
- C. Acute Lymphocytic Leukemia (ALL)
- D. Non-Hodgkin Lymphoma (NHL)
Explanation: **Explanation:** **1. Why AML is the correct answer:** Gum hypertrophy (gingival hyperplasia) is a classic clinical sign associated with **Acute Myeloid Leukemia (AML)**, specifically the monocytic subtypes [1]. Under the French-American-British (FAB) classification, these are **M4 (Acute Myelomonocytic Leukemia)** and **M5 (Acute Monocytic Leukemia)**. The underlying mechanism involves the infiltration of the gingival tissues by malignant leukemic blasts (monoblasts and myeloblasts). This leads to swelling, redness, and sometimes bleeding of the gums. **2. Why the other options are incorrect:** * **Mitral Stenosis (MS):** This is a valvular heart disease. While it can cause "Malar flush" (pinkish-purple patches on the cheeks) due to low cardiac output and systemic vasoconstriction, it has no association with gingival changes. * **Acute Lymphocytic Leukemia (ALL):** While ALL is the most common leukemia in children and presents with bone pain and lymphadenopathy, it rarely causes tissue infiltration like gum hypertrophy. * **Non-Hodgkin Lymphoma (NHL):** NHL primarily presents with painless lymphadenopathy or extranodal involvement (like the GI tract or skin), but gingival hypertrophy is not a characteristic diagnostic feature. **3. NEET-PG High-Yield Pearls:** * **Mnemonic for Gum Hypertrophy in AML:** Remember **"M4 and M5"** as the "Mouth" subtypes. * **Other causes of Gum Hypertrophy:** Often tested as a "Differential Diagnosis" question: 1. **Drugs:** Phenytoin (Antiepileptic) [2], Cyclosporine (Immunosuppressant), and Nifedipine/Verapamil (Calcium Channel Blockers). 2. **Scurvy:** Vitamin C deficiency. 3. **Pregnancy:** Due to hormonal changes. * **Auer Rods:** These are pathognomonic for AML (especially M3) but are **absent** in ALL.
Question 150: What is the preservation solution used for storing blood for transfusion?
- A. Heparin + dextrose
- B. Citrate + glucose
- C. EDTA
- D. CDP-A (Correct Answer)
Explanation: **Explanation:** The correct answer is **CPD-A (Citrate Phosphate Dextrose Adenine)**. This is the standard preservative solution used in blood banking to maintain the viability and function of red blood cells (RBCs) during storage. **Why CPD-A is the correct choice:** Each component of CPD-A serves a specific physiological purpose: * **Citrate:** Acts as an anticoagulant by chelating calcium ions, preventing the coagulation cascade. * **Phosphate:** Acts as a buffer to maintain the pH of the blood, preventing excessive acidity during storage. * **Dextrose (Glucose):** Provides a substrate for glycolysis, allowing the RBCs to generate ATP. * **Adenine:** Enhances ATP synthesis, which extends the shelf life of the blood from 21 days (standard CPD) to **35 days**. **Analysis of Incorrect Options:** * **A & B (Heparin/Citrate + Glucose):** While citrate and glucose are components, they lack the buffering capacity of phosphate and the ATP-boosting properties of adenine, leading to a shorter shelf life and poorer cell survival. Heparin is rarely used as it is not a preservative and activates platelets. * **C (EDTA):** While EDTA is an excellent anticoagulant for laboratory hematology (CBC), it is **never** used for transfusion because it damages RBC membranes and is toxic in large systemic doses [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Shelf Life:** CPD-A extends storage to **35 days**. If SAGM (Saline-Adenine-Glucose-Mannitol) is added, storage extends to **42 days**. * **Storage Temperature:** Whole blood/RBCs must be stored at **2°C to 6°C**. * **Storage Lesion:** During storage, there is a decrease in 2,3-DPG (shifting the oxygen dissociation curve to the left) and an increase in extracellular Potassium (risk of hyperkalemia in neonates/massive transfusions).
Practice by Chapter
Anemia Evaluation and Management
Practice Questions
Hemoglobinopathies
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Thalassemias
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Platelet Disorders
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Coagulation Disorders
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Thrombotic Disorders
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Leukemias
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Lymphomas
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Multiple Myeloma and Plasma Cell Disorders
Practice Questions
Myeloproliferative Neoplasms
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Transfusion Medicine
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Hematopoietic Stem Cell Transplantation
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