Hematology — MCQs
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A 27-year-old female presents with easy fatigue and light-headedness. She also has a dry cough and fever for the past few days. On examination, she is pale, her lungs are clear, and the rest is normal. A chest x-ray shows patchy bilateral infiltrates; the hemoglobin is 8.4 g/dL, reticulocyte count of 6%, and many spherocytes on the peripheral blood film. Which of the following is the most likely significance of the spherocytosis on the blood film?
A 42-year-old male presents with fatigue, pale skin, and exertional dyspnea. Laboratory findings reveal macrocytic, hyperchromic anemia with hyper-segmented neutrophils. Folate levels are normal. The patient reports long-term omeprazole use for gastric reflux disease. Which of the following interventions is indicated for this patient?
In hemophilia, which of the following is raised?
Which of the following statements is NOT true about heparin-induced thrombocytopenia?
Which of the following statements about sickle cell disease is false?
Autoimmune destruction of platelets is seen in which of the following conditions?
All of the following can lead to the development of overt anemia in patients with long-standing compensated hemolytic anemia, EXCEPT:
Which of the following is NOT a side effect of massive blood transfusion?
Which of the following is NOT included in the differential diagnosis of microangiopathic hemolytic anemia?
A 33-year-old alcoholic patient on anti-tuberculosis treatment presents with increased serum iron and increased transferrin saturation. What is the most likely diagnosis?
Hematology Indian Medical PG Practice Questions and MCQs
Question 671: A 27-year-old female presents with easy fatigue and light-headedness. She also has a dry cough and fever for the past few days. On examination, she is pale, her lungs are clear, and the rest is normal. A chest x-ray shows patchy bilateral infiltrates; the hemoglobin is 8.4 g/dL, reticulocyte count of 6%, and many spherocytes on the peripheral blood film. Which of the following is the most likely significance of the spherocytosis on the blood film?
- A. Multiple long bone fractures
- B. Hereditary elliptocytosis
- C. Coombs'-positive hemolytic anemia (Correct Answer)
- D. Glucose-6-phosphate dehydrogenase (G6PD) deficiency
Explanation: ### Explanation The clinical presentation describes a young female with **Autoimmune Hemolytic Anemia (AIHA)**, likely secondary to **Mycoplasma pneumoniae** infection (suggested by the dry cough, fever, and patchy infiltrates on chest X-ray). **1. Why Coombs'-positive Hemolytic Anemia is correct:** The patient has anemia (Hb 8.4 g/dL) with a high reticulocyte count (6%), indicating a hemolytic process. The presence of **spherocytes** on a peripheral smear is a hallmark of two conditions: Hereditary Spherocytosis (HS) and AIHA [1]. In AIHA, antibodies (IgG or IgM) coat the RBCs; as these cells pass through the splenic sinusoids, macrophages "nibble" off portions of the antibody-coated membrane [4]. This reduction in surface area-to-volume ratio forces the cell into a spherical shape. Given the acute respiratory symptoms, **Cold Agglutinin Disease** (a form of AIHA triggered by *Mycoplasma*) is the most likely diagnosis, which would be confirmed by a **Positive Direct Coombs' Test** [1], [3]. **2. Why the other options are incorrect:** * **Multiple long bone fractures:** These are associated with fat embolism syndrome, which presents with petechiae and respiratory distress, not spherocytic hemolytic anemia. * **Hereditary elliptocytosis:** This is a membrane defect characterized by **elliptocytes** (oval-shaped cells), not spherocytes. * **G6PD deficiency:** This typically presents with **Heinz bodies** and **Bite cells** (degmacytes) following oxidative stress, rather than prominent spherocytosis [2]. **3. Clinical Pearls for NEET-PG:** * **Spherocytes + Positive Family History + Splenomegaly** = Hereditary Spherocytosis (Negative Coombs'). * **Spherocytes + Acute onset + Underlying infection/drugs** = AIHA (Positive Coombs') [1]. * *Mycoplasma pneumoniae* is classically associated with **Cold AIHA (IgM)**, which can cause intravascular hemolysis and Raynaud’s phenomenon [3]. * **Warm AIHA (IgG)** is more common and often associated with SLE, CLL, or drugs like Penicillin and Methyldopa [1].
Question 672: A 42-year-old male presents with fatigue, pale skin, and exertional dyspnea. Laboratory findings reveal macrocytic, hyperchromic anemia with hyper-segmented neutrophils. Folate levels are normal. The patient reports long-term omeprazole use for gastric reflux disease. Which of the following interventions is indicated for this patient?
- A. Oral folic acid supplementation
- B. Vitamin B6 injections
- C. Intrinsic factor injections
- D. Vitamin B12 injections (Correct Answer)
Explanation: ### Explanation **Correct Answer: D. Vitamin B12 injections** **1. Why it is correct:** The clinical presentation of **macrocytic anemia** with **hyper-segmented neutrophils** (a hallmark of megaloblastic anemia) combined with normal folate levels points directly to **Vitamin B12 deficiency**. [1] The underlying mechanism here is the patient’s long-term use of **Omeprazole** (a Proton Pump Inhibitor). Gastric acid is essential for releasing Vitamin B12 from dietary proteins. Furthermore, chronic PPI use can lead to atrophic changes in the gastric mucosa. [1] Since the patient has a functional impairment in B12 absorption due to altered gastric pH and potential lack of intrinsic factor, **parenteral (injection) B12** is the preferred route to bypass the gastrointestinal tract and ensure rapid correction of the deficiency. **2. Why the other options are wrong:** * **A. Oral folic acid:** Folate levels are explicitly stated as normal. Giving folic acid in B12 deficiency can improve the anemia but will **not** prevent (and may worsen) subacute combined degeneration of the spinal cord. [2] * **B. Vitamin B6:** B6 (Pyridoxine) is used for sideroblastic anemia (microcytic) or to prevent neuropathy in patients taking Isoniazid, not for megaloblastic anemia. [3] * **C. Intrinsic factor injections:** Intrinsic factor is a protein produced by the stomach; it is not administered via injection as a therapeutic agent. The treatment is to provide the vitamin (B12) itself. **3. NEET-PG High-Yield Pearls:** * **Hyper-segmented neutrophils:** Defined as >5% of neutrophils having 5 lobes or a single neutrophil having ≥6 lobes. This is often the *earliest* sign of megaloblastic anemia. * **Drug-induced B12 deficiency:** Common culprits include **Metformin** (decreases ileal absorption) and **PPIs/H2 Blockers** (decreases acid-pepsin release of B12). * **Schilling Test:** Historically used to differentiate causes of B12 malabsorption (though rarely used in modern practice). * **Neurological symptoms:** Unlike folate deficiency, B12 deficiency presents with neurological deficits (loss of vibration/position sense) due to involvement of the posterior and lateral columns. [2]
Question 673: In hemophilia, which of the following is raised?
- A. Bleeding Time (BT)
- B. Clotting Time (CT)
- C. Prothrombin Time (PT)
- D. Activated Partial Thromboplastin Time (aPTT) (Correct Answer)
Explanation: **Explanation:** Hemophilia (A and B) is a disorder of the **intrinsic pathway** of the coagulation cascade [1]. Hemophilia A is a deficiency of Factor VIII, and Hemophilia B (Christmas disease) is a deficiency of Factor IX [3]. **1. Why aPTT is the correct answer:** The **Activated Partial Thromboplastin Time (aPTT)** measures the integrity of the **intrinsic** and common pathways (Factors XII, XI, IX, VIII, X, V, II, and I) [1]. Since Hemophilia involves a deficiency in Factor VIII or IX, the intrinsic pathway is impaired, leading to a prolonged (raised) aPTT [1]. **2. Why the other options are incorrect:** * **Bleeding Time (BT):** This measures **platelet function** and primary hemostasis (platelet plug formation). In hemophilia, platelet count and function are normal, so BT remains normal. * **Prothrombin Time (PT):** This measures the **extrinsic** and common pathways (specifically Factor VII) [1]. Factors VIII and IX are not involved in the extrinsic pathway; therefore, PT is normal in hemophilia [1]. * **Clotting Time (CT):** While CT can be raised in severe hemophilia, it is a crude, insensitive, and outdated bedside test. In modern clinical practice and medical examinations, **aPTT** is the specific and preferred laboratory parameter for screening coagulation factor deficiencies in the intrinsic pathway. **Clinical Pearls for NEET-PG:** * **Inheritance:** Both Hemophilia A and B are **X-linked recessive** (mostly affecting males) [2]. * **Mixing Study:** If aPTT is prolonged, a mixing study (adding normal plasma) is done [1]. If the aPTT corrects, it indicates a **factor deficiency**; if it doesn't, it suggests an **inhibitor/antibody**. [1] * **vWD vs. Hemophilia:** In von Willebrand Disease, both BT and aPTT can be raised (as vWF stabilizes Factor VIII). In Hemophilia, **only** aPTT is raised. * **Most common site of bleeding:** Hemarthrosis (bleeding into joints, commonly the knee).
Question 674: Which of the following statements is NOT true about heparin-induced thrombocytopenia?
- A. Low molecular weight heparins should not be used for treatment.
- B. It causes both arterial and venous thrombosis.
- C. It is more common with unfractionated heparin than low molecular weight heparin. (Correct Answer)
- D. It typically occurs after about a week of heparin therapy.
Explanation: ### Explanation: Heparin-Induced Thrombocytopenia (HIT) Heparin-Induced Thrombocytopenia (HIT Type II) is an immune-mediated prothrombotic disorder caused by antibodies against the **Platelet Factor 4 (PF4)-Heparin complex**. **1. Analysis of the Correct Answer (Option C):** The question asks for the statement that is **NOT** true. Option C states that HIT is more common with Unfractionated Heparin (UFH) than Low Molecular Weight Heparin (LMWH). **This statement is actually TRUE.** UFH has longer saccharide chains, which more readily form the large, immunogenic complexes with PF4 required to trigger antibody production. Since the statement is true, and the question asks for the "not true" statement, there appears to be a discrepancy in the provided key. In standard medical literature, HIT occurs in ~3–5% of patients on UFH and <1% on LMWH. **2. Analysis of Other Options:** * **Option A (True):** LMWH must **not** be used for treatment because the HIT antibodies cross-react with LMWH, further fueling the prothrombotic state. * **Option B (True):** HIT is paradoxically a **prothrombotic** state [1]. It causes "White Clot Syndrome," leading to both venous (DVT, PE) and arterial (MI, Stroke, limb ischemia) thrombosis. * **Option C (True):** As explained above, UFH is significantly more immunogenic than LMWH. * **Option D (True):** Typical onset is **5–10 days** after starting heparin (the time required for antibody synthesis). **3. High-Yield Clinical Pearls for NEET-PG:** * **Diagnosis:** Use the **4T Score** (Thrombocytopenia, Timing, Thrombosis, and oTher causes). * **Gold Standard Test:** Serotonin Release Assay (SRA). * **Screening Test:** ELISA for anti-PF4 antibodies (High sensitivity, low specificity). * **Management:** Immediately stop all heparin. Start a **Direct Thrombin Inhibitor (DTI)** like **Argatroban** (safe in renal failure) or **Lepirudin/Bivalirudin** [1]. * **Caution:** Do not start Warfarin until the platelet count recovers (>150,000), as it can cause skin necrosis due to rapid Protein C depletion.
Question 675: Which of the following statements about sickle cell disease is false?
- A. Sickle cell trait confers a protective effect against malaria.
- B. There is a replacement of glutamic acid by valine at the beta-6 position.
- C. Hyposthenuria is a characteristic finding.
- D. Hemolysis is predominantly intravascular. (Correct Answer)
Explanation: In Sickle Cell Disease (SCD), the primary mechanism of red cell destruction is extravascular hemolysis [1]. Sickled erythrocytes are rigid and non-deformable; as they pass through the splenic sinusoids, they are recognized as abnormal and sequestered by splenic macrophages [1]. While some minor intravascular hemolysis occurs due to mechanical fragility, the predominant site of destruction is the reticuloendothelial system (spleen and liver). **Analysis of Options:** * **Option A (True):** Sickle cell trait (HbAS) provides a survival advantage against *Plasmodium falciparum* malaria. The parasite consumes oxygen, causing the cell to sickle and be cleared by the spleen, thereby reducing the parasite burden. * **Option B (True):** The molecular basis of SCD is a point mutation (GAG → GTG) in the β-globin gene, resulting in the substitution of **Glutamic acid (polar) by Valine (non-polar)** at the 6th position of the β-chain [2]. * **Option C (True):** **Hyposthenuria** (inability to concentrate urine) is a classic finding. Repeated micro-infarctions in the renal medulla (due to the hypertonic, hypoxic environment) damage the vasa recta, impairing the countercurrent exchange mechanism. **NEET-PG High-Yield Pearls:** 1. **Autosplenectomy:** Repeated splenic infarctions lead to a shrunken, fibrotic spleen by childhood, increasing susceptibility to encapsulated organisms (*S. pneumoniae*, *H. influenzae*) [1]. 2. **Howell-Jolly Bodies:** These nuclear remnants are seen on peripheral smears post-autosplenectomy. 3. **Salmonella Osteomyelitis:** While *S. aureus* is the most common cause of osteomyelitis overall, patients with SCD have a uniquely high predisposition to *Salmonella* species. 4. **Aplastic Crisis:** Most commonly triggered by **Parvovirus B19** infection [1].
Question 676: Autoimmune destruction of platelets is seen in which of the following conditions?
- A. Systemic Lupus Erythematosus (SLE) (Correct Answer)
- B. Polyarteritis Nodosa (PAN)
- C. Rheumatoid Arthritis (RA)
- D. Sarcoidosis
Explanation: **Explanation:** The correct answer is **Systemic Lupus Erythematosus (SLE)**. **1. Why SLE is correct:** SLE is a multisystem autoimmune disorder characterized by the production of various autoantibodies [1]. Hematological involvement is a hallmark of the disease. Thrombocytopenia in SLE occurs primarily due to **immune-mediated destruction of platelets**, where anti-platelet antibodies (IgG) coat the platelets, leading to their premature clearance by the splenic macrophages [2]. This mechanism is identical to **Immune Thrombocytopenic Purpura (ITP)**. In fact, ITP can often be the presenting feature of SLE. **2. Why other options are incorrect:** * **Polyarteritis Nodosa (PAN):** This is a necrotizing vasculitis of medium-sized arteries. While it causes multisystem involvement (renal, GI, skin), it does not typically involve autoantibody-mediated destruction of platelets. * **Rheumatoid Arthritis (RA):** While RA is autoimmune, its primary hematological association is **Felty’s Syndrome** (RA, Splenomegaly, and Neutropenia). Thrombocytopenia is not a classic feature unless secondary to drug toxicity (e.g., methotrexate) or hypersplenism. * **Sarcoidosis:** This is a granulomatous disease. Hematological issues usually involve lymphopenia or anemia of chronic disease. Thrombocytopenia, if present, is usually due to splenic sequestration (splenomegaly) rather than direct autoimmune destruction. **Clinical Pearls for NEET-PG:** * **Evans Syndrome:** The coexistence of Autoimmune Hemolytic Anemia (AIHA) and Immune Thrombocytopenia (ITP); frequently associated with SLE. * **Most common hematological abnormality in SLE:** Anemia of Chronic Disease (however, Lymphopenia is the most *specific* hematologic criteria in the ACR classification) [2]. * **Mechanism:** Type II Hypersensitivity reaction (Antibody-mediated) [3].
Question 677: All of the following can lead to the development of overt anemia in patients with long-standing compensated hemolytic anemia, EXCEPT:
- A. Pregnancy
- B. Renal failure
- C. Folate deficiency
- D. Hypothyroidism (Correct Answer)
Explanation: In patients with **compensated hemolytic anemia**, the bone marrow increases erythropoiesis (up to 6–8 times the normal rate) to match the shortened lifespan of red blood cells. **Overt anemia** occurs when this delicate balance is disrupted, either by an increased demand for RBCs or a decrease in marrow production. ### Why Hypothyroidism is the Correct Answer **Hypothyroidism** typically causes a mild, normocytic, hypoproliferative anemia due to a generalized decrease in metabolic rate and tissue oxygen demand, which leads to reduced erythropoietin (EPO) production. However, it does **not** cause an acute "decompensation" or a sudden crisis in hemolytic states. Unlike the other options, it does not acutely interfere with the high-turnover requirements of a hemolytic marrow. ### Explanation of Incorrect Options * **Pregnancy:** Increases plasma volume (dilutional effect) and significantly raises the demand for RBC production and nutrients. This can tip a compensated state into overt anemia. * **Renal Failure:** Leads to a deficiency in **Erythropoietin (EPO)**. In hemolysis, the marrow requires high levels of EPO to maintain compensation; loss of EPO leads to a rapid drop in hemoglobin. * **Folate Deficiency:** Hemolysis creates a high-turnover state with a massive demand for folate for DNA synthesis. If stores are depleted, a **megaloblastic/aplastic crisis** occurs, causing profound anemia. ### High-Yield Clinical Pearls for NEET-PG * **Aplastic Crisis:** Most commonly caused by **Parvovirus B19**, which infects erythrocyte precursors. * **Megaloblastic Crisis:** Caused by folate deficiency due to chronic hyperactive erythropoiesis. * **Hemolytic Crisis:** An acute acceleration of hemolysis (e.g., G6PD deficiency after oxidant stress). * **Splenic Sequestration:** Common in Sickle Cell Anemia; causes sudden pooling of blood in the spleen and acute anemia.
Question 678: Which of the following is NOT a side effect of massive blood transfusion?
- A. Hypothermia
- B. Hypocalcemia
- C. Hypomagnesemia
- D. Hypokalemia (Correct Answer)
Explanation: Massive blood transfusion (MBT) is defined as the replacement of one total blood volume within 24 hours or 10 units of PRBCs within 24 hours. The correct answer is **Hypokalemia** because MBT typically causes **Hyperkalemia**, not hypokalemia. **1. Why Hypokalemia is the correct (incorrect side effect) answer:** During storage, red blood cells undergo a "storage lesion" where the Na+/K+ ATPase pump fails due to lack of ATP and cold temperatures. This causes potassium to leak out of the cells into the plasma. When multiple units of stored blood are infused rapidly, the high extracellular potassium concentration leads to **Hyperkalemia**, which can cause life-threatening arrhythmias. (Note: Transient hypokalemia may occur later as citrate is metabolized to bicarbonate, causing alkalosis, but hyperkalemia is the classic immediate complication). **2. Why the other options are wrong (actual side effects):** * **Hypothermia (A):** Blood is stored at 4°C. Rapid infusion of large volumes of cold blood lowers the core body temperature, impairing coagulation and increasing the risk of cardiac arrest. * **Hypocalcemia (B):** Citrate is used as an anticoagulant in stored blood. It chelates ionized calcium in the recipient's serum. Rapid transfusion overwhelms the liver's ability to metabolize citrate, leading to symptomatic hypocalcemia (tetany, prolonged QT interval). * **Hypomagnesemia (C):** Similar to calcium, citrate also chelates magnesium, leading to low serum magnesium levels. **Clinical Pearls for NEET-PG:** * **Citrate Toxicity:** Leads to Hypocalcemia and Hypomagnesemia. * **Acid-Base Balance:** Initially, stored blood is acidic (due to lactic acid and citrate); however, the late effect of MBT is **Metabolic Alkalosis** as citrate is converted to bicarbonate by the liver. * **Coagulopathy:** MBT leads to "Dilutional Coagulopathy" (depletion of platelets and clotting factors). * **Lethal Triad of Trauma:** Hypothermia, Acidosis, and Coagulopathy.
Question 679: Which of the following is NOT included in the differential diagnosis of microangiopathic hemolytic anemia?
- A. Sepsis
- B. Hemolytic uremic syndrome
- C. Myocardial infarction (Correct Answer)
- D. Eclampsia
Explanation: **Explanation:** Microangiopathic Hemolytic Anemia (MAHA) is a descriptive term for non-immune hemolytic anemias characterized by **fragmentation of red blood cells (schistocytes)** [1]. This occurs due to mechanical shearing of erythrocytes as they pass through small blood vessels obstructed by fibrin or platelet thrombi [1]. **Why Myocardial Infarction (MI) is the correct answer:** MI is a macrovascular event typically caused by the occlusion of a coronary artery by an atherosclerotic plaque or thrombus. It does not involve systemic microvascular pathology or the mechanical shearing of RBCs. Therefore, it is not a cause of MAHA. **Analysis of Incorrect Options:** * **Sepsis:** Severe sepsis can trigger **Disseminated Intravascular Coagulation (DIC)** [2]. In DIC, widespread fibrin deposition in the microvasculature leads to RBC fragmentation and schistocyte formation [1]. * **Hemolytic Uremic Syndrome (HUS):** This is a classic cause of MAHA, characterized by the triad of microangiopathic anemia, thrombocytopenia, and acute renal failure, typically due to Shiga toxin-induced endothelial damage [1]. * **Eclampsia:** Preeclampsia and eclampsia can lead to **HELLP syndrome** (Hemolysis, Elevated Liver enzymes, Low Platelets), which is a specific form of MAHA occurring in pregnancy [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Hallmark Finding:** The presence of **schistocytes** (helmet cells) on a peripheral blood smear (>1% is significant). * **Laboratory Markers:** Elevated LDH, decreased haptoglobin, and indirect hyperbilirubinemia (all markers of hemolysis), with a **negative Direct Coombs Test** (confirming non-immune etiology). * **Primary Differential (The "Pentad" of TTP):** Fever, Anemia (MAHA), Thrombocytopenia, Neurological symptoms, and Renal failure. * **Other Causes:** Malignant hypertension, Systemic Sclerosis (Scleroderma renal crisis), and prosthetic heart valves (Macroangiopathic) [1].
Question 680: A 33-year-old alcoholic patient on anti-tuberculosis treatment presents with increased serum iron and increased transferrin saturation. What is the most likely diagnosis?
- A. Iron deficiency anemia
- B. Sideroblastic anemia (Correct Answer)
- C. Megaloblastic anemia
- D. Anemia of chronic disease
Explanation: ### Explanation **Correct Answer: B. Sideroblastic Anemia** The clinical presentation points toward **Sideroblastic Anemia**, a defect in heme synthesis. In this condition, iron is available but cannot be incorporated into protoporphyrin to form heme. This leads to iron overload in the mitochondria of erythroid precursors, forming "ringed sideroblasts." * **Underlying Mechanism:** The patient has two major risk factors: **Alcoholism** (a common cause of acquired sideroblastic anemia) and **Anti-Tuberculosis Treatment (Isoniazid)**. Isoniazid is a Vitamin B6 (Pyridoxine) antagonist. Since B6 is a mandatory cofactor for **ALA synthase** (the rate-limiting enzyme in heme synthesis), its deficiency leads to impaired heme production and subsequent iron accumulation. * **Iron Profile:** Because iron is not being utilized, serum iron increases, and transferrin saturation rises, reflecting systemic iron overload. **Why other options are incorrect:** * **A. Iron Deficiency Anemia:** Characterized by *decreased* serum iron and *decreased* transferrin saturation (opposite of this case). * **C. Megaloblastic Anemia:** While common in alcoholics (Folate deficiency), it typically presents with normal or slightly elevated iron; however, it does not explain the specific association with INH or the classic iron-overload profile seen here. * **D. Anemia of Chronic Disease:** Characterized by *decreased* serum iron and *decreased* TIBC due to iron sequestration in macrophages (hepcidin-mediated). **NEET-PG High-Yield Pearls:** * **Gold Standard Diagnosis:** Bone marrow examination showing **Ringed Sideroblasts** (Prussian Blue stain). * **Management:** Discontinue the offending agent (Alcohol/INH) and supplement with **Pyridoxine (Vitamin B6)**. * **Lead Poisoning:** Another cause of sideroblastic anemia; look for "basophilic stippling" and "Burtonian lines" on gums.
Practice by Chapter
Anemia Evaluation and Management
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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
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Myeloproliferative Neoplasms
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Transfusion Medicine
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Hematopoietic Stem Cell Transplantation
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