Hematology — MCQs

Hematology Indian Medical PG Practice Questions and MCQs

Question 771: Thrombocytosis is a recognized feature of which of the following conditions?

A. Myelofibrosis
B. Systemic lupus erythematosus
C. Azidothymidine therapy (Correct Answer)
D. Myelodysplastic syndrome

Explanation: AZT therapy is classically associated with bone marrow suppression, leading to macrocytic anemia and neutropenia [2]. However, a unique and paradoxical hematological feature of AZT therapy is **rebound or reactive thrombocytosis**. While the exact mechanism is not fully elucidated, it is believed to be a compensatory response or a direct stimulatory effect on megakaryopoiesis during the recovery phase of marrow suppression. **Analysis of Incorrect Options:** * **A. Myelofibrosis:** In the early (pre-fibrotic) stage, there may be thrombocytosis; however, the hallmark of established Primary Myelofibrosis is **thrombocytopenia** due to progressive bone marrow fibrosis and splenic sequestration (massive splenomegaly). * **B. Systemic Lupus Erythematosus (SLE):** SLE is typically associated with **thrombocytopenia** (immune-mediated destruction) as part of the ACR diagnostic criteria [1]. While reactive thrombocytosis can occur during acute inflammation, it is not a "recognized feature" compared to the characteristic cytopenias. * **D. Myelodysplastic Syndrome (MDS):** MDS is characterized by ineffective hematopoiesis leading to **cytopenias** (anemia, neutropenia, and thrombocytopenia). An exception is the 5q- syndrome, which may present with normal or elevated platelets, but overall, MDS is synonymous with low counts. **NEET-PG High-Yield Pearls:** * **AZT Side Effects:** Macrocytic anemia (most common), nail hyperpigmentation, and myopathy [2]. * **Reactive Thrombocytosis:** Most commonly caused by iron deficiency anemia, acute hemorrhage, and post-splenectomy states. * **Drug-induced Thrombocytopenia:** Common culprits include Heparin (HIT), Quinine, and Sulfonamides [1].

Question 772: Which of the following is absent in hemolytic anemia?

A. Increased indirect bilirubin
B. Increased direct bilirubin (Correct Answer)
C. Increased reticulocyte count
D. Jaundice

Explanation: In hemolytic anemia, the primary pathology is the accelerated destruction of red blood cells (RBCs). Understanding the metabolic pathway of hemoglobin is key to answering this question. ### **Why "Increased Direct Bilirubin" is the Correct Answer** When RBCs break down, hemoglobin is released and converted into **unconjugated (indirect) bilirubin**. This indirect bilirubin is water-insoluble and travels to the liver to be conjugated. In hemolysis, the liver's capacity to conjugate bilirubin is overwhelmed by the sheer volume of heme breakdown products [3]. However, the liver still functions normally and excretes the conjugated (direct) bilirubin into the bile duct. Therefore, the excess bilirubin circulating in the blood remains in the **unconjugated** form. **Increased direct (conjugated) bilirubin** is a hallmark of obstructive jaundice or hepatocellular injury, not hemolysis [1]. ### **Explanation of Incorrect Options** * **A. Increased indirect bilirubin:** This is the classic laboratory finding in hemolysis. The rapid breakdown of RBCs leads to an accumulation of unconjugated bilirubin before the liver can process it [3]. * **C. Increased reticulocyte count:** This is the bone marrow's physiological response to anemia. To compensate for the loss of RBCs, the marrow increases erythropoiesis, releasing immature RBCs (reticulocytes) into the peripheral blood. * **D. Jaundice:** Jaundice occurs when serum bilirubin levels exceed ~2-2.5 mg/dL. In hemolysis, the high levels of indirect bilirubin lead to "acholuric jaundice" (jaundice without bilirubin in the urine) [3]. ### **NEET-PG High-Yield Pearls** * **Markers of Hemolysis:** ↑ Indirect Bilirubin, ↑ LDH, ↑ Reticulocyte count, and **↓ Haptoglobin** (haptoglobin binds free hemoglobin) [2]. * **Urine Findings:** In hemolytic anemia, you will see **increased urobilinogen** but **absent urinary bilirubin** (because indirect bilirubin is not water-soluble and cannot pass the glomerular basement membrane) [1, 4]. * **Direct vs. Indirect:** If Direct Bilirubin is >50% of total bilirubin, think cholestasis/obstruction. If Indirect is >80-85%, think hemolysis or Gilbert’s syndrome [4].

Question 773: Iron deficiency is best demonstrated by?

A. RDW
B. S. ferritin (Correct Answer)
C. BM examination
D. Differential leucocyte count

Explanation: **Explanation:** **Serum Ferritin** is the single most accurate and reliable non-invasive test for diagnosing Iron Deficiency Anemia (IDA). Ferritin is the primary storage protein for iron; its levels in the blood are directly proportional to the total body iron stores [1]. A low serum ferritin level (<15–30 ng/mL) is highly specific and indicates depleted iron stores, which is the earliest stage of iron deficiency. **Analysis of Options:** * **RDW (Red Cell Distribution Width):** While RDW increases early in IDA (indicating anisocytosis), it is a non-specific marker. It can also be elevated in Vitamin B12/Folate deficiency or sideroblastic anemia. * **BM (Bone Marrow) Examination:** Historically, Prussian blue staining of bone marrow aspirate was the "Gold Standard" for assessing iron stores (hemosiderin) [1]. However, it is an invasive, painful, and expensive procedure. Examination of the marrow may ultimately be required to assess iron stores directly in difficult cases [2]. * **Differential Leucocyte Count (DLC):** This measures white blood cells and has no diagnostic value in assessing iron status. **NEET-PG High-Yield Pearls:** * **Earliest indicator of IDA:** Increased RDW. * **Best biochemical test/Best screening test:** Serum Ferritin [1]. * **Gold Standard (Invasive):** Bone marrow iron (Prussian blue stain) [1][2]. * **Confirmatory test for IDA:** Response to oral iron therapy (increase in Reticulocyte count within 5–7 days) [2]. * **Note:** Ferritin is an **Acute Phase Reactant**. In the presence of inflammation, infection, or malignancy, ferritin levels may be falsely normal or high despite underlying iron deficiency [2]. In such cases, Transferrin Saturation (<16%) is used.

Question 774: What is the first-line treatment for the T315I mutation in Chronic Myeloid Leukemia (CML) management?

A. Bosutinib
B. Tofacitinib
C. Ponatinib (Correct Answer)
D. Nilotinib

Explanation: **Explanation:** Chronic Myeloid Leukemia (CML) is characterized by the BCR-ABL1 fusion gene [2]. While first and second-generation Tyrosine Kinase Inhibitors (TKIs) are effective, resistance often develops due to mutations in the ABL kinase domain [1]. **1. Why Ponatinib is correct:** The **T315I mutation** (often called the "gatekeeper mutation") involves a substitution of threonine with isoleucine at position 315. This change creates a bulky side chain that sterically hinders the binding of most TKIs. **Ponatinib** is a third-generation TKI specifically designed with a carbon-carbon triple bond ethynyl linkage that bypasses this steric hindrance, making it the **first-line and only standard TKI effective against the T315I mutation.** **2. Why other options are incorrect:** * **Bosutinib (Option A):** A second-generation TKI. While effective against many mutations, it is ineffective against T315I. * **Tofacitinib (Option B):** This is a JAK inhibitor used in rheumatoid arthritis and ulcerative colitis; it has no role in BCR-ABL1 inhibition. * **Nilotinib (Option D):** A second-generation TKI. Like Imatinib and Dasatinib, it cannot bind to the ABL kinase domain when the T315I mutation is present [2]. **Clinical Pearls for NEET-PG:** * **Asciminib:** A newer "STAMP" inhibitor (Specifically Targeting the ABL Myristoyl Pocket) is also effective against T315I and is used in resistant cases. * **Side Effect Alert:** Ponatinib is associated with a high risk of **arterial occlusive events** (thrombosis) and hypertension; patients must be monitored for cardiovascular complications. * **Imatinib:** Still the first-line treatment for standard (non-mutated) chronic phase CML [2].

Question 775: Pseudotumor syndrome is seen in which condition?

A. Systemic lupus erythematosus
B. Thalassemia
C. Hemophilia (Correct Answer)
D. Hyperparathyroidism

Explanation: Explanation: Hemophilic Pseudotumor is a rare but serious complication occurring in approximately 1–2% of patients with severe hemophilia (Factor VIII or IX deficiency). Why Hemophilia is correct: A pseudotumor is essentially a chronic, encapsulated, progressive hematoma. It occurs due to repeated subperiosteal or soft tissue hemorrhages, most commonly in the long bones (femur, pelvic bones) or small bones of the hands/feet [1]. The pressure from the expanding hematoma causes pressure necrosis of the surrounding muscles and bone destruction, mimicking a neoplastic process (hence the name "pseudotumor") [1]. On X-ray, it appears as a well-demarcated lytic lesion with cortical thinning. Why other options are incorrect: * Systemic Lupus Erythematosus (SLE): While SLE can cause "Pseudotumor Cerebri" (idiopathic intracranial hypertension) due to venous sinus thrombosis or vasculitis, the term "Pseudotumor syndrome" in a hematological context specifically refers to the hemophilic complication. * Thalassemia: Thalassemia is associated with extramedullary hematopoiesis, which can present as masses (often paravertebral), but these are not referred to as pseudotumors. * Hyperparathyroidism: This condition leads to "Brown Tumors" (osteitis fibrosa cystica) due to increased osteoclast activity, not hematoma formation. High-Yield Clinical Pearls for NEET-PG: * Most common site: The femur is the most common site in adults; small bones of the hand/foot in children. * Management: Conservative management with factor replacement is the first line; however, large pseudotumors often require surgical excision or radiation [1]. * Radiology: Look for a "soap bubble" appearance or large soft tissue mass with adjacent bone erosion [1].

Question 776: A patient underwent bilateral adrenalectomy for bilateral pheochromocytoma. One day later, the patient developed lethargy, fatigue, low blood pressure, and a normal pulse. There are no signs of volume deficit. What is the likely course?

A. Addisonian Crisis (Correct Answer)
B. SIADH
C. Diabetes Insipidus (DI)
D. Cerebral Salt Wasting Syndrome

Explanation: ### Explanation **Correct Option: A. Addisonian Crisis** The patient has undergone a **bilateral adrenalectomy**, which involves the surgical removal of both adrenal glands. This results in an immediate and total deficiency of cortisol and mineralocorticoids. Without immediate glucocorticoid replacement therapy, the patient enters an **acute adrenal crisis (Addisonian Crisis)**. [1] * **Clinical Presentation:** The lethargy, fatigue, and hypotension described are classic signs. The crisis is often precipitated by surgery. [1] * **Key Feature:** The presence of **low blood pressure with a normal pulse** (or lack of compensatory tachycardia) is a high-yield sign of adrenal insufficiency, as cortisol is required for the permissive action of catecholamines on the vasculature. Primary adrenal insufficiency due to destruction of the adrenal cortex is known as Addison disease. [2] **Why Incorrect Options are Wrong:** * **B. SIADH:** While SIADH can cause lethargy due to hyponatremia, it typically presents with normovolemia and *not* hypotension. It is usually a complication of CNS or pulmonary pathology, not adrenal surgery. * **C. Diabetes Insipidus (DI):** DI presents with polyuria, polydipsia, and signs of dehydration (volume deficit). This patient has no signs of volume deficit. * **D. Cerebral Salt Wasting (CSW):** CSW involves renal salt loss leading to hyponatremia and **significant volume depletion**. The question explicitly states there are no signs of volume deficit. **NEET-PG High-Yield Pearls:** 1. **Post-Adrenalectomy Protocol:** Patients undergoing bilateral adrenalectomy require lifelong glucocorticoid and mineralocorticoid replacement. [3] Stress-dose steroids must be administered perioperatively to prevent crisis. 2. **Waterhouse-Friderichsen Syndrome:** Another cause of acute adrenal crisis, usually due to meningococcemia-induced adrenal hemorrhage. 3. **Electrolyte Pattern:** In a crisis, look for **Hyponatremia, Hyperkalemia, and Hypoglycemia** (though not mentioned here, these are classic board findings). 4. **Refractory Hypotension:** Hypotension that does not respond to fluids or vasopressors should always raise suspicion of adrenal insufficiency.

Question 777: Microangiopathic hemolytic anemia is seen in all of the following diseases except?

A. Antiphospholipid antibody syndrome (Correct Answer)
B. Thrombotic thrombocytopenic purpura
C. Microscopic polyangitis
D. Metallic cardiac valves

Explanation: Microangiopathic Hemolytic Anemia (MAHA) is a descriptive term for non-immune hemolytic anemias caused by the mechanical fragmentation of red blood cells (schistocytes) as they pass through narrowed or obstructed small blood vessels [1]. **Why Antiphospholipid Antibody Syndrome (APS) is the correct answer:** While APS is a prothrombotic state, its primary pathology involves **macrovascular** thrombosis (large venous or arterial clots) and obstetric complications. It does not typically cause the mechanical fragmentation of RBCs in the microvasculature. While a rare variant called "Catastrophic APS" can mimic MAHA, classic APS is not a primary cause of microangiopathic hemolysis. **Analysis of Incorrect Options:** * **Thrombotic Thrombocytopenic Purpura (TTP):** This is the classic cause of MAHA. Deficiency of ADAMTS13 leads to large vWF multimers that create "platelet strings" in capillaries, shearing RBCs [1]. * **Microscopic Polyangiitis (MPA):** As a small-vessel vasculitis, MPA causes inflammation and fibrinoid necrosis of arterioles and capillaries [1]. This damaged endovascular surface leads to the formation of schistocytes. * **Metallic Cardiac Valves:** This causes **Macroangiopathic** hemolytic anemia. However, in the context of NEET-PG questions, "mechanical" or "prosthetic valve hemolysis" is frequently grouped under the broad umbrella of fragmentation anemias alongside MAHA due to the shared mechanism of physical RBC destruction. **NEET-PG High-Yield Pearls:** * **Hallmark Lab Finding:** Schistocytes (helmet cells) on peripheral smear and elevated LDH. * **The "Pentad" of TTP:** Fever, Anemia (MAHA), Thrombocytopenia, Neurological symptoms, and Renal failure [1]. * **Differential Diagnosis:** Always consider HUS (especially in children with E. coli O157:H7), HELLP syndrome in pregnancy, and DIC [1]. * **Rule of Thumb:** If the question asks for MAHA, look for conditions causing "micro-thrombi" or "vessel wall roughness."

Question 778: Neurological symptoms and premature graying of hair are associated with which of the following conditions?

A. Folic acid deficiency
B. Pernicious anemia (Correct Answer)
C. Plummer-Vinson syndrome
D. Paterson-Kelly syndrome

Explanation: **Explanation:** The correct answer is **Pernicious Anemia (Option B)**. This condition is an autoimmune disorder characterized by the destruction of gastric parietal cells, leading to a deficiency of **Intrinsic Factor (IF)**. Since IF is essential for the absorption of Vitamin B12 in the terminal ileum, its absence results in Vitamin B12 deficiency [1]. **Why Pernicious Anemia is correct:** 1. **Neurological Symptoms:** Vitamin B12 is crucial for myelin synthesis. Deficiency leads to **Subacute Combined Degeneration (SCD)** of the spinal cord, involving the posterior and lateral columns. Symptoms include loss of vibration/position sense, paresthesia, and ataxia. 2. **Premature Graying of Hair:** Vitamin B12 deficiency is a well-documented cause of reversible premature graying (canities) and skin hyperpigmentation. **Analysis of Incorrect Options:** * **Option A (Folic acid deficiency):** While it causes megaloblastic anemia similar to B12 deficiency, it **does not** cause neurological symptoms or premature graying. * **Options C & D (Plummer-Vinson / Paterson-Kelly syndrome):** These are synonyms for the same condition characterized by the triad of **Iron Deficiency Anemia, esophageal webs, and dysphagia**. It is associated with glossitis and koilonychia, but not neurological deficits or graying hair. **High-Yield Clinical Pearls for NEET-PG:** * **Schilling Test:** Historically used to diagnose Pernicious Anemia (now largely replaced by Anti-Intrinsic Factor and Anti-Parietal cell antibody titers). * **MCV:** Typically >100 fL (Megaloblastic). * **Peripheral Smear:** Shows hypersegmented neutrophils (earliest sign) and macro-ovalocytes. * **Metabolic Markers:** Both **Methylmalonic acid (MMA)** and **Homocysteine** levels are elevated in B12 deficiency (only Homocysteine is elevated in Folate deficiency).

Question 779: All are true in megaloblastic anemia except?

A. Microcytes (Correct Answer)
B. Megakaryocytes
C. Decrease in platelets
D. Neurological symptoms

Explanation: Explanation: Megaloblastic anemia is a type of macrocytic anemia primarily caused by a deficiency in Vitamin B12 or Folic acid [1]. These vitamins are essential cofactors for DNA synthesis. 1. Why "Microcytes" is the correct answer (The Exception): In megaloblastic anemia, impaired DNA synthesis leads to "nuclear-cytoplasmic asynchrony." While the nucleus matures slowly, the cytoplasm continues to grow, resulting in abnormally large cells. Therefore, the hallmark peripheral smear finding is Macrocytes (specifically oval macrocytes), not microcytes. Microcytes are characteristic of iron deficiency anemia or thalassemias. 2. Analysis of other options: * Megakaryocytes: These are the precursor cells for platelets in the bone marrow. In megaloblastic anemia, the marrow is hypercellular and contains giant, abnormal megakaryocytes with multi-lobed nuclei due to defective DNA synthesis. * Decrease in platelets: Severe megaloblastic anemia often leads to pancytopenia (reduction in RBCs, WBCs, and platelets) because the ineffective erythropoiesis affects all cell lines in the bone marrow. * Neurological symptoms: This is a classic feature of Vitamin B12 deficiency (Subacute Combined Degeneration of the spinal cord), presenting as loss of vibration/position sense, paresthesia, and ataxia. Note: Folic acid deficiency does not cause neurological symptoms. NEET-PG High-Yield Pearls: * Peripheral Smear: Look for Hypersegmented Neutrophils (earliest sign) and Howell-Jolly bodies. * Bone Marrow: Shows "sieve-like" chromatin and megaloblastic changes. * Biochemical markers: Increased Homocysteine (both B12 and Folate deficiency) and increased Methylmalonic Acid (MMA) (specific to B12 deficiency only). * Schilling Test: Historically used to determine the cause of B12 malabsorption (e.g., Pernicious Anemia).

Question 780: Which of the following presents with microcytic, hypochromic anemia?

A. Megaloblastic anemia
B. Iron deficiency anemia (Correct Answer)
C. Aplastic anemia
D. All of the above

Explanation: **Explanation:** **1. Why Iron Deficiency Anemia (IDA) is correct:** Microcytic, hypochromic anemia is characterized by a Mean Corpuscular Volume (MCV) < 80 fL and Mean Corpuscular Hemoglobin Concentration (MCHC) < 32 g/dL. In IDA, iron—a critical component of the heme molecule—is deficient. This leads to a decrease in hemoglobin synthesis. To compensate for the lack of hemoglobin, erythroid precursors undergo additional cell divisions, resulting in smaller (microcytic) and paler (hypochromic) red blood cells [1]. **2. Why other options are incorrect:** * **Megaloblastic Anemia:** This is a **macrocytic** anemia (MCV > 100 fL). It is caused by impaired DNA synthesis (usually due to Vitamin B12 or Folate deficiency), leading to nuclear-cytoplasmic asynchrony where the cell grows but cannot divide properly. * **Aplastic Anemia:** This is typically a **normocytic, normochromic** anemia [2]. It involves bone marrow failure leading to pancytopenia (reduction in RBCs, WBCs, and platelets) without a change in the size or color of the individual red cells. **3. NEET-PG High-Yield Pearls:** * **Differential Diagnosis for Microcytic Hypochromic Anemia (Mnemonic: TAILS):** **T**halassemia, **A**nemia of Chronic Disease (late stage), **I**ron Deficiency, **L**ead Poisoning, **S**ideroblastic Anemia [1]. * **Gold Standard Investigation for IDA:** Bone marrow aspiration (Prussian Blue staining for iron stores); however, **Serum Ferritin** is the most sensitive initial biochemical test. * **Mentzer Index:** (MCV/RBC count) — If < 13, it suggests Thalassemia; if > 13, it suggests Iron Deficiency Anemia.

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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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Hematology — MCQs

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