Hematology — MCQs

Hematology Indian Medical PG Practice Questions and MCQs

Question 361: All of the following conditions are acquired causes of iron overload, EXCEPT:

A. Sideroblastic anemia
B. Chronic Hepatitis C
C. Nonalcoholic steatohepatitis
D. Hypothyroidism (Correct Answer)

Explanation: **Explanation:** The correct answer is **Hypothyroidism**. Iron overload is characterized by an excess of iron in the body, which can be either hereditary (Primary Hemochromatosis) or acquired (Secondary Hemochromatosis) [1]. **Why Hypothyroidism is the correct answer:** Hypothyroidism is **not** a cause of iron overload. In fact, it is frequently associated with **iron deficiency anemia** due to decreased gastrointestinal absorption of iron, achlorhydria, or heavy menstrual bleeding (menorrhagia) in women [2]. While endocrine disorders like Diabetes Mellitus are *complications* of iron overload, hypothyroidism does not cause it [1]. **Analysis of Incorrect Options:** * **Sideroblastic Anemia:** This is a classic cause of acquired iron overload. Ineffective erythropoiesis leads to increased iron absorption and frequent blood transfusions, resulting in iron deposition in tissues (hemosiderosis). * **Chronic Hepatitis C:** Chronic liver inflammation can lead to elevated ferritin levels and mild-to-moderate hepatic iron overload. It often involves the downregulation of hepcidin or the release of iron from necrotic hepatocytes. * **Nonalcoholic Steatohepatitis (NASH):** Also known as "Dysmetabolic Iron Overload Syndrome," NASH is frequently associated with increased hepatic iron stores, which can further exacerbate oxidative stress and liver fibrosis. **Clinical Pearls for NEET-PG:** * **Gold Standard Diagnosis:** Liver biopsy with Prussian Blue staining (to calculate the Hepatic Iron Index) is the definitive test, though MRI (T2*) is now the preferred non-invasive method. * **Porphyria Cutanea Tarda (PCT):** This condition is strongly associated with iron overload and Hepatitis C [3]. * **Treatment of Choice:** Therapeutic phlebotomy is the mainstay for most iron overload states; however, in anemias like Sideroblastic anemia, **iron chelators** (e.g., Deferasirox, Deferoxamine) are used instead.

Question 362: Which of the following is best to confirm the diagnosis of thalassemia trait in a patient with a positive family history of thalassemia?

A. Elevated HbA2 (Correct Answer)
B. Reticulocytosis
C. NESTROFT
D. Peripheral smear

Explanation: **Explanation:** **1. Why Elevated HbA2 is the Correct Answer:** The hallmark of **Beta-Thalassemia Trait (Minor)** is a quantitative deficiency in beta-globin chain synthesis. To compensate for the lack of beta chains, there is a relative increase in delta-chain production, which combines with alpha chains to form **Hemoglobin A2 (α2δ2)**. * **Diagnostic Gold Standard:** High-Performance Liquid Chromatography (HPLC) or Hemoglobin Electrophoresis is used to quantify Hb levels. * **Cut-off:** An **HbA2 level >3.5%** is considered diagnostic for Beta-Thalassemia Trait. HbF may also be slightly elevated (1–5%), but HbA2 is the more reliable confirmatory marker. **2. Why Other Options are Incorrect:** * **NESTROFT (Naked Eye Single Tube Red Cell Osmotic Fragility Test):** This is a highly sensitive **screening test** used in field surveys and mass screenings due to its low cost. However, it is not confirmatory as it can be positive in other conditions like iron deficiency anemia (IDA). * **Peripheral Smear:** While it shows characteristic microcytic hypochromic cells, target cells, and basophilic stippling, these findings are non-specific and overlap significantly with IDA. * **Reticulocytosis:** In thalassemia trait, the reticulocyte count is usually normal or only slightly elevated. Significant reticulocytosis is more characteristic of Thalassemia Major or Intermedia. **3. NEET-PG Clinical Pearls:** * **Mentzer Index:** (MCV/RBC count). If **<13**, it suggests Thalassemia; if **>13**, it suggests Iron Deficiency Anemia. * **RBC Count:** In Thalassemia trait, the RBC count is typically **elevated** (polycythemia) despite low hemoglobin, whereas in IDA, the RBC count is low. * **Differential Diagnosis:** Always rule out IDA before diagnosing Thalassemia trait, as iron deficiency can falsely lower HbA2 levels, potentially masking a Thalassemia diagnosis.

Question 363: Which of the following is NOT used in the treatment of thalassemia?

A. Folic acid
B. Iron therapy (Correct Answer)
C. Splenectomy
D. Bone marrow transplant

Explanation: **Explanation:** **Why Iron Therapy is the Correct Answer:** Thalassemia is a genetic disorder characterized by defective globin chain synthesis, leading to ineffective erythropoiesis and chronic hemolysis [1]. Patients with thalassemia major are at a high risk of **iron overload** due to two primary mechanisms: repeated blood transfusions and increased gastrointestinal iron absorption (driven by low hepcidin levels). Administering iron therapy is contraindicated as it would exacerbate systemic hemosiderosis, leading to multi-organ failure (specifically involving the heart, liver, and endocrine glands). Instead, these patients require **iron chelation therapy** (e.g., Deferasirox, Deferoxamine) to remove excess iron. **Why the Other Options are Incorrect:** * **Folic Acid:** Chronic hemolysis leads to increased bone marrow activity and high erythrocyte turnover. This creates a high demand for folate; supplementation is essential to prevent megaloblastic crises. * **Splenectomy:** This is indicated in cases of hypersplenism where increasing transfusion requirements (usually >200-250 ml/kg/year) or symptomatic splenomegaly occur. * **Bone Marrow Transplant (BMT):** Currently, Allogeneic Hematopoietic Stem Cell Transplant is the only **curative** treatment for thalassemia, ideally performed at a young age before significant organ damage from iron overload occurs. **High-Yield Clinical Pearls for NEET-PG:** * **Target Ferritin:** Chelation therapy is typically started when serum ferritin levels exceed **1000 ng/mL** or after approximately 10–20 transfusions. * **Most Common Cause of Death:** In poorly chelated thalassemia patients, the leading cause of mortality is **cardiac failure/arrhythmia** due to secondary hemochromatosis. * **Diagnosis:** Hb Electrophoresis/HPLC is the gold standard; look for increased **HbF** and **HbA2** in Beta-Thalassemia [1].

Question 364: Which one of the following is the most common immunologic type of multiple myeloma?

A. IgG; Kappa light chain (Correct Answer)
B. IgA, Kappa light chain
C. IgD, Lambda light chain
D. IgM, type

Explanation: Multiple Myeloma (MM) is a plasma cell dyscrasia characterized by the neoplastic proliferation of a single clone of plasma cells, which produce a monoclonal (M) protein [1]. The classification of MM is based on the type of heavy chain and light chain produced. **1. Why Option A is Correct:** * **Heavy Chain:** **IgG** is the most common heavy chain isotype, accounting for approximately **50-60%** of all cases. * **Light Chain:** In humans, the normal ratio of **Kappa (κ)** to Lambda (λ) light chains is roughly 2:1. This distribution is mirrored in myeloma; Kappa light chains are significantly more common than Lambda. Therefore, **IgG-Kappa** is the most frequent immunologic subtype encountered in clinical practice [1]. **2. Why Other Options are Incorrect:** * **Option B (IgA):** IgA is the second most common type, seen in about **20-25%** of cases. It is often associated with hypercalcemia and extramedullary involvement. * **Option C (IgD):** IgD myeloma is rare (<2%) and is unique because it is more frequently associated with **Lambda** light chains and often presents at a younger age with a more aggressive course. * **Option D (IgM):** True IgM myeloma is extremely rare. Most cases of monoclonal IgM production are classified as **Waldenström Macroglobulinemia**, not Multiple Myeloma [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Order of Frequency:** IgG > IgA > Light chain only (Bence-Jones) > IgD > IgE. * **Bence-Jones Proteins:** These are free monoclonal light chains filtered into the urine. They are not detected by standard dipsticks (which detect albumin) but require **sulfosalicylic acid (SSA) test** or urine electrophoresis. * **CRAB Criteria:** Remember the classic presentation: **C**alcium (high), **R**enal failure, **A**nemia, and **B**one lesions (lytic). * **Diagnosis:** Clonal bone marrow plasma cells **≥10%** or biopsy-proven extramedullary plasmacytoma PLUS one or more myeloma-defining events [1].

Question 365: Which of the following statements is FALSE regarding hemochromatosis?

A. Prone to fatal Vibrio enteric infections
B. Prone to fatal Yersinia enteric infections
C. Should avoid raw fish
D. Prone to Mycobacterium enteric infections (Correct Answer)

Explanation: The correct answer is **D**. Hemochromatosis is a disorder of iron overload, and certain pathogens thrive in high-iron environments. While patients are highly susceptible to specific "siderophilic" (iron-loving) bacteria, **Mycobacterium** species are not typically associated with increased enteric infection risk specifically due to iron overload in hemochromatosis. **Why the other options are true:** * **Vibrio vulnificus (Option A & C):** This is a high-yield association. *Vibrio* requires free iron for rapid growth and virulence. Patients with hemochromatosis are at a significantly higher risk of fatal septicemia from *Vibrio vulnificus* after consuming **raw seafood/shellfish** or through wound exposure to seawater. * **Yersinia enterocolitica (Option B):** *Yersinia* is a siderophilic organism that cannot produce its own siderophores (iron-binding molecules) efficiently. In an iron-overloaded host, the excess iron facilitates its proliferation, leading to severe enterocolitis or sepsis. * **Listeria monocytogenes:** Though not listed, it is another siderophilic organism to remember. **Clinical Pearls for NEET-PG:** * **The "Bronze Diabetes" Triad:** Skin hyperpigmentation, Diabetes Mellitus, and Cirrhosis [1]. * **Most Common Cause of Death:** Historically cirrhosis; however, currently, **Hepatocellular Carcinoma (HCC)** is the leading cause of death in treated patients [1]. * **Cardiac Involvement:** Most common manifestation is **Restrictive Cardiomyopathy**, though dilated cardiomyopathy can also occur. * **Joints:** Characterized by "hook-like" osteophytes in the 2nd and 3rd MCP joints and pseudogout (CPPD). * **Screening:** Best initial test is **Transferrin Saturation** (>45%) [3]; Gold standard for diagnosis is **HFE gene analysis** [1],[2].

Question 366: Which of the following is preferred in an elderly woman with macrocytic anemia and early signs of neurological deficit?

A. Folic acid
B. Hydroxycobalamine (Correct Answer)
C. Erythropoietin
D. Iron dextran

Explanation: The clinical presentation of **macrocytic anemia** combined with **neurological deficits** (such as paresthesia, loss of vibration/position sense, or ataxia) is a classic hallmark of **Vitamin B12 (Cobalamin) deficiency**. [1] **1. Why Hydroxycobalamine is Correct:** In Vitamin B12 deficiency, neurological symptoms occur due to the failure of myelin synthesis (Subacute Combined Degeneration of the Spinal Cord). **Hydroxycobalamine** is the preferred parenteral form of B12 because it has a longer half-life and better tissue retention compared to cyanocobalamin. In patients with neurological deficits, parenteral administration is mandatory to bypass potential malabsorption (e.g., Pernicious Anemia) and ensure rapid correction to prevent permanent nerve damage. **2. Why Other Options are Incorrect:** * **Folic acid:** While it can correct the megaloblastic anemia, it **cannot** treat the neurological symptoms [2]. In fact, giving folic acid alone in B12 deficiency can "mask" the anemia while allowing the neurological damage to progress irreversibly. * **Erythropoietin:** This is used for anemia of chronic kidney disease or certain malignancies; it has no role in nutritional macrocytic anemia. * **Iron dextran:** This is used for iron-deficiency anemia (microcytic), not macrocytic anemia. **Clinical Pearls for NEET-PG:** * **The "Folate Trap":** Always rule out B12 deficiency before starting Folic acid. * **Earliest Sign:** Hypersegmented neutrophils on a peripheral smear are the earliest sign of megaloblastic anemia. * **Biochemical Markers:** In B12 deficiency, both **Methylmalonic Acid (MMA)** and **Homocysteine** levels are elevated. In Folate deficiency, only Homocysteine is elevated. * **Neurological involvement:** Only B12 deficiency causes neurological symptoms; Folate deficiency does not. [1]

Question 367: Christmas disease is due to deficiency of:

A. Factor IX (Correct Answer)
B. Factor X
C. Factor XI
D. Factor XII

Explanation: Christmas Disease, also known as Hemophilia B, is a hereditary bleeding disorder caused by a deficiency of Factor IX [1]. It is an X-linked recessive condition, meaning it primarily affects males [1]. The name "Christmas Disease" is derived from Stephen Christmas, the first patient described with this specific deficiency in 1952, distinguishing it from classical Hemophilia A. Analysis of Options: * Factor IX (Correct): Deficiency leads to Hemophilia B [1]. Factor IX is a vitamin K-dependent serine protease in the intrinsic pathway of the coagulation cascade [1]. * Factor X: Deficiency is rare and leads to Stuart-Prower factor deficiency, affecting the common pathway. * Factor XI: Deficiency leads to Hemophilia C (Rosenthal syndrome), which is autosomal recessive and most common in Ashkenazi Jews. * Factor XII: Deficiency (Hageman factor deficiency) is unique because it causes a prolonged aPTT in vitro but does not cause clinical bleeding; instead, it may be associated with a risk of thrombosis. High-Yield Clinical Pearls for NEET-PG: 1. Inheritance: Both Hemophilia A (Factor VIII) and B (Factor IX) are X-linked recessive [1]. 2. Lab Findings: Characterized by prolonged aPTT with a normal PT and Bleeding Time. 3. Clinical Presentation: Patients present with deep tissue bleeding, most commonly hemarthrosis (bleeding into joints) and muscle hematomas. 4. Treatment: Managed with recombinant Factor IX concentrate [2]. Unlike Hemophilia A, desmopressin (DDAVP) is not effective for Hemophilia B.

Question 368: Megaloblastic anemia may be caused by all of the following, except?

A. Dilantin toxicity
B. Vitamin B12 deficiency
C. Folic acid deficiency
D. Long term aspirin intake (Correct Answer)

Explanation: **Explanation:** Megaloblastic anemia is characterized by impaired DNA synthesis, leading to a maturation delay between the nucleus and the cytoplasm (nuclear-cytoplasmic asynchrony). [1] This results in large, nucleated RBC precursors in the bone marrow and macrocytic cells in the peripheral blood. [1] **Why Option D is Correct:** **Long-term aspirin intake** is associated with gastrointestinal bleeding and chronic blood loss, which typically leads to **Iron Deficiency Anemia (Microcytic Hypochromic)**. Aspirin does not interfere with DNA synthesis or the metabolism of Vitamin B12 or Folate; therefore, it does not cause megaloblastic changes. **Why the other options are incorrect:** * **Vitamin B12 and Folic Acid Deficiency (Options B & C):** These are the most common causes. [1] Both are essential cofactors for DNA synthesis. B12 is required for the conversion of homocysteine to methionine, and Folate is required for thymidylate synthesis. [1] Deficiency leads to ineffective erythropoiesis. * **Dilantin (Phenytoin) Toxicity (Option A):** Phenytoin is a well-known cause of drug-induced megaloblastic anemia. It interferes with folate metabolism by inhibiting intestinal folate conjugase (reducing absorption) and increasing the catabolism of folate. **NEET-PG High-Yield Pearls:** 1. **Drug-induced Megaloblastic Anemia:** Common culprits include **Methotrexate** (DHFR inhibitor), **Phenytoin**, **Pyrimethamine**, **Trimethoprim**, and **Zidovudine (AZT)**. 2. **Pernicious Anemia:** The most common cause of B12 deficiency, caused by autoimmune destruction of gastric parietal cells (leading to Intrinsic Factor deficiency). [1] 3. **Peripheral Smear Findings:** Look for **Hypersegmented Neutrophils** (>5 lobes) and **Macro-ovalocytes**. 4. **Biochemical Markers:** Both B12 and Folate deficiency show elevated **Homocysteine**, but only B12 deficiency shows elevated **Methylmalonic Acid (MMA)**.

Question 369: Which of the following is a cause of intravascular hemolysis?

A. Cold agglutinin disease
B. Warm type autoimmune hemolytic anemia
C. Paroxysmal nocturnal hemoglobinuria (Correct Answer)
D. Both B and C

Explanation: ### Explanation Hemolysis is broadly classified into **intravascular** (destruction within the blood vessels) and **extravascular** (destruction within the reticuloendothelial system, primarily the spleen) [1]. **Why Paroxysmal Nocturnal Hemoglobinuria (PNH) is correct:** PNH is a classic cause of **intravascular hemolysis**. It is an acquired clonal stem cell disorder caused by a mutation in the *PIGA* gene, leading to a deficiency of GPI-anchored proteins like **CD55 (DAF)** and **CD59 (MIRL)**. These proteins normally protect RBCs from complement-mediated attack [1]. Without them, the **membrane attack complex (MAC)** forms directly on the RBC surface, causing osmotic lysis within the circulation. This leads to hemoglobinemia and hemoglobinuria. **Why the other options are incorrect:** * **Warm type Autoimmune Hemolytic Anemia (WAIHA):** This is the most common form of AIHA, usually mediated by **IgG** antibodies. IgG-coated RBCs are recognized by Fc receptors on splenic macrophages, leading to partial phagocytosis and the formation of **spherocytes**. Thus, the destruction is **extravascular** [1]. * **Cold Agglutinin Disease (CAD):** While CAD involves IgM and complement (C3b) fixation, the destruction is primarily **extravascular**. C3b-coated RBCs are cleared by the Kupffer cells in the **liver**. (Note: While rare, massive complement activation in CAD can occasionally cause minor intravascular hemolysis, but it is classically categorized as extravascular for exam purposes) [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Intravascular Hemolysis Markers:** Low haptoglobin, high LDH, hemoglobinuria, and hemosiderinuria [3]. * **Extravascular Hemolysis Markers:** Splenomegaly and spherocytes on peripheral smear. * **PNH Triad:** Hemolytic anemia, pancytopenia, and venous thrombosis (e.g., Budd-Chiari syndrome). * **Gold Standard Test for PNH:** Flow cytometry (looking for absence of CD55/CD59).

Question 370: Cryoprecipitate is a rich source of which of the following?

A. Thromboplastin
B. Factor VIII (Correct Answer)
C. Factor X
D. Factor VII

Explanation: **Explanation:** Cryoprecipitate is a blood product prepared by thawing one unit of Fresh Frozen Plasma (FFP) at 1–6°C and collecting the insoluble precipitate. It is a concentrated source of specific clotting factors, making it the treatment of choice for specific consumptive coagulopathies [1]. **Why Factor VIII is correct:** Cryoprecipitate is specifically enriched with five key components [1]: 1. **Factor VIII** (Anti-hemophilic factor) 2. **Fibrinogen** (Factor I) – It is the most concentrated source available. 3. **von Willebrand Factor (vWF)** 4. **Factor XIII** (Fibrin stabilizing factor) 5. **Fibronectin** **Why the other options are incorrect:** * **Option A (Thromboplastin):** Also known as Factor III or Tissue Factor, it is not a plasma-derived component found in cryoprecipitate; it is released from damaged tissues to initiate the extrinsic pathway. * **Option C (Factor X) and Option D (Factor VII):** These are vitamin K-dependent clotting factors. Along with Factors II and IX, these remain in the supernatant (the "cryo-poor" plasma) after the cryoprecipitate is removed [1]. To replace these, one would use FFP or Prothrombin Complex Concentrate (PCC). **High-Yield Clinical Pearls for NEET-PG:** * **Primary Indication:** Hypofibrinogenemia (e.g., in DIC or massive hemorrhage). * **Dosage:** One bag of cryoprecipitate typically raises the fibrinogen level by 5–10 mg/dL. * **Storage:** It is stored at -18°C or colder and has a shelf life of 1 year. Once thawed, it must be used within 6 hours (or 4 hours if pooled). * **Note on Hemophilia A:** While it contains Factor VIII, recombinant or plasma-derived Factor VIII concentrates are now preferred over cryoprecipitate to reduce the risk of transfusion-transmitted infections.

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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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Hematology — MCQs

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