Hematology — MCQs

A 45-year-old patient on hemodialysis for one week has noted that his blood pressure is more difficult to control. He reports good compliance with his medications, which include erythropoietin, ferrous sulfate, vancomycin, and vitamin D. His blood pressure is 180/99 mm Hg. Most likely cause for the worsening control of his blood pressure is:

Hematology Indian Medical PG Practice Questions and MCQs

Question 641: Which of the following statements is NOT true regarding multiple myeloma?

A. Plasmacytosis is less than 10% in the bone marrow. (Correct Answer)
B. There is an increase in IgG levels.
C. ANA antibody is commonly positive.
D. There is an increase in M spikes.

Explanation: Multiple Myeloma (MM) is a neoplastic proliferation of a single clone of plasma cells derived from B cells [1]. To understand the correct answer, we must look at the International Myeloma Working Group (IMWG) diagnostic criteria [1]. 1. Why Option A is the correct answer (The "NOT true" statement): In Multiple Myeloma, the bone marrow biopsy must show clonal plasma cells ≥10% (or biopsy-proven extramedullary plasmacytoma) [1]. If plasmacytosis is less than 10%, the diagnosis is more likely MGUS (Monoclonal Gammopathy of Undetermined Significance), provided other criteria are not met. Therefore, the statement that plasmacytosis is <10% in MM is factually incorrect. 2. Analysis of Incorrect Options: * Option B & D: These are characteristic features. Malignant plasma cells produce excessive amounts of a single immunoglobulin (usually IgG in 50% of cases). This results in a "monoclonal protein" or M-spike on Serum Protein Electrophoresis (SPEP) [1]. * Option C: While not a diagnostic marker, patients with plasma cell dyscrasias often show various immunological abnormalities. However, in the context of this specific question, Option A is the definitive "false" statement regarding diagnostic pathology. NEET-PG High-Yield Pearls: * CRAB Criteria: Used to define end-organ damage in MM: Calcium elevation, Renal insufficiency, Anemia, and Bone lesions (lytic) [1]. * Most common immunoglobulin: IgG > IgA > Light chain only. * Peripheral Smear: Shows Rouleaux formation due to high protein levels. * Urine: Bence-Jones proteins (free light chains) are detected via heat precipitation or electrophoresis, not by standard dipstick. * Radiology: "Punched-out" lytic lesions on a skeletal survey; Bone scans are usually negative as they detect osteoblastic activity [1].

Question 642: Which of the following conditions can cause pancytopenia?

A. Aplastic anemia
B. Myelodysplastic syndromes (MDS)
C. Megaloblastic anemia
D. All of the above (Correct Answer)

Explanation: **Explanation:** Pancytopenia is defined as a simultaneous decrease in all three peripheral blood cell lines: red blood cells (anemia), white blood cells (leukopenia), and platelets (thrombocytopenia). It is not a disease itself but a clinical manifestation of various underlying pathologies affecting the bone marrow [1]. **Why "All of the above" is correct:** 1. **Aplastic Anemia:** This is the classic cause of pancytopenia due to **bone marrow failure**. There is a replacement of hematopoietic tissue with fat cells (hypocellular marrow), leading to decreased production of all cell lines. 2. **Myelodysplastic Syndromes (MDS):** These are clonal stem cell disorders characterized by **ineffective hematopoiesis**. While the marrow may be hypercellular, the cells are dysplastic and undergo premature apoptosis, failing to reach the peripheral circulation. 3. **Megaloblastic Anemia:** Severe Vitamin B12 or Folate deficiency impairs DNA synthesis [2]. This leads to **nuclear-cytoplasmic asynchrony**, causing intramedullary hemolysis (ineffective erythropoiesis). While anemia is most prominent, severe cases frequently present with leukopenia and thrombocytopenia. **Clinical Pearls for NEET-PG:** * **Most common cause of pancytopenia in India:** Megaloblastic anemia (followed by Aplastic anemia). * **Bone Marrow Biopsy:** Essential to differentiate causes. Look for "dry tap" in myelofibrosis or "hypocellularity" in aplastic anemia. * **Pancytopenia with Splenomegaly:** Think of Hypersplenism [1], Kala-azar (Visceral Leishmaniasis), or Cirrhosis with portal hypertension. * **Pancytopenia without Splenomegaly:** Think of Aplastic anemia or Vitamin B12 deficiency. * **High-Yield Tip:** Always check the Reticulocyte Count; a low count indicates a production marrow failure, while a high count suggests peripheral destruction or sequestration.

Question 643: Hereditary spherocytosis is characterized by all the following features, except:

A. Increased osmotic fragility
B. Autosomal dominant inheritance
C. Increased surface area to volume ratio (Correct Answer)
D. Direct Coombs test is diagnostic

Explanation: **Explanation:** Hereditary Spherocytosis (HS) is a common inherited hemolytic anemia caused by defects in red blood cell (RBC) membrane proteins (most commonly **Ankyrin**, followed by Spectrin and Band 3) [2]. **1. Why "Increased surface area to volume ratio" is the correct answer (False statement):** In HS, the protein defect leads to the loss of membrane fragments (microvesiculation). This results in a **decreased surface area to volume ratio** [1]. As the cell loses membrane but retains its cytoplasmic volume, it is forced into the most geometrically efficient shape—a **sphere** [2]. Unlike the normal biconcave disc, a sphere cannot expand further, making it rigid and prone to splenic sequestration [1]. **2. Analysis of other options:** * **Increased osmotic fragility:** Because spherocytes have a decreased surface area-to-volume ratio, they have no "reserve" to expand when placed in hypotonic solutions. They lyse much earlier than normal cells, making this a hallmark finding. * **Autosomal dominant inheritance:** Approximately 75% of cases follow an autosomal dominant pattern, though autosomal recessive and de novo mutations also occur. * **Direct Coombs test:** This test is used to identify autoimmune hemolytic anemia (AIHA). HS is a genetic membrane defect, not an immune-mediated process; therefore, the **Coombs test is negative**. (Note: While the question asks for the "except," if Option D were "Direct Coombs test is positive," it would also be a false statement. In this specific MCQ format, Option C is the classic physiological hallmark tested). **NEET-PG High-Yield Pearls:** * **MCHC:** Characteristically **increased** (often >36 g/dL) due to relative cellular dehydration [1]. * **Confirmatory Test:** Eosin-5-maleimide (EMA) binding test (Flow cytometry) is now the gold standard. * **Clinical Triad:** Anemia, Jaundice, and Splenomegaly. * **Complication:** Pigment gallstones (calcium bilirubinate) are common due to chronic hemolysis. * **Treatment:** Splenectomy is the definitive treatment for moderate-to-severe cases (usually delayed until after age 6) [2].

Question 644: Plasmapheresis is recommended in all of the following conditions except?

A. Hyperviscosity syndrome
B. Macroglobulinaemia
C. Immune complex glomerulonephritis
D. Chronic active hepatitis (Correct Answer)

Explanation: Plasmapheresis (Therapeutic Plasma Exchange) is a procedure used to remove high-molecular-weight substances, such as autoantibodies, immune complexes, or paraproteins, from the plasma. **Why Chronic Active Hepatitis is the correct answer:** Chronic active hepatitis is primarily an inflammatory and fibrotic liver disease managed with immunosuppressants (like corticosteroids) [1] or antiviral therapy [2]. Plasmapheresis has no established therapeutic role in its management as the pathology is not driven by circulating macromolecules that require mechanical removal. **Analysis of other options:** * **Hyperviscosity Syndrome:** This is a classic indication. Plasmapheresis rapidly reduces blood viscosity by removing excess proteins (usually IgM), preventing complications like stroke or retinal hemorrhage. * **Macroglobulinaemia (Waldenström’s):** This condition involves high levels of monoclonal IgM. Because IgM is large and mostly intravascular (80%), plasmapheresis is highly effective at removing it to treat associated hyperviscosity. * **Immune Complex Glomerulonephritis:** Conditions like Goodpasture’s syndrome or rapidly progressive glomerulonephritis (RPGN) utilize plasmapheresis to physically remove circulating nephrotoxic autoantibodies or immune complexes to prevent irreversible renal damage. **NEET-PG High-Yield Pearls:** * **ASFA Category I Indications (First-line):** Guillain-Barré Syndrome (GBS), Myasthenia Gravis (crisis), TTP (Thrombotic Thrombocytopenic Purpura), and Goodpasture’s Syndrome. * **TTP Fact:** Plasmapheresis is the treatment of choice for TTP; it removes ADAMTS13 inhibitors and replenishes the enzyme. * **IgM vs. IgG:** Plasmapheresis is more efficient for IgM-mediated diseases (like Waldenström’s) because IgM is primarily intravascular, whereas IgG is distributed in the extravascular space.

Question 645: A 60-year-old man presents with a 6-month history of increasing fatigue. Physical examination reveals marked pallor, and a CBC shows a macrocytic anemia. Which of the following is the most likely cause of anemia in this patient?

A. Alcoholism (Correct Answer)
B. Chronic disease
C. Iron deficiency
D. Renal disease

Explanation: ### Explanation **Correct Option: A. Alcoholism** The key to this question lies in the **MCV (Mean Corpuscular Volume)**. The patient presents with **macrocytic anemia** (MCV >100 fL). Alcoholism is one of the most common causes of non-megaloblastic macrocytosis [1]. Alcohol has a direct toxic effect on the bone marrow (interfering with erythrocyte maturation) and is often associated with poor nutrition, leading to secondary **folate deficiency** [1]. In chronic alcoholics, macrocytosis can occur even in the absence of anemia or liver disease [3]. **Why Incorrect Options are Wrong:** * **B. Chronic Disease:** Anemia of Chronic Disease (ACD) is typically **normocytic, normochromic**, though it can become microcytic in long-standing cases [2], [4]. It is never macrocytic. * **C. Iron Deficiency:** This is the most common cause of **microcytic, hypochromic** anemia (MCV <80 fL) due to impaired hemoglobin synthesis [2]. * **D. Renal Disease:** Anemia in chronic kidney disease (CKD) is primarily due to decreased erythropoietin production [2]. It is characteristically **normocytic and normochromic**. **NEET-PG High-Yield Pearls:** 1. **Macrocytic Anemia Classification:** * **Megaloblastic:** (Hypersegmented neutrophils present) – Vitamin B12 and Folate deficiency [1], [5]. * **Non-megaloblastic:** Alcoholism, Liver disease, Hypothyroidism, and Myelodysplastic Syndrome (MDS). 2. **Alcohol & MCV:** An unexplained increase in MCV is often an early biochemical marker of occult alcohol abuse. 3. **Round vs. Oval:** Macrocytes in alcoholism/liver disease are usually **round**, whereas in B12/Folate deficiency, they are **oval** (macro-ovalocytes).

Question 646: All of the following are seen in sickle cell anemia EXCEPT:

A. Target cells
B. Jaundice
C. Reticulocytosis
D. High hematocrit (Correct Answer)

Explanation: **Explanation:** Sickle Cell Anemia (SCA) is a chronic hemolytic anemia caused by a point mutation in the $\beta$-globin gene (Glu $\to$ Val at position 6) [1]. The fundamental pathophysiology involves the polymerization of deoxygenated Hemoglobin S (HbS), leading to red blood cell (RBC) distortion and premature destruction [1]. **Why "High hematocrit" is the correct answer:** In SCA, the continuous destruction of sickled RBCs (extravascular and intravascular hemolysis) leads to a **low hematocrit** and low hemoglobin levels (typically 6–9 g/dL) [2]. A high hematocrit is characteristic of polycythemia, not a hemolytic state. **Analysis of incorrect options:** * **Target cells (Codocytes):** These are commonly seen on peripheral smears in SCA. They occur due to a decrease in hemoglobin volume relative to the cell membrane surface area, often exacerbated by functional asplenia. * **Jaundice:** Chronic hemolysis leads to increased breakdown of heme, resulting in **unconjugated hyperbilirubinemia**. This clinically manifests as icterus (jaundice) and predisposes patients to pigment gallstones. * **Reticulocytosis:** To compensate for the shortened lifespan of RBCs (10–20 days instead of 120), the bone marrow increases erythropoiesis, resulting in an elevated reticulocyte count. **Clinical Pearls for NEET-PG:** * **Peripheral Smear:** Look for Sickle cells (drepanocytes), Target cells, and **Howell-Jolly bodies** (indicating functional asplenia due to repeated splenic infarctions) [2]. * **Aplastic Crisis:** Usually triggered by **Parvovirus B19** infection, characterized by a sudden drop in hemoglobin and a *low* reticulocyte count [2]. * **Diagnosis:** Gold standard is **Hemoglobin Electrophoresis** (HbS >80%, HbF variable, HbA absent) [1]. * **Acute Chest Syndrome:** The leading cause of death in adult SCA patients.

Question 647: Autoimmune hemolytic anemia is seen in which of the following conditions?

A. Acute lymphoblastic leukemia (ALL)
B. Acute myeloid leukemia (AML)
C. Cold agglutinin induced hemolytic anemia (CIL) (Correct Answer)
D. Chronic myeloid leukemia (CML)

Explanation: Explanation Correct Answer: C. Cold agglutinin induced hemolytic anemia (CIL) Autoimmune Hemolytic Anemia (AIHA) is a condition where the body produces antibodies against its own red blood cell (RBC) antigens, leading to premature destruction [1]. AIHA is broadly classified into Warm AIHA (IgG-mediated) and Cold AIHA (IgM-mediated) [1]. Cold Agglutinin Disease (CAD) is a specific subtype of AIHA where IgM antibodies bind to RBCs at low temperatures (typically <30°C), causing complement-mediated hemolysis [1]. Therefore, CIL is, by definition, a form of autoimmune hemolytic anemia. Why the other options are incorrect: * Acute Lymphoblastic Leukemia (ALL): While ALL can cause anemia due to bone marrow infiltration (myelophthisis), it is rarely associated with AIHA. AIHA is much more characteristically associated with Chronic Lymphocytic Leukemia (CLL). * Acute Myeloid Leukemia (AML): Anemia in AML is primarily due to the "crowding out" of normal erythroid precursors by malignant blasts in the marrow, not an autoimmune process. * Chronic Myeloid Leukemia (CML): CML typically presents with massive splenomegaly and a high white cell count. While it can cause anemia, it is almost never autoimmune in nature. NEET-PG High-Yield Pearls: * CLL & AIHA: Chronic Lymphocytic Leukemia is the most common leukemia associated with Warm AIHA (IgG). * Infections: Cold AIHA is classically associated with Mycoplasma pneumoniae (anti-I antibodies) and Infectious Mononucleosis (anti-i antibodies) [1]. * Direct Coombs Test: This is the gold standard investigation for diagnosing AIHA; it detects antibodies or complement components on the RBC surface [1]. * Treatment: Warm AIHA responds well to steroids; Cold AIHA generally does not and is managed by avoiding cold exposure or using Rituximab [1].

Question 648: Iron overload occurs in all of the following conditions except?

A. Thalassemia
B. Myelodysplastic syndrome
C. Polycythemia vera (Correct Answer)
D. Sideroblastic anemia

Explanation: **Explanation:** The core concept behind iron overload in hematological disorders is **ineffective erythropoiesis** and **chronic transfusion requirements**. **Why Polycythemia Vera (PV) is the correct answer:** Polycythemia Vera is a myeloproliferative neoplasm characterized by the autonomous overproduction of red blood cells. Unlike the other conditions listed, PV is actually associated with **iron deficiency**, not overload [1]. This occurs because the massive expansion of the red cell mass consumes the body's iron stores. In fact, therapeutic phlebotomy (the mainstay of treatment for PV) further depletes iron to help control the hematocrit levels. **Analysis of Incorrect Options:** * **Thalassemia:** Iron overload occurs due to two mechanisms: chronic blood transfusions and increased intestinal iron absorption triggered by suppressed hepcidin (due to ineffective erythropoiesis) [1]. * **Myelodysplastic Syndrome (MDS):** Patients often become transfusion-dependent. Additionally, ineffective erythropoiesis leads to the suppression of hepcidin, increasing dietary iron absorption [1]. * **Sideroblastic Anemia:** This is a classic cause of iron overload. It involves a defect in heme synthesis, leading to iron accumulation in the mitochondria of erythroblasts (forming "ringed sideroblasts"). **Clinical Pearls for NEET-PG:** * **Hepcidin Connection:** Ineffective erythropoiesis releases "Erythroferrone," which inhibits Hepcidin. Low Hepcidin levels lead to increased ferroportin activity, causing excessive iron absorption even without transfusions [1]. * **Hereditary Hemochromatosis:** The most common genetic cause of primary iron overload (HFE gene mutation). * **Diagnostic Gold Standard:** While serum ferritin is a screening tool, **MRI T2*** is the non-invasive gold standard for quantifying cardiac and hepatic iron overload.

Question 649: What is the most common presentation of sickle cell anemia?

A. Priapism
B. Bone pain (Correct Answer)
C. Fever
D. Splenomegaly

Explanation: **Explanation:** The hallmark of Sickle Cell Anemia (SCA) is the **Vaso-occlusive Crisis (VOC)**, which occurs when sickle-shaped erythrocytes obstruct microvasculature, leading to tissue ischemia and infarction. **Bone pain** (often referred to as a "painful crisis") is the most common clinical presentation and the leading cause of emergency department visits and hospitalizations in these patients. It typically involves the long bones, ribs, and spine. **Analysis of Options:** * **B. Bone pain (Correct):** It is the most frequent manifestation. In infants, this often presents as **Dactylitis** (Hand-Foot Syndrome), characterized by symmetrical painful swelling of the hands and feet due to infarcts in the small bones. * **A. Priapism:** While a classic and serious complication due to stasis in the corpora cavernosa, it occurs in approximately 30-40% of males and is not as frequent as bone pain. * **C. Fever:** Fever is common during crises or due to secondary infections (e.g., *S. pneumoniae*), but it is a non-specific symptom rather than the primary presenting feature of the disease itself. * **D. Splenomegaly:** In SCA, splenomegaly is usually seen only in early childhood. Due to repeated infarctions, the spleen undergoes fibrosis and shrinkage, leading to **autosplenectomy** by adulthood (Howell-Jolly bodies on peripheral smear). **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause of death:** Acute Chest Syndrome (Adults); Infection (Children). * **Most common organism for Osteomyelitis:** *Salmonella* (though *S. aureus* is still common). * **Triggers for Sickling:** Hypoxia, dehydration, acidosis, and cold exposure. * **Management:** Hydroxyurea is used to increase **HbF** levels, which inhibits the polymerization of HbS.

Question 650: A 45-year-old patient on hemodialysis for one week has noted that his blood pressure is more difficult to control. He reports good compliance with his medications, which include erythropoietin, ferrous sulfate, vancomycin, and vitamin D. His blood pressure is 180/99 mm Hg. Most likely cause for the worsening control of his blood pressure is:

A. Erythropoietin (Correct Answer)
B. Ferrous sulfate
C. Vancomycin
D. Vitamin D

Explanation: **Explanation:** The correct answer is **Erythropoietin (EPO)**. Hypertension is the most common and significant side effect of Recombinant Human Erythropoietin (rhEPO) therapy, occurring in approximately 20-30% of patients on dialysis. **Mechanism of EPO-induced Hypertension:** 1. **Increased Peripheral Resistance:** EPO has a direct vasoconstrictive effect on vascular smooth muscle cells and increases the production of Endothelin-1 (a potent vasoconstrictor) while decreasing Nitric Oxide (a vasodilator). 2. **Increased Blood Viscosity:** As EPO stimulates erythropoiesis, the rising hematocrit increases blood viscosity, leading to higher peripheral resistance. 3. **Vascular Remodeling:** Chronic use can lead to structural changes in the vessel walls. **Why the other options are incorrect:** * **Ferrous sulfate:** Oral iron supplementation commonly causes gastrointestinal side effects (constipation, nausea, metallic taste) but does not impact systemic blood pressure. * **Vancomycin:** This antibiotic is associated with "Red Man Syndrome" (infusion-related flushing) and nephrotoxicity/ototoxicity, but it does not cause hypertension. * **Vitamin D:** While excessive Vitamin D can lead to hypercalcemia (which may cause mild hypertension), it is not a classic or frequent cause of acute blood pressure elevation in the setting of dialysis initiation compared to EPO [1]. **NEET-PG High-Yield Pearls:** * **Rate of Rise:** The risk of hypertension is higher when the hematocrit rises rapidly (>4 points in 2 weeks). * **Route of Administration:** Subcutaneous EPO is associated with a lower risk of hypertension compared to Intravenous (IV) administration. * **Management:** If BP becomes uncontrollable, the EPO dose should be reduced or withheld. * **Other EPO Side Effects:** Pure Red Cell Aplasia (PRCA) due to anti-EPO antibodies and increased risk of thromboembolic events [2].

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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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