Hematology — MCQs

Hematology Indian Medical PG Practice Questions and MCQs

Question 31: Moeller's glossitis is due to a deficiency in which of the following?

A. Pernicious anemia (Correct Answer)
B. Riboflavin deficiency
C. Acute monocytic leukemia
D. Late acquired syphilis

Explanation: **Explanation:** **Moeller’s glossitis** (also known as Hunter’s glossitis) is a classic clinical finding characterized by a smooth, red, and "glazed" appearance of the tongue, often accompanied by a burning sensation or pain. 1. **Why Pernicious Anemia is correct:** Pernicious anemia results from a deficiency of Vitamin B12 (cobalamin) due to a lack of intrinsic factor [1]. Vitamin B12 is essential for DNA synthesis in rapidly dividing cells. In the oral cavity, this deficiency leads to the atrophy of the filiform and fungiform papillae. The loss of these papillae results in the characteristic smooth, beefy red tongue seen in Moeller’s glossitis. 2. **Why other options are incorrect:** * **Riboflavin (B2) deficiency:** Typically presents with **Magenta tongue**, angular cheilitis, and corneal vascularization. * **Acute Monocytic Leukemia (AML-M5):** Characteristically associated with **gingival hypertrophy** or hyperplasia due to leukemic infiltration, rather than atrophic glossitis. * **Late Acquired Syphilis:** Associated with **interstitial glossitis**, which may present with leukoplakia and carries a risk of malignant transformation, but it does not cause the diffuse papillary atrophy of Moeller’s glossitis. **NEET-PG High-Yield Pearls:** * **Hunter’s/Moeller’s Glossitis:** Pathognomonic for Vitamin B12 deficiency/Pernicious Anemia [1]. * **Plummer-Vinson Syndrome:** Characterized by Iron deficiency anemia, esophageal webs, and atrophic glossitis. * **Bald Tongue of Sandwith:** Seen in Pellagra (Niacin/B3 deficiency). * **Strawberry Tongue:** Seen in Scarlet Fever and Kawasaki Disease.

Question 32: Which of the following drugs has the least bone marrow suppression?

A. Cisplatin
B. Vincristine (Correct Answer)
C. Cyclophosphamide
D. Methotrexate

Explanation: The correct answer is **Vincristine**. ### **Explanation** The primary dose-limiting toxicity of most cytotoxic chemotherapy agents is **myelosuppression** (bone marrow suppression). However, certain drugs are known for being "bone marrow sparing." **Vincristine**, a Vinca alkaloid that inhibits microtubule assembly (mitotic inhibitor), is unique because it causes **minimal to no bone marrow suppression**. Its dose-limiting toxicity is instead **peripheral neuropathy** (paresthesia, loss of deep tendon reflexes, and autonomic dysfunction like constipation). ### **Analysis of Incorrect Options** * **Cisplatin:** A platinum compound known for being highly emetogenic and nephrotoxic, but it also causes significant cumulative myelosuppression. * **Cyclophosphamide:** An alkylating agent that causes significant neutropenia. Its other classic side effect is hemorrhagic cystitis (prevented by Mesna). * **Methotrexate:** An antimetabolite (folate antagonist) that is highly myelosuppressive. This effect is managed using "Leucovorin rescue." ### **High-Yield Clinical Pearls for NEET-PG** * **Bone Marrow Sparing Agents:** Remember the mnemonic **"V-B-L-S"** for drugs with minimal myelosuppression: **V**incristine, **B**leomycin (Lung fibrosis), **L**-Asparaginase (Pancreatitis/Thrombosis), and **S**teroids. * **Vincristine vs. Vinblastine:** While they belong to the same class, **V**inblastine "**B**lasts" the bone marrow (highly myelosuppressive), whereas **V**incristine spares it. * **Vincristine Warning:** It is **fatal if given intrathecally**; it must only be administered intravenously.

Question 33: JAK-2 mutation is strongly associated with which of the following conditions?

A. Burkitt's lymphoma
B. Polycythemia vera (Correct Answer)
C. Multiple myeloma
D. Mantle cell lymphoma

Explanation: **Explanation:** **JAK2 (Janus Kinase 2)** is a non-receptor tyrosine kinase involved in the signal transduction pathway of hematopoietic growth factor receptors (like erythropoietin and thrombopoietin). The **V617F mutation** leads to constitutive activation of this pathway, causing autonomous production of blood cells independent of growth factors. * **Polycythemia Vera (PV):** This is the correct answer because the JAK2 V617F mutation is found in **>95% of cases**. It is a major diagnostic criterion according to WHO classification. It is also found in Essential Thrombocythemia (ET) and Primary Myelofibrosis (PMF), but with lower frequency (~50-60%). **Why other options are incorrect:** * **Burkitt’s Lymphoma:** Characterized by the **t(8;14)** translocation involving the **c-myc** oncogene. * **Multiple Myeloma:** A plasma cell dyscrasia primarily associated with chromosomal abnormalities like trisomies or translocations involving the IgH locus (e.g., t(11;14), t(4;14)). * **Mantle Cell Lymphoma:** Defined by the **t(11;14)** translocation, leading to the overexpression of **Cyclin D1**. **High-Yield Clinical Pearls for NEET-PG:** 1. **JAK2 V617F:** Substitution of Valine (V) by Phenylalanine (F) at codon 617. 2. **PV Diagnosis:** Low serum Erythropoietin (EPO) levels + JAK2 mutation + Increased Red Cell Mass. 3. **Aquagenic Pruritus:** Itching after a hot bath is a classic clinical sign of PV. 4. **Treatment:** Ruxolitinib is a JAK1/2 inhibitor used in patients resistant to hydroxyurea.

Question 34: A 68-year-old patient developed atrophic gastritis and, 2 years later, developed a macrocytic, hyperchromic anemia. His anemia has most likely occurred due to which one of the following reasons?

A. The atrophic gastritis leads to vitamin B12 malabsorption. (Correct Answer)
B. The atrophic gastritis raises the pH in the duodenum, leading to folate malabsorption.
C. The terminal ileum is also involved, so iron is malabsorbed.
D. The atrophic gastritis leads to increased red blood cell absorption by the spleen.

Explanation: **Explanation:** **1. Why Option A is correct:** Atrophic gastritis involves the chronic inflammation and subsequent destruction of gastric parietal cells [4]. These cells are responsible for secreting **Intrinsic Factor (IF)**. Vitamin B12 (cobalamin) requires IF to form a complex that can be absorbed in the terminal ileum. Without IF, B12 malabsorption occurs, leading to Megaloblastic Anemia [2]. This is characterized by **macrocytic** (high MCV) and **hyperchromic** (due to increased hemoglobin concentration in a larger cell) indices. When this process is autoimmune-mediated, it is specifically termed **Pernicious Anemia**. **2. Why the other options are incorrect:** * **Option B:** Folate absorption occurs primarily in the jejunum and is not significantly dependent on gastric pH or Intrinsic Factor. While atrophic gastritis causes achlorhydria, it does not typically cause folate deficiency. * **Option C:** Iron is absorbed in the duodenum and proximal jejunum, not the terminal ileum [3]. While achlorhydria can impair iron absorption (leading to microcytic anemia), the question specifies macrocytic anemia, pointing directly to B12/Folate issues. * **Option D:** Atrophic gastritis does not cause hypersplenism or increased sequestration of RBCs. The anemia is due to ineffective erythropoiesis in the bone marrow, not peripheral destruction. **Clinical Pearls for NEET-PG:** * **Schilling Test:** Historically used to diagnose B12 malabsorption (now largely replaced by anti-parietal and anti-IF antibody titers). * **Neurological Symptoms:** B12 deficiency causes **Subacute Combined Degeneration (SCD)** of the spinal cord (dorsal columns and lateral corticospinal tracts), whereas folate deficiency does NOT cause neurological deficits. * **Peripheral Smear:** Look for **hypersegmented neutrophils** (>5 lobes) and macro-ovalocytes. * **Biochemical markers:** Both B12 and Folate deficiency raise Homocysteine levels, but only B12 deficiency raises **Methylmalonic Acid (MMA)** levels [1].

Question 35: Which of the following is NOT a feature of polycythemia rubra vera?

A. Increased red cell mass
B. Low arterial oxygen saturation (Correct Answer)
C. Presence of JAK2 mutation
D. Splenomegaly

Explanation: **Explanation:** Polycythemia Vera (PV) is a chronic myeloproliferative neoplasm characterized by the autonomous overproduction of red blood cells. The fundamental concept to understand here is the distinction between **Primary Polycythemia** (PV) and **Secondary Polycythemia**. **Why "Low arterial oxygen saturation" is the correct answer:** In PV, the increase in red cell mass is "primary," meaning it is driven by a genetic mutation (JAK2) rather than a physiological response to hypoxia. Therefore, **arterial oxygen saturation ($SaO_2$) remains normal (typically $\geq$ 92%)**. In contrast, low arterial oxygen saturation is a hallmark of *Secondary Polycythemia*, where the body increases erythropoiesis in response to chronic hypoxia (e.g., high altitude, COPD, or cyanotic heart disease) [1]. **Analysis of Incorrect Options:** * **A. Increased red cell mass:** This is the defining feature of PV, leading to hyperviscosity and clinical symptoms like headache and plethora [1]. * **C. Presence of JAK2 mutation:** This is a major WHO diagnostic criterion. Approximately 95% of patients carry the **JAK2 V617F** mutation, while most of the remainder have JAK2 exon 12 mutations [1]. * **D. Splenomegaly:** Found in about 70% of patients at diagnosis, it occurs due to the sequestration of excess blood cells and extramedullary hematopoiesis [1]. **NEET-PG High-Yield Pearls:** * **Serum Erythropoietin (EPO):** In PV, EPO levels are characteristically **low** (suppressed by high RBC mass). High EPO suggests secondary polycythemia. * **Pruritus:** Aquagenic pruritus (itching after a warm bath) is a classic, highly specific symptom of PV due to mast cell degranulation [1]. * **Treatment of Choice:** Therapeutic phlebotomy (target Hct <45%) and low-dose aspirin. Hydroxyurea is used for high-risk patients. * **Complications:** Increased risk of both arterial/venous thrombosis and transformation to myelofibrosis or Acute Myeloid Leukemia (AML) [1].

Question 36: What are the characteristic laboratory findings of hemophilia A?

A. Prolonged prothrombin time (PT)
B. Prolonged activated partial thromboplastin time (aPTT)
C. X-linked recessive inheritance
D. Presence of 30% of factor level expressing the disease (Correct Answer)

Explanation: **Explanation:** Hemophilia A is an X-linked recessive bleeding disorder caused by a deficiency of **Coagulation Factor VIII** [1]. **Why the correct answer is right:** In Hemophilia, the severity of clinical bleeding is directly proportional to the plasma level of the deficient factor. Normal factor levels range from 50% to 150%. Symptoms typically manifest when factor levels fall below **30% to 35%**. Patients with levels between 5% and 30% are classified as having "Mild Hemophilia," where bleeding usually occurs only after significant trauma or surgery. Levels <1% indicate "Severe Hemophilia," characterized by spontaneous hemarthrosis. **Analysis of incorrect options:** * **Option A:** Prothrombin Time (PT) measures the extrinsic and common pathways (Factors VII, X, V, II, and I). Since Factor VIII is part of the **intrinsic pathway**, the PT remains **normal** in Hemophilia A [1]. * **Option B:** While a **prolonged aPTT** is a hallmark laboratory finding of Hemophilia A, the question asks for "characteristic laboratory findings" in the context of disease expression [1]. While aPTT is prolonged, it is a non-specific screening test [1]; the definitive diagnosis and expression of the disease are defined by the specific **Factor VIII assay level**. * **Option C:** While Hemophilia A does follow an **X-linked recessive** inheritance pattern, this is a genetic characteristic, not a "laboratory finding" [1]. **NEET-PG High-Yield Pearls:** * **Mixing Studies:** If aPTT is prolonged, a mixing study (1:1 with normal plasma) is performed [1]. If the aPTT corrects, it indicates a factor deficiency; if it fails to correct, it suggests an inhibitor (e.g., Factor VIII antibodies). * **Bleeding Time (BT) & Platelet Count:** Both are **normal** in Hemophilia A, as primary hemostasis is unaffected. * **Most common cause of death:** Intracranial hemorrhage. * **Most common site of bleeding:** Knee joint (Hemarthrosis).

Question 37: Cell of origin of hairy cell leukemia is?

A. B-cell (Correct Answer)
B. T-cell
C. NK-cell
D. Dendritic reticulum cell

Explanation: Hairy Cell Leukemia (HCL) is a rare, chronic lymphoproliferative disorder characterized by the proliferation of mature B-lymphocytes. **1. Why B-cell is correct:** The cell of origin in HCL is a **mature memory B-cell** (post-germinal center). These cells exhibit characteristic "hairy" cytoplasmic projections. They express pan-B-cell markers such as **CD19, CD20, and CD22**. Crucially, they also express highly specific markers like **CD103** (most specific), **CD11c, CD25, and Annexin A1**. Almost all cases (approx. 95%) harbor the **BRAF V600E mutation**, which is a key diagnostic feature. **2. Why other options are incorrect:** * **T-cell & NK-cell:** While some rare T-cell leukemias can mimic the morphology of HCL (e.g., T-cell prolymphocytic leukemia), HCL is strictly a B-cell malignancy. T-cell and NK-cell markers (like CD3, CD4, CD8, or CD56) are negative in HCL. * **Dendritic reticulum cell:** These are antigen-presenting cells found in lymphoid follicles. While they interact with B-cells, they are not the progenitors of HCL. **High-Yield Clinical Pearls for NEET-PG:** * **Clinical Triad:** Splenomegaly (often massive), Pancytopenia, and "Dry Tap" on bone marrow aspiration (due to increased reticulin fibrosis). * **Diagnosis:** TRAP (Tartrate-Resistant Acid Phosphatase) positive staining; "Fried egg appearance" on bone marrow biopsy. * **Treatment:** Cladribine (2-Chlorodeoxyadenosine) is the drug of choice. * **Key Association:** Increased risk of atypical mycobacterial infections (e.g., *Mycobacterium avium-intracellulare*).

Question 38: What is the most common cause of precipitation of renal failure in multiple myeloma?

A. Hyperuricemia
B. Infection
C. Hypercalcemia (Correct Answer)
D. Amyloidosis

Explanation: **Explanation:** Renal failure is a common complication of Multiple Myeloma (MM), occurring in approximately 25-50% of patients [1]. While the classic "Myeloma Kidney" (Cast Nephropathy) is caused by the deposition of Bence-Jones proteins, the **most common reversible and precipitating cause** of acute renal failure in these patients is **Hypercalcemia** [1]. **1. Why Hypercalcemia is Correct:** Hypercalcemia causes renal impairment through two primary mechanisms: * **Renal Vasoconstriction:** High calcium levels lead to direct constriction of the afferent arterioles, reducing the Glomerular Filtration Rate (GFR). * **Polyuria and Dehydration:** It induces a form of nephrogenic diabetes insipidus, leading to volume depletion, which further worsens pre-renal azotemia and promotes the precipitation of light-chain casts in the tubules. **2. Why other options are incorrect:** * **Hyperuricemia (A):** While it can occur due to high cell turnover or tumor lysis, it is a less frequent cause of acute renal failure compared to hypercalcemia in MM. * **Infection (B):** Patients with MM are prone to infections (due to hypogammaglobulinemia), which can lead to sepsis-induced AKI, but it is not the primary metabolic precipitant. * **Amyloidosis (D):** AL-Amyloidosis occurs in ~10% of MM patients. It typically presents as **nephrotic syndrome** (chronic proteinuric renal failure) rather than an acute precipitating event. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for MM:** **CRAB** (Calcium elevation, Renal insufficiency, Anemia, Bone lesions). * **Cast Nephropathy:** The most common *pathological* cause of chronic renal failure in MM. * **Urinalysis Hint:** In Myeloma Kidney, the dipstick is often **negative** for protein (as it detects albumin), but the 24-hour urine collection shows high protein (Bence-Jones proteins). * **First-line treatment for Hypercalcemia in MM:** Aggressive hydration with Normal Saline, followed by Bisphosphonates (Zoledronic acid).

Question 39: Platelet count is decreased in all of the following conditions except?

A. Henoch-Schönlein purpura (Correct Answer)
B. Idiopathic thrombocytopenic purpura
C. Thrombotic thrombocytopenic purpura
D. Systemic lupus erythematosus

Explanation: **Explanation:** The core concept tested here is the distinction between **quantitative** and **qualitative** platelet disorders. **1. Why Henoch-Schönlein Purpura (HSP) is the correct answer:** HSP is a **small-vessel vasculitis** mediated by IgA immune complex deposition. The hallmark of HSP is **palpable purpura** occurring in the presence of a **normal platelet count** [1]. The bleeding into the skin occurs because the blood vessel walls are inflamed and "leaky," not because platelets are deficient. Therefore, it is a vascular cause of purpura, not a thrombocytopenic one. **2. Analysis of Incorrect Options:** * **Idiopathic Thrombocytopenic Purpura (ITP):** Characterized by isolated thrombocytopenia due to anti-platelet antibodies (IgG) leading to premature destruction of platelets in the spleen [2]. * **Thrombotic Thrombocytopenic Purpura (TTP):** A pentad of symptoms (including microangiopathic hemolytic anemia and thrombocytopenia) caused by a deficiency of ADAMTS13, leading to extensive platelet-rich microthrombi that consume platelets [2]. * **Systemic Lupus Erythematosus (SLE):** An autoimmune condition where hematological abnormalities are common. Thrombocytopenia in SLE is usually immune-mediated (secondary ITP) or part of Evans syndrome [2]. **NEET-PG High-Yield Pearls:** * **HSP Tetrad:** Palpable purpura (buttocks/legs), Arthralgia, Abdominal pain (intussusception risk), and Renal involvement (IgA nephropathy). * **Platelet Count in Vasculitis:** Always remember that in most vasculitides (like HSP or Polyarteritis Nodosa), the platelet count is normal or even elevated (as an acute phase reactant) [1]. * **Rule of Thumb:** If the question mentions "palpable purpura," think Vasculitis (Normal Platelets). If it mentions "flat/non-palpable purpura/petechiae," think Thrombocytopenia (Low Platelets) [2].

Question 40: Which of the following is NOT a feature of hemolytic anemia?

A. Hemoglobinuria
B. Jaundice
C. Increased haptoglobin (Correct Answer)
D. Hemosiderinuria

Explanation: ### Explanation In hemolytic anemia, the hallmark is the premature destruction of red blood cells (RBCs). This process leads to the release of free hemoglobin into the plasma [1]. **Why "Increased haptoglobin" is the correct answer:** Haptoglobin is a plasma protein produced by the liver whose primary function is to bind free hemoglobin to prevent oxidative damage and iron loss. In hemolytic states (especially intravascular hemolysis), large amounts of hemoglobin are released. Haptoglobin binds to this hemoglobin, and the resulting **haptoglobin-hemoglobin complex** is rapidly cleared by the reticuloendothelial system (liver). Consequently, serum **haptoglobin levels decrease** (often becoming undetectable), not increase. **Analysis of incorrect options:** * **A. Hemoglobinuria:** When the hemoglobin-binding capacity of haptoglobin is saturated, free hemoglobin is filtered by the renal glomeruli, appearing in the urine [1]. * **B. Jaundice:** Hemolysis leads to an increase in unconjugated bilirubin (a byproduct of heme breakdown). When this exceeds the liver's conjugating capacity, acholuric jaundice occurs. * **D. Hemosiderinuria:** This is a sign of chronic intravascular hemolysis. Iron from reabsorbed hemoglobin accumulates in renal tubular cells as hemosiderin; when these cells slough off into the urine, it is detected via Prussian blue staining [1]. **Clinical Pearls for NEET-PG:** * **Best initial test for hemolysis:** Peripheral blood smear (look for schistocytes or spherocytes) and Reticulocyte count (increased). * **Most specific biochemical marker for intravascular hemolysis:** Decreased serum haptoglobin. * **Markers of Hemolysis:** ↑ Indirect Bilirubin, ↑ LDH, ↑ Reticulocytes, ↓ Haptoglobin. * **Intravascular vs. Extravascular:** Hemoglobinuria and Hemosiderinuria are specific to **intravascular** hemolysis [1].

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Thalassemias

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Coagulation 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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Hematology — MCQs

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