Hematology — MCQs

Hematology Indian Medical PG Practice Questions and MCQs

Question 561: All are features of hemolytic anemia except?

A. Thrombocytopenia (Correct Answer)
B. Hemosiderinuria
C. Decreased haptoglobin
D. Raised indirect bilirubin

Explanation: Explanation: Hemolytic anemia is characterized by the premature destruction of red blood cells (RBCs) [1]. The hallmarks of this condition are related to the release of intracellular contents and the body’s compensatory response to anemia. Why Thrombocytopenia is the correct answer: Thrombocytopenia (low platelet count) is **not** a standard feature of hemolytic anemia. In most hemolytic processes, the pathology is specific to the erythrocyte lineage. While certain conditions like Evans Syndrome (AIHA + ITP) or Microangiopathic Hemolytic Anemias (TTP/HUS) involve both low RBCs and platelets, they are specific syndromes rather than general features of hemolysis [2]. Why the other options are incorrect: * **Decreased Haptoglobin:** Haptoglobin is a transport protein that binds to free hemoglobin. In intravascular hemolysis, haptoglobin is rapidly consumed as it clears hemoglobin, making it a highly sensitive marker for hemolysis. * **Raised Indirect Bilirubin:** When RBCs break down, heme is converted into unconjugated (indirect) bilirubin. The liver's conjugating capacity is overwhelmed, leading to unconjugated hyperbilirubinemia and clinical jaundice. * **Hemosiderinuria:** In chronic intravascular hemolysis, filtered hemoglobin is reabsorbed by renal tubular cells. When these cells slough off into the urine, they contain iron deposits (hemosiderin), which can be detected by Prussian blue staining. NEET-PG High-Yield Pearls: * **Best initial test for hemolysis:** Peripheral smear (look for schistocytes or spherocytes) and Reticulocyte count (will be elevated). * **Most specific marker for intravascular hemolysis:** Low serum Haptoglobin. * **Intravascular vs. Extravascular:** Hemoglobinuria and Hemosiderinuria are features of **intravascular** hemolysis only. Splenomegaly is more common in **extravascular** hemolysis [1]. * **LDH:** Serum Lactate Dehydrogenase is typically elevated due to release from ruptured RBCs.

Question 562: Which of the following is NOT a feature of chronic leukemia?

A. Often diagnosed incidentally
B. Splenomegaly is common
C. Leukocytosis with circulating blasts and cytopenias are common (Correct Answer)
D. Lymphadenopathy is common

Explanation: The fundamental distinction between acute and chronic leukemias lies in the **maturation arrest** of the cells. **Why Option C is the correct answer:** Leukocytosis with a high percentage of **circulating blasts** (>20%) and significant **cytopenias** (anemia, thrombocytopenia) are hallmark features of **Acute Leukemias** (AML/ALL) [1]. In acute leukemia, the bone marrow is "crowded out" by immature, non-functional blasts, leading to rapid bone marrow failure. In contrast, **Chronic Leukemias** (CML/CLL) are characterized by the proliferation of **mature, differentiated cells** [2]. While a few blasts may be seen in CML (chronic phase <10%), a "blast crisis" is required to see the picture described in Option C [1]. **Analysis of Incorrect Options:** * **Option A (Incidental Diagnosis):** Chronic leukemias often have an indolent course [2]. Many patients are asymptomatic and are diagnosed via routine CBC showing elevated WBC counts [1]. * **Option B (Splenomegaly):** This is a classic feature, especially in **CML**, where massive splenomegaly is common due to extramedullary hematopoiesis [1, 2]. * **Option D (Lymphadenopathy):** This is a hallmark of **CLL** (Chronic Lymphocytic Leukemia), where painless, generalized lymphadenopathy is a frequent presenting sign [2]. **NEET-PG High-Yield Pearls:** * **CML:** Characterized by the Philadelphia chromosome $t(9;22)$ and the *BCR-ABL* fusion gene [1]. Low Leukocyte Alkaline Phosphatase (LAP) score is diagnostic. * **CLL:** Most common leukemia in the elderly; characterized by "Smudge cells" on peripheral smear and CD5+ B-cells. * **Blast Count:** In Chronic Myeloid Leukemia, the "Accelerated Phase" is 10-19% blasts, while the "Blast Crisis" is $\geq$20% blasts [1].

Question 563: Which of the following is associated with Bence Jones myeloma?

A. gamma chain disease
B. alpha chain disease
C. kappa or lambda light chain disease (Correct Answer)
D. heavy chain disease

Explanation: **Explanation:** **Bence Jones Myeloma** (also known as Light Chain Myeloma) is a variant of Multiple Myeloma where the malignant plasma cells produce only monoclonal free light chains (FLCs) rather than complete immunoglobulin molecules [1]. 1. **Why Option C is Correct:** In this condition, there is a failure to produce heavy chains. Instead, the plasma cells secrete either **kappa (κ) or lambda (λ) light chains**. Because of their low molecular weight (approx. 22-44 kDa), these light chains are easily filtered by the renal glomeruli and excreted in the urine, where they are known as **Bence Jones proteins** [2]. These proteins are unique because they precipitate when heated to 40–60°C and redissolve upon boiling (100°C). 2. **Why Other Options are Incorrect:** * **Options A, B, and D:** These refer to **Heavy Chain Diseases (HCDs)**, such as Franklin’s disease (gamma), Seligmann’s disease (alpha), and Mu-chain disease. In these rare B-cell proliferative disorders, the plasma cells produce truncated heavy chains without associated light chains. This is the exact opposite of Bence Jones Myeloma. **High-Yield Clinical Pearls for NEET-PG:** * **Diagnosis:** Bence Jones proteins are **not detected by standard urine dipsticks** (which primarily sense albumin) [2]. They require **Sulphosalicylic acid (SSA) test** or Urine Protein Electrophoresis (UPEP) [1]. * **Renal Impact:** The filtration of these light chains can lead to "Myeloma Kidney" (Cast Nephropathy), where light chains precipitate with Tamm-Horsfall protein in the distal tubules. * **Frequency:** Light chain myeloma accounts for approximately 15–20% of all Multiple Myeloma cases. * **CRAB Criteria:** Remember the classic presentation of Multiple Myeloma: **C**alcium elevation, **R**enal insufficiency, **A**nemia, and **B**one lesions [1].

Question 564: In Von Willebrand disease, what is the primary defect?

A. Factor VII deficiency
B. Factor VIII C deficiency
C. Factor X deficiency
D. Defects in von Willebrand factor (Correct Answer)

Explanation: **Explanation:** **Von Willebrand Disease (vWD)** is the most common inherited bleeding disorder. The primary defect is a quantitative or qualitative deficiency of **von Willebrand Factor (vWF)**. **Why the correct answer is right:** vWF is a large multimeric glycoprotein synthesized by endothelial cells and megakaryocytes. It serves two critical functions: 1. **Platelet Adhesion:** It acts as a bridge between platelet surface receptors (GpIb) and the subendothelial collagen at the site of vascular injury [1]. 2. **Carrier for Factor VIII:** It stabilizes Factor VIII (FVIII:C) in the circulation, protecting it from rapid proteolytic degradation [2]. Therefore, a defect in vWF leads to both impaired primary hemostasis (platelet plug formation) and secondary hemostasis (due to low FVIII levels). **Why other options are incorrect:** * **Factor VII deficiency:** This is a rare autosomal recessive disorder affecting the extrinsic pathway, characterized by an isolated prolonged Prothrombin Time (PT). * **Factor VIII C deficiency:** This is the hallmark of **Hemophilia A**. While vWD can lead to secondary low levels of Factor VIII, the *primary* genetic defect in vWF gene, not the Factor VIII gene [2]. * **Factor X deficiency:** This affects the common pathway of coagulation and is unrelated to the pathophysiology of vWD. **High-Yield Clinical Pearls for NEET-PG:** * **Inheritance:** Most types (Type 1 and 2) are Autosomal Dominant [2]; Type 3 is Autosomal Recessive. * **Lab Findings:** Prolonged Bleeding Time (BT) and often a prolonged aPTT (due to low Factor VIII). PT and Platelet count are typically normal (except in Type 2B where thrombocytopenia may occur). * **Screening Test:** Ristocetin Cofactor Assay (measures vWF-induced platelet agglutination) [2]. * **Treatment:** Desmopressin (DDAVP) is used for Type 1 as it releases stored vWF from Weibel-Palade bodies [2]. For severe cases, vWF-containing concentrates are used.

Question 565: All of the following are good prognostic features of Hodgkin's disease except?

A. Hemoglobin > 10 gm/dL
B. WBC count < 15000/mm³
C. Absolute lymphocyte count < 600/µL (Correct Answer)
D. Age < 45 years

Explanation: This question pertains to the **International Prognostic Score (IPS)** for Advanced Hodgkin Lymphoma (Hasenclever Index). The IPS identifies seven independent risk factors that predict a poorer prognosis. [1] ### **Explanation of the Correct Option** * **Option C: Absolute lymphocyte count < 600/µL:** This is a **poor** prognostic factor, not a good one. In Hodgkin’s Lymphoma, lymphopenia (ALC < 600/µL or < 8% of WBC count) indicates a more advanced disease state and a weakened immune response, leading to lower progression-free survival rates. Therefore, it is the "except" in this list. ### **Explanation of Incorrect Options (Good Prognostic Features)** The following are considered favorable because they represent the absence of the IPS risk factors: * **Option A: Hemoglobin > 10 gm/dL:** Anemia (Hb < 10.5 g/dL) is a poor prognostic factor. Thus, a normal or mildly reduced Hb is a positive sign. [1] * **Option B: WBC count < 15,000/mm³:** Leukocytosis (WBC ≥ 15,000/mm³) is associated with higher tumor burden and inflammation, making a lower count a good prognostic feature. [1] * **Option D: Age < 45 years:** Older age (≥ 45 years) is an independent predictor of worse outcomes; hence, younger age is favorable. [1] ### **High-Yield Clinical Pearls for NEET-PG** To master the **Hasenclever Index (IPS)**, remember the 7 adverse prognostic factors (Mnemonic: **"ALBUMIN"**): 1. **A**lbumin < 4 g/dL 2. **L**ymphocytes < 600/µL (or < 8%) 3. **B**lood (Hemoglobin) < 10.5 g/dL 4. **U**nder (Age) ≥ 45 years 5. **M**ale Gender 6. **I**ncreased WBC ≥ 15,000/mm³ 7. **N**odal Stage IV (Ann Arbor Classification) * **Note:** For **Early-stage** Hodgkin Lymphoma, the most important prognostic factor is the presence of **B-symptoms** and **Bulky disease** (mediastinal mass > 1/3 of chest diameter). [1]

Question 566: Anti-phospholipid antibody syndrome is characterized by all the following features except?

A. Thrombocytosis (Correct Answer)
B. Arterial and venous thrombosis
C. Recurrent abortions
D. Livedo reticularis

Explanation: **Explanation:** Antiphospholipid Antibody Syndrome (APS) is an autoimmune hypercoagulable state characterized by the presence of antiphospholipid antibodies (Lupus anticoagulant, Anti-cardiolipin, and Anti-β2 glycoprotein I). **Why Thrombocytosis is the correct answer:** APS is typically associated with **Thrombocytopenia** (low platelet count), not thrombocytosis [1]. The reduction in platelets occurs because they are consumed during the formation of thrombi or cleared by the reticuloendothelial system due to antibody coating. Thrombocytosis is not a feature of APS and often suggests an alternative diagnosis like a myeloproliferative neoplasm. **Analysis of other options:** * **Arterial and venous thrombosis:** This is the hallmark of APS. It can affect any vessel size, leading to Deep Vein Thrombosis (DVT), pulmonary embolism, or strokes. * **Recurrent abortions:** APS causes placental insufficiency and placental infarctions, leading to recurrent pregnancy loss (typically >10 weeks), premature births, or pre-eclampsia. * **Livedo reticularis:** This is the most common cutaneous manifestation of APS, presenting as a mottled, purplish, net-like pattern on the skin caused by swelling of the venules due to obstruction of capillaries by small blood clots [2]. **High-Yield Clinical Pearls for NEET-PG:** * **The Paradox:** APS causes a **prolonged aPTT** *in vitro* (due to antibody interference with phospholipids in the test), but it causes **thrombosis** *in vivo*. * **Catastrophic APS (Asherson’s Syndrome):** Rapidly progressive multiorgan failure due to small vessel occlusion. * **Treatment:** Long-term anticoagulation with Warfarin (Target INR 2.0–3.0). Note: DOACs are generally avoided in triple-positive APS patients.

Question 567: Which of the following is a common feature in multiple myeloma?

A. Body ache and pain
B. Elevated serum globulin
C. Renal failure
D. Hypocalcemia (Correct Answer)

Explanation: **Explanation:** Multiple Myeloma (MM) is a plasma cell dyscrasia characterized by the neoplastic proliferation of a single clone of plasma cells [1]. The hallmark features are summarized by the mnemonic **CRAB**: **C**alcium (Hypercalcemia), **R**enal failure, **A**nemia, and **B**one lesions. **Why the correct answer is D (Hypocalcemia):** Actually, there appears to be a discrepancy in the question's marking. In Multiple Myeloma, **Hypercalcemia** is the classic feature, not hypocalcemia. Hypercalcemia occurs due to increased osteoclast activity mediated by RANK-L and various cytokines (IL-6, TNF-β) secreted by myeloma cells, leading to extensive bone resorption. If the question intended to identify a "common feature," **Hypocalcemia is incorrect**; however, if we must analyze the options provided: * **A. Body ache and pain:** This is the **most common presenting symptom** (present in >70% of patients) due to lytic bone lesions and pathological fractures [1]. * **B. Elevated serum globulin:** This is a **hallmark finding**. The "M-spike" on electrophoresis represents the monoclonal globulin (paraprotein), leading to a reversed Albumin:Globulin (A:G) ratio [1]. * **C. Renal failure:** A common complication (up to 25-50% of patients) caused by Bence-Jones proteinuria (cast nephropathy), hypercalcemia, and amyloidosis. * **D. Hypocalcemia:** This is **NOT** a feature of Multiple Myeloma. Patients characteristically present with **Hypercalcemia**. **NEET-PG High-Yield Pearls:** * **Most common cause of death:** Infection (due to hypogammaglobulinemia), followed by Renal Failure. * **Diagnosis:** Bone marrow plasma cells ≥10% + CRAB features or specific biomarkers (SLiM criteria: **S**ixty percent plasma cells, **L**ight chain ratio >100, **M**RI >1 focal lesion) [1]. * **Peripheral Smear:** Rouleaux formation (due to high globulin levels). * **X-ray:** "Punched-out" lytic lesions (Skull X-ray is classic) [1]. Note: Bone scans are often negative because there is no osteoblastic activity.

Question 568: Which of the following is NOT a component of POEMS syndrome?

A. Polyneuropathy
B. Organomegaly
C. Endocrinopathy
D. Multiple osteolytic lesions (Correct Answer)

Explanation: **Explanation:** POEMS syndrome is a rare multisystemic disorder caused by an underlying plasma cell dyscrasia. The diagnosis is based on the acronym itself, which represents its core clinical features. **Why "Multiple osteolytic lesions" is the correct answer:** In POEMS syndrome, the characteristic bone involvement is **osteosclerotic lesions** (bone-forming), not osteolytic (bone-destroying). This is a critical distinction from Multiple Myeloma, where punched-out osteolytic lesions are the hallmark [1]. In POEMS, the plasma cell proliferative disorder is typically associated with high levels of Vascular Endothelial Growth Factor (VEGF), which contributes to the unique sclerotic bone changes. **Analysis of other options:** * **A. Polyneuropathy:** This is a mandatory major criterion. It is typically a chronic, symmetric, sensorimotor polyradiculoneuropathy. * **B. Organomegaly:** Commonly involves hepatomegaly, splenomegaly, or lymphadenopathy (often associated with Castleman disease). * **C. Endocrinopathy:** Frequent manifestations include hypothyroidism, hypogonadism, adrenal insufficiency, and diabetes mellitus. **High-Yield Clinical Pearls for NEET-PG:** * **The Acronym:** **P**olyneuropathy, **O**rganomegaly, **E**ndocrinopathy, **M**onoclonal protein (M-spike), and **S**kin changes (e.g., hyperpigmentation, hypertrichosis). * **Key Biomarker:** Elevated serum **VEGF** levels are highly sensitive and specific for monitoring disease activity. * **Mandatory Criteria for Diagnosis:** 1. Polyneuropathy AND 2. Monoclonal plasma cell proliferative disorder (usually Lambda light chain). * **Association:** Frequently associated with **Castleman disease**. * **Treatment:** Targeted at the underlying plasma cell clone (e.g., radiation for localized lesions, systemic chemotherapy, or autologous stem cell transplant).

Question 569: Which of the following is NOT an example of massive splenomegaly?

A. Chronic myeloid leukemia
B. Chronic malaria
C. Tropical splenomegaly
D. Acute lymphoblastic leukemia (Correct Answer)

Explanation: The classification of splenomegaly is a high-yield topic for NEET-PG. Splenomegaly is categorized by the distance the spleen extends below the left costal margin: **Mild** (<4 cm), **Moderate** (4–8 cm), and **Massive** (>8 cm or weight >1000g). **Why Acute Lymphoblastic Leukemia (ALL) is the correct answer:** In **Acute Lymphoblastic Leukemia**, the disease progression is rapid. The spleen does not have sufficient time to undergo the massive compensatory hypertrophy or extensive infiltration seen in chronic conditions. Splenomegaly in ALL is typically **mild to moderate**. Massive splenomegaly is almost exclusively a feature of chronic myeloproliferative disorders or chronic infections [1]. **Analysis of Incorrect Options:** * **Chronic Myeloid Leukemia (CML):** This is the classic cause of massive splenomegaly. * **Chronic Malaria:** Repeated infections lead to persistent congestion and hyperplasia of the reticuloendothelial system. * **Tropical Splenomegaly (Hyperreactive Malarial Splenomegaly):** This is an exaggerated immune response to malaria characterized by massive IgM production and huge splenic enlargement. **Clinical Pearls for NEET-PG:** * **Mnemonic for Massive Splenomegaly (The "3 C's and 3 M's"):** 1. **C**ML (Most common) 2. **C**LL (Less common than CML) [3] 3. **C**irrhosis (with portal hypertension - though usually moderate) 4. **M**yelofibrosis [2] 5. **M**alaria (Chronic/Tropical) 6. **M**ala-azar (Visceral Leishmaniasis) 7. *Bonus:* **G**aucher’s disease (Storage disorder) * **Note:** In **Polycythemia Vera**, splenomegaly is common, but it is rarely "massive" unless it transforms into myelofibrosis.

Question 570: A 35-year-old female presents with bilateral deep vein thrombosis in her legs. She has a past history of recurrent fetal loss and one episode of pulmonary embolism. Screening tests of coagulation reveal a prolonged aPTT. What is the likely diagnosis?

A. Factor VIII deficiency
B. Inherited Protein C and S deficiency
C. Antiphospholipid syndrome (Correct Answer)
D. Hereditary excess of Antithrombin III

Explanation: The clinical presentation of recurrent venous thromboembolism (DVT and PE) combined with a history of recurrent fetal loss in a young female is a classic triad for **Antiphospholipid Syndrome (APS)** [2]. **1. Why Antiphospholipid Syndrome (APS) is correct:** APS is an autoimmune prothrombotic state. The "paradox" of APS is that while it causes **thrombosis in vivo** (inside the body), it causes **prolonged aPTT in vitro** (in the lab). This occurs because antiphospholipid antibodies (specifically Lupus Anticoagulant) interfere with the phospholipids used in the aPTT reagent, artificially delaying clot formation in the test tube [3]. **2. Why other options are incorrect:** * **Factor VIII deficiency (Hemophilia A):** This leads to a bleeding diathesis, not thrombosis. While aPTT is prolonged, the clinical history of DVT and fetal loss contradicts this. * **Protein C and S deficiency:** These are common causes of inherited thrombophilia, but they typically present with a **normal aPTT** [1]. * **Hereditary excess of Antithrombin III:** Antithrombin III is a natural anticoagulant. An *excess* would lead to a bleeding tendency, whereas a *deficiency* leads to thrombosis [1]. **3. High-Yield Clinical Pearls for NEET-PG:** * **Diagnostic Criteria (Sapporo):** At least one clinical criteria (vascular thrombosis or pregnancy morbidity) + one laboratory criteria (Lupus anticoagulant, Anti-cardiolipin, or Anti-β2 glycoprotein I antibodies). * **Mixing Study:** In APS, the prolonged aPTT **does not correct** upon mixing with normal plasma (indicating the presence of an inhibitor), whereas in factor deficiencies, it does correct [3]. * **False Positive VDRL:** Patients with APS may show a false positive test for Syphilis due to cross-reactivity with cardiolipin. * **Treatment:** Long-term anticoagulation with Warfarin (INR 2.0–3.0) [4]. Note: DOACs are currently not recommended for "triple-positive" APS.

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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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Hematology — MCQs

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