Hematology — MCQs

A 26-year-old woman presents with weakness, dyspnea, and palpitations. Examination reveals severe pallor. She recently experienced a viral infection. Liver function tests show elevated bilirubin levels. Ultrasound reveals splenomegaly and gallstones. Her mother, who is standing nearby, also appears pale and has splenomegaly. What is the probable diagnosis?

Q416Medium

All are TRUE about paroxysmal cold hemoglobinuria (PCH), EXCEPT:

Q417Medium

A patient receiving low molecular weight heparin (LMWH) suddenly develops hemorrhage. What is the next step in management?

Q418Medium

Acute myeloid leukemia (AML) with the best prognosis is typically associated with which subtype?

Q419Easy

Which of the following is a feature of pernicious anemia?

Q420Medium

What type of anemia is typically caused by pulmonary tuberculosis?

Hematology Indian Medical PG Practice Questions and MCQs

Question 411: Which of the following is NOT an intrinsic cause of hemolytic anemia?

A. G6PD deficiency
B. Hereditary spherocytosis
C. Hypersplenism (Correct Answer)
D. Pyruvate kinase deficiency

Explanation: ### Explanation Hemolytic anemias are broadly classified into **Intrinsic (Intracorpuscular)** and **Extrinsic (Extracorpuscular)** causes. This distinction is based on whether the defect resides within the red blood cell (RBC) itself or is caused by external factors [1]. **Why Hypersplenism is the Correct Answer:** Hypersplenism is an **extrinsic** cause of hemolysis. In this condition, an enlarged or overactive spleen prematurely traps and destroys otherwise normal RBCs as they pass through the splenic sinusoids [1]. The defect is in the environment (the spleen), not the cell. Other extrinsic causes include autoimmune hemolytic anemia, microangiopathic hemolytic anemia (MAHA), and infections like Malaria [1]. **Analysis of Incorrect Options:** * **G6PD Deficiency:** An intrinsic defect involving the **hexose monophosphate shunt** [2]. The lack of G6PD enzyme makes RBCs susceptible to oxidative stress, leading to hemoglobin denaturation (Heinz bodies) [2]. * **Hereditary Spherocytosis:** An intrinsic defect of the **RBC membrane proteins** (most commonly Ankyrin or Spectrin) [3]. This leads to a loss of membrane surface area, resulting in spherical, fragile cells [3]. * **Pyruvate Kinase (PK) Deficiency:** An intrinsic **enzymatic defect** in the glycolytic pathway. Without PK, the cell cannot generate sufficient ATP, leading to rigid cells and premature destruction. **Clinical Pearls for NEET-PG:** * **Rule of Thumb:** Almost all intrinsic hemolytic anemias are **hereditary** (except Paroxysmal Nocturnal Hemoglobinuria/PNH), while almost all extrinsic causes are **acquired** [1]. * **PNH Exception:** Always remember PNH is an *acquired* intrinsic defect (due to a PIGA gene mutation). * **Peripheral Smear:** Look for **Bite cells** in G6PD deficiency and **Spherocytes** in Hereditary Spherocytosis. * **Coombs Test:** Usually negative in intrinsic defects and positive in immune-mediated extrinsic defects.

Question 412: Which of the following parameters will fall the earliest in iron deficiency?

A. MCV (Correct Answer)
B. MCH
C. MCHC
D. Red cell distribution width

Explanation: In iron deficiency anemia (IDA), the depletion of iron stores occurs in a predictable sequence. Understanding the kinetics of red cell indices is crucial for NEET-PG. **Why MCV is the correct answer:** As iron stores are exhausted, the bone marrow begins to produce smaller red cells (microcytosis) before the hemoglobin concentration within those cells significantly drops [1]. **Mean Corpuscular Volume (MCV)** measures the average size of the RBC. In the progression of IDA, microcytosis (low MCV) typically precedes hypochromia (low MCH/MCHC) [1]. Therefore, MCV is the first of the standard indices (MCV, MCH, MCHC) to fall below the reference range. **Analysis of Incorrect Options:** * **B. MCH (Mean Corpuscular Hemoglobin):** This measures the average amount of hemoglobin per RBC. While it falls early, it generally follows the decrease in MCV. * **C. MCHC (Mean Corpuscular Hemoglobin Concentration):** This is the last index to decrease. It reflects the "concentration" of hemoglobin; cells become smaller first to maintain concentration before eventually becoming pale (hypochromic). * **D. Red Cell Distribution Width (RDW):** RDW actually **increases** (not falls) in iron deficiency. It is often the very first sign of IDA on a CBC, representing anisocytosis (variation in cell size) as new small cells mix with older normal-sized cells. **High-Yield Clinical Pearls for NEET-PG:** 1. **Earliest Biochemical Marker:** Serum Ferritin (reflects storage iron). 2. **Earliest Hematological Change:** Increased RDW (Red Cell Distribution Width). 3. **Earliest Index to Fall:** MCV. 4. **Gold Standard Diagnosis:** Bone marrow aspiration (Perl’s Prussian Blue stain) showing absent haemosiderin [1]. 5. **Mentzer Index:** MCV/RBC count. If <13, suggests Thalassemia trait; if >13, suggests Iron Deficiency Anemia.

Question 413: A patient presents with MCV = 60 fL, Hb = 5 gm%, MCHC = 20 pg/cell, and PCV = 32%. What are the potential causes of anemia in this patient?

A. Phenytoin
B. Blind loop syndrome
C. Hookworm infection (Correct Answer)
D. Chronic renal failure (CRF)

Explanation: ### Explanation The patient’s laboratory parameters indicate **Microcytic Hypochromic Anemia**. * **MCV (Mean Corpuscular Volume) = 60 fL:** Low (Normal: 80–100 fL), indicating microcytosis [1]. * **MCHC (Mean Corpuscular Hemoglobin Concentration) = 20 pg/cell:** Low (Normal: 27–33 pg/cell), indicating hypochromia [1]. * **Hb = 5 gm%:** Severe anemia. **1. Why Hookworm Infection is Correct:** Hookworm infection (*Ancylostoma duodenale* and *Necator americanus*) is a leading cause of **Iron Deficiency Anemia (IDA)** in developing countries [2]. The worms attach to the intestinal mucosa and suck blood, leading to chronic occult blood loss [1]. Over time, iron stores are depleted, resulting in the classic microcytic hypochromic picture seen in this patient [1]. **2. Why Other Options are Incorrect:** * **Phenytoin:** This drug interferes with folate metabolism, leading to **Megaloblastic Anemia**, which is characterized by a *high* MCV (>100 fL) [1]. * **Blind Loop Syndrome:** This condition causes bacterial overgrowth, which leads to Vitamin B12 deficiency. Like phenytoin, this results in **Macrocytic Anemia** (High MCV). * **Chronic Renal Failure (CRF):** Anemia in CRF is primarily due to decreased erythropoietin production [3]. It typically presents as **Normocytic Normochromic Anemia** (Normal MCV and MCHC). **High-Yield Clinical Pearls for NEET-PG:** * **Differential Diagnosis for Microcytic Anemia (TAILS):** **T**halassemia, **A**nemia of chronic disease (late stage), **I**ron deficiency, **L**ead poisoning, **S**ideroblastic anemia. * **Hookworm Fact:** *Ancylostoma duodenale* causes more blood loss (0.15–0.2 ml/day) than *Necator americanus* (0.03 ml/day). * **Mentzer Index:** MCV/RBC count. If <13, it suggests Thalassemia; if >13, it suggests Iron Deficiency Anemia.

Question 414: Which of the following statements is not true about Von Willebrand disease?

A. Von Willebrand factor (VWF) is synthesized by endothelial cells and megakaryocytes.
B. VWF may be located in the plasma and subendothelial tissue.
C. VWF causes platelet adhesion and prevents the degradation of factor VIII in plasma.
D. Deficiency of VWF causes prolonged prothrombin time. (Correct Answer)

Explanation: Explanation: **Why Option D is the correct (false) statement:** Von Willebrand Factor (VWF) is primarily involved in primary hemostasis (platelet adhesion) and the stabilization of Factor VIII. A deficiency in VWF leads to a prolonged **Bleeding Time (BT)** and potentially a prolonged **Activated Partial Thromboplastin Time (aPTT)** due to decreased Factor VIII levels [1]. However, it has no effect on the extrinsic pathway. **Prothrombin Time (PT)** measures the extrinsic and common pathways (Factors I, II, V, VII, X); since VWF does not interact with these factors, the PT remains **normal** in Von Willebrand Disease (vWD). **Analysis of other options:** * **Option A:** Correct. VWF is synthesized in **endothelial cells** (stored in Weibel-Palade bodies) and **megakaryocytes** (stored in α-granules of platelets). * **Option B:** Correct. VWF circulates in the plasma as multimers and is also present in the subendothelial connective tissue, where it awaits vascular injury to facilitate platelet binding. * **Option C:** Correct. VWF acts as a "bridge" between platelet GpIb receptors and subendothelial collagen (adhesion). It also serves as a carrier protein for **Factor VIII**, protecting it from rapid proteolytic degradation by Activated Protein C [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Most Common:** vWD is the most common inherited bleeding disorder. * **Inheritance:** Most types (Type 1 and 2) are **Autosomal Dominant**, unlike Hemophilia (X-linked). * **Diagnostic Test:** The **Ristocetin Cofactor Assay** is the gold standard for functional assessment (measures VWF-dependent platelet agglutination) [1]. * **Treatment:** **Desmopressin (DDAVP)** is the treatment of choice for Type 1 as it releases endogenous VWF stores from endothelial cells [1].

Question 415: A 26-year-old woman presents with weakness, dyspnea, and palpitations. Examination reveals severe pallor. She recently experienced a viral infection. Liver function tests show elevated bilirubin levels. Ultrasound reveals splenomegaly and gallstones. Her mother, who is standing nearby, also appears pale and has splenomegaly. What is the probable diagnosis?

A. Gilbert's syndrome
B. Hereditary spherocytosis (Correct Answer)
C. G6PD deficiency
D. Paroxysmal nocturnal hemoglobinuria

Explanation: **Explanation:** The clinical presentation points toward **Hereditary Spherocytosis (HS)**, an autosomal dominant disorder caused by defects in red blood cell (RBC) membrane proteins (most commonly **Ankyrin**, followed by Spectrin) [1]. **Why Option B is correct:** 1. **Hemolytic Anemia:** Weakness, pallor, and elevated bilirubin indicate hemolysis [1]. 2. **Triad:** The classic triad of HS is **anemia, jaundice, and splenomegaly**. 3. **Complications:** Chronic hemolysis leads to increased bilirubin excretion, resulting in **pigment gallstones** (cholelithiasis), even in young patients. 4. **Family History:** The mother’s similar symptoms suggest an autosomal dominant inheritance pattern. 5. **Trigger:** Viral infections (like Parvovirus B19) can trigger "aplastic crises" or "hemolytic crises," worsening the symptoms. **Why other options are incorrect:** * **A. Gilbert’s Syndrome:** Causes isolated indirect hyperbilirubinemia without anemia, splenomegaly, or gallstones. * **C. G6PD Deficiency:** An X-linked recessive disorder (rare in females) characterized by episodic hemolysis triggered by oxidative stress (drugs/fava beans) [2]. It does not typically cause chronic splenomegaly. * **D. Paroxysmal Nocturnal Hemoglobinuria (PNH):** An acquired stem cell defect presenting with intravascular hemolysis and venous thrombosis; it lacks a strong family history. **NEET-PG High-Yield Pearls:** * **Gold Standard Test:** Eosin-5-maleimide (EMA) binding test via flow cytometry. * **Screening Test:** Osmotic Fragility Test (increased fragility). * **Peripheral Smear:** Spherocytes (small, dark RBCs lacking central pallor) and increased MCHC (>36 g/dL) [1]. * **Treatment of Choice:** Splenectomy (usually deferred until after age 6 to reduce sepsis risk) [1].

Question 416: All are TRUE about paroxysmal cold hemoglobinuria (PCH), EXCEPT:

A. It occurs mostly in children
B. It is self-limited
C. Donath-Landsteiner antibody is present
D. Lysis of red blood cells occurs at low temperatures (Correct Answer)

Explanation: Explanation: Paroxysmal Cold Hemoglobinuria (PCH) is a rare form of autoimmune hemolytic anemia characterized by the presence of the **Donath-Landsteiner antibody**, a biphasic IgG autoantibody directed against the P-antigen on red blood cells (RBCs). **Why Option D is the Correct Answer (The False Statement):** The hallmark of PCH is its **biphasic** nature. The Donath-Landsteiner antibodies bind to RBCs only at **low temperatures** (cold phase), but the actual **lysis (complement-mediated hemolysis) occurs at 37°C** (warm phase) when the blood recirculates to the body's core. Therefore, stating that lysis occurs at low temperatures is physiologically incorrect. **Analysis of Other Options:** * **Option A:** PCH is most commonly seen in **children**, often following a viral (e.g., Measles, Mumps, EBV) or upper respiratory infection. * **Option B:** In its acute form (post-viral), PCH is typically **self-limited**, resolving within a few days to weeks once the inciting infection clears. * **Option C:** The **Donath-Landsteiner antibody** is the pathognomonic finding. It is an IgG antibody that fixes complement (C3) in the cold [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Antibody Type:** IgG (unlike Cold Agglutinin Disease, which is typically IgM) [1]. * **Specificity:** Anti-P antibody. * **Direct Antiglobulin Test (DAT):** Usually positive for **C3** only; negative for IgG (as the antibody dissociates at warmer temperatures) [1]. * **Historical Context:** Historically associated with late-stage syphilis; currently most common in pediatric post-viral settings. * **Clinical Presentation:** Sudden onset of dark "cola-colored" urine (hemoglobinuria) after cold exposure, accompanied by fever and chills.

Question 417: A patient receiving low molecular weight heparin (LMWH) suddenly develops hemorrhage. What is the next step in management?

A. Level of Factor Xa activity (Correct Answer)
B. Activated partial thromboplastin time (APTT)
C. Platelet count
D. Prothrombin time (PT)

Explanation: The correct management for monitoring or assessing complications of **Low Molecular Weight Heparin (LMWH)** is the measurement of **Factor Xa activity**. [1] **1. Why Factor Xa activity is correct:** LMWH (e.g., Enoxaparin) acts primarily by inhibiting Factor Xa rather than Thrombin (Factor IIa), with a ratio of approximately 3:1 to 4:1. [1] Unlike Unfractionated Heparin (UFH), LMWH has a predictable pharmacokinetic profile and usually does not require routine monitoring. [4] However, in specific scenarios—such as **active hemorrhage**, renal failure, pregnancy, or extreme obesity—monitoring is essential. Since LMWH does not significantly prolong global coagulation tests, the **anti-Xa assay** is the only reliable method to quantify its anticoagulant effect. **2. Why other options are incorrect:** * **APTT (Option B):** This is the standard test for monitoring **Unfractionated Heparin (UFH)**. [3], [4] LMWH molecules are too short to bridge antithrombin to thrombin effectively, resulting in minimal to no change in APTT even at therapeutic doses. * **Platelet Count (Option C):** While used to screen for Heparin-Induced Thrombocytopenia (HIT), it does not measure the anticoagulant intensity or explain an acute hemorrhage caused by drug overdose. * **Prothrombin Time (Option D):** PT/INR is used to monitor Warfarin (extrinsic pathway) [2] and is not affected by LMWH. **Clinical Pearls for NEET-PG:** * **Antidote:** Protamine sulfate only partially neutralizes LMWH (approx. 60-75%), whereas it completely reverses UFH. * **Renal Clearance:** LMWH is renally excreted; thus, it is contraindicated in patients with ESRD (CrCl <30 ml/min). UFH is preferred in such cases. * **Monitoring:** Routine monitoring is NOT required for LMWH, unlike UFH. Anti-Xa levels should be drawn 4 hours after the dose (peak level). [4]

Question 418: Acute myeloid leukemia (AML) with the best prognosis is typically associated with which subtype?

A. Acute myelomonocytic leukemia
B. Acute monocytic leukemia
C. Acute promyelocytic leukemia (M3) (Correct Answer)
D. Erythroleukemia

Explanation: **Explanation:** **Acute Promyelocytic Leukemia (APL/M3)** is associated with the best prognosis among all AML subtypes due to its unique molecular target and highly effective targeted therapy [1]. It is characterized by the **t(15;17)** translocation, which results in the **PML-RARα** fusion gene [1]. This fusion protein arrests myeloid differentiation at the promyelocyte stage. The introduction of **All-Trans Retinoic Acid (ATRA)** and **Arsenic Trioxide (ATO)** has revolutionized treatment, allowing for differentiation of these cells into mature granulocytes, leading to complete remission rates exceeding 90%. **Analysis of Incorrect Options:** * **A & B (Acute Myelomonocytic/Monocytic Leukemia):** These subtypes (M4 and M5) are often associated with intermediate to poor prognosis. They frequently present with hyperleukocytosis and extramedullary involvement (e.g., gingival hyperplasia), which can complicate management. * **D (Erythroleukemia):** Previously classified as M6, this subtype is generally associated with a poor prognosis, often arising from prior myelodysplastic syndromes (MDS) and exhibiting complex cytogenetics [1]. **High Yield Clinical Pearls for NEET-PG:** * **DIC Risk:** APL is a medical emergency because the promyelocytic granules contain procoagulants; starting ATRA immediately is vital to prevent fatal **Disseminated Intravascular Coagulation (DIC)**. * **Morphology:** Look for **Auer rods** (often in bundles called "Faggot cells") on peripheral smears. * **Differentiation Syndrome:** A key complication of ATRA/ATO therapy, presenting with fever, respiratory distress, and pulmonary infiltrates. * **Molecular Marker:** Monitoring the PML-RARα transcript via PCR is the gold standard for assessing Minimal Residual Disease (MRD).

Question 419: Which of the following is a feature of pernicious anemia?

A. Glossitis
B. Tingling or numbness of extremities
C. Nervous system involvement in 75% of cases
D. All of the above (Correct Answer)

Explanation: Pernicious anemia is an autoimmune condition characterized by the destruction of gastric parietal cells, leading to a deficiency of **Intrinsic Factor (IF)**. This results in the malabsorption of Vitamin B12 (Cobalamin), which is essential for DNA synthesis and myelin maintenance [1]. **Analysis of Options:** * **Glossitis (Option A):** Vitamin B12 deficiency leads to megaloblastic changes in the rapidly dividing cells of the gastrointestinal tract. This manifests clinically as a "beefy red," sore, and smooth tongue (Hunter’s glossitis) due to the atrophy of lingual papillae. * **Tingling or numbness (Option B):** These are early sensory symptoms of peripheral neuropathy. Vitamin B12 is a cofactor in the conversion of methylmalonyl-CoA to succinyl-CoA. Deficiency leads to an accumulation of methylmalonic acid (MMA), causing abnormal myelin synthesis and subsequent **Subacute Combined Degeneration (SCD)** of the spinal cord. * **Nervous system involvement (Option C):** Neurological symptoms (paresthesia, loss of vibratory sense, ataxia, or dementia) are highly prevalent in pernicious anemia, occurring in approximately **70-90% of symptomatic cases**. Notably, neurological symptoms can occur even in the absence of overt anemia. [2] Since all three features are characteristic of the disease, **Option D** is the correct answer. **High-Yield Clinical Pearls for NEET-PG:** * **Diagnostic Triad:** Hypersegmented neutrophils, macro-ovalocytes, and increased serum homocysteine/MMA levels. [1] * **Antibodies:** Anti-parietal cell antibodies (sensitive) and Anti-intrinsic factor antibodies (highly specific). * **Schilling Test:** Historically used to differentiate B12 malabsorption etiologies (now largely replaced by serology). * **Association:** Increased risk of **Gastric Adenocarcinoma** and Carcinoid tumors due to chronic atrophic gastritis.

Question 420: What type of anemia is typically caused by pulmonary tuberculosis?

A. Iron-deficiency anemia
B. Megaloblastic anemia
C. Sideroblastic anemia
D. Anemia of chronic disease (Correct Answer)

Explanation: **Explanation:** **1. Why Anemia of Chronic Disease (ACD) is the correct answer:** Pulmonary Tuberculosis (TB) is a chronic inflammatory infection. The primary mediator in ACD is **Hepcidin**, an acute-phase reactant produced by the liver in response to inflammatory cytokines like **IL-6** [1]. * **Mechanism:** Hepcidin binds to and degrades **ferroportin** (the iron export channel) on enterocytes and macrophages [2]. This leads to iron sequestration within the Reticuloendothelial System (RES), meaning iron is present in the body but "locked away" and unavailable for erythropoiesis [3]. Additionally, cytokines directly suppress erythropoietin (EPO) production and shorten red cell survival. **2. Why the other options are incorrect:** * **Iron-deficiency anemia (IDA):** While TB can cause nutritional depletion, the primary mechanism is functional iron deficiency (sequestration) rather than absolute iron loss. In IDA, ferritin is low; in ACD, ferritin is normal or high [3]. * **Megaloblastic anemia:** This is caused by Vitamin B12 or Folate deficiency. TB does not directly interfere with these vitamins, though it may occur in severely malnourished patients as a secondary finding. * **Sideroblastic anemia:** This involves a defect in heme synthesis (e.g., lead poisoning or Vitamin B6 deficiency). While the anti-TB drug **Isoniazid (INH)** can cause sideroblastic anemia by antagonizing Vitamin B6, the *disease itself* (TB) causes ACD. **3. Clinical Pearls for NEET-PG:** * **Lab Findings in ACD:** Low Serum Iron, **Low TIBC** (Total Iron Binding Capacity), and **High/Normal Ferritin** [3]. * **Morphology:** Initially Normocytic Normochromic, but can become Microcytic Hypochromic in long-standing cases [1]. * **Treatment:** The definitive treatment for ACD is managing the underlying condition (i.e., ATT for Tuberculosis) [3]. * **High-Yield Association:** If a patient on ATT develops peripheral neuropathy or sideroblastic anemia, the culprit is **Isoniazid (INH)**; prevent this by co-administering **Pyridoxine (B6)**.

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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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