Hematology — MCQs

Hematology Indian Medical PG Practice Questions and MCQs

Question 131: What is the most likely cause of hypochromic anisocytosis in a 37-year-old multipara construction labourer?

A. Iron deficiency
B. Folic acid deficiency
C. Combined iron and folic acid deficiency (Correct Answer)
D. Chronic disease

Explanation: The correct answer is **Combined iron and folic acid deficiency**. This diagnosis is reached by synthesizing the clinical profile with the morphologic description provided. **1. Why it is correct:** The patient is a **multipara** (multiple pregnancies deplete iron and folate stores) [3], [4] and a **construction laborer** (high physical demand and likely low socioeconomic status/poor nutrition). * **Hypochromic:** Indicates low hemoglobin content, characteristic of **Iron Deficiency Anemia (IDA)** [1], [2]. * **Anisocytosis:** Refers to a high Red Cell Distribution Width (RDW), meaning a high variation in cell size. In nutritional deficiencies, especially "dimorphic anemia" (combined deficiency), the presence of both microcytes (from iron deficiency) and macrocytes (from folate/B12 deficiency) leads to a significantly high RDW (anisocytosis). In India, this combination is the most common cause of nutritional anemia in women of reproductive age. **2. Why other options are incorrect:** * **Iron deficiency (A):** While it causes hypochromia, pure IDA typically presents with microcytosis [1]. While anisocytosis occurs, the combination with folate deficiency in this specific demographic is more "classic" for a NEET-PG clinical vignette. * **Folic acid deficiency (B):** This typically causes **macrocytic normochromic** anemia [3]. It would not explain the hypochromia. * **Chronic disease (D):** Anemia of chronic disease is usually **normocytic normochromic** (though it can become microcytic) [2]. It typically presents with low RDW (minimal anisocytosis) because the cell size is uniform. **Clinical Pearls for NEET-PG:** * **Dimorphic Anemia:** Look for a "double population" on the peripheral smear or a high RDW with a normal or slightly altered Mean Corpuscular Volume (MCV). * **RDW:** It is the earliest indicator of iron deficiency anemia, rising before the hemoglobin drops. * **Hookworm infestation:** In a laborer, always consider this as a contributing factor to iron deficiency in the Indian context [1].

Question 132: What is the most common presentation of Hodgkin's lymphoma?

A. Painless enlargement of lymph nodes (Correct Answer)
B. Pruritus
C. Fever
D. Leukocytosis

Explanation: **Explanation:** **1. Why Option A is Correct:** The hallmark clinical presentation of Hodgkin’s Lymphoma (HL) is **painless, rubbery, non-tender lymphadenopathy** [1]. In approximately 60-80% of cases, the involvement begins in the **cervical or supraclavicular nodes**. The disease typically follows a predictable, contiguous pattern of spread through the lymphatic chain. While systemic symptoms occur, the physical discovery of an enlarged, painless node is the most frequent initial complaint [1]. **2. Why Other Options are Incorrect:** * **B. Pruritus:** While severe, generalized itching is a recognized "paraneoplastic" feature of HL (sometimes preceding diagnosis), it occurs in only about 10-15% of patients. It is not as common as lymphadenopathy. * **C. Fever:** Fever is one of the classic **"B-symptoms"** (along with night sweats and weight loss) [2]. While clinically significant for staging and prognosis, B-symptoms are present in only about 25-30% of patients at the time of diagnosis. * **D. Leukocytosis:** While a mild-to-moderate neutrophilia or eosinophilia can be seen in HL, it is a non-specific laboratory finding and not a primary clinical presentation [3]. **3. NEET-PG High-Yield Pearls:** * **Pel-Ebstein Fever:** A rare but classic pattern of high fever for 1-2 weeks followed by an afebrile period. * **Alcohol-Induced Pain:** Pain in the lymph nodes specifically after drinking alcohol is a highly specific (though uncommon) sign of HL. * **B-Symptoms:** Defined as Fever (>38°C), drenching night sweats, and unexplained weight loss (>10% in 6 months) [2]. Their presence indicates a worse prognosis (Stage B). * **Bimodal Age Distribution:** HL typically shows two peaks—one in the 20s and another after age 50.

Question 133: Which of the following laboratory evaluations is NOT included in the differential diagnosis of chronic myeloproliferative disorders?

A. Chromosomal evaluation
B. Bone marrow aspiration
C. Flow-cytometric analysis (Correct Answer)
D. Determination of red blood cell mass

Explanation: ### Explanation **Chronic Myeloproliferative Neoplasms (MPNs)**, such as Chronic Myeloid Leukemia (CML), Polycythemia Vera (PV), Essential Thrombocythemia (ET), and Primary Myelofibrosis (PMF), are characterized by the clonal expansion of mature myeloid elements. **Why Flow-cytometric analysis is the correct answer:** Flow cytometry is primarily used to identify **cell surface markers (CD markers)**. It is the gold standard for diagnosing **acute leukemias** (to differentiate AML from ALL) and **lymphoproliferative disorders** (like CLL or Lymphoma) [1]. In chronic MPNs, the cells are mature and do not typically express a specific "leukemic" immunophenotype that flow cytometry can distinguish from normal mature cells [4]. Therefore, it is not a routine part of the MPN diagnostic workup. **Why the other options are incorrect:** * **Chromosomal evaluation:** Essential for identifying the **Philadelphia chromosome [t(9;22)]** to diagnose CML and to rule out other clonal abnormalities in BCR-ABL negative MPNs [3]. * **Bone marrow aspiration/biopsy:** Crucial for assessing cellularity, morphology, and the degree of **fibrosis** (especially in PMF) or megakaryocyte clusters [2], [4]. * **Determination of red blood cell mass:** Historically used to differentiate **absolute polycythemia** (increased RBC mass) from relative polycythemia (decreased plasma volume). While replaced by JAK2 testing in newer WHO criteria, it remains a classic physiological evaluation for erythrocytosis. **High-Yield Clinical Pearls for NEET-PG:** * **JAK2 V617F mutation:** Present in >95% of PV cases and ~50-60% of ET and PMF cases [2]. * **CML Hallmark:** Translocation t(9;22) creating the *BCR-ABL1* fusion gene [3]. * **LAP Score:** Low in CML; high in Leukemoid reaction and Polycythemia Vera. * **Primary Myelofibrosis:** Characterized by "Dry tap" on aspiration and "Teardrop cells" (Dacrocytes) on peripheral smear [2].

Question 134: Which of the following is NOT true about polycythemia vera?

A. Bleeding
B. Thrombosis
C. Decreased ESR
D. Infection (Correct Answer)

Explanation: **Explanation:** Polycythemia Vera (PV) is a chronic myeloproliferative neoplasm characterized by the autonomous overproduction of all three myeloid cell lines (erythrocytosis, leukocytosis, and thrombocytosis), primarily driven by the **JAK2 V617F mutation** [1]. **Why "Infection" is the correct answer:** While PV involves an increase in the total white blood cell count (leukocytosis), these cells are generally mature and functional. Unlike conditions like leukemia or myelodysplastic syndromes where cells are dysfunctional, or states of neutropenia, **infection is not a characteristic feature or a common complication of PV.** Patients are more likely to suffer from vascular events than infectious ones. **Analysis of incorrect options:** * **Bleeding:** Paradoxically, despite high platelet counts, PV patients are at risk for bleeding. This is often due to **acquired von Willebrand Syndrome**, where high shear stress and massive platelet surfaces lead to the depletion of large vWF multimers. * **Thrombosis:** This is the **most common cause of morbidity and mortality** in PV. Hyperviscosity (due to high hematocrit) and qualitative platelet abnormalities lead to both arterial (stroke, MI) and venous (DVT, Budd-Chiari syndrome) thrombosis [1]. * **Decreased ESR:** The Erythrocyte Sedimentation Rate (ESR) is essentially zero in PV. Since ESR depends on the rate at which RBCs fall, the extreme overcrowding of cells (high hematocrit) prevents them from settling, resulting in a **near-zero ESR**. **High-Yield Clinical Pearls for NEET-PG:** * **Hallmark symptom:** Aquagenic pruritus (itching after a warm bath) due to mast cell degranulation [1]. * **Physical Exam:** Splenomegaly (present in 75% of cases) and facial plethora [1]. * **Diagnosis:** Low serum Erythropoietin (EPO) levels and JAK2 mutation (95% of cases) [1]. * **Treatment of choice:** Phlebotomy (target Hct <45%) and low-dose Aspirin. Hydroxyurea is used for high-risk patients.

Question 135: In iron deficiency anemia, after hemoglobin levels have returned to normal and iron stores are replenished, for how long should iron tablets be recommended?

A. 0-3 months (Correct Answer)
B. 3-6 months
C. 6-12 months
D. 12-24 months

Explanation: ### Explanation The management of Iron Deficiency Anemia (IDA) involves two distinct phases: correcting the anemia (restoring hemoglobin) and replenishing the body’s iron stores (ferritin). **Why Option A is correct:** The standard protocol for IDA treatment is to continue oral iron therapy for **3 to 6 months after the hemoglobin level has normalized**. However, the question specifically asks for the duration of treatment **after** both hemoglobin levels have returned to normal **and** iron stores (ferritin) have been replenished. Once the iron stores are fully replenished (indicated by a serum ferritin >30–50 µg/L), there is no physiological benefit to continuing supplementation [1]. Therefore, the additional duration required is **0–3 months** (essentially stopping once the target store is reached). **Why the other options are incorrect:** * **Options B, C, and D:** These durations (3–24 months) are excessive once stores are already confirmed to be replenished. Prolonged, unnecessary iron intake increases the risk of gastrointestinal side effects (constipation, nausea) and oxidative stress without providing further therapeutic benefit. **NEET-PG High-Yield Pearls:** * **First sign of response:** The earliest laboratory sign of response to iron therapy is an increase in **reticulocyte count**, which peaks at **7–10 days**. * **Hemoglobin rise:** Expect Hb to rise by approximately **1 g/dL every 7–10 days**. * **Best absorption:** Oral iron is best absorbed on an empty stomach or with Vitamin C (Ascorbic acid). * **Failure of therapy:** If Hb does not rise after 3 weeks of compliant therapy, investigate for malabsorption (e.g., Celiac disease), ongoing occult blood loss, or an incorrect diagnosis (e.g., Thalassemia trait).

Question 136: Which of the following is NOT a component of POEMS syndrome?

A. Polyneuropathy
B. Esophageal atresia (Correct Answer)
C. Endocrinopathy
D. Multiple myeloma

Explanation: POEMS syndrome is a rare multisystemic paraneoplastic syndrome associated with an underlying plasma cell proliferative disorder. The diagnosis is based on a specific constellation of clinical features, which are represented by its acronym. ### **Why "Esophageal Atresia" is the Correct Answer** The "E" in POEMS stands for **Endocrinopathy**, not Esophageal atresia. Esophageal atresia is a congenital structural defect typically diagnosed in neonates and has no pathophysiological link to plasma cell dyscrasias or the cytokine-mediated systemic involvement seen in POEMS. ### **Analysis of Other Options** * **P – Polyneuropathy:** Usually the presenting symptom; it is typically chronic, progressive, distal, and symmetric (sensorimotor). * **O – Organomegaly:** Primarily hepatomegaly, splenomegaly, or lymphadenopathy. * **E – Endocrinopathy:** Common manifestations include hypogonadism, hypothyroidism, and adrenal insufficiency. * **M – Monoclonal Plasma Cell Proliferative Disorder:** Often presents as osteosclerotic myeloma (rather than the typical osteolytic lesions seen in classic Multiple Myeloma). [1] * **S – Skin Changes:** Includes hyperpigmentation, hypertrichosis, and glomeruloid hemangiomas. ### **High-Yield Clinical Pearls for NEET-PG** * **VEGF:** Elevated serum levels of **Vascular Endothelial Growth Factor (VEGF)** are a hallmark of the disease and correlate with disease activity. * **Bone Lesions:** Unlike classic Multiple Myeloma (which has lytic lesions), POEMS is associated with **osteosclerotic lesions**. * **Castleman Disease:** A significant proportion of patients with POEMS syndrome also have co-existing Castleman disease. * **Major Diagnostic Criteria:** Mandatory criteria include Polyneuropathy and Monoclonal plasma cell protein (usually IgA or IgG lambda).

Question 137: Fanconi's anemia is characterized by which of the following?

A. An inherited form of aplastic anemia with autosomal recessive inheritance. (Correct Answer)
B. A form of iron deficiency anemia.
C. A form of white blood cell abnormality.
D. All of the above.

Explanation: **Explanation:** **Fanconi’s Anemia (FA)** is the most common cause of **inherited bone marrow failure syndrome**. It is primarily an **autosomal recessive** disorder (though rare X-linked forms exist) caused by mutations in genes responsible for DNA repair. This leads to genomic instability, resulting in progressive pancytopenia and an evolution into **aplastic anemia**, typically manifesting in the first decade of life. * **Why Option A is correct:** FA is defined by its genetic predisposition to chromosomal breakage. The inability to repair DNA interstrand cross-links leads to the depletion of hematopoietic stem cells, causing aplastic anemia. * **Why Option B is incorrect:** Iron deficiency anemia is a microcytic nutritional anemia caused by blood loss or poor intake, unrelated to the genetic DNA-repair defects seen in FA. * **Why Option C is incorrect:** While FA involves a decrease in white blood cells (as part of pancytopenia), it is not primarily a "WBC abnormality" (like leukemia or functional neutrophil defects); it is a global failure of the bone marrow to produce all three cell lines. **High-Yield Clinical Pearls for NEET-PG:** * **Physical Findings:** Short stature, **absent or hypoplastic radii/thumbs**, microcephaly, and **café-au-lait spots**. * **Gold Standard Diagnosis:** The **Chromosomal Breakage Test** (using Diepoxybutane or Mitomycin C) shows increased sensitivity of lymphocytes to DNA cross-linking agents. * **Malignancy Risk:** Patients have a significantly increased risk of developing **AML** and squamous cell carcinomas (especially of the head, neck, and anogenital region). * **Treatment:** Hematopoietic stem cell transplant (HSCT) is the definitive treatment for hematologic manifestations.

Question 138: Which of the following can cause secondary polycythemia?

A. Chronic cor pulmonale
B. Renal carcinoma
C. Cerebellar haemangioblastoma
D. All of the above (Correct Answer)

Explanation: **Explanation:** Polycythemia (erythrocytosis) is classified into **Primary** (Polycythemia Vera), where the bone marrow autonomously produces excess RBCs, and **Secondary**, where RBC production is driven by elevated levels of **Erythropoietin (EPO)** [1]. Secondary polycythemia occurs via two main mechanisms, both represented in the options: 1. **Physiologic Compensation (Hypoxia-driven):** When the body senses low arterial oxygen saturation, the kidneys increase EPO production to improve oxygen-carrying capacity [1][2]. **Chronic cor pulmonale (Option A)**, resulting from chronic lung diseases (like COPD), leads to chronic hypoxemia, triggering this compensatory response [2]. 2. **Inappropriate EPO Secretion (Tumor-driven):** Certain tumors autonomously secrete EPO regardless of oxygen levels [1]. * **Renal Cell Carcinoma (Option B):** The most common tumor associated with ectopic EPO production. * **Cerebellar Haemangioblastoma (Option C):** A classic "high-yield" association in exams; these tumors are often seen in Von Hippel-Lindau (VHL) syndrome and can secrete EPO. Since all three conditions lead to increased EPO and subsequent erythrocytosis, **Option D** is the correct answer. **High-Yield Clinical Pearls for NEET-PG:** * **Differential Diagnosis:** To distinguish Primary from Secondary polycythemia, check **Serum EPO levels**. EPO is **low** in Polycythemia Vera (due to feedback inhibition) and **high** in Secondary polycythemia [2]. * **Other EPO-secreting tumors:** Hepatocellular carcinoma (HCC), Uterine fibroids (leiomyomas) [1], and Pheochromocytoma. * **Gaisbock Syndrome:** Also known as "Relative Polycythemia," where RBC mass is normal but plasma volume is decreased (commonly seen in stressed, hypertensive, obese males) [2].

Question 139: Osteomyelitis in sickle cell anemia is most commonly caused by which organism?

A. Salmonella (Correct Answer)
B. Streptococcus
C. Haemophilus
D. Neisseria

Explanation: **Explanation:** In the general population, *Staphylococcus aureus* is the most common cause of osteomyelitis. However, in patients with **Sickle Cell Anemia (SCA)**, **Salmonella** species are the most common causative organisms (followed by *S. aureus*). **Why Salmonella?** The predisposition to Salmonella in SCA is due to several factors: 1. **Autosplenectomy:** Chronic splenic infarction leads to functional asplenia, impairing the clearance of encapsulated and intracellular organisms [1]. 2. **Vaso-occlusive Crises:** Micro-infarctions in the intestinal mucosa allow Salmonella (normal gut flora) to enter the bloodstream. 3. **Bone Infarction:** Ischemic areas in the bone marrow serve as a nidus for bacteria to settle during transient bacteremia [1]. 4. **Complement Deficiency:** Impaired alternative complement pathway activity reduces the opsonization of Salmonella. **Analysis of Incorrect Options:** * **B. Streptococcus:** While *S. pneumoniae* is a major cause of sepsis and meningitis in SCA due to asplenia, it is not the leading cause of osteomyelitis. * **C. Haemophilus:** *H. influenzae* was a common cause of infection in asplenic children, but its incidence has significantly decreased due to widespread vaccination. * **D. Neisseria:** Patients with terminal complement deficiency are at risk for Neisserial infections, but it is not a primary pathogen in sickle cell-related osteomyelitis. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause of Osteomyelitis in SCA:** *Salmonella* (unique association). * **Most common cause of Osteomyelitis overall:** *Staphylococcus aureus*. * **Most common cause of death in SCA (Children):** *S. pneumoniae* sepsis [1]. * **Most common cause of death in SCA (Adults):** Acute Chest Syndrome. * **Radiology:** It is often difficult to distinguish between a bone infarct and osteomyelitis on X-ray; MRI or bone scans are preferred.

Question 140: All of the following cause microcytic anemia except?

A. Hookworm infestation
B. Thalassemia
C. Orotic aciduria (Correct Answer)
D. Pyridoxine deficiency

Explanation: **Explanation:** The classification of anemia is primarily based on the **Mean Corpuscular Volume (MCV)**. Microcytic anemias (MCV < 80 fL) typically result from defects in hemoglobin synthesis, whereas macrocytic anemias (MCV > 100 fL) result from defects in DNA synthesis or erythrocyte maturation. **Why Orotic Aciduria is the correct answer:** Orotic aciduria is a rare autosomal recessive disorder caused by a deficiency of **UMP synthase**. This enzyme is crucial for **de novo pyrimidine synthesis**. A defect leads to impaired DNA synthesis, which manifests as **Megaloblastic Anemia** (a type of macrocytic anemia). Unlike nutritional megaloblastic anemias, it does not respond to Vitamin B12 or Folate but responds to **Uridine supplementation**. **Analysis of Incorrect Options (Causes of Microcytic Anemia):** * **Hookworm infestation:** Causes chronic gastrointestinal blood loss, leading to **Iron Deficiency Anemia (IDA)**, the most common cause of microcytic hypochromic anemia worldwide [2]. * **Thalassemia:** A genetic defect in the synthesis of globin chains (alpha or beta), leading to ineffective erythropoiesis and microcytosis [1]. * **Pyridoxine (Vitamin B6) deficiency:** Vitamin B6 is a mandatory cofactor for **ALAS**, the rate-limiting enzyme in heme synthesis. Deficiency leads to **Sideroblastic Anemia**, which is characteristically microcytic. **NEET-PG High-Yield Pearls:** * **Mnemonic for Microcytic Anemia (TAILS):** **T**halassemia, **A**nemia of chronic disease (some cases), **I**ron deficiency, **L**ead poisoning, **S**ideroblastic anemia [2]. * **Orotic Aciduria vs. OTC Deficiency:** Both present with high orotic acid in urine. However, **OTC deficiency** (Urea cycle defect) presents with **hyperammonemia** and NO megaloblastic anemia, whereas **Orotic Aciduria** presents with **megaloblastic anemia** and NO hyperammonemia.

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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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