Hematology Practice Questions

Q: A 45-year-old lady diagnosed to have anemia presents with Hb of 7.8 g/dL and MCV of 72 fL. Her serum ferritin is 8 ng/mL. After one month of adequate iron therapy, her Hb is still 8.0 g/dL. What is the most probable cause for treatment failure?

Non-compliance. **Explanation:** The patient presents with **Microcytic Hypochromic Anemia** (Hb 7.8 g/dL, MCV 72 fL) and a low serum ferritin (8 ng/mL), which is the most specific biochemical marker for **Iron Deficiency Anemia (IDA)**. [1] In a patient with confirmed IDA, oral iron therapy typically results in a reticulocyte count peak within 7–10 days and a rise in Hemoglobin (Hb) of approximately **1–2 g/dL every 2–3 weeks**. After one month of "adequate" therapy, this patient’s Hb has remained stagnant (7.8 to 8.0 g/dL). **1. Why Non-compliance is the Correct Answer:** Statistically, **non-compliance** is the most common cause of failure to respond to oral iron therapy. Oral iron (especially ferrous sulfate) frequently causes gastrointestinal side effects like nausea, epigastric pain, constipation, or metallic taste, leading many patients to discontinue the medication or take it irregularly. **2. Why other options are incorrect:** * **Acquired Sideroblastic Anemia:** This would typically present with *increased* serum ferritin (iron overload) and ring sideroblasts in the bone marrow, not the low ferritin seen here. * **Inadequate intake of iron:** While a cause of IDA, the question states the patient was put on "adequate iron therapy." [1] Failure to respond to prescribed treatment points toward compliance or absorption issues rather than dietary intake. * **Folate deficiency:** This causes Macrocytic anemia (high MCV), which contradicts the microcytic (low MCV) picture provided. [2] **Clinical Pearls for NEET-PG:** * **First sign of response to iron:** Increase in Reticulocyte count (5–10 days). * **Most specific test for IDA:** Serum Ferritin (<15 ng/mL). * **Gold Standard for IDA:** Bone marrow iron stores (Perl’s Prussian Blue stain)—though rarely done. * **Malabsorption:** If compliance is confirmed but Hb still doesn't rise, consider Celiac disease or *H. pylori* infection.

Q: Megaloblastic anemia develops in which of the following conditions?

Infants fed on goat's milk. **Explanation:** **Megaloblastic anemia** is primarily caused by a deficiency in Vitamin B12 or Folic acid, leading to impaired DNA synthesis while RNA synthesis remains unaffected [1]. This results in "nuclear-cytoplasmic asynchrony." **Why Option C is Correct:** Infants fed exclusively on **goat’s milk** are at a high risk of developing **Folate deficiency**. Goat’s milk is notoriously low in folic acid (containing only about 6 µg/L compared to 50 µg/L in cow's milk) and is also deficient in Vitamin B12 and Vitamin C. Without supplementation, this leads to macrocytic, megaloblastic anemia. **Why Other Options are Incorrect:** * **A. Sideroblastic Anemia:** This is a microcytic hypochromic anemia characterized by the failure to incorporate iron into protoporphyrin IX, leading to "ringed sideroblasts" in the bone marrow. * **B. Thalassaemia:** This is a quantitative defect in globin chain synthesis, resulting in microcytic hypochromic anemia with characteristic target cells. * **D. Vitamin C Deficiency:** While Vitamin C aids iron absorption, its deficiency primarily causes **Scurvy**. While it can coexist with anemia (due to bleeding or decreased iron absorption), it does not directly cause megaloblastic changes. **High-Yield Clinical Pearls for NEET-PG:** * **Pernicious Anemia:** The most common cause of Vitamin B12 deficiency (autoimmune destruction of parietal cells). * **Drug-induced Megaloblastosis:** Common culprits include Methotrexate, Phenytoin, and Zidovudine. * **Peripheral Smear:** Look for **Hypersegmented Neutrophils** (earliest sign) and Macro-ovalocytes. * **Biochemical markers:** Increased Homocysteine is seen in both B12 and Folate deficiency, but **increased Methylmalonic Acid (MMA)** is specific to Vitamin B12 deficiency.

Q: All of the following are poor prognostic factors in a case of acute myeloid leukemia, except?

Presence of t(8:21). In Acute Myeloid Leukemia (AML), prognosis is primarily determined by cytogenetic abnormalities, molecular markers, and patient-related factors [1]. **1. Why t(8;21) is the Correct Answer:** Translocation **t(8;21)**, which involves the *RUNX1-RUNX1T1* gene fusion, is classified as a **favorable-risk** cytogenetic abnormality [1]. It belongs to the group of "Core Binding Factor" (CBF) leukemias. Patients with this translocation generally have high rates of complete remission and better overall survival compared to other AML subtypes [1]. Therefore, it is a **good** prognostic factor, not a poor one. **2. Explanation of Incorrect Options (Poor Prognostic Factors):** * **Age > 60 years:** Advanced age is a significant poor prognostic factor due to a higher frequency of unfavorable cytogenetics, decreased tolerance to intensive chemotherapy, and increased comorbidities [1]. * **Secondary Leukemias:** AML arising from a prior myelodysplastic syndrome (MDS), myeloproliferative neoplasm, or following exposure to chemotherapy/radiation (therapy-related AML) carries a much worse prognosis and often shows multi-drug resistance. * **Hyperleukocytosis (>1,00,000/µL):** A very high white cell count at presentation increases the risk of tumor lysis syndrome and leukostasis (causing respiratory or neurological distress), correlating with early mortality and lower remission rates. **Clinical Pearls for NEET-PG:** * **Favorable Prognosis:** t(8;21), inv(16), t(15;17) [APML], and isolated *NPM1* or *CEBPA* mutations [1]. * **Poor Prognosis:** Monosomy 5 or 7, del(5q), *FLT3-ITD* mutation, and complex karyotypes (≥3 abnormalities) [1]. * **Treatment Note:** While t(8;21) is favorable, the presence of a concurrent **c-KIT mutation** in these patients can worsen the prognosis.

Q: ADAMTS deficiency is seen in which condition?

Thrombotic thrombocytopenic purpura. **Explanation:** **Thrombotic Thrombocytopenic Purpura (TTP)** is the correct answer because its primary pathophysiology involves a deficiency of **ADAMTS13**, a metalloproteinase enzyme. Under normal conditions, ADAMTS13 cleaves large **von Willebrand Factor (vWF) multimers** into smaller, less active fragments. In TTP, a deficiency of this enzyme (either congenital or, more commonly, acquired via autoantibodies) leads to the persistence of "Ultra-Large" vWF multimers. These multimers cause spontaneous platelet aggregation and microthrombi formation, resulting in microangiopathic hemolytic anemia (MAHA) and consumptive thrombocytopenia [1]. **Why other options are incorrect:** * **Essential Thrombocythemia (ET):** A myeloproliferative neoplasm characterized by autonomous overproduction of platelets, usually associated with mutations in *JAK2*, *CALR*, or *MPL* genes. * **Idiopathic Thrombocytopenic Purpura (ITP):** An immune-mediated destruction of platelets by anti-GP IIb/IIIa antibodies [1]. It does not involve the vWF-cleaving protease. * **Chronic Lymphocytic Leukemia (CLL):** A B-cell neoplasm characterized by the accumulation of mature monoclonal B-lymphocytes; it is not related to ADAMTS13 [1]. **High-Yield Clinical Pearls for NEET-PG:** * **The Classic Pentad of TTP:** (Mnemonic: **FAT RN**) **F**ever, **A**nemia (MAHA), **T**hrombocytopenia, **R**enal failure, and **N**eurological symptoms. * **Diagnosis:** Schistocytes (fragmented RBCs) on peripheral smear and decreased ADAMTS13 activity (<10%). * **Treatment:** **Plasmapheresis (Plasma Exchange)** is the gold standard as it removes antibodies and replenishes the ADAMTS13 enzyme. [1] Brian Walker. Davidson's Principles and Practice of Medicine. 22E ed. Coagulation factor deficiency, pp. 1028-1029.

Q: Richter transformation in Chronic Lymphocytic Leukemia (CLL) transforms into which of the following?

Diffuse large B-cell lymphoma. **Explanation:** **Richter Transformation (RT)** refers to the sudden clinical deterioration of a patient with Chronic Lymphocytic Leukemia (CLL) or Small Lymphocytic Lymphoma (SLL) into a more aggressive, high-grade non-Hodgkin lymphoma. [1] 1. **Why Option A is Correct:** In approximately **90–95% of cases**, Richter transformation manifests as **Diffuse Large B-cell Lymphoma (DLBCL)**. [1] It is characterized by a rapid increase in lymph node size, worsening systemic (B) symptoms, and a sharp rise in Serum LDH. Pathologically, it involves the transformation of small, mature B-cells into large, malignant lymphoid blasts. 2. **Why Other Options are Incorrect:** * **Anaplastic Large Cell Lymphoma (B):** This is a T-cell lymphoma characterized by CD30 expression and the t(2;5) translocation. CLL is a B-cell malignancy and does not transform into T-cell lineages. * **Burkitt Lymphoma (C):** This is an aggressive B-cell lymphoma associated with c-MYC translocation [t(8;14)]. While aggressive, it is not the standard pathway for CLL transformation. * **Multiple Myeloma (D):** This is a plasma cell dyscrasia. While both CLL and Myeloma involve B-cell lineages, one does not typically "transform" into the other in the context of Richter’s. **High-Yield Clinical Pearls for NEET-PG:** * **Clinical Trigger:** Suspect RT if a stable CLL patient develops localized lymphadenopathy, fever, weight loss, and **elevated LDH**. * **Diagnosis:** PET-CT is useful to identify the most metabolic node (highest SUV), but **Excisional Biopsy** is the gold standard. * **Prognosis:** RT carries a poor prognosis with a median survival of less than 1 year. * **Genetic Association:** Often associated with mutations in **TP53** and **NOTCH1**.

Q: The MOST severe complication of idiopathic hyper-eosinophilic syndrome is:

Endocardial fibrosis. **Explanation:** **Idiopathic Hypereosinophilic Syndrome (HES)** is characterized by a persistent absolute eosinophil count >1500/µL for more than 6 months, leading to multi-organ damage. **Why Endocardial Fibrosis is Correct:** The most severe and life-threatening complication of HES is cardiac involvement, specifically **Loeffler’s Endocarditis**. Eosinophils release toxic granules (Major Basic Protein and Eosinophil Peroxidase) that cause direct endomyocardial damage. This progresses through three stages: 1. **Acute Necrotic Stage:** Myocardial damage. 2. **Thrombotic Stage:** Formation of mural thrombi. 3. **Fibrotic Stage:** Development of **Endocardial Fibrosis**, leading to restrictive cardiomyopathy and congestive heart failure. This is the primary cause of morbidity and mortality in these patients. **Why Other Options are Incorrect:** * **B. Eosinophilic gastroenteritis:** While the GI tract is frequently involved (causing diarrhea or pain), it is rarely fatal compared to cardiac failure. * **C. Interstitial pneumonia:** Pulmonary involvement (Loeffler’s syndrome/infiltrates) is common but usually responds well to steroids and is less severe than permanent cardiac remodeling. * **D. Bone marrow failure:** HES is a proliferative disorder, not an aplastic one. While it can evolve into myeloid leukemia, marrow failure is not a characteristic complication. **NEET-PG High-Yield Pearls:** * **Target Organ Damage:** Heart > Lungs > Skin > CNS. * **Cardiac Hallmark:** Restrictive cardiomyopathy with apical obliteration on Echo. * **Treatment:** Corticosteroids are the first-line treatment; Imatinib is used in cases with the *FIP1L1-PDGFRA* fusion gene.

Q: A 47-year-old man presents with a 6-week history of increasing fatigue and dark-colored stools. Complete blood count shows hemoglobin of 8.6 g/dL and microcytic, hypochromic RBCs. Upper gastrointestinal endoscopy reveals a peptic ulcer along the lesser curvature of the stomach. This patient's anemia is most likely caused by deficiency of which of the following?

Iron. **Explanation:** The patient presents with classic features of **Iron Deficiency Anemia (IDA)** secondary to chronic gastrointestinal blood loss [1]. **1. Why Iron is correct:** The clinical triad of **fatigue** (anemic symptom), **dark-colored stools** (melena indicating upper GI bleed), and a confirmed **peptic ulcer** points toward chronic blood loss [3]. In adults, the most common cause of iron deficiency is occult GI bleeding [1]. Laboratory findings of **microcytic, hypochromic RBCs** (low MCV, low MCHC) are the hallmark of IDA [2], as iron is a critical component of heme synthesis. Without iron, hemoglobin production is impaired, leading to smaller, paler red cells [1]. **2. Why the other options are incorrect:** * **Folic acid & Vitamin B12:** Deficiency of these vitamins leads to **Megaloblastic Anemia**, characterized by **macrocytic** (high MCV) RBCs and hypersegmented neutrophils, not microcytic cells [4]. * **Thiamine (Vitamin B1):** Thiamine deficiency typically presents as Beriberi (cardiovascular or neurological symptoms) or Wernicke-Korsakoff syndrome; it does not cause microcytic anemia. **Clinical Pearls for NEET-PG:** * **Rule of Thumb:** In any adult male or post-menopausal female with iron deficiency anemia, **GI malignancy** or **peptic ulcer disease** must be ruled out via endoscopy/colonoscopy [1]. * **Mentzer Index:** (MCV/RBC count) 13** suggests Iron Deficiency Anemia. * **Earliest Marker:** A decrease in **Serum Ferritin** is the earliest laboratory sign of iron deficiency. * **Pica and Koilonychia** (spoon-shaped nails) are specific physical exam findings associated with chronic IDA.

Question 1

A 45-year-old lady diagnosed to have anemia presents with Hb of 7.8 g/dL and MCV of 72 fL. Her serum ferritin is 8 ng/mL. After one month of adequate iron therapy, her Hb is still 8.0 g/dL. What is the most probable cause for treatment failure?

Accepted Answer

Non-compliance

Answer

Acquired sideroblastic anemia

Answer

Inadequate intake of iron

Answer

Folate deficiency

Question 2

Megaloblastic anemia develops in which of the following conditions?

Accepted Answer

Infants fed on goat's milk

Answer

Sideroblastic anemia

Answer

Thalassaemia

Answer

Vitamin C deficiency

Question 3

A patient with cirrhosis of the liver has the following coagulation parameters: Platelet count 2,00,000, Prothrombin time 25s/12s, Activated partial thromboplastin time 60s/35s, and thrombin time 15s/15s. Which of the following laboratory findings can also be seen in this patient?

Accepted Answer

D-dimer will be normal

Answer

Fibrinogen will be low

Answer

Antithrombin III will be high

Answer

Protein C will be elevated

Question 4

All of the following are poor prognostic factors in a case of acute myeloid leukemia, except?

Accepted Answer

Presence of t(8:21)

Answer

Age more than 60 years

Answer

Secondary leukemias

Answer

Leukocyte count more than 1,00,000/microliter

Question 5

ADAMTS deficiency is seen in which condition?

Accepted Answer

Thrombotic thrombocytopenic purpura

Answer

Essential thrombocythemia

Answer

Idiopathic thrombocytopenic purpura

Answer

Chronic lymphocytic leukemia

Question 6

Richter transformation in Chronic Lymphocytic Leukemia (CLL) transforms into which of the following?

Accepted Answer

Diffuse large B-cell lymphoma

Answer

Anaplastic Large Cell Lymphoma

Answer

Burkitt lymphoma

Answer

Multiple myeloma

Question 7

What is the treatment of choice for Idiopathic Thrombocytopenic Purpura?

Accepted Answer

Steroids

Answer

Intravenous immunoglobulin

Answer

Blood transfusion

Answer

Splenectomy

Question 8

What is an evidence that splenectomy might benefit a patient with idiopathic thrombocytopenic purpura?

Accepted Answer

An increase in platelet count on corticosteroid therapy

Answer

A significant enlargement of the spleen

Answer

A high reticulocyte count

Answer

Patient's age less than five years

Question 9

The MOST severe complication of idiopathic hyper-eosinophilic syndrome is:

Accepted Answer

Endocardial fibrosis

Answer

Eosinophilic gastroenteritis

Answer

Interstitial pneumonia

Answer

Bone marrow failure

Question 10

A 47-year-old man presents with a 6-week history of increasing fatigue and dark-colored stools. Complete blood count shows hemoglobin of 8.6 g/dL and microcytic, hypochromic RBCs. Upper gastrointestinal endoscopy reveals a peptic ulcer along the lesser curvature of the stomach. This patient's anemia is most likely caused by deficiency of which of the following?

Accepted Answer

Iron

Answer

Folic acid

Answer

Thiamine

Answer

Vitamin B12

Hematology — MCQs

Hematology — MCQs

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