Hematology Practice Questions

Q: A 56-year-old male presents with low back pain, weight loss, fatigue, and recurrent sinus infections. He has no history of trauma. Examination reveals focal tenderness at the T10 level. Laboratory investigations show Hb of 9 g/dl and deranged renal function tests. A skull X-ray was performed. Bone marrow biopsy and serum protein electrophoresis are planned. What is the characteristic abnormality expected on the peripheral blood film?

Rouleaux formation. The clinical presentation of bone pain (low back pain), constitutional symptoms (weight loss, fatigue), recurrent infections, and renal impairment in an elderly male is highly suggestive of **Multiple Myeloma (MM)** [1]. The "CRAB" features (Calcium elevation, Renal insufficiency, Anemia, and Bone lesions) are classic indicators [1]. **1. Why Rouleaux formation is correct:** In Multiple Myeloma, there is a monoclonal proliferation of plasma cells leading to the overproduction of monoclonal (M) proteins (immunoglobulins) [1]. These high levels of paraproteins reduce the zeta potential (negative charge) on the surface of Red Blood Cells (RBCs). This allows RBCs to stack together like a "pile of coins," a phenomenon known as **Rouleaux formation** [2]. This is the characteristic peripheral smear finding in MM and is also responsible for the characteristically high ESR seen in these patients [1]. **2. Analysis of Incorrect Options:** * **Anemia (A):** While the patient has anemia (Hb 9 g/dl), it is a *finding*, not a *characteristic morphological abnormality* on the film. * **Pelger-Huet anomaly (B):** This refers to hyposegmented neutrophils, typically seen in Myelodysplastic Syndromes (MDS) or congenital conditions, not MM. * **Neutrophilia (D):** Patients with MM are often neutropenic due to marrow infiltration or have normal counts; neutrophilia is not a characteristic feature. **Clinical Pearls for NEET-PG:** * **Skull X-ray:** Look for "punched-out" lytic lesions [1]. * **Diagnosis:** Gold standard is Bone Marrow Biopsy (>10% clonal plasma cells) [1]. * **Bence-Jones Proteins:** These are free light chains found in urine; they do not show up on standard dipsticks [1]. * **M-Spike:** Seen on Serum Protein Electrophoresis (SPEP), usually in the Gamma globulin region [1].

Q: Schilling's test may be used to establish a diagnosis of:

Intrinsic factor deficiency. The **Schilling test** is a classic diagnostic tool used to determine the cause of Vitamin B12 (cobalamin) malabsorption. It is performed in stages to pinpoint the specific anatomical or physiological defect. **1. Why Option A is Correct:** Intrinsic Factor (IF) deficiency is the hallmark of **Pernicious Anemia** [1]. In the Schilling test, Stage I involves giving oral radiolabeled B12. If excretion in the urine is low, Stage II is performed by co-administering oral B12 with **exogenous Intrinsic Factor**. If the B12 absorption normalizes (increased urinary excretion) during Stage II, it confirms that the primary pathology was a lack of IF, thereby establishing the diagnosis. **2. Why Other Options are Incorrect:** * **Option B:** While pancreatic **exocrine** insufficiency (lack of proteases to cleave R-binder from B12) can cause malabsorption, the option specifies **endocrine** dysfunction (e.g., Diabetes), which does not affect B12 absorption. * **Option C:** Folic acid deficiency is a cause of megaloblastic anemia, but its absorption is independent of Intrinsic Factor and the B12-specific pathways tested by the Schilling test [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Stage III** of the Schilling test uses antibiotics to check for **Small Intestinal Bacterial Overgrowth (SIBO)**. * **Stage IV** uses pancreatic enzymes to check for **Chronic Pancreatitis**. * **Prerequisite:** Before starting the test, a

Q: Which of the following is a nutritional deficiency anemia?

Megaloblastic anemia. **Explanation:** **Megaloblastic anemia** is the correct answer because it is primarily caused by a deficiency of essential nutrients—specifically **Vitamin B12 (Cobalamin)** and **Vitamin B9 (Folic Acid)** [1]. These nutrients are critical cofactors for DNA synthesis. When they are deficient, there is a "nuclear-cytoplasmic asynchrony" where the cell's nucleus matures slower than the cytoplasm, leading to the formation of large, immature red blood cell precursors (megaloblasts) in the bone marrow and macrocytic cells in the peripheral blood [1]. **Analysis of Incorrect Options:** * **Aplastic Anemia:** This is a bone marrow failure syndrome characterized by pancytopenia and a hypocellular marrow. It is usually caused by autoimmune destruction of stem cells, toxins, or drugs, rather than a lack of dietary nutrients. * **Sickle Cell Anemia:** This is a genetic (hereditary) hemoglobinopathy caused by a point mutation in the ̢-globin gene (Glu → Val at the 6th position), leading to the production of abnormal Hemoglobin S. * **Hemolytic Anemia:** This refers to a group of disorders where red blood cells are destroyed prematurely. Causes can be intrinsic (e.g., G6PD deficiency, Spherocytosis) or extrinsic (e.g., Autoimmune hemolytic anemia), but it is not fundamentally a nutritional deficiency. **High-Yield Clinical Pearls for NEET-PG:** * **Peripheral Smear:** Look for **macro-ovalocytes** and **hypersegmented neutrophils** (≥ 5 lobes in > 5% of neutrophils or a single neutrophil with ≥ 6 lobes). * **Neurological Symptoms:** Only Vitamin B12 deficiency causes Subacute Combined Degeneration (SCD) of the spinal cord (dorsal columns and lateral corticospinal tracts). Pure Folate deficiency does **not** cause neurological deficits [1]. * **Schilling Test:** Historically used to differentiate causes of B12 malabsorption (e.g., Pernicious anemia vs. dietary deficiency).

Q: Which of the following is the most common cause of transfusion-associated hepatitis?

Hepatitis B. The correct answer is **Hepatitis B (HBV)**. While Hepatitis C was historically the most common cause of post-transfusion hepatitis before the discovery of the virus and the implementation of rigorous screening, modern nucleic acid testing (NAT) has significantly reduced the risk for both HBV and HCV. However, **Hepatitis B remains the most common** transfusion-transmitted viral infection (TTI) globally and in India. This is primarily due to the "occult" HBV infection (HBsAg negative but DNA positive) and the longer window period compared to other viruses, which allows it to occasionally bypass standard screening protocols. **Analysis of Incorrect Options:** * **Hepatitis A:** It is primarily transmitted via the fecal-oral route [1]. While transient viremia occurs, it is an extremely rare cause of transfusion-associated hepatitis because it does not have a chronic carrier state. * **Hepatitis C:** Formerly the leading cause of "Non-A, Non-B" post-transfusion hepatitis. Since the introduction of highly sensitive NAT, the risk has plummeted to less than 1 in 2 million units in developed regions, making it less common than HBV. * **Hepatitis D:** This is a defective virus that requires the presence of HBsAg to replicate. It is only transmitted alongside HBV and is not considered an independent primary cause of transfusion-associated hepatitis. **High-Yield Pearls for NEET-PG:** * **Most common TTI overall:** Hepatitis B. * **Most common cause of post-transfusion purpura:** Antibodies against HPA-1a. * **Most common cause of transfusion-related mortality:** TRALI (Transfusion-Related Acute Lung Injury). * **Window Period:** HBV has a longer window period (~30-60 days) compared to HIV (~7-10 days) or HCV (~3-5 days) when using NAT. [2]

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.

Q: All of the following are inherited platelet function disorders except?

Weber-Christian disease. The question asks to identify the condition that is **not** an inherited platelet function disorder. **Weber-Christian disease** (Relapsing febrile non-suppurative panniculitis) is the correct answer because it is an inflammatory condition characterized by recurrent nodules of the subcutaneous fat (panniculitis), often accompanied by systemic symptoms like fever. It is **not** a hematological disorder of platelet function. **Analysis of Incorrect Options:** * **Bernard-Soulier Syndrome:** An autosomal recessive disorder caused by a deficiency of the **GpIb-IX-V complex** (the receptor for von Willebrand factor) [1]. It is characterized by giant platelets and failure of platelets to aggregate with Ristocetin. * **Glanzmann Thrombasthenia:** An autosomal recessive disorder caused by a deficiency or dysfunction of **GpIIb/IIIa** (the receptor for fibrinogen) [1]. Platelets fail to aggregate with all agonists (ADP, collagen, epinephrine) except Ristocetin. * **Wiskott-Aldrich Syndrome:** An X-linked recessive disorder characterized by the triad of **thrombocytopenia (with small platelets)**, eczema, and immunodeficiency. It involves a defect in the WASP protein, affecting the platelet cytoskeleton. **NEET-PG High-Yield Pearls:** * **Adhesion Defect:** Bernard-Soulier Syndrome (GpIb deficiency) [1]. * **Aggregation Defect:** Glanzmann Thrombasthenia (GpIIb/IIIa deficiency) [1]. * **Platelet Size:** Giant platelets are seen in Bernard-Soulier; **Small platelets** are a hallmark of Wiskott-Aldrich Syndrome. * **Ristocetin Test:** In Bernard-Soulier, the Ristocetin cofactor assay is abnormal and **does not** correct with the addition of normal plasma (unlike von Willebrand Disease).

Question 1

A 56-year-old male presents with low back pain, weight loss, fatigue, and recurrent sinus infections. He has no history of trauma. Examination reveals focal tenderness at the T10 level. Laboratory investigations show Hb of 9 g/dl and deranged renal function tests. A skull X-ray was performed. Bone marrow biopsy and serum protein electrophoresis are planned. What is the characteristic abnormality expected on the peripheral blood film?

Accepted Answer

Rouleaux formation

Answer

Anemia

Answer

Pelger-Huet anomaly

Answer

Neutrophilia

Question 2

Schilling's test may be used to establish a diagnosis of:

Accepted Answer

Intrinsic factor deficiency

Answer

Pancreatic endocrine dysfunction

Answer

Megaloblastic anemia from folic acid deficiency

Answer

All of the above

Question 3

Which of the following is a nutritional deficiency anemia?

Accepted Answer

Megaloblastic anemia

Answer

Aplastic anemia

Answer

Sickle cell anemia

Answer

Hemolytic anemia

Question 4

Which of the following is the most common cause of transfusion-associated hepatitis?

Accepted Answer

Hepatitis B

Answer

Hepatitis A

Answer

Hepatitis C

Answer

Hepatitis D

Question 5

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 6

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

Question 7

A 62-year-old man reports early satiety, fatigue, and generally feeling unwell. The symptoms started gradually and are getting worse. He notes no chest discomfort, respiratory symptoms, or abdominal pain. On physical examination, he appears pale, the vital signs are normal, and the pertinent findings are a large spleen, absence of lymph nodes, and normal heart and lungs. His blood count is abnormal; the WBC is 50,000/mL with increased mature granulocytes, hemoglobin is 9.5 g/dL, and platelets are 450,000/mL. Which of the following cytogenetic changes is most characteristic of his condition?

Accepted Answer

Reciprocal translocation of 9 and 22 (Philadelphia chromosome)

Answer

Deletion of chromosome 14

Answer

Translocation of the renal artery stenosis (RAS) oncogene

Answer

Trisomy 21

Question 8

All of the following are inherited platelet function disorders except?

Accepted Answer

Weber-Christian disease

Answer

Bernard-Soulier syndrome

Answer

Glanzmann thrombasthenia

Answer

Wiskott-Aldrich syndrome

Question 9

Which of the following statements regarding hematological malignancies is true?

Accepted Answer

Acute lymphoid leukemia in infants less than 1 year of age has a poor prognosis.

Answer

Chronic myeloid leukemia characteristically occurs in individuals over 50 years of age.

Answer

Hairy cell leukemia in individuals less than 50 years of age generally has a good prognosis.

Answer

Chronic lymphocytic leukemia characteristically occurs in individuals less than 50 years of age.

Question 10

What is the intermediate form of Non-Hodgkin's lymphoma?

Accepted Answer

Diffuse, small cleaved cell

Answer

Small noncleaved cell

Answer

Lymphoblastic

Answer

Large cell immunoblastic

Hematology — MCQs

Hematology — MCQs

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