Hematology Practice Questions

Q: Which of the following is not a type of hypoproliferative anemia?

G6PD deficiency. Anemias are broadly classified based on the reticulocyte count into **hypoproliferative** (low production) and **hyperproliferative** (increased destruction or loss). **Why G6PD Deficiency is the Correct Answer:** G6PD deficiency is a **hemolytic anemia**, which falls under the **hyperproliferative** category [1]. In this condition, the deficiency of the G6PD enzyme leads to inadequate production of NADPH, making red blood cells vulnerable to oxidative stress [2]. This results in episodic hemolysis. Because the bone marrow is healthy, it responds to the low hemoglobin by increasing erythropoiesis, leading to an **elevated reticulocyte count**. **Why the other options are Hypoproliferative:** * **Parvovirus B19:** This virus specifically infects and destroys erythroid progenitor cells in the bone marrow, leading to a transient cessation of RBC production (Pure Red Cell Aplasia). * **Anemia of Chronic Disease (ACD):** Driven by high levels of **Hepcidin**, this condition involves iron sequestration and a blunted erythropoietin response, resulting in decreased RBC production [3]. * **Fanconi Anemia:** This is an inherited form of **Aplastic Anemia** (pancytopenia). It is a primary bone marrow failure syndrome where the marrow cannot produce sufficient cells. **NEET-PG High-Yield Pearls:** * **Reticulocyte Production Index (RPI):** RPI 3% indicates hemolysis or acute blood loss. * **G6PD Hallmark:** Look for **"Heinz bodies"** (denatured hemoglobin) and **"Bite cells"** (degluticytes) on a peripheral smear. * **ACD Hallmark:** Characterized by **High Ferritin** and **Low TIBC** (Total Iron Binding Capacity) [3]. * **Parvovirus B19:** Classically causes "Aplastic Crisis" in patients with pre-existing hemolytic conditions like Sickle Cell Anemia or Hereditary Spherocytosis.

Q: A 20-year-old female presents with features of anemia. Blood tests show Hb of 5 g/dL, MCV of 52 fL, MCHC of 20 g/dL, and PCV of 32%. What is the most likely diagnosis?

Hookworm infection. ### Explanation **1. Analysis of the Correct Answer (Hookworm Infection)** The patient presents with severe anemia (Hb 5 g/dL) characterized by a low **MCV (52 fL)** and low **MCHC (20 g/dL)**. These findings are diagnostic of **Microcytic Hypochromic Anemia**. In the context of a young female in a tropical setting, the most common cause of microcytic hypochromic anemia is **Iron Deficiency Anemia (IDA)** [3]. Hookworms (*Ancylostoma duodenale* and *Necator americanus*) are a leading cause of chronic intestinal blood loss [1]. They attach to the intestinal mucosa and suck blood, leading to a progressive depletion of iron stores [1][2]. This results in the classic laboratory profile seen here: decreased hemoglobin, decreased cell volume (MCV), and decreased hemoglobin concentration within the cells (MCHC). **2. Analysis of Incorrect Options** * **Phenytoin Toxicity:** Phenytoin interferes with folate metabolism, typically causing **Megaloblastic (Macrocytic) Anemia**, where the MCV would be >100 fL. * **Fish Tapeworm Infection (*Diphyllobothrium latum*):** This parasite competes for Vitamin B12 absorption in the ileum, leading to Vitamin B12 deficiency and **Megaloblastic Anemia** (Macrocytic). * **Blind Loop Syndrome:** This condition causes bacterial overgrowth, which leads to Vitamin B12 malabsorption (due to bacterial utilization of B12), resulting in **Megaloblastic Anemia** (Macrocytic). **3. NEET-PG High-Yield Pearls** * **Mentzer Index:** (MCV/RBC count) 13 suggests Iron Deficiency Anemia. * **Hookworm Fact:** *Ancylostoma duodenale* causes more blood loss (0.15–0.2 ml/day) than *Necator americanus* (0.03 ml/day). * **Classic Triad of Hookworm:** Ground itch (dermatitis), Loeffler’s syndrome (pneumonitis), and Iron deficiency anemia [1]. * **MCHC:** This is the most specific indicator of true hypochromia. Normal range is 32–36 g/dL; a value of 20 g/dL is severely low.

Q: A 16-year-old girl has had frequent nosebleeds since childhood. Her gums bleed easily even with routine tooth brushing. She has experienced menorrhagia since menarche at age 13 years. On physical examination, there are no abnormal findings. Laboratory studies show hemoglobin, 14.1 g/dL; hematocrit, 42.5%; MCV, 90 mm3; platelet count, 277,400/mm3; and WBC count, 5920/mm3. Her platelets fail to aggregate in response to ADP, collagen, epinephrine, and thrombin. The ristocetin agglutination test result is normal. There is a deficiency of glycoprotein IIb/IIIa. Prothrombin time is 12 seconds, and partial thromboplastin time is 28 seconds. What is the most likely diagnosis?

Glanzmann thrombasthenia. The clinical presentation of mucosal bleeding (epistaxis, gingival bleeding, and menorrhagia) in a young patient with a **normal platelet count** and **normal PT/PTT** points toward a qualitative platelet disorder rather than a quantitative deficiency or a coagulation factor defect [1]. **Why Glanzmann Thrombasthenia (GT) is correct:** GT is an autosomal recessive disorder caused by a deficiency or dysfunction of **Glycoprotein IIb/IIIa (GPIIb/IIIa)**, a receptor essential for platelet-to-platelet aggregation via fibrinogen bridging [2]. * **Key Diagnostic Feature:** Platelets in GT **fail to aggregate** with all physiological agonists (ADP, collagen, epinephrine, thrombin). * **The Ristocetin Clue:** The **Ristocetin agglutination test is normal** in GT because ristocetin-induced binding depends on GPIb and von Willebrand Factor (vWF), which are intact in this condition. **Why the other options are incorrect:** * **DIC:** Characterized by consumption of platelets (thrombocytopenia) and clotting factors (prolonged PT/PTT), usually in an acutely ill patient [3]. * **ITP:** Presents with isolated **thrombocytopenia** (low platelet count) due to immune destruction [3]; platelet function is typically normal. * **Vitamin C Deficiency (Scurvy):** Causes bleeding due to defective collagen synthesis in blood vessel walls (perifollicular hemorrhages, corkscrew hairs); it does not involve GPIIb/IIIa deficiency. **NEET-PG High-Yield Pearls:** * **Glanzmann Thrombasthenia:** Defect in **Aggregation** (GPIIb/IIIa); Normal Ristocetin test [2]. * **Bernard-Soulier Syndrome:** Defect in **Adhesion** (GPIb-IX-V); **Abnormal** Ristocetin test (not corrected by adding normal plasma); characterized by **Giant Platelets** and mild thrombocytopenia [2], [3]. * **Von Willebrand Disease:** Most common inherited bleeding disorder; **Abnormal** Ristocetin test (corrected by adding normal plasma) [2].

Q: The TRUE statement about B cell Prolymphocytic leukemia is:

The cells express surface IgM and CD19, 20, 22. **Explanation:** **B-cell Prolymphocytic Leukemia (B-PLL)** is a rare, aggressive mature B-cell neoplasm characterized by a high count of circulating prolymphocytes (usually >55%). **Why Option C is Correct:** B-PLL cells represent a mature B-cell phenotype. They characteristically show **strong expression of surface IgM** (with or without IgD) and pan-B-cell markers including **CD19, CD20, and CD22**. Unlike Chronic Lymphocytic Leukemia (CLL), B-PLL cells typically express high density surface immunoglobulins and are usually **CD5 negative** and **CD23 negative** (though CD5 can be positive in 20-30% of cases). **Why Other Options are Incorrect:** * **Option A:** The median age at diagnosis is **65–70 years**. It is a disease of the elderly and is extremely rare in patients under 50. * **Option B:** The hallmark clinical feature is **massive splenomegaly** with a rapidly rising white blood cell count (often >100,000/µL). In contrast to CLL, **lymphadenopathy is typically minimal or absent**. * **Option D:** While splenectomy or splenic irradiation may provide symptomatic relief for massive, painful splenomegaly or hypersplenism, it is a palliative measure and **does not improve overall survival**. **High-Yield Clinical Pearls for NEET-PG:** * **Morphology:** Prolymphocytes are larger than mature lymphocytes, featuring a vesicular nucleus and a **single, prominent, central nucleolus**. * **Cytogenetics:** The most common abnormality is **17p deletion (TP53 mutation)**, which contributes to its poor prognosis and resistance to conventional chemotherapy. * **Differential Diagnosis:** Must be distinguished from "CLL in prolymphocytoid transformation," where prolymphocytes exceed 10% but are less than 55%.

Q: During an evaluation of hypoproliferative anemia, a patient was found to have mild normocytic anemia, serum iron was low (< 50), increased TIBC, with elevated serum ferritin and adequate bone marrow iron stores. What is the most likely diagnosis in this scenario?

Anemia of chronic inflammation. The clinical scenario describes **Anemia of Chronic Inflammation (ACI)**, also known as Anemia of Chronic Disease. The hallmark of ACI is the **sequestration of iron** within the reticuloendothelial system (macrophages), mediated by **Hepcidin** [1], [3]. 1. **Why ACI is correct:** In response to inflammation (IL-6), the liver produces Hepcidin, which degrades ferroportin [2]. This prevents iron release from macrophages and absorption from the gut. Consequently, **Serum Iron is low**, but **Serum Ferritin is high** (reflecting trapped iron stores) [3]. Bone marrow examination shows **adequate iron stores** but poor incorporation into RBC precursors [3]. 2. **Why other options are wrong:** * **Iron Deficiency Anemia (IDA):** While IDA also has low serum iron and high TIBC, it is characterized by **low Serum Ferritin** and **absent bone marrow iron stores**. * **Thalassemia:** This is a microcytic anemia with **normal or high serum iron** and ferritin levels due to ineffective erythropoiesis and hemolysis. * **Renal Disease:** Anemia in chronic kidney disease is primarily due to **Erythropoietin (EPO) deficiency**. While it is normocytic, it does not typically present with the classic "iron trapping" profile unless comorbid inflammation is present. **High-Yield Pearls for NEET-PG:** * **Hepcidin** is the "Master Regulator" of iron metabolism; it is an acute-phase reactant [2]. * **TIBC vs. Ferritin:** In IDA, TIBC is high and Ferritin is low. In ACI, TIBC is low/normal and Ferritin is high [3]. * **Soluble Transferrin Receptor (sTfR):** This is the best test to differentiate IDA from ACI. sTfR is **elevated in IDA** but **normal in ACI**. * ACI is typically **normocytic normochromic**, but can become microcytic in long-standing cases [1].

Q: A 35-year-old man was admitted with a history of painless cervical and axillary lymphadenopathy. He had a history of loss of weight, fever, and night sweats and was found to have cutaneous allergy. There was no hepatosplenomegaly. What is the most likely diagnosis?

Hodgkin's lymphoma. The clinical presentation of painless cervical and axillary lymphadenopathy associated with "B symptoms" (fever, night sweats, and weight loss) in a young adult is classic for Hodgkin’s Lymphoma (HL) [1]. A key diagnostic clue in this question is "cutaneous anergy" (implied by cutaneous allergy/lack of delayed-type hypersensitivity). In HL, there is a progressive defect in T-cell mediated immunity, even in early stages, leading to a failure to respond to skin antigens (like Tuberculin). Unlike Non-Hodgkin Lymphomas (NHL), HL typically spreads in a predictable, contiguous fashion and often involves the mediastinal or cervical nodes without early hepatosplenomegaly [1]. **Why other options are incorrect:** * **Diffuse Large B-cell Lymphoma (DLBCL):** While it can present with B symptoms, it is usually more aggressive, often involves extranodal sites, and does not characteristically present with cutaneous anergy as a primary feature [2]. * **Burkitt Lymphoma:** This is a very high-grade B-cell lymphoma [2]. It typically presents as a rapidly growing jaw mass (Endemic/African) or abdominal mass (Sporadic), rather than chronic painless peripheral lymphadenopathy. * **Follicular Lymphoma:** This is an indolent (slow-growing) lymphoma usually seen in older adults (median age >60) [2]. B symptoms and cutaneous anergy are uncommon in the early stages. **High-Yield Pearls for NEET-PG:** * **Bimodal Age Distribution:** HL has peaks in the 20s and 50s. * **Reed-Sternberg (RS) Cells:** The hallmark "Owl’s eye" appearance (CD15+ and CD30+) [1]. * **Alcohol-induced pain:** Pain in the lymph nodes after drinking alcohol is a rare but highly specific sign of HL. * **Pel-Ebstein Fever:** Characterized by alternating bouts of high fever and afebrile periods.

Q: All of the following statements characterize chronic lymphocytic leukemia (CLL), EXCEPT:

Hypergammaglobulinemia is usually present.. **Explanation:** Chronic Lymphocytic Leukemia (CLL) is a monoclonal proliferation of mature-appearing but functionally incompetent B-lymphocytes. **Why Option D is the Correct Answer (The Exception):** In CLL, the neoplastic B-cells do not differentiate into plasma cells effectively. Instead of hypergammaglobulinemia, patients typically develop **Hypogammaglobulinemia** (low antibody levels) as the disease progresses [1]. This occurs due to the suppression of normal B-cell function, leading to an increased risk of recurrent bacterial infections (e.g., *S. pneumoniae*) [1]. **Analysis of Incorrect Options:** * **Option A:** CLL is primarily a disease of the **elderly**, with a median age at diagnosis of approximately 70-72 years. It is rare in individuals under 40. * **Option B:** Approximately 50-70% of patients are **asymptomatic** at the time of diagnosis [1]. The condition is often discovered incidentally during routine blood work showing isolated lymphocytosis. * **Option C:** Physical examination often reveals painless generalized lymphadenopathy and **hepatosplenomegaly** due to the infiltration of lymphoid organs by leukemic cells [1]. **NEET-PG High-Yield Pearls:** * **Peripheral Smear:** Characterized by mature small lymphocytes and **Smudge cells** (basket cells), which are fragile lymphocytes ruptured during slide preparation. * **Immunophenotype:** CLL cells characteristically express **CD5** (a T-cell marker), **CD19, CD20, and CD23**. * **Complications:** Watch for **Richter Transformation**, where CLL evolves into a high-grade Large B-cell Lymphoma, and **Autoimmune Hemolytic Anemia (AIHA)** [1]. * **Staging:** The **Rai** and **Binet** staging systems are used to determine prognosis and treatment initiation [1].

Q: Intravenous immunoglobulin therapy is effective in some patients with which of the following conditions?

Pure red cell aplasia. **Explanation:** **Pure Red Cell Aplasia (PRCA)** is a clinical syndrome characterized by a severe reduction in erythroid precursors in the bone marrow, leading to isolated anemia. The underlying pathophysiology is often immune-mediated (T-cell or antibody-driven). Intravenous Immunoglobulin (IVIG) is specifically effective in cases of PRCA caused by **persistent Parvovirus B19 infection**, particularly in immunocompromised patients (e.g., HIV, transplant recipients). IVIG provides neutralizing antibodies against the virus, allowing erythropoiesis to resume. It is also sometimes used in refractory autoimmune PRCA. **Analysis of Incorrect Options:** * **Myelodysplasia (MDS):** This is a clonal stem cell disorder characterized by ineffective hematopoiesis and cytopenias. Treatment involves growth factors (EPO), hypomethylating agents (Azacitidine), or bone marrow transplant, but not IVIG. * **Paroxysmal Nocturnal Hemoglobinuria (PNH):** This is a stem cell defect involving a mutation in the *PIGA* gene, leading to a deficiency of GPI-anchored proteins (CD55/CD59) and complement-mediated hemolysis. The treatment of choice is Eculizumab (C5 inhibitor). * **G6PD Deficiency:** This is an X-linked enzymatic defect causing episodic oxidative hemolysis. Management focuses on avoiding triggers (e.g., fava beans, certain drugs) and supportive care; IVIG has no role here. **High-Yield Clinical Pearls for NEET-PG:** * **PRCA Associations:** Thymoma (most common association), Parvovirus B19, SLE, and drugs (e.g., Phenytoin, EPO-alpha). * **Diagnostic Hallmark:** Bone marrow shows a selective absence of erythroid precursors with normal myeloid and megakaryocytic lines. * **First-line treatment for autoimmune PRCA:** Cyclosporine or Corticosteroids. * **Parvovirus B19** specifically targets the **P-antigen** on proerythroblasts.

Q: A patient presents with an Hb of 6 g/dL, WBC count of 2000/mm³, normal differential count except for 6% blasts, and platelets reduced to 80,000/mm³. Moderate splenomegaly is also noted. What is the most likely diagnosis?

Leukemia. ### Explanation The clinical presentation describes **pancytopenia** (anemia, leukopenia, and thrombocytopenia) associated with **splenomegaly** and the presence of **circulating blasts**. **1. Why Leukemia is the Correct Answer:** The defining feature in this case is the presence of **6% blasts** in the peripheral blood. In a patient with pancytopenia, the presence of any significant number of blasts (immature cells) strongly suggests a primary bone marrow pathology, most commonly **Acute Leukemia** [1]. While a definitive diagnosis of Acute Myeloid Leukemia (AML) requires ≥20% blasts in the marrow or blood, the presence of 6% blasts in the context of cytopenias and **splenomegaly** (which indicates extramedullary involvement or marrow infiltration) makes leukemia the most likely diagnosis among the choices [2]. **2. Why Other Options are Incorrect:** * **Aplastic Anemia:** While it presents with pancytopenia, it is characterized by an "empty" marrow. Crucially, **splenomegaly is typically absent** in aplastic anemia, and blasts are never seen. * **Hemolysis:** This usually presents with anemia and jaundice. While it can cause splenomegaly, it does not cause leukopenia, thrombocytopenia, or the presence of blasts. * **Immune Thrombocytopenic Purpura (ITP):** This is characterized by isolated thrombocytopenia. The Hb and WBC counts remain normal, and there is no splenomegaly. **3. NEET-PG Clinical Pearls:** * **Pancytopenia + Splenomegaly:** Think of Leukemia, Myelofibrosis [3], Hypersplenism, or Kala-azar. * **Pancytopenia - Splenomegaly:** Think of Aplastic Anemia or Megaloblastic Anemia. * **Blast Cells:** Their presence in peripheral blood is always pathological and usually indicates a "leukemic gap" or marrow "spill-over" from a hematological malignancy [1]. * **Gold Standard:** Bone marrow aspiration and biopsy are essential to differentiate between "hypocellular" (Aplastic) and "hypercellular" (Leukemic) causes of pancytopenia.

Q: All of the following can be associated with paroxysmal nocturnal hemoglobinuria (PNH) except?

Massive splenomegaly. Paroxysmal Nocturnal Hemoglobinuria (PNH) is an acquired clonal hematopoietic stem cell disorder caused by a somatic mutation in the PIGA gene. This leads to a deficiency of Glycosylphosphatidylinositol (GPI) anchor proteins, resulting in the absence of complement regulatory proteins CD55 and CD59 on the surface of blood cells. Why Massive Splenomegaly is the Correct Answer: In PNH, hemolysis is primarily intravascular (due to complement-mediated membrane attack complex formation) [1]. Unlike extravascular hemolysis (e.g., Hereditary Spherocytosis), where the spleen destroys abnormal cells, PNH does not typically cause significant organomegaly. If splenomegaly is present, it is usually mild or suggests a complication like splenic vein thrombosis. Massive splenomegaly is a hallmark of myeloproliferative neoplasms or visceral leishmaniasis [2], not PNH. Analysis of Incorrect Options: * A & B (Cerebral Thrombosis & Budd-Chiari Syndrome): Thrombosis is the leading cause of death in PNH. It occurs due to nitric oxide depletion and platelet activation. PNH has a predilection for unusual venous sites, including the hepatic veins (Budd-Chiari syndrome), cerebral sinuses, and mesenteric veins. * C (Pancytopenia): PNH is a stem cell disorder. It frequently overlaps with Aplastic Anemia, and bone marrow failure leading to pancytopenia is a common clinical presentation. NEET-PG High-Yield Pearls: * Gold Standard Diagnosis: Flow cytometry (shows absence of CD55/CD59). * Classic Triad: Hemolytic anemia, pancytopenia, and thrombosis. * Treatment: Eculizumab (Monoclonal antibody against C5 complement). * Screening Test: Ham’s test (Acidified serum lysis) and Sucrose lysis test (now largely replaced by flow cytometry).

Question 1

Which of the following is not a type of hypoproliferative anemia?

Accepted Answer

G6PD deficiency

Answer

Anemia caused by Parvovirus B19 infection

Answer

Anemia of chronic disease/inflammation

Answer

Fanconi anemia

Question 2

A 20-year-old female presents with features of anemia. Blood tests show Hb of 5 g/dL, MCV of 52 fL, MCHC of 20 g/dL, and PCV of 32%. What is the most likely diagnosis?

Accepted Answer

Hookworm infection

Answer

Phenytoin toxicity

Answer

Fish tapeworm infection

Answer

Blind loop syndrome

Question 3

A 16-year-old girl has had frequent nosebleeds since childhood. Her gums bleed easily even with routine tooth brushing. She has experienced menorrhagia since menarche at age 13 years. On physical examination, there are no abnormal findings. Laboratory studies show hemoglobin, 14.1 g/dL; hematocrit, 42.5%; MCV, 90 mm3; platelet count, 277,400/mm3; and WBC count, 5920/mm3. Her platelets fail to aggregate in response to ADP, collagen, epinephrine, and thrombin. The ristocetin agglutination test result is normal. There is a deficiency of glycoprotein IIb/IIIa. Prothrombin time is 12 seconds, and partial thromboplastin time is 28 seconds. What is the most likely diagnosis?

Accepted Answer

Glanzmann thrombasthenia

Answer

Disseminated intravascular coagulation

Answer

Immune thrombocytopenic purpura

Answer

Vitamin C deficiency

Question 4

The TRUE statement about B cell Prolymphocytic leukemia is:

Accepted Answer

The cells express surface IgM and CD19, 20, 22

Answer

The median age is 40

Answer

Generalised lymphadenopathy is the presenting symptom

Answer

Splenectomy improves survival

Question 5

During an evaluation of hypoproliferative anemia, a patient was found to have mild normocytic anemia, serum iron was low (< 50), increased TIBC, with elevated serum ferritin and adequate bone marrow iron stores. What is the most likely diagnosis in this scenario?

Accepted Answer

Anemia of chronic inflammation

Answer

Thalassemia

Answer

Iron deficiency anemia

Answer

Renal disease

Question 6

A 35-year-old man was admitted with a history of painless cervical and axillary lymphadenopathy. He had a history of loss of weight, fever, and night sweats and was found to have cutaneous allergy. There was no hepatosplenomegaly. What is the most likely diagnosis?

Accepted Answer

Hodgkin's lymphoma

Answer

Diffuse large B-cell lymphoma

Answer

Burkitt lymphoma

Answer

Follicular lymphoma

Question 7

All of the following statements characterize chronic lymphocytic leukemia (CLL), EXCEPT:

Accepted Answer

Hypergammaglobulinemia is usually present.

Answer

It is a malignancy of elderly persons.

Answer

Patients may be asymptomatic at diagnosis.

Answer

Patients may exhibit hepatosplenomegaly.

Question 8

Intravenous immunoglobulin therapy is effective in some patients with which of the following conditions?

Accepted Answer

Pure red cell aplasia

Answer

Myelodysplasia

Answer

Paroxysmal nocturnal hemoglobinuria (PNH)

Answer

Glucose-6-phosphate dehydrogenase (G6PD) deficiency

Question 9

A patient presents with an Hb of 6 g/dL, WBC count of 2000/mm³, normal differential count except for 6% blasts, and platelets reduced to 80,000/mm³. Moderate splenomegaly is also noted. What is the most likely diagnosis?

Accepted Answer

Leukemia

Answer

Aplastic anemia

Answer

Hemolysis

Answer

Immune thrombocytopenic purpura (ITP)

Question 10

All of the following can be associated with paroxysmal nocturnal hemoglobinuria (PNH) except?

Accepted Answer

Massive splenomegaly

Answer

Cerebral thrombosis

Answer

Budd-Chiari syndrome

Answer

Pancytopenia

Hematology — MCQs

Hematology — MCQs

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