Hematology — MCQs

Hematology Indian Medical PG Practice Questions and MCQs

Question 961: Why does iron deficiency anemia cause increased platelet count despite decreased erythropoiesis?

A. Enhanced iron utilization
B. Compensatory bone marrow response
C. Increased TPO production (Correct Answer)
D. Decreased platelet destruction

Explanation: Increased TPO production - **Iron deficiency** stimulates the production of **thrombopoietin (TPO)**, a cytokine that promotes megakaryocyte proliferation and platelet production. - This elevated TPO, often mediated by inflammatory cytokines, overrides the bone marrow's overall reduced activity in erythropoiesis. *Enhanced iron utilization* - While the body attempts to maximize iron utilization during deficiency, this mechanism primarily benefits erythropoiesis and does not directly cause **thrombocytosis**. - **Iron's role** in platelet production is indirect, mainly through its impact on overall cellular function rather than a direct stimulus for increased numbers. *Compensatory bone marrow response* - The bone marrow *does* attempt to compensate for anemia, but this primarily focuses on increasing red blood cell production, which is hindered by the **lack of iron**. - The *specific* increase in platelets is due to a distinct signaling pathway involving **TPO**, not a general compensatory response for all cell lines. *Decreased platelet destruction* - **Iron deficiency anemia** does not typically lead to a decrease in platelet destruction. - Platelet lifespan and clearance mechanisms are generally unaffected by **iron status**. *Note: Current medical literature, including leading hematology and biochemistry texts, acknowledges that iron deficiency is associated with reactive thrombocytosis, often linked to structural similarity between erythropoietin and thrombopoietin or common progenitor stimulation, though specific molecular pathways regarding hepcidin and iron-sensing are primarily focused on the erythroid lineage [1].*

Question 962: Direct Coombs test is positive in all EXCEPT:

A. G6PD deficiency (Correct Answer)
B. Rh incompatibility
C. Autoimmune hemolysis
D. ABO incompatibility

Explanation: ***G6PD deficiency*** - **G6PD deficiency** is an intrinsic red blood cell defect that leads to hemolytic anemia, but it does **not involve immune-mediated destruction** of red blood cells. - The **Direct Coombs test** detects antibodies or complement components bound to the surface of red blood cells; since G6PD deficiency is not immune-mediated, the test will be negative. *Rh incompatibility* - **Rh incompatibility** occurs when maternal antibodies cross the placenta and target fetal red blood cells, leading to **immune-mediated hemolysis** [1]. - The anti-D antibodies bind to fetal red blood cells, resulting in a **positive Direct Coombs test** (detecting antibody-coated fetal RBCs) [1]. *Autoimmune hemolysis* - **Autoimmune hemolysis** involves the body producing **autoantibodies** against its own red blood cells, leading to their premature destruction [3]. - These autoantibodies (e.g., IgG, IgM) bind to the red blood cell surface, making the **Direct Coombs test positive** [3]. *ABO incompatibility* - **ABO incompatibility** involves the presence of naturally occurring antibodies (e.g., anti-A, anti-B) in a recipient's plasma that react with donor red blood cells [2]. - When incompatible red blood cells are transfused, or in cases of **hemolytic disease of the newborn** due to ABO incompatibility, antibodies bind to the RBCs, resulting in a **positive Direct Coombs test** [2].

Question 963: A patient presents with elevated serum iron, low TIBC, and high ferritin. Which of the following conditions is most likely?

A. Lead poisoning
B. Acute hepatitis
C. Iron-deficiency anemia
D. Hemochromatosis (Correct Answer)

Explanation: ***Hemochromatosis*** - **Hereditary hemochromatosis** is characterized by excessive iron absorption, leading to **iron overload** in tissues and organs [1][3]. - The classic lab findings include **elevated serum iron**, **elevated ferritin** (reflecting increased iron stores), and **low total iron-binding capacity (TIBC)** due to increased iron saturation of transferrin [1]. *Lead poisoning* - **Lead poisoning** can cause **microcytic anemia** due to inhibition of heme synthesis enzymes, but it does not typically present with elevated serum iron or ferritin. - It's more commonly associated with **basophilic stippling** on peripheral blood smear and **elevated lead levels** in the blood. *Acute hepatitis* - **Acute hepatitis** can cause an elevation in **ferritin** as an acute phase reactant due to inflammation and liver cell damage [1]. - However, it typically does not present with simultaneously **elevated serum iron** and **low TIBC** in the same pattern as hemochromatosis, and iron metabolism disorders are not its primary feature. *Iron-deficiency anemia* - **Iron-deficiency anemia** is characterized by **low serum iron**, **low ferritin** (reflecting depleted iron stores), and **elevated TIBC** as the body tries to maximize iron absorption [2]. - These findings are directly opposite to the laboratory values presented in the question [2].

Question 964: Which vitamin deficiency leads to megaloblastic anemia?

A. Riboflavin
B. Folate (Correct Answer)
C. Vitamin C
D. Niacin

Explanation: ***Folate*** - **Folate** is essential for DNA synthesis; a deficiency impairs erythrocyte maturation, leading to the production of **large, immature red blood cells** (megaloblasts) [3]. - This vitamin deficiency also presents with symptoms like **fatigue, glossitis**, and neurologic manifestations are absent unlike vitamin B12 deficiency [1]. *Riboflavin* - **Riboflavin (Vitamin B2)** deficiency can cause **normocytic anemia**, but generally not megaloblastic anemia. - Its deficiency is mainly associated with **angular stomatitis, cheilosis**, and ocular symptoms. *Vitamin C* - **Vitamin C** deficiency (scurvy) is associated with impaired collagen synthesis, leading to **gingival bleeding, petechiae**, and poor wound healing. - While it can cause some anemia, it is typically **microcytic** due to impaired iron absorption if it affects iron metabolism, not megaloblastic [2]. *Niacin* - **Niacin (Vitamin B3)** deficiency causes **pellagra**, characterized by the "3 D's": **dermatitis, diarrhea, and dementia**. - It does not directly lead to megaloblastic anemia, as it is not involved in a critical step of DNA synthesis in the same way folate is.

Question 965: A 25-year-old male presents with jaundice, fatigue, and dark urine after taking antimalarial drugs. Labs show elevated bilirubin, reticulocytosis, and splenomegaly. Peripheral smear shows bite cells and Heinz bodies. Which enzyme deficiency is most likely?

A. Glucose-6-phosphatase
B. Glucose-6-phosphate dehydrogenase (Correct Answer)
C. Pyruvate kinase
D. Aldolase A

Explanation: ***Glucose-6-phosphate dehydrogenase*** - The combination of **jaundice**, **fatigue**, **dark urine** after antimalarial drug exposure, along with **reticulocytosis**, **splenomegaly**, **bite cells**, and **Heinz bodies**, is highly indicative of **G6PD deficiency** [1], [4]. - **G6PD deficiency** impairs the hexose monophosphate shunt, leading to reduced NADPH production and increased oxidative stress in red blood cells when exposed to certain drugs or stressors, resulting in **hemolytic anemia** [2], [3]. *Glucose-6-phosphatase* - Deficiency in **glucose-6-phosphatase** is associated with **Von Gierke disease** (Type I glycogen storage disease). - This condition primarily presents with **hypoglycemia**, **lactic acidosis**, and **hepatomegaly**, not hemolytic anemia with bite cells. *Pyruvate kinase* - **Pyruvate kinase deficiency** also causes **hemolytic anemia**, but it typically presents with **echinocytes** (burr cells) on peripheral smear, rather than bite cells and Heinz bodies. - The hemolysis is ongoing and not acutely precipitated by oxidative stressors in the same manner as G6PD deficiency. *Aldolase A* - **Aldolase A deficiency** is a rare cause of **hemolytic anemia** with associated **myopathy**. - It would not typically present with **bite cells** and **Heinz bodies** in response to oxidative stress from antimalarial drugs.

Question 966: Which is not a feature of G6PD deficiency?

A. Presence of Heinz bodies
B. Males and females are equally affected (Correct Answer)
C. Absence of NADPH
D. Oxidative stress

Explanation: ***Males and females are equally affected*** - G6PD deficiency is an **X-linked recessive disorder**, meaning males are predominantly and more severely affected because they have only one X chromosome [2]. - Females are typically carriers and are less commonly affected, or may experience milder symptoms, due to **X-chromosome inactivation** (Lyonization). *Presence of Heinz bodies* - **Heinz bodies** are formed from denatured hemoglobin precipitates within red blood cells, a characteristic feature of **oxidative stress** in G6PD deficiency [2]. - These bodies are removed by the spleen, contributing to **hemolytic anemia**. *Absence of NADPH* - G6PD is the rate-limiting enzyme in the **pentose phosphate pathway**, which generates **NADPH** [1], [2]. - Without sufficient G6PD, the production of **NADPH** is severely impaired, leading to a deficiency in this critical reducing agent. *Oxidative stress* - **NADPH** is crucial for reducing **glutathione**, which in turn detoxifies reactive oxygen species [2]. - The lack of NADPH makes red blood cells vulnerable to **oxidative damage**, manifesting as hemolytic anemia upon exposure to oxidative agents [3].

Question 967: All of the following are causes of normocytic anemia, EXCEPT:

A. Hemolysis
B. Aplastic anemia
C. Iron deficiency (Correct Answer)
D. Chronic kidney disease

Explanation: ***Iron deficiency*** - **Iron deficiency anemia** is typically a **microcytic hypochromic anemia**, meaning red blood cells are smaller than normal with reduced hemoglobin [1], [2]. - While it can initially present with normocytic indices in very early stages or mixed deficiencies, it classically causes microcytosis as it progresses [2]. *Hemolysis* - **Hemolytic anemias** usually present as **normocytic anemias** because the red blood cells are destroyed prematurely without affecting their size. - The bone marrow compensates by releasing new but normally sized red blood cells. *Aplastic anemia* - **Aplastic anemia** is characterized by bone marrow failure, leading to a decrease in all blood cell lines, including red blood cells, which are typically **normocytic** in size. - The problem is insufficient production, not abnormal cell size. *Chronic kidney disease* - **Anemia of chronic kidney disease** is commonly a **normocytic, normochromic anemia** due to decreased erythropoietin production by the kidneys [1]. - Erythropoietin stimulates red blood cell production in the bone marrow, so its deficiency leads to fewer, but normally sized, red blood cells.

Question 968: Which of the following is a risk factor for deep vein thrombosis (DVT)?

A. Hypertension
B. Chronic kidney disease
C. Hyperthyroidism
D. Prolonged immobility (Correct Answer)

Explanation: Detailed understanding of deep vein thrombosis (DVT) and its risk factors is essential for clinical practice. **Prolonged immobility**, such as during long flights, bed rest, or surgery, significantly increases the risk of DVT due to **venous stasis** [1]. **Reduced blood flow** allows clotting factors to accumulate, promoting the formation of a thrombus. *Hypertension*, while a risk factor for **atherosclerosis** and cardiovascular disease, is **not directly a primary risk factor for DVT**. Its effects on blood vessels are generally distinct from the venous stasis and hypercoagulability mechanisms primarily involved in DVT. *Chronic kidney disease* (CKD) can lead to a **prothrombotic state** due to various factors like endothelial dysfunction and inflammation; specific conditions like Nephrotic syndrome are noted risk factors [1]. However, CKD is not as direct or strong a risk factor for DVT as immobility, and many deaths are related to coexisting medical conditions [1]. *Hyperthyroidism* can cause a **hypercoagulable state**, increasing the risk of both arterial and venous thrombosis, but it is less commonly emphasized as a primary DVT risk factor compared to prolonged immobility.

Question 969: A patient presents with jaundice, dark urine, and high unconjugated bilirubin. Most likely cause?

A. Biliary obstruction due to pancreatic cancer
B. Extrahepatic cholestasis
C. Hemolysis (Correct Answer)
D. Viral hepatitis

Explanation: ***Hemolysis*** - **Jaundice** and **dark urine** with **high unconjugated bilirubin** are classic signs of hemolysis [1]. - **Unconjugated bilirubin** levels rise because the liver cannot process the increased load from red blood cell breakdown. *Biliary obstruction due to pancreatic cancer* - Would primarily cause a rise in **conjugated bilirubin** due to impaired bile flow, not unconjugated bilirubin [2]. - Patients often experience **pruritus** and **pale stools** in addition to jaundice. *Extrahepatic cholestasis* - This condition involves impaired bile flow outside the liver, leading to an increase in **conjugated bilirubin** [1]. - The presence of **unconjugated hyperbilirubinemia** argues against this diagnosis. *Viral hepatitis* - Typically causes an increase in both **conjugated and unconjugated bilirubin**, but especially **conjugated bilirubin**, as liver cells are damaged and cannot properly excrete bile [3]. - Often associated with elevated **liver enzymes (ALT, AST)**, which are not mentioned here [3].

Question 970: A patient presents with recurrent pneumonia and splenomegaly. Peripheral smear shows smudge cells. What is the likely diagnosis?

A. Acute myeloid leukemia
B. Hodgkin's lymphoma
C. Multiple myeloma
D. Chronic lymphocytic leukemia (CLL) (Correct Answer)

Explanation: ***Chronic lymphocytic leukemia (CLL)*** - The presence of **smudge cells** on a peripheral smear is a classic diagnostic feature of CLL, representing fragile lymphocytes that rupture during smear preparation. - Recurrent infections (like **pneumonia**) are common due to **hypogammaglobulinemia** and impaired immune function, and **splenomegaly** is a frequent physical finding [1]. *Acute myeloid leukemia* - Characterized by the presence of **myeloblasts** (immature myeloid cells) with **Auer rods** on the peripheral smear, which are not described here. - While it can cause anemia and thrombocytopenia, **splenomegaly** and **smudge cells** are not typical primary features. *Hodgkin's lymphoma* - This is a **lymphoma** (a solid tumor of lymphoid tissue) primarily diagnosed by **lymph node biopsy** showing **Reed-Sternberg cells** [2]. - It does not typically present with **smudge cells** on the peripheral smear or recurrent infections in the same manner as CLL. *Multiple myeloma* - This is a **plasma cell malignancy** characterized by **monoclonal protein (M-protein)** in serum or urine, **bone lesions**, and **renal dysfunction**. - The peripheral smear typically shows **rouleaux formation**, not smudge cells, and splenomegaly is not a common primary feature.

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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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