Hematology Practice Questions

Q: Elevated serum ferritin, decreased serum iron, and decreased % transferrin saturation are most consistent with which diagnosis?

Anemia of chronic disease. **Explanation:** The laboratory profile described is the classic presentation of **Anemia of Chronic Disease (ACD)**, also known as Anemia of Inflammation [1]. **1. Why Anemia of Chronic Disease is Correct:** The pathophysiology of ACD is driven by **Hepcidin**, an acute-phase reactant [1]. In chronic inflammatory states (infections, malignancy, autoimmune diseases), cytokines like IL-6 stimulate the liver to produce hepcidin. Hepcidin degrades **ferroportin** (the iron export channel), leading to [2]: * **Sequestration of iron** within macrophages and hepatocytes (reflected by **elevated serum ferritin**) [2]. * **Decreased serum iron** because iron cannot be released into the plasma [2]. * **Decreased % Transferrin Saturation** because there is less iron available to bind to transferrin. **2. Why the other options are incorrect:** * **Iron Deficiency Anemia (IDA):** Characterized by **decreased ferritin** (the most sensitive marker) and increased Total Iron Binding Capacity (TIBC) [3]. * **Thalassemia:** Typically presents with **normal to elevated serum iron and ferritin** because the defect is in globin chain synthesis, not iron metabolism. * **Sideroblastic Anemia:** Characterized by iron overload. You would see **elevated serum iron, elevated ferritin,** and increased transferrin saturation, along with ringed sideroblasts in the bone marrow. **High-Yield Clinical Pearls for NEET-PG:** * **Ferritin** is the key differentiator: It is **low** in IDA and **normal/high** in ACD [3]. * **TIBC** (Total Iron Binding Capacity) is **increased** in IDA but **decreased** in ACD [3]. * **Soluble Transferrin Receptor (sTfR) assay:** This is the most reliable test to distinguish IDA from ACD when both coexist; sTfR is **elevated in IDA** but **normal in ACD** [3].

Q: A 30-year-old male, undergoing platelet apheresis for the first time, experiences tingling around the mouth and numbness in his arm. An ECG shows ST segment elevation. What is the most likely cause of these symptoms?

Citrate toxicity. The correct answer is **Citrate toxicity**. During platelet apheresis, **sodium citrate** is used as an anticoagulant. When returned to the donor's circulation, citrate chelates free ionized calcium, leading to **hypocalcemia**. The classic presentation of hypocalcemia includes neuromuscular irritability, such as perioral tingling (paresthesia) and numbness [1]. Crucially, hypocalcemia affects cardiac conduction. While it typically causes QT interval prolongation, severe electrolyte imbalances during apheresis can lead to coronary vasospasm or conduction abnormalities that manifest as **ST-segment changes** on an ECG. **Analysis of Incorrect Options:** * **A & B (Blood phobia/Anxiety):** While common in first-time donors, these typically present with vasovagal symptoms (bradycardia, hypotension, syncope) or hyperventilation. While hyperventilation can cause tingling due to respiratory alkalosis, it does not typically cause the specific ECG changes associated with electrolyte shifts. * **D (Hypothermia):** Though large volume exchanges can lower body temperature, the primary symptoms would be shivering and "J" waves (Osborn waves) on ECG, not acute perioral numbness. **High-Yield Clinical Pearls for NEET-PG:** * **Mechanism:** Citrate binds to ionized Calcium ($Ca^{2+}$) $\rightarrow$ Hypocalcemia. * **Management:** Slowing the infusion rate or administering oral/IV calcium gluconate. * **ECG Hallmark:** The most common ECG finding in hypocalcemia is **prolonged QT interval** (specifically the ST segment). * **Apheresis vs. Whole Blood:** Citrate toxicity is significantly more common in apheresis and massive blood transfusions because of the high volume of citrate-anticoagulated plasma involved.

Q: All of the following are conditions that precipitate hemolysis in G6PD deficiency, except?

Intake of acetaminophen and aspirin. **Explanation:** Glucose-6-Phosphate Dehydrogenase (G6PD) deficiency is an X-linked recessive disorder where the RBCs are unable to regenerate reduced glutathione, making them vulnerable to oxidative stress [3][4]. When exposed to oxidizing agents, hemoglobin denatures into **Heinz bodies**, leading to episodic hemolysis [1][3]. **Why Option D is Correct:** Acetaminophen and Aspirin (at standard therapeutic doses) are considered **safe** in G6PD deficiency. While high-dose aspirin was historically debated, current hematological guidelines list these as non-oxidizing agents that do not precipitate clinically significant hemolysis. **Why Other Options are Incorrect:** * **A. Ingestion of fava beans:** This causes "Favism." Fava beans contain vicine and covicine, which produce free radicals that overwhelm the limited antioxidant capacity of G6PD-deficient cells [1]. * **B. Viral hepatitis:** Infection is the **most common trigger** for hemolysis in G6PD deficiency [1]. Inflammatory responses generate reactive oxygen species (ROS) from polymorphonuclear leukocytes, causing oxidative damage to RBCs. * **C. Antimalarials:** Primaquine is the classic "textbook" trigger [1]. It undergoes redox cycling, generating superoxide anions that cause rapid hemolysis in deficient individuals [2]. **NEET-PG High-Yield Pearls:** * **Inheritance:** X-linked Recessive (Common in Mediterranean and African populations) [1][3]. * **Peripheral Smear:** Look for **Heinz Bodies** (denatured Hb) and **Bite Cells/Degmacytes** (formed when splenic macrophages pluck out Heinz bodies) [3]. * **Diagnosis:** Be careful! G6PD levels may be **falsely normal** during an acute hemolytic episode because the most deficient (older) cells have already lysed [1]. Re-testing should be done 6–8 weeks later. * **Key Contraindicated Drugs:** Primaquine, Dapsone, Nitrofurantoin, Rasburicase, and Sulfonamides [1].

Q: Hunter's glossitis is a feature of which condition?

Pernicious anemia. **Explanation:** **Hunter’s glossitis** (also known as Moeller’s glossitis) is a classic clinical sign of **Pernicious anemia**, which results from Vitamin B12 deficiency due to a lack of intrinsic factor. 1. **Why Pernicious Anemia is correct:** Vitamin B12 is essential for DNA synthesis and the rapid turnover of mucosal cells [3]. In its absence, the lingual papillae undergo atrophy. This results in a characteristic **"beefy red," smooth, and shiny appearance** of the tongue, often accompanied by a burning sensation or soreness [1]. 2. **Why other options are incorrect:** * **Leukemia:** Typically presents with gingival hypertrophy (especially in AML-M5) [1], oral candidiasis, or petechiae due to thrombocytopenia, rather than isolated atrophic glossitis. * **Sickle cell anemia:** Oral manifestations are usually related to bone changes (e.g., "crew-cut" appearance on X-ray) or mucosal pallor due to chronic hemolysis [4], not specific glossitis. * **HIV infection:** Common oral findings include Hairy Leukoplakia (caused by EBV), Kaposi sarcoma, or Oral Candidiasis, but not Hunter’s glossitis. **High-Yield Clinical Pearls for NEET-PG:** * **Triad of Vitamin B12 Deficiency:** Megaloblastic anemia, Hunter’s glossitis, and Neurological symptoms (Subacute Combined Degeneration of the Spinal Cord). * **Peripheral Smear:** Look for **Hypersegmented neutrophils** (earliest sign) and Macro-ovalocytes. * **Schilling Test:** Historically used to differentiate B12 malabsorption causes (now largely replaced by antibody testing for Anti-Intrinsic Factor and Anti-Parietal Cell antibodies) [2]. * **Other causes of Atrophic Glossitis:** Iron deficiency anemia (Plummer-Vinson Syndrome), sprue, and other B-complex deficiencies [1].

Question 1

Elevated serum ferritin, decreased serum iron, and decreased % transferrin saturation are most consistent with which diagnosis?

Accepted Answer

Anemia of chronic disease

Answer

Iron deficiency anemia

Answer

Thalassemia

Answer

Sideroblastic anemia

Question 2

A 30-year-old male, undergoing platelet apheresis for the first time, experiences tingling around the mouth and numbness in his arm. An ECG shows ST segment elevation. What is the most likely cause of these symptoms?

Accepted Answer

Citrate toxicity

Answer

Blood phobia

Answer

Anxiety related to first-time transfusion

Answer

Hypothermia

Question 3

A 40-year-old chronic alcoholic is investigated for anemia. Tests reveal increased serum iron and increased transferrin saturation. What is the probable diagnosis?

Accepted Answer

Hemosiderosis

Answer

Iron deficiency anemia

Answer

Sideroblastic anemia

Answer

Megaloblastic anemia

Question 4

All of the following are conditions that precipitate hemolysis in G6PD deficiency, except?

Accepted Answer

Intake of acetaminophen and aspirin

Answer

Ingestion of fava beans

Answer

Viral hepatitis

Answer

Antimalarials such as primaquine and chloroproguanil

Question 5

What is the positive finding in a patient with anemia due to chronic inflammation?

Accepted Answer

Serum iron is increased

Answer

Serum ferritin is decreased

Answer

Total iron-binding capacity (TIBC) is decreased

Answer

Presence of normal iron in blasts

Question 6

Hunter's glossitis is a feature of which condition?

Accepted Answer

Pernicious anemia

Answer

Leukemia

Answer

Sickle cell anemia

Answer

HIV infection

Question 7

A 65-year-old man presents with tingling in his hands and feet and increased forgetfulness. A CBC shows mild anemia. The patient reports no change in diet, other than increased consumption of red meat. What is the most appropriate treatment for this patient?

Accepted Answer

Intramuscular vitamin B12 injections

Answer

Oral vitamin B12

Answer

Oral folic acid

Answer

Oral methionine

Question 8

Spherocytes are not seen in which of the following conditions?

Accepted Answer

Plasmodium falciparum infection

Answer

Splenectomy

Answer

Hereditary spherocytosis

Answer

Autoimmune hemolytic anemia

Question 9

A 15-year-old boy presents with acute onset of right flank pain that developed after physical exercise. Physical examination demonstrates an area of ecchymosis in the right flank that is tender to palpation. The patient has a lifelong history of easy bruising, and a sibling has the same symptoms. The serum level of clotting factor VIII is less than 2% of normal. Which of the following is the most likely underlying mechanism for the bleeding tendency in this patient?

Accepted Answer

Genetic defect involving the factor VIII gene

Answer

Deficiency of vitamin K

Answer

Decreased hepatic synthesis of multiple coagulation factors

Answer

Circulating antibodies directed against factor VIII

Question 10

A 48-year-old woman presents with a 3-week history of fatigue and yellow skin and sclerae. Physical examination reveals mild jaundice. Laboratory findings include a serum bilirubin level of 3.7 mg/dL (predominantly unconjugated), normal serum AST, ALT, and alkaline phosphatase, and a hemoglobin level of 6.0 g/dL. Jaundice resolved after administration of corticosteroids. What is the most likely cause of hyperbilirubinemia in this patient?

Accepted Answer

Autoimmune hemolytic anemia

Answer

Acute hepatitis B infection

Answer

Gallstone in the common bile duct

Answer

Primary biliary cirrhosis

Hematology — MCQs

Hematology — MCQs

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