Hematology — MCQs
On this page
All of the following are features of hemolytic anemia, EXCEPT:
A 27-year-old woman complains of constant back pain. She recently had an episode of severe chest and back pain that required narcotic medications, blood transfusions, and fluids to treat. On examination, she is afebrile, with midthoracic tenderness on palpation. X-rays of the spine reveal periosteal reaction of the eighth thoracic vertebra. She has a chronic blood disorder where bone infarction can occur that may be difficult to distinguish from osteomyelitis. For the above patient with a hemoglobin abnormality, select the most likely diagnosis.
What is the recommended daily elemental iron supplementation for iron deficiency anemia?
The threshold for prophylactic platelet transfusion is __________ platelets/mL.
Alkaline phosphatase is elevated in all the following conditions except?
Spontaneous mouth petechiae and gingival bleeding typically occur at which platelet level?
Cryoprecipitate cannot be used in which of the following conditions?
Which of the following drugs is NOT associated with pure red cell aplasia?
Which viral infection is characterized by hemolysis?
Which of the following conditions can result in dactylitis?
Hematology Indian Medical PG Practice Questions and MCQs
Question 421: All of the following are features of hemolytic anemia, EXCEPT:
- A. Increased LDH
- B. Increased AST
- C. Increased ALT (Correct Answer)
- D. Increased urobilinogen in stool
Explanation: **Explanation:** Hemolytic anemia is characterized by the premature destruction of red blood cells (RBCs). When RBCs rupture, their intracellular contents are released into the plasma, and the body’s metabolic pathways for processing heme are accelerated. **Why "Increased ALT" is the correct answer:** Alanine Aminotransferase (ALT) is a highly specific marker for **liver parenchyma**. Unlike other enzymes, ALT is present in very negligible amounts within red blood cells. Therefore, hemolysis does not significantly elevate serum ALT levels. If ALT is elevated, it typically points toward primary hepatic injury rather than a hematologic process [1]. **Analysis of incorrect options:** * **Increased LDH:** Lactate Dehydrogenase (specifically LDH-1 and LDH-2) is abundant in RBCs. It is a highly sensitive, though non-specific, marker of hemolysis. * **Increased AST:** Aspartate Aminotransferase (AST) is found in the liver, heart, and **skeletal muscle/RBCs**. In cases of significant hemolysis, AST levels rise alongside LDH. * **Increased Urobilinogen in stool:** Hemolysis leads to increased unconjugated bilirubin. This is processed by the liver [2] and excreted into the gut, where bacteria convert it into stercobilinogen (urobilinogen in stool). This causes the characteristic dark stools seen in hemolytic states. **High-Yield NEET-PG Pearls:** 1. **Best initial test for hemolysis:** Peripheral blood smear (look for schistocytes or spherocytes) and Reticulocyte count. 2. **Most specific marker for intravascular hemolysis:** Decreased **Haptoglobin** levels (as it binds free hemoglobin). 3. **Urine findings:** In intravascular hemolysis, you will see hemoglobinuria and hemosiderinuria, but **never** bilirubinuria (unconjugated bilirubin is water-insoluble) [2]. 4. **The LDH/AST ratio:** A high LDH with a mildly elevated AST and normal ALT is a classic biochemical "fingerprint" of hemolysis [1].
Question 422: A 27-year-old woman complains of constant back pain. She recently had an episode of severe chest and back pain that required narcotic medications, blood transfusions, and fluids to treat. On examination, she is afebrile, with midthoracic tenderness on palpation. X-rays of the spine reveal periosteal reaction of the eighth thoracic vertebra. She has a chronic blood disorder where bone infarction can occur that may be difficult to distinguish from osteomyelitis. For the above patient with a hemoglobin abnormality, select the most likely diagnosis.
- A. beta-thalassemia major
- B. HbH disease
- C. sickle cell disease (Correct Answer)
- D. HbC disease
Explanation: ### Explanation **Correct Option: C. Sickle Cell Disease (SCD)** The clinical presentation is classic for **Sickle Cell Disease (SCD)**. The patient’s history of severe chest and back pain requiring narcotics and fluids describes a **Vaso-occlusive Crisis (VOC)**. In SCD, deoxygenated Hemoglobin S (HbS) polymerizes, causing red cell distortion and rigidity [1][2]. These rigid cells obstruct microvasculature, leading to tissue ischemia and **bone infarction** [1]. A critical diagnostic challenge in SCD is distinguishing **bone infarction from osteomyelitis**, as both present with localized pain, tenderness, and periosteal reactions on X-ray. While *Salmonella* is the most specific cause of osteomyelitis in SCD patients, *Staphylococcus aureus* remains the most common overall. The "midthoracic tenderness" and "periosteal reaction" in this young patient with a history of transfusions point directly to SCD-related bone complications. **Why Other Options are Incorrect:** * **A & B (Beta-thalassemia major & HbH disease):** These are disorders of globin chain synthesis (quantitative defects) [2]. While they cause severe anemia and "crew-cut" skull appearance due to extramedullary hematopoiesis, they do not typically cause acute vaso-occlusive crises or bone infarctions. * **D (HbC disease):** This usually presents as a mild hemolytic anemia with splenomegaly [2]. While HbSC disease can cause crises, pure HbC disease does not typically present with the severe, narcotic-requiring VOCs seen in SCD. **Clinical Pearls for NEET-PG:** * **Hand-Foot Syndrome (Dactylitis):** The earliest manifestation of SCD in infants. * **Radiology:** Look for "H-shaped vertebrae" (Codman sign) due to central vertebral endplate infarction. * **Osteomyelitis:** SCD patients have an increased susceptibility to *Salmonella* osteomyelitis due to functional asplenia [1]. * **Acute Chest Syndrome:** Defined by a new pulmonary infiltrate on X-ray plus fever, chest pain, or dyspnea; it is a leading cause of mortality [3].
Question 423: What is the recommended daily elemental iron supplementation for iron deficiency anemia?
- A. 300 – 400 mg
- B. 150 – 200 mg
- C. 100 – 150 mg (Correct Answer)
- D. less than 100 mg
Explanation: The goal of oral iron therapy in Iron Deficiency Anemia (IDA) is to provide enough elemental iron to maximize erythropoiesis while minimizing gastrointestinal side effects. [1] **Why 100 – 150 mg is correct:** Standard clinical guidelines (including Harrison’s Principles of Internal Medicine) traditionally recommend **100 to 200 mg of elemental iron daily** in divided doses to achieve a maximal hemoglobin rise (0.7–1.0 g/dL per week). In the context of this question, **100–150 mg** represents the optimal therapeutic range that balances efficacy with patient tolerance. It is important to distinguish between the weight of the iron salt (e.g., Ferrous Sulfate 325 mg) and the actual **elemental iron** content (which is 65 mg per 325 mg tablet). **Analysis of Incorrect Options:** * **A (300 – 400 mg):** This dose is excessively high. The intestinal iron transporter (DMT-1) becomes saturated, and excess unabsorbed iron causes severe oxidative stress to the gut mucosa, leading to nausea, cramping, and constipation. * **B (150 – 200 mg):** While technically within the upper limit of traditional teaching, most modern protocols favor the lower end of this spectrum (or even alternate-day dosing) to improve compliance. * **D (Less than 100 mg):** While doses as low as 60 mg can be effective in some patients, it may not provide the "maximal" rate of replacement required for symptomatic anemia in a standard clinical setting. **NEET-PG High-Yield Pearls:** * **Absorption:** Iron is best absorbed in the **duodenum and proximal jejunum** in the ferrous ($Fe^{2+}$) state. * **Enhancers/Inhibitors:** Vitamin C (Ascorbic acid) enhances absorption; tea, coffee, and antacids inhibit it. * **Hepcidin Factor:** Recent studies suggest that high daily doses increase **Hepcidin** levels, which actually *blocks* further iron absorption for 24–48 hours. This is why **alternate-day dosing** is becoming a popular clinical recommendation. * **Response Marker:** The first hematological sign of response to iron therapy is an **increase in Reticulocyte count** (usually within 5–7 days). [1]
Question 424: The threshold for prophylactic platelet transfusion is __________ platelets/mL.
- A. 5000
- B. 10000 (Correct Answer)
- C. 15000
- D. 50000
Explanation: ### Explanation The correct answer is **10,000 platelets/µL** (Option B). **1. Why 10,000 is the Correct Answer:** In patients with bone marrow failure (e.g., leukemia or post-chemotherapy) who are otherwise stable, the standard threshold for prophylactic platelet transfusion is **10,000/µL** [1]. Clinical trials (such as the TOPPS trial) have demonstrated that this threshold is as safe as higher triggers (like 20,000/µL) in preventing major spontaneous hemorrhage while significantly reducing the total number of transfusions and associated risks (alloimmunization, infections, and transfusion reactions). **2. Analysis of Incorrect Options:** * **5,000/µL (Option A):** While some studies suggest this may be safe in very stable patients, it is not the standard clinical guideline. Spontaneous intracranial hemorrhage risk increases significantly below this level [1]. * **15,000/µL (Option C):** This is an intermediate value not supported by major hematological guidelines (ASCO/ASH) as a standard trigger. * **50,000/µL (Option D):** This is the target threshold for patients undergoing **major surgery**, lumbar punctures, or those with active bleeding. It is not the threshold for *prophylaxis* in stable patients. **3. High-Yield Clinical Pearls for NEET-PG:** * **Threshold for Major Surgery/Liver Biopsy:** >50,000/µL. * **Threshold for Neurosurgery/Ophthalmic Surgery:** >100,000/µL. * **Threshold in Febrile/Infected Patients:** The trigger is often raised to **20,000/µL** due to increased platelet consumption. * **ITP Exception:** Prophylactic transfusion is generally **avoided** in Immune Thrombocytopenic Purpura (ITP) regardless of the count, unless there is life-threatening bleeding, as the transfused platelets are rapidly destroyed. * **Dose:** One unit of Random Donor Platelets (RDP) typically increases the count by 5,000–10,000/µL.
Question 425: Alkaline phosphatase is elevated in all the following conditions except?
- A. Rickets
- B. Hypophosphatemia
- C. Osteomalacia
- D. Hypoparathyroidism (Correct Answer)
Explanation: Serum **Alkaline Phosphatase (ALP)** is a marker of osteoblastic activity. Its levels rise whenever there is increased bone turnover or remodeling [3]. **Why Hypoparathyroidism is the correct answer:** In **Hypoparathyroidism**, there is a deficiency of Parathyroid Hormone (PTH). PTH is the primary stimulator of bone remodeling; without it, bone turnover becomes abnormally low (adynamic bone). Consequently, osteoblastic activity is minimal, leading to **low or normal ALP levels**. This distinguishes it from most other metabolic bone diseases where ALP is typically elevated [1]. **Analysis of Incorrect Options:** * **Rickets & Osteomalacia:** These conditions involve defective mineralization of the osteoid [4]. To compensate for the weak bone matrix, osteoblasts increase their activity, leading to a significant **elevation in ALP** [2]. This is a hallmark diagnostic feature. * **Hypophosphatemia:** Low serum phosphate (as seen in Vitamin D resistant rickets or Fanconi syndrome) impairs mineralization, similarly triggering a compensatory increase in osteoblastic activity and **elevated ALP**. **NEET-PG High-Yield Pearls:** 1. **ALP is NOT elevated in:** Multiple Myeloma (punched-out lesions have no osteoblastic reaction), Scurvy, and Hypoparathyroidism. 2. **Highest ALP levels:** Seen in **Paget’s Disease of bone** and Hyperparathyroidism (Osteitis fibrosa cystica). 3. **Hypophosphatasia:** A rare genetic disorder where ALP is pathologically **low**, leading to rickets-like symptoms. 4. **Isoenzymes:** Remember that ALP also originates from the liver (biliary tract), placenta (Regan isoenzyme), and intestine. To confirm bone origin, check Heat stability (Bone ALP is heat-labile) or GGT levels.
Question 426: Spontaneous mouth petechiae and gingival bleeding typically occur at which platelet level?
- A. Between 300,000 - 500,000/mm3
- B. Between 20,000-30,000/mm3 (Correct Answer)
- C. Between 150,000-170,000/mm3
- D. Between 70,000-185,000/mm3
Explanation: The clinical manifestation of thrombocytopenia (low platelet count) is directly correlated with the degree of deficiency. The correct answer is **Option B (20,000–30,000/mm³)** because this range represents the critical threshold where the primary hemostatic mechanism fails to maintain capillary integrity under normal physiological stress [1]. * **Why Option B is correct:** While the normal platelet count is 150,000–450,000/mm³, surgical bleeding usually doesn't occur until levels fall below 50,000/mm³. However, **spontaneous** bleeding—manifesting as petechiae, ecchymosis, and mucosal bleeding (gingival/epistaxis)—typically emerges when the count drops below **20,000–30,000/mm³** [1], [2]. Below 10,000/mm³, the risk of life-threatening internal hemorrhage (e.g., intracranial) increases significantly. * **Why other options are incorrect:** * **Option A & C:** These ranges are either normal or represent very mild thrombocytopenia where patients remain entirely asymptomatic. * **Option D:** Counts above 70,000/mm³ are generally sufficient to prevent spontaneous bleeding and are even adequate for most minor surgical procedures. **High-Yield Clinical Pearls for NEET-PG:** 1. **First Sign:** Petechiae are the hallmark of primary hemostatic defects (platelet issues), whereas deep muscle hematomas and hemarthrosis suggest secondary hemostatic defects (clotting factor issues) [2]. 2. **Wet Purpura:** The presence of blood blisters in the mouth (bullae) is a sign of severe thrombocytopenia and a predictor of imminent intracranial hemorrhage [3]. 3. **Transfusion Threshold:** In stable patients without bleeding, prophylactic platelet transfusion is usually indicated when the count falls below **10,000/mm³**.
Question 427: Cryoprecipitate cannot be used in which of the following conditions?
- A. Von Willebrand disease
- B. Hemophilia A
- C. Hemophilia B (Correct Answer)
- D. Disseminated Intravascular Coagulation (DIC)
Explanation: **Explanation:** The correct answer is **Hemophilia B**. To understand why, we must look at the specific composition of Cryoprecipitate. **Why Hemophilia B is the correct answer:** Cryoprecipitate is a concentrated fraction of plasma obtained by thawing fresh frozen plasma (FFP) at 4°C. It contains only five specific factors: **Factor VIII, Von Willebrand Factor (vWF), Fibrinogen (Factor I), Factor XIII, and Fibronectin.** Hemophilia B is caused by a deficiency of **Factor IX** (Christmas factor) [4]. Since Cryoprecipitate does not contain Factor IX, it is ineffective for treating Hemophilia B. These patients require Factor IX concentrates or FFP [1]. **Analysis of incorrect options:** * **Von Willebrand Disease (vWD):** Cryoprecipitate contains high concentrations of vWF and was historically the mainstay of treatment before the availability of virus-inactivated concentrates. * **Hemophilia A:** It contains Factor VIII, making it an effective (though now secondary to recombinant factors) treatment for Factor VIII deficiency [2]. * **DIC:** In DIC, there is massive consumption of fibrinogen. Cryoprecipitate is the treatment of choice to rapidly replenish fibrinogen levels when they fall below 100 mg/dL [3]. **NEET-PG High-Yield Pearls:** * **Composition Mnemonic:** Remember **"1, 8, 13, and vWF"** (Factors I, VIII, XIII, and vWF). * **Fibrinogen Source:** Cryoprecipitate is the most concentrated source of fibrinogen available (approx. 200-250 mg per unit). * **Storage:** It is stored at -18°C or colder and has a shelf life of 1 year. Once thawed, it must be used within 6 hours. * **Indication:** It is specifically indicated in **Hypofibrinogenemia** and **Uremic bleeding** (due to its effect on platelet adhesion via vWF).
Question 428: Which of the following drugs is NOT associated with pure red cell aplasia?
- A. Phenytoin
- B. Isoniazid
- C. Erythropoietin
- D. None of the above (Correct Answer)
Explanation: ### Explanation **Pure Red Cell Aplasia (PRCA)** is a rare hematological syndrome characterized by a severe reduction in erythroid precursors in the bone marrow, leading to normocytic normochromic anemia with a very low reticulocyte count, while white blood cell and platelet counts remain normal. #### Why "None of the above" is correct: All three drugs listed (Phenytoin, Isoniazid, and Erythropoietin) are well-documented causes of secondary acquired PRCA. Therefore, none of them can be excluded as an association. * **Phenytoin (Option A):** This antiepileptic drug is a classic cause of drug-induced PRCA. The mechanism is thought to be an immune-mediated toxicity against erythroid progenitor cells. * **Isoniazid (Option B):** Used in the treatment of Tuberculosis, INH is another frequently cited culprit in drug-induced marrow suppression specifically targeting the red cell line. * **Erythropoietin (Option C):** This is a high-yield fact for NEET-PG. Recombinant human erythropoietin (EPO) can lead to the development of **neutralizing anti-erythropoietin antibodies**. This occurs most commonly with subcutaneous administration (notably the Eprex brand in the past), leading to a sudden "resistance" to the drug and severe PRCA. #### Clinical Pearls for NEET-PG: * **Most common association:** PRCA is most famously associated with **Thymoma**. Surgical removal of the thymoma leads to remission in about 30% of cases. * **Viral Trigger:** **Parvovirus B19** is the most common viral cause, especially in patients with underlying hemolytic anemias (e.g., Sickle Cell Disease), leading to a transient aplastic crisis. * **Diagnosis:** Bone marrow biopsy is essential, showing a near-total absence of erythroid precursors (<0.5%) but normal myeloid and megakaryocytic lines. * **Treatment:** Immunosuppression (Cyclosporine, Corticosteroids) is the mainstay for acquired cases.
Question 429: Which viral infection is characterized by hemolysis?
- A. Hepatitis B (Correct Answer)
- B. Hepatitis C
- C. Prolonged fever
- D. Hepatitis A
Explanation: Explanation: Hepatitis B (Option A) is the correct answer because it is uniquely associated with various extrahepatic hematological manifestations, most notably Autoimmune Hemolytic Anemia (AIHA) and Aplastic Anemia. The underlying mechanism involves the formation of immune complexes and the production of autoantibodies against erythrocyte antigens triggered by the viral infection [2]. In chronic Hepatitis B, hypersplenism secondary to cirrhosis can also lead to the sequestration and destruction of red blood cells, further contributing to hemolysis. Why other options are incorrect: * Hepatitis C (Option B): While HCV is strongly associated with Mixed Cryoglobulinemia and B-cell Lymphomas, it is less commonly linked to direct hemolysis compared to HBV. * Prolonged Fever (Option C): This is a non-specific clinical symptom rather than a specific viral etiology. While some infections causing prolonged fever (like Malaria or Leishmaniasis) cause hemolysis, it is not a viral infection itself. * Hepatitis A (Option D): HAV is typically an acute, self-limiting infection. While rare cases of hemolysis in patients with G6PD deficiency have been reported during HAV infection, it is not a classic or characteristic feature of the virus [2]. NEET-PG High-Yield Pearls: * Hepatitis B & Hematology: Always remember the triad of HBV-associated extrahepatic issues: Polyarteritis Nodosa (PAN), Membranous Nephropathy, and Aplastic Anemia/Hemolysis. * Viral Hemolysis: Apart from HBV, other viruses frequently tested for causing hemolysis (via AIHA) include Epstein-Barr Virus (EBV) and Cytomegalovirus (CMV) [2]. * Parvovirus B19: High-yield for causing "Aplastic Crisis" specifically in patients with pre-existing hemolytic anemias (like Hereditary Spherocytosis or Sickle Cell Disease) [1].
Question 430: Which of the following conditions can result in dactylitis?
- A. Hemophilia
- B. Von Willebrand disease
- C. Thalassemia
- D. Sickle cell anemia (Correct Answer)
Explanation: ### Explanation **Correct Answer: D. Sickle cell anemia** **Mechanism:** Dactylitis, also known as **Hand-Foot Syndrome**, is often the first clinical manifestation of Sickle Cell Anemia (SCA) in infants (typically aged 6 months to 2 years). It is caused by **vaso-occlusive crises** in the small bones of the hands and feet [1]. The rapid expansion of bone marrow in these small bones, combined with sluggish blood flow, leads to infarction of the bone marrow and cortical bone [1]. This triggers an inflammatory response, resulting in symmetrical, painful swelling of the dorsum of the hands and feet, often accompanied by low-grade fever. **Why other options are incorrect:** * **A & B (Hemophilia and Von Willebrand Disease):** These are primary bleeding disorders. While Hemophilia commonly causes **hemarthrosis** (bleeding into large joints like the knee), it does not cause vaso-occlusive infarction or dactylitis. * **C (Thalassemia):** While Thalassemia involves ineffective erythropoiesis and bone marrow expansion (leading to "chipmunk facies"), it does not involve the sickling phenomenon [2] or acute vaso-occlusion required to produce dactylitis. **High-Yield Clinical Pearls for NEET-PG:** * **Radiology:** In the acute phase of dactylitis, X-rays are often normal. After 1–2 weeks, subperiosteal new bone formation or "moth-eaten" appearances may be seen. * **Differential Diagnosis:** The primary differential for dactylitis is **Osteomyelitis** (specifically *Salmonella* in SCA patients). However, dactylitis is usually bilateral and symmetrical, whereas osteomyelitis is typically focal. * **Other causes of dactylitis:** Beyond SCA, dactylitis is a hallmark of **Sero-negative Spondyloarthropathies** (e.g., Psoriatic arthritis—"Sausage digits"), Sarcoidosis, and Syphilis (clutton's joints). * **Management:** Treatment is supportive, involving aggressive hydration and analgesia [3].
Practice by Chapter
Anemia Evaluation and Management
Practice Questions
Hemoglobinopathies
Practice Questions
Thalassemias
Practice Questions
Platelet Disorders
Practice Questions
Coagulation Disorders
Practice Questions
Thrombotic Disorders
Practice Questions
Leukemias
Practice Questions
Lymphomas
Practice Questions
Multiple Myeloma and Plasma Cell Disorders
Practice Questions
Myeloproliferative Neoplasms
Practice Questions
Transfusion Medicine
Practice Questions
Hematopoietic Stem Cell Transplantation
Practice Questions
Want unlimited practice?
Get full access to all questions, explanations, and performance tracking.
Start For Free