Hematology — MCQs

Hematology Indian Medical PG Practice Questions and MCQs

Question 71: Which of the following is true for von Willebrand disease?

A. Normal partial thromboplastin time
B. Decreased platelets
C. Normal prothrombin time (Correct Answer)
D. Normal bleeding time

Explanation: Von Willebrand Disease (vWD) is the most common inherited bleeding disorder, characterized by a deficiency or dysfunction of von Willebrand Factor (vWF) [2]. vWF has two primary roles: mediating platelet adhesion to subendothelial collagen (primary hemostasis) and acting as a carrier protein to stabilize Factor VIII (secondary hemostasis) [2]. **Why Option C is correct:** The **Prothrombin Time (PT)** measures the extrinsic and common pathways (Factors VII, X, V, II, and I) [3]. Since vWD only affects vWF and potentially Factor VIII (intrinsic pathway), the PT remains **normal** [3]. **Why other options are incorrect:** * **A. Normal PTT:** This is incorrect because vWF stabilizes Factor VIII. In many cases of vWD (especially Type 1 and 2N), Factor VIII levels are low, leading to a **prolonged Activated Partial Thromboplastin Time (aPTT)** [2]. * **B. Decreased platelets:** Platelet count is typically **normal** in most types of vWD [2]. The exception is Type 2B vWD (gain-of-function mutation), where increased binding to platelets leads to mild thrombocytopenia, but this is not the general rule. * **D. Normal bleeding time:** Bleeding time (BT) measures primary hemostasis. Since vWF is essential for platelet-vessel wall adhesion, the **BT is characteristically prolonged**. **High-Yield Clinical Pearls for NEET-PG:** * **Inheritance:** Most types are Autosomal Dominant (Type 3 is Autosomal Recessive) [2]. * **Screening Tests:** Prolonged BT, normal/prolonged aPTT, and normal PT/Platelet count [2], [3]. * **Confirmatory Test:** Ristocetin Cofactor Assay (measures vWF activity) [2]. * **Treatment:** **Desmopressin (DDAVP)** is the drug of choice for Type 1 as it releases stored vWF from Weibel-Palade bodies [1], [2]. For Type 3 or severe cases, vWF-containing concentrates are used [2].

Question 72: Which cell count increases earliest following splenectomy?

A. Lymphocytes
B. Monocytes
C. Neutrophils
D. Platelets (Correct Answer)

Explanation: The spleen acts as the primary reservoir for blood cells, particularly platelets. Approximately **one-third (30%) of the total body platelet pool** is sequestered within the splenic red pulp at any given time. **Why Platelets are the correct answer:** Immediately following a splenectomy, the sequestration site is removed, leading to a rapid redistribution of these stored platelets into the systemic circulation. This results in an increase in platelet count within **hours** of the procedure. This transient reactive thrombocytosis usually peaks between 7–10 days post-surgery. **Analysis of Incorrect Options:** * **Neutrophils:** While a transient neutrophilic leukocytosis occurs post-splenectomy (due to demargination and stress response), it is generally less pronounced and less immediate than the redistribution of the sequestered platelet pool. * **Lymphocytes & Monocytes:** These cells may show a mild, chronic increase (lymphocytosis and monocytosis) as the spleen is a major lymphoid organ, but these changes occur much later and are not the earliest hematological finding. **High-Yield Clinical Pearls for NEET-PG:** 1. **Post-Splenectomy Blood Picture:** Look for **Howell-Jolly bodies** (nuclear remnants), **Pappenheimer bodies** (iron granules), **Heinz bodies** (denatured hemoglobin), and **Target cells**. 2. **Infections:** Patients are at lifelong risk of **OPSI (Overwhelming Post-Splenectomy Infection)**, primarily from encapsulated organisms: *Streptococcus pneumoniae* (most common), *Haemophilus influenzae*, and *Neisseria meningitidis*. 3. **Vaccination Protocol:** Ideally, vaccines should be administered **2 weeks before** elective surgery or **2 weeks after** emergency surgery to ensure optimal immune response.

Question 73: A 50-year-old male patient complains of pain in the back and legs. On routine investigations, it is found that he is anemic and his ESR is also raised. Which of the following is the most probable diagnosis for this patient?

A. Sickle cell anemia
B. Polycythemia
C. Waldenstrom macroglobulinemia
D. Multiple myeloma (Correct Answer)

Explanation: **Explanation:** The clinical presentation of bone pain (back and legs) in an elderly patient, combined with anemia and a significantly raised ESR, is a classic triad for **Multiple Myeloma (MM)** [1]. **Why Multiple Myeloma is correct:** Multiple Myeloma is a plasma cell dyscrasia characterized by the neoplastic proliferation of a single clone of plasma cells producing monoclonal (M) protein [1]. * **Bone Pain:** Caused by the activation of osteoclasts (via RANKL), leading to lytic lesions, pathological fractures, and bone resorption [1]. * **Anemia:** Usually normocytic, normochromic, resulting from bone marrow infiltration by plasma cells and cytokine-induced suppression of erythropoiesis. * **Raised ESR:** The high levels of monoclonal paraproteins (M-spike) neutralize the negative charge on RBCs, leading to **Rouleaux formation**, which causes a characteristically "extreme" elevation of ESR (often >100 mm/hr) [1]. **Why other options are incorrect:** * **Sickle cell anemia:** While it causes bone pain (vaso-occlusive crises), the ESR is typically **very low** because sickled cells cannot form Rouleaux. * **Polycythemia:** Characterized by an increased RBC mass; the ESR is typically **low or zero** due to increased blood viscosity and crowding. * **Waldenstrom Macroglobulinemia:** While it involves an M-spike (IgM) and high ESR, it typically presents with hyperviscosity symptoms and lymphadenopathy/splenomegaly rather than lytic bone lesions and bone pain [2]. **High-Yield Clinical Pearls for NEET-PG:** * **CRAB Criteria:** **C**alcium (High), **R**enal insufficiency, **A**nemia, **B**one lesions. * **Diagnosis:** Bone marrow biopsy shows >10% plasma cells; Serum Protein Electrophoresis (SPEP) shows an **M-spike** [1]. * **Urine:** Bence-Jones proteins (light chains) may be present (not detected on standard dipstick) [1]. * **X-ray:** "Punched-out" lytic lesions (Skull X-ray is a classic exam image) [1].

Question 74: A 25-year-old male presented with high-grade fever and hypotension. His Hb is 5 g/dL and TLC is 9000/mm³. What should be included in the management, except?

A. Oral ciprofloxacin (Correct Answer)
B. Packed cell transfusion
C. IV ciprofloxacin
D. Colony stimulating factor

Explanation: ### Explanation The patient presents with **Febrile Neutropenia** (implied by high-grade fever and potential bone marrow suppression suggested by severe anemia) and **Septic Shock** (hypotension). **1. Why "Oral ciprofloxacin" is the correct answer (The Exception):** In a patient with hypotension (septic shock), oral medications are contraindicated. Hypotension leads to splanchnic vasoconstriction and reduced gastrointestinal perfusion, resulting in unpredictable and inadequate absorption of drugs. Furthermore, patients with hemodynamic instability or high-risk features (MASCC score <21) require **Intravenous (IV)** broad-spectrum antibiotics immediately to achieve rapid therapeutic levels. **2. Analysis of Incorrect Options:** * **Packed cell transfusion:** The patient has severe anemia (Hb 5 g/dL). In the presence of hemodynamic instability (hypotension), a blood transfusion is indicated to improve oxygen-carrying capacity and stabilize the patient. * **IV ciprofloxacin:** Fluoroquinolones are often part of the regimen for febrile neutropenia, especially when targeting Gram-negative organisms. In a state of shock, the **IV route** is the mandatory standard of care. * **Colony stimulating factor (G-CSF):** While not always first-line for all fevers, G-CSF is indicated in "high-risk" febrile neutropenia (e.g., sepsis, hypotension, or multi-organ failure) to accelerate neutrophil recovery and improve clinical outcomes. **Clinical Pearls for NEET-PG:** * **Definition of Febrile Neutropenia:** Single oral temp >38.3°C (101°F) or >38.0°C (100.4°F) for 1 hour + ANC <500 cells/mm³. * **Initial Choice:** Monotherapy with an anti-pseudomonal beta-lactam (e.g., Piperacillin-Tazobactam, Cefepime, or Meropenem) is standard. * **Route Rule:** Always choose **IV over Oral** if the patient is hypotensive, vomiting, or has severe mucositis.

Question 75: Which of the following is NOT typically seen in a chronic case of sickle cell anemia?

A. Hepatomegaly
B. Pulmonary hypertension
C. Cardiomegaly
D. Splenomegaly (Correct Answer)

Explanation: **Explanation:** The correct answer is **Splenomegaly**. In chronic cases of Sickle Cell Anemia (SCA), the spleen undergoes a process known as **autosplenectomy**. While children with SCA may initially present with splenomegaly due to sequestration of sickled cells, recurrent splenic infarcts over time lead to progressive fibrosis and shrinkage of the organ. By adulthood, the spleen is typically small, calcified, and non-functional. **Analysis of Incorrect Options:** * **Hepatomegaly:** This is a common finding in chronic SCA. It occurs due to compensatory extramedullary hematopoiesis, chronic passive congestion from heart failure, or iron overload (hemosiderosis) resulting from frequent blood transfusions. * **Pulmonary Hypertension:** This is a major chronic complication and a leading cause of death in adult SCA patients. It results from chronic hemolysis, which depletes nitric oxide, leading to vasoconstriction and vascular remodeling. * **Cardiomegaly:** Chronic anemia leads to a hyperdynamic circulation. To compensate for the low oxygen-carrying capacity, the stroke volume and heart rate increase, eventually resulting in eccentric left ventricular hypertrophy and cardiomegaly. **NEET-PG High-Yield Pearls:** * **Autosplenectomy** usually occurs by age 6–8 years in HbSS patients. * The presence of **Howell-Jolly bodies** on a peripheral smear is a hallmark of functional asplenia. * Patients with autosplenectomy are at high risk for infections by **encapsulated organisms** (*S. pneumoniae, H. influenzae, N. meningitidis*). * If an adult with sickle cell disease has splenomegaly, consider **Sickle Cell-Thalassemia (HbSβ+)** or **HbSC disease**, where sickling is less severe and the spleen is preserved longer.

Question 76: A patient has normal prothrombin time (PT) and platelet count. The activated partial thromboplastin time (aPTT) is increased, and factor VIII levels are observed to be 60% (normal). There is no associated history of bleeding even after a surgical procedure. What is the most likely diagnosis?

A. Factor IX deficiency
B. Factor VIII inhibitors
C. Lupus anticoagulant (Correct Answer)
D. Thalassemia

Explanation: The clinical scenario describes an **isolated prolonged aPTT** with a normal PT, normal platelet count, and normal Factor VIII levels (60% is within the low-normal range). The most critical clue is the **absence of bleeding**, even after surgical stress. **1. Why Lupus Anticoagulant (LA) is correct:** Lupus anticoagulant is an antiphospholipid antibody. In *vitro* (in the lab), these antibodies interfere with the phospholipids used in the aPTT reagent, causing a paradoxical prolongation of the clotting time [1]. However, in *vivo* (in the body), LA is **pro-thrombotic**, not pro-hemorrhagic. Therefore, patients do not bleed; instead, they are at risk for arterial and venous thrombosis. This "asymptomatic prolongation of aPTT" is a classic board exam presentation for LA. **2. Why other options are incorrect:** * **Factor IX deficiency (Hemophilia B):** This would cause a prolonged aPTT, but it is characterized by a significant **bleeding tendency** (hemarthrosis, post-surgical bleeding). * **Factor VIII inhibitors:** These are antibodies against Factor VIII. They cause a prolonged aPTT and **severe bleeding** manifestations [1]. Furthermore, Factor VIII levels would be significantly low, not 60%. * **Thalassemia:** This is a hemoglobinopathy affecting red blood cells. It does not affect the coagulation cascade, PT, or aPTT. **Clinical Pearls for NEET-PG:** * **Mixing Study:** If aPTT remains prolonged after mixing the patient's plasma with normal plasma (1:1), it indicates the presence of an **inhibitor** (like LA) rather than a factor deficiency [1]. * **The "Silent" Prolonged aPTT:** Always consider **Factor XII deficiency** or **Lupus Anticoagulant** when aPTT is high but the patient has no bleeding symptoms. * **Paradox:** LA causes a "long aPTT" in the lab but "clots" in the patient.

Question 77: What is the most sensitive indicator for iron deficiency anemia?

A. Serum ferritin (Correct Answer)
B. TIBC (Total Iron-Binding Capacity)
C. Percentage saturation of transferrin
D. Bone marrow iron

Explanation: **Explanation:** Iron deficiency anemia (IDA) develops in stages: first, iron stores are depleted, followed by a decrease in transport iron, and finally, a drop in hemoglobin. **1. Why Serum Ferritin is the Correct Answer:** Serum ferritin is the **most sensitive and specific initial laboratory indicator** for iron deficiency. It directly reflects the body's total iron stores. A low serum ferritin level (<15–30 ng/mL) is virtually diagnostic of iron deficiency, as it is the first parameter to decrease before clinical anemia or changes in red cell morphology (microcytosis/hypochromia) occur. **2. Why Other Options are Incorrect:** * **TIBC (Total Iron-Binding Capacity):** While TIBC increases in IDA, it is less specific than ferritin and can be affected by nutritional status and liver function. * **Percentage Saturation of Transferrin:** This measures transport iron. It decreases in IDA but also fluctuates in other conditions like anemia of chronic disease (ACD) and is less sensitive for early storage depletion. * **Bone Marrow Iron:** While the **"Gold Standard"** for diagnosing iron deficiency (Prussian blue staining), it is an invasive procedure. In the context of "most sensitive indicator" in routine clinical practice, serum ferritin is the preferred non-invasive test. **High-Yield Clinical Pearls for NEET-PG:** * **The "Rule of Ferritin":** Ferritin is an **acute-phase reactant**. In the presence of inflammation, infection, or malignancy, ferritin levels may be falsely normal or elevated even if iron deficiency exists. * **Earliest Sign of IDA:** Depletion of bone marrow iron stores (but Serum Ferritin is the earliest biochemical marker). * **Earliest Sign of Response to Iron Therapy:** Increase in **Reticulocyte count** (usually seen within 5–7 days). * **Soluble Transferrin Receptor (sTfR) Assay:** Useful to differentiate IDA from Anemia of Chronic Disease (sTfR is elevated in IDA but normal in ACD).

Question 78: A patient has received 8 blood transfusions in the last few years, with Hb: 6.0 g/dL and RBCs 2 lakh/cu mm with MCV=64 fL. Which of the following investigations is not required for evaluating this patient?

A. Tests for pulmonary hemosiderosis
B. GI endoscopy
C. Urine hemosiderin
D. Bone marrow examination (Correct Answer)

Explanation: This patient presents with severe **microcytic anemia** (Hb 6.0 g/dL, MCV 64 fL [2]) and a history of multiple transfusions, suggesting a chronic iron deficiency or blood loss state [1]. ### Why Bone Marrow Examination is NOT required: In modern hematology, **Bone Marrow Examination** is rarely indicated for the primary evaluation of iron deficiency anemia (IDA) [3]. While it was once the "gold standard" (using Prussian blue stain for hemosiderin), it is invasive and expensive [3]. Diagnosis is now reliably established through peripheral blood counts, iron studies (Serum Ferritin), and identifying the source of loss. It provides no additional diagnostic value in this clinical scenario. ### Evaluation of Other Options: * **GI Endoscopy (B):** This is a mandatory investigation in any adult with unexplained IDA to rule out occult gastrointestinal bleeding (e.g., peptic ulcers, malignancy, or hookworm infestation), which is the most common cause of chronic blood loss [2]. * **Urine Hemosiderin (C):** This is a sensitive marker for **chronic intravascular hemolysis** (e.g., PNH). If the patient is losing iron via the kidneys, this test helps localize the site of iron loss. * **Tests for Pulmonary Hemosiderosis (A):** Idiopathic pulmonary hemosiderosis involves recurrent alveolar hemorrhage leading to iron sequestration in the lungs. If GI and renal sources are ruled out, evaluating the lungs is necessary to explain the microcytic anemia. ### Clinical Pearls for NEET-PG: * **Gold Standard for Iron Stores:** Bone marrow aspirate (Prussian blue stain), but **Serum Ferritin** is the best initial non-invasive test [3]. * **Mentzer Index:** MCV/RBC count. If **<13**, it suggests Thalassemia trait; if **>13**, it suggests Iron Deficiency Anemia. In this patient, $64 / 0.2 = 320$, strongly pointing towards IDA [2]. * **Pica:** A specific clinical sign of iron deficiency. * **Plummer-Vinson Syndrome:** Triad of IDA, esophageal webs, and glossitis.

Question 79: A 23-year-old male presented with epistaxis. Lab parameters show Hb= 5 g/dl, Platelet count = 23,000/mm3 and absolute neutrophil count = 176/mm3. Bone marrow is hypocellular with fatty infiltration. Which of the following statements regarding this condition is FALSE?

A. Hematopoietic stem cell transplantation can be curative.
B. Lymphadenopathy and splenomegaly are highly typical. (Correct Answer)
C. Bleeding is the most common symptom.
D. Immunosuppressants are used in treatment.

Explanation: ### Explanation The clinical presentation of pancytopenia (anemia, thrombocytopenia, and neutropenia) combined with a hypocellular bone marrow showing fatty replacement is diagnostic of **Aplastic Anemia**. **Why Option B is the Correct Answer (False Statement):** In Aplastic Anemia, the primary pathology is the failure of the bone marrow to produce cells. It is **not** a proliferative or infiltrative disorder. Therefore, physical findings such as **lymphadenopathy and splenomegaly are characteristically absent**. If these are present, clinicians must suspect alternative diagnoses like leukemia, lymphoma, or myelofibrosis. **Analysis of Other Options:** * **Option A (True):** Allogeneic Hematopoietic Stem Cell Transplantation (HSCT) is the treatment of choice for young patients (usually <40 years) with a matched sibling donor and can be curative. * **Option C (True):** While patients present with symptoms of anemia (fatigue) and infection (fever), **bleeding** due to severe thrombocytopenia (epistaxis, petechiae, mucosal bleeds) is often the most common and distressing presenting symptom. * **Option D (True):** For patients who are older or lack a donor, immunosuppressive therapy (IST) using **Antithymocyte Globulin (ATG)** and **Cyclosporine** is the standard of care, as the disease is often T-cell mediated. ### Clinical Pearls for NEET-PG: * **Severity Criteria (Camitta Criteria):** Severe Aplastic Anemia is defined by marrow cellularity <25% plus at least two of: 1. ANC < 500/mm³ (Very severe if < 200/mm³—as seen in this patient). 2. Platelets < 20,000/mm³. 3. Reticulocyte count < 1% (or < 60,000/mm³). * **Drug of Choice:** Eltrombopag (TPO receptor agonist) is now frequently added to IST to improve response rates. * **Most common cause:** Idiopathic (immune-mediated). Secondary causes include drugs (Chloramphenicol, Sulfa), viruses (Hepatitis, EBV), and toxins (Benzene).

Question 80: Which of the following is a finding in functional platelet defects?

A. Normal platelet count and prolonged bleeding time (Correct Answer)
B. Normal platelet count and bleeding time
C. Prolonged bleeding time, prothrombin time, and PTT
D. Thrombocytopenia and prolonged bleeding time

Explanation: ### Explanation **1. Understanding the Core Concept** Functional platelet defects (Thrombocytopathies) are disorders where the **number** of platelets is typically normal, but their **function** (adhesion, aggregation, or secretion) is impaired [2]. * **Bleeding Time (BT):** This is a clinical marker of primary hemostasis (platelet-vessel wall interaction). Since the platelets cannot form an effective primary plug, the BT is **prolonged** [2]. * **Platelet Count:** In classic functional defects like Glanzmann Thrombasthenia or Bernard-Soulier Syndrome (usually), the quantitative count remains within the **normal** range [4]. **2. Analysis of Incorrect Options** * **Option B:** Normal BT would imply intact primary hemostasis, which contradicts a functional defect. * **Option C:** Prothrombin Time (PT) and Partial Thromboplastin Time (PTT) measure the coagulation cascade (secondary hemostasis) [1]. These are typically normal in isolated platelet disorders unless there is a dual pathology (e.g., von Willebrand Disease, where PTT may be elevated due to low Factor VIII). * **Option D:** This describes **Thrombocytopenia**. While BT is prolonged here, it is due to a lack of quantity, not necessarily a functional defect of the existing cells. **3. NEET-PG High-Yield Pearls** * **Glanzmann Thrombasthenia:** Deficiency of **GPIIb/IIIa**; failure of platelet **aggregation** (Normal count, prolonged BT) [4]. * **Bernard-Soulier Syndrome:** Deficiency of **GPIb-IX-V**; failure of platelet **adhesion** [4]. Key finding: **Giant Platelets** and mild thrombocytopenia (exception to the "normal count" rule, but primarily a functional defect) [3]. * **Ristocetin Test:** Aggregation is absent in Bernard-Soulier and vWD. It corrects with the addition of normal plasma in vWD, but **not** in Bernard-Soulier. * **Drug-induced defect:** Aspirin causes irreversible inhibition of COX-1, leading to a functional defect (prolonged BT) despite a normal count.

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Anemia Evaluation and Management

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Hemoglobinopathies

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Thalassemias

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Platelet Disorders

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Coagulation Disorders

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Thrombotic Disorders

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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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Transfusion Medicine

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Hematopoietic Stem Cell Transplantation

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Hematology — MCQs

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