Hematology — MCQs

A 74-year-old man presents with fatigue, shortness of breath on exertion, and back and rib pain, which is made worse with movement. Investigations reveal he is anemic, calcium, urea, and creatinine are elevated. X-rays reveal multiple lytic lesions in the long bones and ribs, and protein electrophoresis is positive for an immunoglobulin G (IgG) paraprotein. Which of the following is the most likely mechanism for the renal injury?

Hematology Indian Medical PG Practice Questions and MCQs

Question 21: What is the earliest hematological response to iron supplementation in iron deficiency anemia?

A. Increase in serum ferritin
B. Increase in reticulocyte count (Correct Answer)
C. Increase in total iron-binding capacity
D. Increase in hemoglobin

Explanation: **Explanation:** The correct answer is **B. Increase in reticulocyte count.** **Why it is correct:** When iron is administered to a patient with iron deficiency anemia (IDA), the bone marrow—which was previously "starved" of iron—rapidly utilizes the new supply to produce new red blood cells. The earliest measurable hematological response is an increase in the **reticulocyte count** (immature RBCs). This typically begins within **3 to 5 days** and peaks around **7 to 10 days** after starting therapy. This "reticulocyte response" serves as a clinical indicator that the patient is responding to treatment. **Why the other options are incorrect:** * **A. Increase in serum ferritin:** Ferritin reflects the body's iron stores. It is the **last** parameter to normalize because the body prioritizes hemoglobin synthesis over storage. It usually takes 3 to 6 months of therapy to replenish stores. * **C. Increase in TIBC:** In IDA, TIBC is high. Successful treatment leads to a **decrease** in TIBC as iron saturation improves, not an increase. * **D. Increase in hemoglobin:** While hemoglobin begins to rise shortly after the reticulocyte peak, a significant increase (usually ~1-2 g/dL) is typically seen after **2 to 3 weeks**, and it takes about 2 months to reach normal levels. [1] **High-Yield Clinical Pearls for NEET-PG:** * **Subjective Improvement:** The very first sign of recovery is often the patient's **subjective feeling of well-being** (increased appetite/energy), occurring within 24–48 hours. * **Sequence of Recovery:** Reticulocytosis (Days 3–7) → Rise in Hb (Weeks 2–3) → Normalization of Hb (Month 2) → Replenishment of Stores/Ferritin (Months 3–6). * **Failure to respond:** If the reticulocyte count does not rise, consider poor compliance, malabsorption (e.g., Celiac disease), or ongoing occult blood loss. [1]

Question 22: In a case of polycythemia vera, which of the following receptor overactivities is seen?

A. Tyrosine kinase
B. JAK2 (Correct Answer)
C. cGMP
D. None of the above

Explanation: **Explanation:** **Polycythemia Vera (PV)** is a chronic myeloproliferative neoplasm characterized by the autonomous overproduction of red blood cells. The hallmark of PV is a somatic mutation in the **JAK2 (Janus Kinase 2)** gene [2], most commonly the **V617F mutation** (found in >95% of cases). 1. **Why JAK2 is correct:** JAK2 is a non-receptor **tyrosine kinase** that associates with the cytoplasmic tails of cytokine receptors (like the Erythropoietin receptor). In PV, the mutation leads to constitutive activation of the JAK-STAT signaling pathway. This means the bone marrow precursors proliferate independently of erythropoietin levels, leading to panmyelosis (increased RBCs, WBCs, and platelets). 2. **Why other options are incorrect:** * **Tyrosine Kinase (Option A):** While JAK2 is technically a type of tyrosine kinase, "JAK2" is the specific and most accurate answer for PV. In exams, if a specific kinase is mentioned alongside the general class, the specific one is the preferred answer. * **cGMP (Option C):** Cyclic GMP is a second messenger involved in vasodilation (via Nitric Oxide) and phototransduction, not in the pathogenesis of myeloproliferative disorders. **High-Yield Clinical Pearls for NEET-PG:** * **Major WHO Criteria for PV:** Elevated Hemoglobin (>16.5 g/dL in men, >16.0 g/dL in women), Bone marrow hypercellularity, and the presence of **JAK2 V617F** [2] or **JAK2 exon 12** mutation. * **Erythropoietin (EPO) Levels:** Characteristically **low** in PV (useful to differentiate from secondary polycythemia where EPO is high). * **Clinical Sign:** **Aquagenic pruritus** (itching after a warm bath) [2] is a classic symptom. * **Complication:** Increased risk of thrombosis (Budd-Chiari syndrome) and transformation to myelofibrosis [1] or AML.

Question 23: Spontaneous muscle bleeding is typically seen in which of the following conditions?

A. Hemophilia (Correct Answer)
B. Afibrinogenemia
C. Von Willebrand's disease
D. Scott's syndrome

Explanation: The clinical presentation of bleeding disorders is divided into two main patterns: **Primary Hemostasis defects** (Platelet/Vessel wall issues) and **Secondary Hemostasis defects** (Coagulation factor deficiencies). [1] **1. Why Hemophilia is Correct:** Hemophilia A (Factor VIII deficiency) and Hemophilia B (Factor IX deficiency) are classic examples of secondary hemostasis defects. In these conditions, the initial platelet plug forms normally, but the fibrin meshwork fails to stabilize it. This leads to **deep-seated bleeding**. The hallmark of severe hemophilia is spontaneous **Hemarthrosis** (joint bleeding) and **Hematomas** (muscle bleeding, such as in the psoas or gastrocnemius). [1] **2. Why the other options are incorrect:** * **Afibrinogenemia:** While a severe deficiency of fibrinogen (Factor I) can cause significant bleeding, it typically presents with umbilical cord bleeding at birth or mucosal bleeding. Spontaneous muscle/joint bleeding is far more characteristic of the "Hemophilia" group. * **Von Willebrand’s Disease (vWD):** This is the most common inherited bleeding disorder. It primarily affects platelet adhesion. Therefore, it presents with **mucocutaneous bleeding** (epistaxis, menorrhagia, easy bruising) rather than deep muscle bleeds. [1], [2] (Note: Type 3 vWD can mimic hemophilia, but it is not the "typical" presentation). * **Scott’s Syndrome:** This is a rare platelet coagulant disorder where platelets fail to flip phosphatidylserine to their outer surface. It presents with mild to moderate skin/mucosal bleeding, not spontaneous muscle hematomas. **Clinical Pearls for NEET-PG:** * **Hemarthrosis/Muscle Bleed:** Think Coagulation Factor Deficiency (Hemophilia). [1] * **Petechiae/Purpura/Mucosal Bleed:** Think Platelet Disorders (ITP, vWD). [1] * **Delayed Bleeding (after trauma/surgery):** Characteristic of Factor XIII deficiency or Hemophilia. * **Mixing Study:** If the aPTT corrects, it’s a factor deficiency; if it doesn’t, it’s an inhibitor.

Question 24: All of the following are true about beta-thalassemia trait, except?

A. Microcytic hypochromic picture
B. Increased HbA2
C. Increased HbF
D. Patient requires blood transfusion (Correct Answer)

Explanation: **Explanation:** **Beta-thalassemia trait (Beta-thalassemia minor)** is a heterozygous state where there is a mutation in only one of the two beta-globin genes [1]. This condition is typically **asymptomatic** or presents with mild anemia that does not require clinical intervention. 1. **Why Option D is the correct answer:** Patients with beta-thalassemia trait have sufficient hemoglobin production from the single functional beta gene to maintain near-normal levels. Unlike Thalassemia Major (Cooley’s anemia), which is transfusion-dependent, the trait is a **benign carrier state**. Transfusions are not required and, if given unnecessarily, could lead to iatrogenic iron overload. 2. **Analysis of Incorrect Options:** * **Option A (Microcytic hypochromic picture):** This is a classic finding. Due to reduced beta-chain synthesis, RBCs are smaller (Low MCV) and pale (Low MCH). A key differentiator from iron deficiency is a high RBC count despite low Hb (Mentzer Index < 13). * **Option B (Increased HbA2):** This is the **diagnostic hallmark**. In the absence of sufficient beta chains, delta chain pairing increases, leading to HbA2 levels typically >3.5% (normal is <3%). * **Option C (Increased HbF):** While HbA2 is the primary marker, HbF (alpha2-gamma2) is also mildly elevated in about 50% of cases (usually 1–5%). **NEET-PG High-Yield Pearls:** * **Mentzer Index:** MCV/RBC count. If **<13**, it suggests Thalassemia trait; if **>13**, it suggests Iron Deficiency Anemia. * **Target Cells:** Commonly seen on the peripheral blood smear. * **NEVER** treat thalassemia trait with iron unless co-existing iron deficiency is proven; it can lead to lead to secondary hemochromatosis.

Question 25: HbA2 levels are increased in which of the following conditions?

A. Alpha-thalassemia
B. Iron deficiency anemia
C. Beta-thalassemia (Correct Answer)
D. Sickle cell trait

Explanation: **Explanation:** The correct answer is **C. Beta-thalassemia.** **Mechanism of Increased HbA2:** Normal adult hemoglobin consists primarily of **HbA (̢2̢2)**, with small amounts of **HbA2 (̢2̤2)** and **HbF (̢2̣2)** [3]. In Beta-thalassemia, there is a reduced or absent production of ̢-globin chains [1]. To compensate for this deficiency, the body increases the production of alternative non-̢ chains (delta and gamma) [4]. This leads to an increased proportion of HbA2 (typically >3.5%). This elevation is a hallmark diagnostic feature used to identify **Beta-thalassemia trait**. **Analysis of Incorrect Options:** * **Alpha-thalassemia:** Since HbA2 (̢2̤2) requires alpha chains, a deficiency in alpha-globin leads to **decreased or normal** HbA2 levels. * **Iron deficiency anemia (IDA):** IDA is the most common cause of a **falsely decreased** HbA2 level. Iron is a necessary cofactor for globin chain synthesis; its absence disproportionately affects delta chain production. * **Sickle cell trait (HbAS):** Patients with sickle cell trait typically have **normal** HbA2 levels. Their electrophoresis shows HbA and HbS [2]. **High-Yield Clinical Pearls for NEET-PG:** * **Diagnostic Cut-off:** HbA2 >3.5% is diagnostic for Beta-thalassemia minor. * **The "Masking" Effect:** Co-existing Iron Deficiency Anemia can lower HbA2 levels into the normal range in a patient who actually has Beta-thalassemia trait. Therefore, iron stores should be replenished before testing for thalassemia. * **HbF levels:** While HbA2 is the primary marker for Beta-thalassemia minor, HbF is significantly elevated in Beta-thalassemia major. * **Mentzer Index:** (MCV/RBC count) <13 suggests Thalassemia, while >13 suggests IDA [4].

Question 26: A young patient is hospitalized with petechiae of the oral mucous membrane, marginal gingival hemorrhage, and a platelet count of 45,000/cc. The bleeding time (BT) and clot retraction time are increased, while RBC and TLC are normal. What condition is the patient likely suffering from?

A. Infectious mononucleosis
B. Thrombocytopenic purpura (Correct Answer)
C. Leukemia
D. Hemophilia

Explanation: The clinical presentation of petechiae and mucosal bleeding (gingival hemorrhage) points toward a **primary hemostatic defect** [1]. The laboratory findings of a low platelet count (**45,000/cc**; normal: 1.5–4.5 lakh/cc) and a prolonged **Bleeding Time (BT)** are classic hallmarks of **Thrombocytopenic Purpura** [2]. In this condition, the reduction in platelet numbers impairs the formation of the primary platelet plug. Furthermore, **Clot Retraction Time** is increased because clot retraction is a platelet-dependent process (mediated by the protein thrombosthenin). Normal RBC and TLC counts help rule out generalized bone marrow failure or malignancy. [3] **Analysis of Incorrect Options:** * **Infectious Mononucleosis:** While it can occasionally cause mild thrombocytopenia, it typically presents with a triad of fever, pharyngitis, and lymphadenopathy, with characteristic atypical lymphocytes on a blood smear (increased TLC). * **Leukemia:** Although leukemia causes thrombocytopenia, it is almost always accompanied by significant abnormalities in the **RBC count** (anemia) and **TLC** (either marked leukocytosis with blasts or leukopenia), which are normal in this patient. [3] * **Hemophilia:** This is a secondary hemostatic defect (clotting factor deficiency). It presents with deep tissue hematomas or hemarthrosis [1]. The **Bleeding Time and platelet count are normal** in hemophilia; only the aPTT is prolonged. **NEET-PG High-Yield Pearls:** * **BT vs. CT:** Bleeding Time (BT) assesses platelet function/number; Clotting Time (CT) assesses the coagulation cascade. * **Clot Retraction:** Directly proportional to the platelet count and inversely proportional to the red cell mass. * **Dry vs. Wet Purpura:** Mucosal bleeding (as seen here) is termed "wet purpura" and indicates a higher risk of life-threatening intracranial hemorrhage compared to "dry purpura" (skin only). [3]

Question 27: A patient of multiple myeloma presents with bony lesions. What is the best marker for prognosis of the disease?

A. Bone marrow plasma cell percentage
B. Serum calcium level
C. Beta-2 microglobulin (Correct Answer)
D. Beta microglobulin

Explanation: **Explanation:** The prognosis of Multiple Myeloma (MM) is currently determined by the **International Staging System (ISS)**, which relies primarily on two serum markers: **Beta-2 microglobulin (β2M)** and **Serum Albumin** [1]. **Why Beta-2 microglobulin is the correct answer:** β2M is a component of the MHC Class I molecule found on the surface of nucleated cells. In MM, its serum level reflects the **tumor burden** and **renal function**. It is considered the single most important independent prognostic factor. High levels (>5.5 mg/L) indicate a high tumor mass and poor prognosis (ISS Stage III) [1]. **Analysis of Incorrect Options:** * **Bone marrow plasma cell percentage:** While used for diagnosis (≥10% for MM), it does not correlate as accurately with overall survival or prognosis as serum biochemical markers do [1]. * **Serum calcium level:** Hypercalcemia is a feature of the CRAB criteria used for diagnosis and indicates end-organ damage, but it is not a standardized marker for staging or long-term prognosis. * **Beta microglobulin:** This is a distractor term. The specific protein used in clinical practice and staging systems is "Beta-**2** microglobulin." **High-Yield Clinical Pearls for NEET-PG:** * **Revised ISS (R-ISS):** The modern staging system adds **Serum LDH** and **High-risk Cytogenetics** [t(4;14), t(14;16), and del(17p)] to the standard ISS. * **Most common cause of death:** Infection (due to hypogammaglobulinemia), followed by renal failure. * **M-Spike:** Usually IgG (>50%) followed by IgA. * **Best Initial Test:** Skeletal survey (X-rays) to look for punched-out lytic lesions [1]. * **Most Sensitive Imaging:** Whole-body MRI or PET-CT.

Question 28: A patient with bleeding due to platelet function defects typically presents with which of the following features?

A. Normal platelet count and normal bleeding time
B. Normal platelet count and increased bleeding time (Correct Answer)
C. Decreased platelet count and increased bleeding time
D. Normal platelet count and decreased bleeding time

Explanation: ### Explanation **1. Understanding the Core Concept** In hematology, bleeding disorders are broadly categorized into **Primary Hemostasis** defects (platelets and vessel wall) and **Secondary Hemostasis** defects (clotting factors). [1] Platelet function defects (e.g., Glanzmann Thrombasthenia, Bernard-Soulier Syndrome, or aspirin use) fall under primary hemostasis. In these conditions, the **number** of platelets is usually sufficient, but their **ability to aggregate or adhere** is impaired. [2] * **Platelet Count:** Measures quantity (Normal in functional defects). * **Bleeding Time (BT):** Measures the efficiency of the primary platelet plug formation (Prolonged/Increased in functional defects). **2. Analysis of Options** * **Option B (Correct):** Since the defect is qualitative (function) rather than quantitative (number), the count remains normal while the BT increases because the platelets cannot form an effective plug. * **Option A:** This describes a healthy individual or a patient with a mild secondary hemostasis defect (like Hemophilia), where primary hemostasis is intact. * **Option C:** This describes **Thrombocytopenia** (e.g., ITP). While BT is increased here, the primary issue is the low count, not just a functional defect. * **Option D:** A decreased bleeding time is clinically rare and usually suggests a hypercoagulable state; it is never a feature of a bleeding disorder. **3. NEET-PG High-Yield Clinical Pearls** * **Glanzmann Thrombasthenia:** Deficiency of **Gp IIb/IIIa** (Failure of aggregation). * **Bernard-Soulier Syndrome:** Deficiency of **Gp Ib-IX-V** (Failure of adhesion). *Note: This is an exception where you may see mild thrombocytopenia and "Giant Platelets."* [2] * **Drug-induced:** Aspirin causes irreversible inhibition of COX-1, leading to increased BT with a normal count. * **VWD (von Willebrand Disease):** The most common inherited bleeding disorder; presents with increased BT and may have a prolonged aPTT (due to Factor VIII association). [3]

Question 29: A 23-year-old man with hemophilia is recently wheelchair bound. Which of the following best accounts for this development?

A. Hemarthrosis (Correct Answer)
B. Hematemesis
C. Hematocephalus
D. Hematochezia

Explanation: Explanation: 1. Why Hemarthrosis is Correct: Hemophilia (Factor VIII or IX deficiency) is characterized by a bleeding diathesis, primarily affecting deep tissues. Hemarthrosis (bleeding into joint spaces) is the most common clinical manifestation, occurring in up to 80% of patients. Recurrent bleeding into the same joint (target joint) leads to Chronic Hemophilic Arthropathy [1]. This involves synovial hypertrophy, cartilage destruction, and joint fibrosis, eventually causing permanent deformity and loss of mobility [1]. In a young patient, this progression is the leading cause of becoming wheelchair-bound. The knee is the most commonly affected joint, followed by the elbow and ankle [1]. 2. Why Incorrect Options are Wrong: * Hematemesis (B) and Hematochezia (D): While gastrointestinal bleeding can occur in hemophilia, it usually presents as an acute emergency rather than a chronic condition leading to long-term physical disability or immobilization. * Hematocephalus (C): Intracranial hemorrhage is the most common cause of death in hemophiliacs, but it typically presents with acute neurological deficits or sudden mortality rather than progressive orthopedic impairment leading to wheelchair use. 3. Clinical Pearls for NEET-PG: * Most common joint involved: Knee joint [1]. * Earliest sign on X-ray: Soft tissue swelling. * Late X-ray findings: Subchondral cysts, narrowing of joint space, and "squared-off" patella (Jordan's sign). * Management: Acute bleeds require immediate factor replacement (aim for 40-50% levels). Prophylactic factor replacement is the gold standard to prevent arthropathy. * Note: Avoid NSAIDs (except COX-2 inhibitors) and intramuscular injections in these patients.

Question 30: A 74-year-old man presents with fatigue, shortness of breath on exertion, and back and rib pain, which is made worse with movement. Investigations reveal he is anemic, calcium, urea, and creatinine are elevated. X-rays reveal multiple lytic lesions in the long bones and ribs, and protein electrophoresis is positive for an immunoglobulin G (IgG) paraprotein. Which of the following is the most likely mechanism for the renal injury?

A. Plasma cell infiltrates
B. Tubular damage by light chains (Correct Answer)
C. Glomerular injury
D. Vascular injury by light chains

Explanation: ### Explanation **Correct Answer: B. Tubular damage by light chains** The clinical presentation of anemia, bone pain (lytic lesions), hypercalcemia, and renal impairment in an elderly patient is classic for **Multiple Myeloma (MM)** [1]. The presence of an IgG paraprotein (M-spike) confirms the diagnosis. The most common cause of renal failure in MM is **Myeloma Kidney (Cast Nephropathy)**. In this condition, excessive free light chains (Bence-Jones proteins) are filtered by the glomerulus. These light chains are directly toxic to the **proximal tubular epithelium**. Furthermore, they bind with **Tamm-Horsfall protein** in the distal tubules to form large, waxy, intratubular casts that cause obstruction and inflammation. **Analysis of Incorrect Options:** * **A. Plasma cell infiltrates:** While plasma cells infiltrate the bone marrow, they rarely infiltrate the renal parenchyma. Even when present, they are not the primary cause of renal failure. * **C. Glomerular injury:** Although light chains can cause glomerular damage via **AL Amyloidosis** or **Light Chain Deposition Disease (LCDD)**, these typically present with nephrotic-range proteinuria. Cast nephropathy (tubular damage) is the more frequent cause of acute/subacute renal injury in MM. * **D. Vascular injury by light chains:** Light chains do not primarily target the renal vasculature. Renal impairment is predominantly a tubulointerstitial process. **High-Yield Clinical Pearls for NEET-PG:** * **CRAB Criteria for MM:** **C**alcium (elevated), **R**enal insufficiency, **A**nemia, **B**one lesions [2]. * **Bence-Jones Proteins:** These are light chains that precipitate at 40–60°C and redissolve on boiling. They are **not** detected by standard urine dipsticks (which detect albumin). * **Diagnosis:** Bone marrow biopsy showing **>10% clonal plasma cells** is the gold standard. * **Peripheral Smear:** Characterized by **Rouleaux formation** due to high protein levels decreasing the zeta potential of RBCs.

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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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