Hematology — MCQs
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Which chromosomal abnormality is associated with a good prognosis in multiple myeloma?
A 20-year-old female presented with complaints of easy bruising, frequent episodes of nose bleed, menorrhagia, and few episodes of upper gastrointestinal bleeding. On examination, purpura and petechial rash were noted. Laboratory findings revealed thrombocytopenia, normal prothrombin time (PT), and normal activated partial thromboplastin time (aPTT). Platelets do not aggregate in response to ristocetin after adding normal plasma, but have normal aggregation in response to adenosine diphosphate, epinephrine, and collagen. Platelet granules are normal. What is the most likely diagnosis in the above patient?
A 58-year-old woman presents with a six-month history of backache and recurrent chest infections. She develops sudden leg weakness and urinary retention. Investigations reveal a hemoglobin of 7.3 gm/dL, serum calcium of 12.6 mg/dL, phosphate of 2.5 mg/dL, alkaline phosphatase of 100 U/L, serum albumin of 3 gm/dL, globulin of 7.1 gm/dL, and urea of 178 mg/dL. What is the most likely diagnosis?
Autosplenectomy is a feature of which of the following conditions?
Priapism can be due to which of the following conditions?
A 30-year-old epileptic female on phenytoin presents with weakness and fatigue. Blood examination reveals Hb = 4.6 gm/dL, MCV = 102 fL, and MCH = 40 pg/dL. What is the most probable diagnosis?
Hemoptysis can be seen in which of the following conditions?
A 30-year-old female presents with mucosal bleeding upon minor trauma and a history of menorrhagia. Both bleeding time and prothrombin time are elevated. The ristocetin assay is positive. What is the most likely diagnosis?
All of the following are X-linked except?
Which of the following is absent in hemolytic anemia?
Hematology Indian Medical PG Practice Questions and MCQs
Question 271: Which chromosomal abnormality is associated with a good prognosis in multiple myeloma?
- A. t(11;14) (Correct Answer)
- B. deletion of 13q
- C. del 17p
- D. t(14;16)
Explanation: **Explanation:** In Multiple Myeloma (MM), cytogenetic abnormalities are the most significant predictors of clinical outcome and are used to risk-stratify patients into standard, intermediate, and high-risk categories. **1. Why t(11;14) is the Correct Answer:** The translocation **t(11;14)(q13;q32)** involves the fusion of the *CCND1* (Cyclin D1) gene with the immunoglobulin heavy chain (*IgH*) locus. This abnormality is found in approximately 15–20% of MM patients. It is considered a **standard-risk** (favorable) marker associated with improved progression-free survival and overall survival compared to other translocations. Interestingly, this translocation is also the hallmark of Mantle Cell Lymphoma. **2. Analysis of Incorrect Options:** * **del 17p (Option C):** This involves the loss of the **TP53 tumor suppressor gene**. It is considered the most significant **high-risk** genetic marker in MM, associated with aggressive disease, extramedullary involvement, and poor response to standard therapy. * **t(14;16) (Option D):** This translocation involves the *MAF* gene. It is categorized as a **high-risk** cytogenetic abnormality. * **deletion of 13q (Option B):** Historically considered a poor prognostic factor when detected by conventional metaphase cytogenetics, it is often associated with other high-risk features. It is not a "good" prognostic marker. **High-Yield Clinical Pearls for NEET-PG:** * **Standard Risk (Good Prognosis):** t(11;14), t(6;14), and hyperdiploidy. * **High Risk (Poor Prognosis):** del 17p, t(14;16), t(14;20), and Gain 1q. * **Gold Standard Investigation:** Interphase **FISH** (Fluorescence In Situ Hybridization) on bone marrow aspirate is the preferred method for detecting these abnormalities. * **Revised ISS (R-ISS):** Prognosis in MM is currently determined by combining Serum Albumin, Beta-2 Microglobulin, LDH, and high-risk cytogenetics [1]. **Prognosis and Staging:** The International Staging System (ISS) identifies prognostic features including beta-2 microglobulin and albumin levels [1].
Question 272: A 20-year-old female presented with complaints of easy bruising, frequent episodes of nose bleed, menorrhagia, and few episodes of upper gastrointestinal bleeding. On examination, purpura and petechial rash were noted. Laboratory findings revealed thrombocytopenia, normal prothrombin time (PT), and normal activated partial thromboplastin time (aPTT). Platelets do not aggregate in response to ristocetin after adding normal plasma, but have normal aggregation in response to adenosine diphosphate, epinephrine, and collagen. Platelet granules are normal. What is the most likely diagnosis in the above patient?
- A. Bernard-Soulier syndrome (Correct Answer)
- B. Platelet function disorder
- C. Wiskott-Aldrich syndrome
- D. Glanzmann thrombasthenia
Explanation: **Explanation:** The clinical presentation of mucosal bleeding (epistaxis, menorrhagia, GI bleed) and petechiae in a young patient suggests a **disorder of primary hemostasis** [1]. **1. Why Bernard-Soulier Syndrome (BSS) is correct:** BSS is caused by a deficiency or dysfunction of the **GPIb-IX-V receptor** complex on the platelet surface [3]. This receptor is essential for platelet adhesion to the subendothelial von Willebrand factor (vWF). * **Key Diagnostic Feature:** Platelets fail to aggregate with **Ristocetin**. Crucially, unlike von Willebrand Disease (vWD), this defect **cannot be corrected** by adding normal plasma (which contains vWF) because the defect lies in the platelet receptor itself, not the plasma factor. * **Laboratory Findings:** Characterized by **thrombocytopenia** and **Giant Platelets** (though not explicitly mentioned here, it is a hallmark) [2]. PT and aPTT remain normal as secondary hemostasis is intact. **2. Why incorrect options are wrong:** * **Glanzmann Thrombasthenia:** Caused by a deficiency of **GPIIb/IIIa** [3]. While it presents with similar bleeding, aggregation is **absent** with ADP, epinephrine, and collagen, but **normal** with Ristocetin (the exact opposite of this case). * **Wiskott-Aldrich Syndrome:** An X-linked recessive disorder characterized by the triad of eczema, immunodeficiency, and thrombocytopenia with **micro-platelets** (small platelets) [2]. * **Platelet Function Disorder:** This is a broad category; the specific Ristocetin pattern provided points specifically to BSS. **Clinical Pearls for NEET-PG:** * **BSS:** Giant Platelets + Thrombocytopenia + No aggregation with Ristocetin (not corrected by plasma). * **vWD:** Normal Platelet count + No aggregation with Ristocetin (**Corrected** by adding normal plasma) [4]. * **Glanzmann:** Normal Platelet count + No aggregation with ADP/Collagen/Epinephrine.
Question 273: A 58-year-old woman presents with a six-month history of backache and recurrent chest infections. She develops sudden leg weakness and urinary retention. Investigations reveal a hemoglobin of 7.3 gm/dL, serum calcium of 12.6 mg/dL, phosphate of 2.5 mg/dL, alkaline phosphatase of 100 U/L, serum albumin of 3 gm/dL, globulin of 7.1 gm/dL, and urea of 178 mg/dL. What is the most likely diagnosis?
- A. Lung cancer
- B. Disseminated tuberculosis
- C. Multiple myeloma (Correct Answer)
- D. Osteoporosis
Explanation: ### **Explanation** The clinical presentation and laboratory findings are classic for **Multiple Myeloma (MM)**, a plasma cell dyscrasia characterized by the neoplastic proliferation of a single clone of plasma cells [1]. **Why Multiple Myeloma is the Correct Answer:** The patient exhibits the classic **CRAB** features: * **C (Calcium elevation):** Serum calcium is 12.6 mg/dL (Hypercalcemia). * **R (Renal insufficiency):** Urea is significantly elevated (178 mg/dL), indicating "Myeloma Kidney." * **A (Anemia):** Hemoglobin is 7.3 gm/dL (Normocytic normochromic anemia) [1]. * **B (Bone lesions/Backache):** The history of backache and sudden leg weakness/urinary retention suggests a **pathological vertebral fracture** leading to **spinal cord compression**, a common emergency in MM [1]. * **Hyperglobulinemia:** The "Albumin-Globulin (A:G) ratio reversal" (Albumin 3, Globulin 7.1) indicates a massive production of monoclonal immunoglobulins (M-protein) [1]. * **Recurrent Infections:** Due to functional hypogammaglobulinemia (loss of normal antibody diversity). * **Normal Alkaline Phosphatase (ALP):** In MM, bone lesions are purely **osteolytic** (mediated by RANKL); since there is no osteoblastic activity, ALP remains normal—a key differentiator from bone metastases. **Why Other Options are Incorrect:** * **Lung Cancer:** While it can cause hypercalcemia (PTHrP) and bone metastasis [2], it usually presents with elevated ALP and would not typically cause such a profound reversal of the A:G ratio. * **Disseminated Tuberculosis:** Can cause back pain (Pott’s spine) and anemia, but it does not cause significant hypercalcemia or the massive hyperglobulinemia seen here. * **Osteoporosis:** Causes fractures and back pain [2] in elderly women, but laboratory parameters (Calcium, Urea, Globulin) remain normal. **NEET-PG High-Yield Pearls:** 1. **M-Spike:** Seen on Serum Protein Electrophoresis (SPEP). 2. **Bence-Jones Proteins:** Free light chains in urine (detected by sulfosalicylic acid test, not dipstick). 3. **Peripheral Smear:** Shows **Rouleaux formation** due to high globulin levels. 4. **Bone Marrow:** Presence of >10% clonal plasma cells (Fried-egg appearance). 5. **Imaging:** X-rays show "punched-out" lytic lesions [1]. **Note:** Bone scans are often negative as they detect osteoblastic activity.
Question 274: Autosplenectomy is a feature of which of the following conditions?
- A. Beta thalassemia
- B. Sickle cell disease (Correct Answer)
- C. G6PD deficiency
- D. All of the above
Explanation: **Explanation:** **1. Why Sickle Cell Disease (SCD) is correct:** Autosplenectomy is a hallmark of **Sickle Cell Anemia (HbSS)**. The underlying mechanism involves the repeated sickling of red blood cells in the hypoxic, acidic, and slow-flow environment of the splenic sinusoids [1]. These rigid, sickle-shaped cells cause microvascular occlusion (vaso-occlusion), leading to recurrent **splenic infarctions**. Over time, the splenic tissue is replaced by fibrous scar tissue, causing the spleen to shrink and become non-functional (fibrotic nubbin) [1]. This process is usually complete by age 5–8 in HbSS patients. **2. Why other options are incorrect:** * **Beta Thalassemia:** Unlike SCD, Beta Thalassemia typically presents with **massive splenomegaly**. This occurs due to extramedullary hematopoiesis and the constant clearance of abnormal RBCs (excess alpha chains) by the splenic macrophages. * **G6PD Deficiency:** This condition presents as episodic hemolysis triggered by oxidative stress (e.g., fava beans, drugs). It does not cause chronic vaso-occlusion or splenic infarction; therefore, the spleen size usually remains normal or slightly enlarged during acute episodes. **3. Clinical Pearls for NEET-PG:** * **Howell-Jolly Bodies:** The presence of these nuclear remnants on a peripheral smear is a classic sign of functional asplenia/autosplenectomy. * **Infection Risk:** Autosplenectomy increases susceptibility to **encapsulated organisms** (*S. pneumoniae, H. influenzae, N. meningitidis*). Prophylactic penicillin and vaccinations are mandatory. * **SCD vs. SC Disease:** While HbSS leads to autosplenectomy early, patients with **HbSC disease** or Sickle-Thalassemia may maintain an enlarged spleen into adulthood. * **Radiology:** On X-ray or CT, an autosplenectomized spleen may appear as a small, shrunken, and sometimes **calcified** mass in the left upper quadrant.
Question 275: Priapism can be due to which of the following conditions?
- A. Chronic Myeloid Leukemia (CML) (Correct Answer)
- B. Myelofibrosis
- C. Autoimmune Hemolytic Anemia (AIHA)
- D. Thrombocytopenia
Explanation: **Explanation:** **1. Why Chronic Myeloid Leukemia (CML) is correct:** Priapism (a prolonged, painful erection lasting >4 hours) is a known complication of CML, occurring in approximately 1–5% of male patients. The underlying mechanism is **Hyperleukocytosis** (Leukostasis). In CML, the massive elevation of the White Blood Cell (WBC) count—often exceeding 100,000/µL—increases blood viscosity. This leads to the sludging of leukemic cells within the *corpora cavernosa*, obstructing venous outflow and resulting in an ischemic, low-flow state. **2. Why the other options are incorrect:** * **Myelofibrosis:** While it is a myeloproliferative neoplasm, it is characterized by bone marrow fibrosis and cytopenias (or modest leukocytosis) rather than the extreme hyperleukocytosis seen in CML. Thus, it rarely causes leukostasis-induced priapism. * **Autoimmune Hemolytic Anemia (AIHA):** This involves the destruction of RBCs by antibodies. While Sickle Cell Anemia is a classic cause of priapism (due to sickled RBCs obstructing flow), AIHA does not cause the mechanical vascular obstruction required to trigger priapism. * **Thrombocytopenia:** A low platelet count leads to bleeding tendencies (epistaxis, petechiae), not the thrombotic or obstructive events that cause priapism. **Clinical Pearls for NEET-PG:** * **High-Yield Association:** Priapism is most commonly associated with **CML** among leukemias and **Sickle Cell Anemia** among hemoglobinopathies. * **Management:** In CML-induced priapism, the priority is reducing the WBC count via **Leukapheresis** and cytoreduction (e.g., Hydroxyurea) [1], alongside local urological intervention (aspiration/shunts). * **Leukostasis triad:** Often presents with CNS symptoms (headache/confusion), Respiratory distress (hypoxemia), and Priapism.
Question 276: A 30-year-old epileptic female on phenytoin presents with weakness and fatigue. Blood examination reveals Hb = 4.6 gm/dL, MCV = 102 fL, and MCH = 40 pg/dL. What is the most probable diagnosis?
- A. Heart failure
- B. Iron deficiency anemia
- C. Phenytoin-induced agranulocytosis
- D. Megaloblastic anemia (Correct Answer)
Explanation: **Explanation:** The clinical presentation and laboratory findings point directly to **Megaloblastic Anemia**. [1] **1. Why the correct answer is right:** The patient has severe anemia (Hb 4.6 g/dL) with an elevated **Mean Corpuscular Volume (MCV = 102 fL)** and **Mean Corpuscular Hemoglobin (MCH = 40 pg/dL)**. An MCV >100 fL indicates **macrocytic anemia**. Phenytoin is a well-known cause of folate deficiency because it interferes with intestinal folate absorption and increases its catabolism. [1] Folate deficiency impairs DNA synthesis, leading to the characteristic "megaloblastic" changes in the bone marrow and macrocytosis in the peripheral blood. **2. Why the incorrect options are wrong:** * **A. Heart failure:** While severe anemia can lead to high-output heart failure, it is a complication, not the primary diagnosis for the hematological findings. [2] * **B. Iron deficiency anemia:** This typically presents as **microcytic hypochromic** anemia (MCV <80 fL, MCH <27 pg), which contradicts the macrocytosis seen here. [2] * **C. Phenytoin-induced agranulocytosis:** This refers to a severe reduction in white blood cell counts (neutrophils), not a macrocytic reduction in hemoglobin. **3. NEET-PG High-Yield Pearls:** * **Drug-induced Megaloblastic Anemia:** Common culprits include **Phenytoin**, Methotrexate, Trimethoprim, and Zidovudine. [1] * **Peripheral Smear:** Look for **hypersegmented neutrophils** (≥ 5 lobes) as the earliest sign of megaloblastic changes. * **Phenytoin Side Effects (Mnemonic: PHENYTOIN):** **P**-P450 inducer, **H**-Hyperplasia of gums, **E**-Erythroblasts (Megaloblastic anemia), **N**-Neuropathy, **Y**-Yellow-brown skin (pigmentation), **T**-Teratogenicity (Fetal Hydantoin Syndrome), **O**-Osteomalacia, **I**-Interference with B12/Folate, **N**-Nystagmus.
Question 277: Hemoptysis can be seen in which of the following conditions?
- A. Leukemia
- B. Hemophilia
- C. Anticoagulant therapy
- D. All of the above (Correct Answer)
Explanation: Hemoptysis (expectoration of blood from the lower respiratory tract) occurs when there is a disruption of the pulmonary or bronchial vasculature [1]. In the context of hematological disorders, this is typically due to **coagulopathy** or **thrombocytopenia**, leading to alveolar hemorrhage or mucosal bleeding [3]. * **Leukemia (Option A):** Patients with leukemia can develop hemoptysis through multiple mechanisms: severe thrombocytopenia (low platelet count), secondary infections (like invasive Aspergillosis which erodes vessels), or leukostasis in the pulmonary microvasculature. * **Hemophilia (Option B):** While hemophilia primarily presents with hemarthrosis (joint bleeds), any severe deficiency in clotting factors (Factor VIII or IX) can lead to spontaneous or trauma-induced bleeding in the pulmonary parenchyma or bronchial tree [3]. * **Anticoagulant Therapy (Option C):** Drugs like Warfarin, Heparin, or DOACs increase the bleeding diathesis. Over-anticoagulation (high INR) is a well-recognized cause of diffuse alveolar hemorrhage (DAH) and hemoptysis [2]. Since all three conditions impair the body's ability to maintain hemostasis, they can all manifest with hemoptysis. Therefore, **Option D** is correct. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause of hemoptysis in India:** Tuberculosis. * **Most common cause of massive hemoptysis:** Bronchiectasis (due to hypertrophied bronchial arteries) [1]. * **Definition of Massive Hemoptysis:** Usually defined as >200–600 mL of blood within 24 hours. * **Diagnostic Gold Standard:** CT Angiography is preferred for localizing the site, while Bronchoscopy is used for real-time visualization.
Question 278: A 30-year-old female presents with mucosal bleeding upon minor trauma and a history of menorrhagia. Both bleeding time and prothrombin time are elevated. The ristocetin assay is positive. What is the most likely diagnosis?
- A. Immune thrombocytopenic purpura (ITP)
- B. Hemophilia A
- C. Hemophilia B
- D. Von Willebrand disease (Correct Answer)
Explanation: The correct answer is **Von Willebrand Disease (vWD)**. **1. Why Von Willebrand Disease is correct:** vWD is the most common inherited bleeding disorder. Von Willebrand Factor (vWF) has two primary roles: it acts as a bridge for platelet adhesion to subendothelial collagen (via GpIb) and serves as a carrier protein to stabilize **Factor VIII** [1]. * **Bleeding Time (BT):** Elevated because deficient vWF impairs primary hemostasis (platelet plug formation) [3]. * **Prothrombin Time (PT) / aPTT:** While the question mentions elevated PT, in classic vWD, the **aPTT** is more commonly prolonged due to low Factor VIII levels [1]. However, mucosal bleeding and a **positive Ristocetin assay** (which induces vWF-mediated platelet agglutination) are pathognomonic for vWD [1]. [2] **2. Why the other options are incorrect:** * **ITP (Option A):** Characterized by isolated thrombocytopenia. While BT is increased, PT and aPTT are strictly normal. * **Hemophilia A & B (Options B & C):** These are X-linked recessive disorders affecting the intrinsic pathway (Factor VIII and IX respectively). They typically present with deep-seated bleeds (hemarthrosis) rather than mucosal bleeding. In Hemophilia, BT is normal because platelet function is unaffected. **3. NEET-PG High-Yield Pearls:** * **Most common type:** Type 1 (Quantitative deficiency; Autosomal Dominant). * **Ristocetin Cofactor Activity:** The gold standard diagnostic test [1]. * **Treatment of choice:** **Desmopressin (DDAVP)**, which releases stored vWF from Weibel-Palade bodies in endothelial cells [1]. * **Clinical Clue:** Always suspect vWD in a female with menorrhagia and a normal platelet count but prolonged bleeding time [2].
Question 279: All of the following are X-linked except?
- A. G6PD deficiency
- B. Hemophilia A
- C. Von Willebrand's disease (Correct Answer)
- D. Fragile X syndrome
Explanation: **Explanation:** The correct answer is **Von Willebrand's disease (vWD)** because it is primarily an **autosomal dominant** disorder (Type 1 and 2) or autosomal recessive (Type 3). The gene for Von Willebrand Factor (vWF) is located on **chromosome 12**, not on a sex chromosome. **Analysis of Options:** * **Von Willebrand's Disease (vWD):** As the most common inherited bleeding disorder, it affects both males and females equally due to its autosomal inheritance [1]. It is characterized by a deficiency or dysfunction of vWF, leading to impaired platelet adhesion and a secondary decrease in Factor VIII levels [1]. * **G6PD Deficiency:** This is a classic **X-linked recessive** enzymopathy. It primarily affects males, leading to episodic hemolytic anemia triggered by oxidative stress (e.g., fava beans, infections, or drugs like Primaquine). * **Hemophilia A:** This is an **X-linked recessive** deficiency of Factor VIII [2]. It is the most common "true" hemophilia, characterized by deep tissue bleeds and hemarthrosis. * **Fragile X Syndrome:** This is an **X-linked dominant** condition (with variable expressivity) caused by a CGG trinucleotide repeat expansion in the *FMR1* gene. It is the most common inherited cause of intellectual disability. **NEET-PG High-Yield Pearls:** * **Inheritance Shortcut:** Most enzyme deficiencies are Autosomal Recessive, but **G6PD deficiency** and **Hunter Syndrome** are notable X-linked exceptions. * **vWD vs. Hemophilia:** In vWD, the **Bleeding Time (BT)** is prolonged, whereas in Hemophilia, the BT is normal. Both may show a prolonged **aPTT** (due to low Factor VIII). * **Ristocetin Cofactor Assay:** This is the gold standard diagnostic test for vWD; it measures vWF-mediated platelet agglutination.
Question 280: Which of the following is absent in hemolytic anemia?
- A. Increased indirect bilirubin
- B. Jaundice
- C. Increased reticulocyte count
- D. Increased hematocrit (Correct Answer)
Explanation: Hemolytic anemia is characterized by the premature destruction of red blood cells (RBCs). The core pathophysiology involves a decrease in the total RBC mass, which leads to a **decreased hematocrit** and hemoglobin level. Therefore, an **increased hematocrit (Option D)** is physiologically impossible in anemia and is the correct answer. **Analysis of Options:** * **Increased indirect bilirubin (Option A):** When RBCs break down, heme is converted into unconjugated (indirect) bilirubin. * **Jaundice (Option B):** This is a clinical manifestation of increased indirect bilirubin [1]. It is a classic feature of hemolytic anemia, often described as "acholuric jaundice" (no bilirubin in urine). * **Increased reticulocyte count (Option C):** This represents the bone marrow's compensatory response to anemia. Erythropoietin levels rise, stimulating the marrow to release immature RBCs (reticulocytes) into the peripheral blood. **NEET-PG High-Yield Pearls:** 1. **Markers of Hemolysis:** Increased LDH (most sensitive), increased indirect bilirubin, and **decreased Serum Haptoglobin** (haptoglobin binds free hemoglobin). 2. **Intravascular vs. Extravascular:** Hemoglobinuria and hemosiderinuria are specific to *intravascular* hemolysis (e.g., G6PD deficiency, PNH) [2]. 3. **Peripheral Smear:** Look for **Schistocytes** (fragmented cells) in microangiopathic hemolytic anemia (TTP/HUS) and **Spherocytes** in Hereditary Spherocytosis or AIHA. 4. **Corrected Reticulocyte Count (CRC):** In anemia, always calculate the CRC to determine if the marrow response is adequate (>2% suggests hemolysis or acute blood loss).
Practice by Chapter
Anemia Evaluation and Management
Practice Questions
Hemoglobinopathies
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Thalassemias
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Platelet Disorders
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Coagulation Disorders
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Thrombotic Disorders
Practice Questions
Leukemias
Practice Questions
Lymphomas
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Multiple Myeloma and Plasma Cell Disorders
Practice Questions
Myeloproliferative Neoplasms
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Transfusion Medicine
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Hematopoietic Stem Cell Transplantation
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