Hematology — MCQs
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Coomb's positive hemolytic anemia is seen in all except?
Which of the following causes neutrophilia?
Which antibody class is primarily involved in Idiopathic Thrombocytopenic Purpura (ITP)?
A 60-year-old man presented with fatigue, weight loss, and heaviness in the left hypochondrium for 6 months. The hemogram showed Hb 10 g/dL, TLC 5 lakhs/mm³, platelet count 4 lakhs/mm³, DLC: neutrophils 55%, lymphocytes 4%, monocytes 2%, basophils 6%, metamyelocytes 10%, myelocytes 18%, promyelocytes 2%, and blasts 3%. What is the most likely cytogenetic abnormality in this case?
A 19-year-old man presents with a swollen and painful knee after an injury while playing football. He has no history of bleeding disorders. Arthrocentesis of the knee revealed hemarthrosis. Investigations show: Platelets 170,000/mL, PT normal, PTT elevated, bleeding time normal, factor VIII normal, factor IX reduced, and ristocetin cofactor assay normal. What is the most likely diagnosis for this patient's bleeding disorder?
Evans syndrome refers to the presence of which of the following hematologic changes?
The Donath-Landsteiner phenomenon is characteristic of which condition?
A 26-year-old woman presents with severe menorrhagia. She reports that both her father and sister have a bleeding disorder. What is the most likely diagnosis, given an autosomal-dominant mode of inheritance for the hemostatic disorder?
Which of the following is NOT a feature seen in hemolytic anemia?
Which of the following is the least common feature of Multiple Myeloma?
Hematology Indian Medical PG Practice Questions and MCQs
Question 381: Coomb's positive hemolytic anemia is seen in all except?
- A. Alcoholic cirrhosis (Correct Answer)
- B. Chronic active hepatitis
- C. Primary biliary cirrhosis
- D. Primary sclerosing cholangitis
Explanation: The Coombs test (Antiglobulin test) detects antibodies or complement proteins attached to the surface of red blood cells. A positive result indicates **Autoimmune Hemolytic Anemia (AIHA)** [1]. **1. Why Alcoholic Cirrhosis is the correct answer:** Hemolytic anemia in alcoholic cirrhosis is typically **Coombs-negative**. It is primarily caused by **Zieve’s Syndrome** (triad of alcohol consumption, hemolytic anemia, and hyperlipidemia) or **Spur Cell Anemia**. In these cases, hemolysis occurs due to metabolic disturbances and changes in the RBC membrane lipid composition (acanthocytosis), leading to splenic sequestration, rather than an antibody-mediated process. **2. Why the other options are incorrect:** * **Chronic Active Hepatitis (Autoimmune Hepatitis):** This is a classic autoimmune condition frequently associated with other systemic autoimmune phenomena, including Warm-type AIHA (Coombs positive) [1]. * **Primary Biliary Cholangitis (PBC) & Primary Sclerosing Cholangitis (PSC):** Both are chronic cholestatic liver diseases with an underlying autoimmune pathophysiology. They are known to be associated with various extrahepatic autoimmune disorders, including AIHA, making them Coombs positive. **Clinical Pearls for NEET-PG:** * **Warm AIHA (IgG):** Associated with SLE, CLL, and drugs like α-methyldopa [1]. * **Cold AIHA (IgM):** Associated with *Mycoplasma pneumoniae* and Infectious Mononucleosis [1] [2]. * **Spur Cell Anemia:** A poor prognostic sign in end-stage liver disease; it is non-immune (Coombs negative). * **Zieve’s Syndrome:** Characterized by rapid improvement in hemolysis upon alcohol cessation.
Question 382: Which of the following causes neutrophilia?
- A. Epinephrine
- B. Glucocorticoids (Correct Answer)
- C. NSAIDs
- D. Clozapine
Explanation: No relevant citations found in the provided sources. Glucocorticoids cause neutrophilia primarily through a process called demargination. Under normal conditions, a significant portion of neutrophils (the "marginal pool") adheres to the vascular endothelium. Glucocorticoids decrease the expression of adhesion molecules (like L-selectin), causing these neutrophils to detach and enter the circulating pool. Additionally, steroids stimulate the release of mature neutrophils from the bone marrow and inhibit their migration into peripheral tissues (extravasation). **Analysis of Options:** * **A. Epinephrine:** While epinephrine can cause a transient, rapid increase in neutrophil count via demargination (due to increased cardiac output and blood flow), **Glucocorticoids** are the classic, more sustained pharmacological cause of neutrophilia frequently tested in exams. * **C. NSAIDs:** These are generally not associated with neutrophilia. In rare idiosyncratic cases, some NSAIDs (like Phenylbutazone) are actually associated with agranulocytosis (decreased counts). * **D. Clozapine:** This is a high-yield cause of **agranulocytosis** (severe neutropenia). Patients on Clozapine require mandatory serial monitoring of Absolute Neutrophil Counts (ANC). **High-Yield Clinical Pearls for NEET-PG:** * **Steroid-Induced Leucocytosis:** While steroids increase neutrophils, they **decrease** the counts of Eosinophils, Monocytes, and Lymphocytes ("Steroids sweep the EML away"). * **Left Shift:** Neutrophilia due to infection usually shows a "left shift" (increased band cells/immature forms), whereas steroid-induced neutrophilia typically involves mature neutrophils. * **Other causes of Neutrophilia:** Acute bacterial infections, tissue necrosis (MI, burns), and Lithium therapy. *Note: While the provided references describe the physiology of neutrophils and glucocorticoid secretion, they do not explicitly detail the mechanism of demargination for this specific question.*
Question 383: Which antibody class is primarily involved in Idiopathic Thrombocytopenic Purpura (ITP)?
- A. IgG (Correct Answer)
- B. IgM
- C. IgE
- D. IgD
Explanation: **Explanation:** **Idiopathic Thrombocytopenic Purpura (ITP)**, now more commonly referred to as Immune Thrombocytopenic Purpura, is an acquired autoimmune disorder characterized by isolated thrombocytopenia [2]. **Why IgG is Correct:** The pathogenesis of ITP involves the production of **autoantibodies (predominantly of the IgG class)** directed against platelet surface antigens, most commonly the **GPIIb/IIIa** or **GPIb/IX** complexes. These IgG-coated platelets are recognized by the Fc receptors on splenic macrophages, leading to their premature sequestration and destruction in the **spleen**. **Why other options are incorrect:** * **IgM:** While IgM is the first antibody produced in a primary immune response and is involved in Cold Agglutinin Disease [1], it is not the primary mediator of platelet destruction in ITP. * **IgE:** This antibody class is associated with Type I hypersensitivity reactions (allergies, asthma) and parasitic infections, not autoimmune platelet destruction [2]. * **IgD:** Found on the surface of B-cells, its precise physiological function is less defined, but it plays no role in the pathogenesis of ITP. **High-Yield Clinical Pearls for NEET-PG:** * **Site of Destruction:** The **Spleen** is the primary site of both antibody production and platelet destruction in ITP. * **Bone Marrow Findings:** Characterized by **increased or normal megakaryocytes** (a compensatory response to peripheral destruction). * **First-line Treatment:** Corticosteroids (e.g., Prednisolone). In emergencies or prior to surgery, IVIG (Intravenous Immunoglobulin) is used to "clog" splenic Fc receptors [3]. * **Splenectomy:** Indicated in chronic/refractory cases as it removes the primary site of destruction.
Question 384: A 60-year-old man presented with fatigue, weight loss, and heaviness in the left hypochondrium for 6 months. The hemogram showed Hb 10 g/dL, TLC 5 lakhs/mm³, platelet count 4 lakhs/mm³, DLC: neutrophils 55%, lymphocytes 4%, monocytes 2%, basophils 6%, metamyelocytes 10%, myelocytes 18%, promyelocytes 2%, and blasts 3%. What is the most likely cytogenetic abnormality in this case?
- A. t(1;21)
- B. t(9;22) (Correct Answer)
- C. t(15;17)
- D. Trisomy 21
Explanation: ### Explanation **Diagnosis: Chronic Myeloid Leukemia (CML)** The clinical presentation of a 60-year-old male with massive splenomegaly (heaviness in the left hypochondrium) and a massive leukocytosis (TLC 5 lakhs/mm³) is classic for CML [2]. The differential leukocyte count (DLC) shows a **"myelocyte bulge"** (predominance of myelocytes and metamyelocytes) and **basophilia (6%)**, which are hallmark features of CML in the chronic phase. **1. Why t(9;22) is correct:** The cytogenetic hallmark of CML is the **Philadelphia (Ph) chromosome**, resulting from a reciprocal translocation between chromosomes 9 and 22, **t(9;22)(q34;q11)** [2]. This creates the *BCR-ABL1* fusion gene, which encodes a constitutive tyrosine kinase responsible for uncontrolled myeloid proliferation [2]. **2. Why the other options are incorrect:** * **t(1;21):** This is not a standard translocation associated with common leukemias. * **t(15;17):** This is the characteristic translocation for **Acute Promyelocytic Leukemia (APL - AML M3)**, involving the *PML-RARA* fusion [1]. Patients typically present with DIC and a high percentage of promyelocytes with Auer rods. * **Trisomy 21:** Associated with Down Syndrome, which carries an increased risk of **Acute Megakaryoblastic Leukemia (AML M7)** and Transient Myeloproliferative Disorder (TMD) in neonates. **Clinical Pearls for NEET-PG:** * **LAP Score:** Leukocyte Alkaline Phosphatase (LAP) score is characteristically **decreased** in CML (helps differentiate it from a Leukemoid reaction where it is increased). * **Basophilia:** The presence of increased basophils in a peripheral smear is a strong clue for a Myeloproliferative Neoplasm (MPN), specifically CML. * **Treatment of Choice:** Tyrosine Kinase Inhibitors (TKIs) like **Imatinib** [2]. * **Blast Crisis:** Defined as ≥20% blasts in blood or bone marrow.
Question 385: A 19-year-old man presents with a swollen and painful knee after an injury while playing football. He has no history of bleeding disorders. Arthrocentesis of the knee revealed hemarthrosis. Investigations show: Platelets 170,000/mL, PT normal, PTT elevated, bleeding time normal, factor VIII normal, factor IX reduced, and ristocetin cofactor assay normal. What is the most likely diagnosis for this patient's bleeding disorder?
- A. von Willebrand disease
- B. hemophilia A
- C. hemophilia B (Correct Answer)
- D. thrombotic thrombocytopenic purpura (TTP)
Explanation: The clinical presentation of a young male with **hemarthrosis** (bleeding into joints) following minor trauma is a classic hallmark of a coagulation factor deficiency [1]. **1. Why Hemophilia B is correct:** The laboratory profile provided is the key to the diagnosis: * **Elevated PTT (aPTT):** Indicates a defect in the intrinsic pathway (Factors VIII, IX, XI, or XII). * **Normal PT and Bleeding Time:** Rules out extrinsic pathway defects and platelet/vessel wall disorders [1]. * **Factor IX reduced:** This is the definitive finding. Hemophilia B (Christmas Disease) is an X-linked recessive disorder caused by a deficiency of Factor IX [1]. **2. Why other options are incorrect:** * **von Willebrand Disease (vWD):** While it can cause an elevated aPTT (due to low Factor VIII), it typically presents with mucosal bleeding (epistaxis, menorrhagia) and an **abnormal Ristocetin Cofactor Assay**. Hemarthrosis is rare except in Type 3 vWD [2]. * **Hemophilia A:** This also presents with hemarthrosis and elevated aPTT, but it is caused by a deficiency of **Factor VIII**. The question explicitly states Factor VIII levels are normal [1]. * **Thrombotic Thrombocytopenic Purpura (TTP):** This is a microangiopathic hemolytic anemia characterized by the pentad of fever, anemia, thrombocytopenia, renal failure, and neurological symptoms. It would show a **low platelet count**, which is normal in this patient. **Clinical Pearls for NEET-PG:** * **Inheritance:** Both Hemophilia A and B are **X-linked recessive** (affecting males) [1]. * **Mixing Study:** If aPTT is prolonged, a mixing study is done. If it corrects, it indicates a factor deficiency; if not, it suggests an inhibitor. * **Treatment:** Hemophilia B is treated with recombinant Factor IX concentrate. Fresh Frozen Plasma (FFP) is used if specific concentrates are unavailable.
Question 386: Evans syndrome refers to the presence of which of the following hematologic changes?
- A. Autoimmune thrombocytopenia in autoimmune hemolytic anemia (Correct Answer)
- B. Disseminated intravascular coagulation in autoimmune hemolytic anemia
- C. Thrombocytopenia in hairy cell leukemia
- D. Thrombocytosis in autoimmune hemolytic anemia
Explanation: **Explanation:** **Evans Syndrome** is a rare autoimmune disorder characterized by the simultaneous or sequential development of **Autoimmune Hemolytic Anemia (AIHA)** and **Immune Thrombocytopenic Purpura (ITP)** [1]. In some cases, autoimmune neutropenia may also be present. 1. **Why Option A is Correct:** The pathophysiology involves the production of autoantibodies (usually IgG) directed against antigens on both red blood cells and platelets [1]. This leads to their premature destruction in the spleen. It is often associated with underlying conditions like SLE, CLL, or Primary Immunodeficiency (e.g., CVID) [1]. 2. **Why the Other Options are Incorrect:** * **Option B:** DIC involves a consumptive coagulopathy with low fibrinogen and elevated D-dimer, triggered by systemic inflammation or sepsis, not a primary autoimmune attack on RBCs and platelets [1]. * **Option C:** Thrombocytopenia in Hairy Cell Leukemia is typically due to bone marrow infiltration and hypersplenism, not an isolated autoimmune mechanism. * **Option D:** Evans syndrome is defined by a *deficiency* (thrombocytopenia), not an excess (thrombocytosis). **High-Yield Clinical Pearls for NEET-PG:** * **Coombs Test:** The Direct Antiglobulin Test (DAT) is typically **positive** (usually for IgG) [1]. * **Treatment:** First-line therapy is **Corticosteroids**. Refractory cases may require Rituximab, IVIG, or Splenectomy. * **Key Association:** Always screen patients with Evans Syndrome for **Systemic Lupus Erythematosus (SLE)**, as it is a common secondary cause [1]. * **Peripheral Smear:** Look for **Spherocytes** (due to AIHA) and a lack of platelets [1]. Unlike TTP, schistocytes are absent.
Question 387: The Donath-Landsteiner phenomenon is characteristic of which condition?
- A. Paroxysmal Nocturnal Hemoglobinuria (PNH)
- B. Waldenstrom's Macroglobulinemia
- C. Paroxysmal Cold Hemoglobinuria (Correct Answer)
- D. Malaria
Explanation: **Explanation:** The **Donath-Landsteiner phenomenon** is the hallmark of **Paroxysmal Cold Hemoglobinuria (PCH)**. It involves a unique **biphasic IgG antibody** (an anti-P autoantibody) that binds to red blood cells (RBCs) at low temperatures (cold phase) and fixes complement. When the blood subsequently warms to 37°C (warm phase), the complement cascade is activated, leading to intravascular hemolysis [1]. **Analysis of Options:** * **Paroxysmal Cold Hemoglobinuria (PCH):** Correct. Historically associated with late-stage syphilis, it is now more commonly seen as a self-limiting post-viral syndrome in children (e.g., after URI, measles, or mumps). * **Paroxysmal Nocturnal Hemoglobinuria (PNH):** Incorrect. PNH is caused by an acquired mutation in the *PIGA* gene leading to a deficiency of GPI-anchored proteins (CD55/CD59) [2]. The screening test is Flow Cytometry (formerly Ham’s test or Sucrose Lysis test). * **Waldenstrom’s Macroglobulinemia:** Incorrect. This is a B-cell lymphoproliferative disorder characterized by monoclonal IgM. While it can be associated with Cold Agglutinin Disease (IgM-mediated), it does not involve the biphasic Donath-Landsteiner antibody [1]. * **Malaria:** Incorrect. While malaria causes episodic hemolysis and "Blackwater fever," the mechanism is direct parasitic rupture of RBCs [2], not a biphasic autoantibody. **NEET-PG High-Yield Pearls:** * **Antibody Type:** PCH involves **IgG** (unusual for "cold" disorders, which are typically IgM). * **Specificity:** The antibody is specific for the **P-antigen** on RBCs. * **Clinical Presentation:** Sudden onset of hemoglobinuria (dark urine) following cold exposure, often accompanied by fever and chills. * **Diagnosis:** The **Donath-Landsteiner Test** is the gold standard.
Question 388: A 26-year-old woman presents with severe menorrhagia. She reports that both her father and sister have a bleeding disorder. What is the most likely diagnosis, given an autosomal-dominant mode of inheritance for the hemostatic disorder?
- A. Factor X deficiency
- B. von Willebrand's disease (Correct Answer)
- C. Factor VIII deficiency (hemophilia A)
- D. Factor IX deficiency (hemophilia B)
Explanation: The patient presents with **menorrhagia** (mucocutaneous bleeding) and a strong family history involving both genders (father and sister), which points toward an **Autosomal Dominant (AD)** inheritance pattern. [1] **1. Why von Willebrand’s Disease (vWD) is correct:** vWD is the most common inherited bleeding disorder. It typically presents with mucocutaneous bleeding (epistaxis, menorrhagia, gingival bleeding). [1] Most types (specifically Type 1 and Type 2A, 2B, and 2M) follow an **Autosomal Dominant** inheritance. Since it affects both males and females equally, it perfectly matches the clinical scenario. **2. Why the other options are incorrect:** * **Factor VIII (Hemophilia A) and Factor IX (Hemophilia B) deficiency:** These are **X-linked recessive** disorders. They primarily affect males, while females are typically asymptomatic carriers. They usually present with deep-seated bleeds (hemarthrosis/muscle hematomas) rather than mucosal bleeding. [1] * **Factor X deficiency:** This is a rare coagulation disorder that follows an **Autosomal Recessive** inheritance pattern, making it less likely in a multi-generational family history unless consanguinity is present. **Clinical Pearls for NEET-PG:** * **Screening Tests in vWD:** Prolonged Bleeding Time (BT) and often a prolonged Activated Partial Thromboplastin Time (aPTT) (due to low Factor VIII levels, as vWF stabilizes Factor VIII). [2] Platelet count is usually normal (except in Type 2B). * **Confirmatory Test:** Ristocetin Cofactor Assay (measures vWF activity). [2] * **Treatment of Choice:** Desmopressin (DDAVP) for Type 1; Factor VIII concentrates containing vWF for severe cases. [2] * **Inheritance Rule:** If a bleeding disorder affects both father and daughter, think AD (vWD); if it skips females and affects maternal uncles/nephews, think X-linked (Hemophilia).
Question 389: Which of the following is NOT a feature seen in hemolytic anemia?
- A. Tear drop and Burr cells (Correct Answer)
- B. Reduced haptoglobin
- C. Reticulocytosis
- D. Hemoglobinuria
Explanation: In hemolytic anemia, the hallmark is the premature destruction of red blood cells (RBCs), leading to compensatory bone marrow activity and the release of breakdown products [1]. **Explanation of the Correct Option:** * **Option A (Tear drop and Burr cells):** These are not characteristic of hemolysis. **Tear drop cells (Dacrocytes)** are typically seen in **Myelofibrosis** (extramedullary hematopoiesis) or marrow infiltrative disorders. **Burr cells (Echinocytes)** are associated with **Uremia**, liver disease, or pyruvate kinase deficiency [2] (though the latter is hemolytic, Burr cells are not a general feature of hemolysis). The characteristic cell seen in hemolysis is the **Schistocyte** (fragmented cell) or **Spherocyte** [2]. **Explanation of Incorrect Options:** * **Option B (Reduced haptoglobin):** In intravascular hemolysis, free hemoglobin binds to haptoglobin. This complex is cleared by the liver, leading to a marked **decrease** in serum haptoglobin levels. * **Option C (Reticulocytosis):** To compensate for the loss of RBCs, the bone marrow increases production, releasing immature RBCs (reticulocytes) into the peripheral blood. * **Option D (Hemoglobinuria):** When the haptoglobin-binding capacity is saturated, free hemoglobin is filtered by the glomerulus, appearing in the urine (common in intravascular hemolysis) [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Intravascular Hemolysis:** Look for Hemoglobinuria, Hemosiderinuria, and very low Haptoglobin [2]. * **Extravascular Hemolysis:** Look for Splenomegaly and Jaundice (unconjugated hyperbilirubinemia) without hemoglobinuria [1]. * **Most sensitive marker for hemolysis:** Increased **LDH** and decreased **Haptoglobin**. * **Direct Coombs Test:** Used to differentiate autoimmune hemolytic anemia from other causes.
Question 390: Which of the following is the least common feature of Multiple Myeloma?
- A. Bone pain
- B. Normocytic normochromic anemia
- C. Susceptibility to bacterial infection
- D. Hyperviscosity syndrome (Correct Answer)
Explanation: **Explanation:** Multiple Myeloma (MM) is a plasma cell dyscrasia characterized by the neoplastic proliferation of a single clone of plasma cells producing monoclonal (M) protein [1]. **Why Hyperviscosity Syndrome is the correct answer:** Hyperviscosity syndrome is relatively **uncommon** in Multiple Myeloma, occurring in only about **2-6%** of patients. It is much more characteristic of **Waldenström Macroglobulinemia**, where large IgM pentamers significantly increase blood viscosity [1]. In MM, hyperviscosity typically only occurs if the M-protein concentration is very high (usually IgA or IgG3 subtypes) or if the protein forms large polymers. **Analysis of Incorrect Options:** * **Bone Pain (Option A):** This is the **most common presenting symptom** (seen in ~70% of patients). It results from osteolytic "punched-out" lesions caused by the activation of osteoclasts via the RANKL pathway [1]. * **Normocytic Normochromic Anemia (Option B):** This is the most common hematologic abnormality (~80% of patients). It occurs due to bone marrow infiltration by plasma cells and the "anemia of chronic disease" mechanism (hepcidin elevation) [1]. * **Susceptibility to Bacterial Infection (Option C):** This is a leading cause of morbidity and mortality. It is due to **hypogammaglobulinemia** (suppression of normal B-cell function) and neutropenia. Common pathogens include *S. pneumoniae* and *S. aureus*. **NEET-PG High-Yield Pearls:** * **CRAB Criteria:** **C**alcium elevation, **R**enal insufficiency, **A**nemia, **B**one lesions [1]. * **Diagnosis:** Clonal bone marrow plasma cells ≥10% or biopsy-proven extramedullary plasmacytoma PLUS one or more myeloma-defining events [1]. * **Blood Smear:** **Rouleaux formation** (due to decreased zeta potential between RBCs by M-protein). * **Urinalysis:** Bence-Jones proteins (free light chains) are **not** detected on a standard dipstick (which detects albumin); they require sulfasalicylic acid testing or electrophoresis.
Practice by Chapter
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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