Hematology — MCQs

A patient presents with renal failure and bone pain. X-rays show evidence of skeletal destruction. Laboratory evaluation reveals hypercalcemia. Serum electrophoresis shows a prominent M spike. Tissue biopsy shows plasmacytoma. Bone marrow shows plasmacytosis with 35 percent plasma cells. What is the most likely diagnosis?

Q188Medium

What is the best prognostic type of Hodgkin's lymphoma?

Q189Medium

Laboratory monitoring of which of the following is desirable with low molecular weight heparin therapy in a patient with renal failure?

Q190Easy

A 19-year-old man presents with recurrent knee bleeding during contact sports. He has no history of spontaneous bleeding, but his brother has similar issues. He is diagnosed with "mild" hemophilia A. Which of the following factor abnormalities is consistent with this diagnosis?

Hematology Indian Medical PG Practice Questions and MCQs

Question 181: Complement deficiency predisposes to infection with which of the following microorganisms?

A. Pseudomonas aeruginosa
B. Cytomegalovirus
C. Neisseria meningitidis (Correct Answer)
D. Giardia lamblia

Explanation: The complement system is a vital component of innate immunity, responsible for opsonization, chemotaxis, and direct cell lysis via the **Membrane Attack Complex (MAC)** [1]. **Why Neisseria meningitidis is correct:** The MAC (formed by complement components **C5b-C9**) is specifically essential for the destruction of Gram-negative bacteria with thin cell walls, most notably the *Neisseria* species (*N. meningitidis* and *N. gonorrhoeae*) [1]. Patients with deficiencies in terminal complement components (C5–C9) or Properdin (alternative pathway) have a **1,000 to 10,000-fold increased risk** of invasive meningococcal disease. Patients should be vaccinated with meningococcal vaccines to boost adaptive responses [2]. **Analysis of Incorrect Options:** * **A. Pseudomonas aeruginosa:** Susceptibility to *Pseudomonas* is primarily associated with **neutropenia** (e.g., post-chemotherapy) or qualitative neutrophil defects (e.g., Chronic Granulomatous Disease), rather than isolated complement deficiency. * **B. Cytomegalovirus (CMV):** Defense against viruses like CMV depends on **T-cell mediated (cellular) immunity** [3]. Deficiencies here are seen in HIV/AIDS or transplant recipients. * **C. Giardia lamblia:** Resistance to this intestinal parasite depends on **Humoral immunity (IgA)** [3]. Deficiencies are common in patients with Common Variable Immunodeficiency (CVID) or Selective IgA deficiency. **NEET-PG High-Yield Pearls:** * **C1, C2, C4 deficiency:** Strongly associated with **Systemic Lupus Erythematosus (SLE)** and pyogenic infections (S. pneumoniae). * **C3 deficiency:** The most severe; predisposes to recurrent pyogenic infections and Type II Hypersensitivity reactions. * **C1 Esterase Inhibitor deficiency:** Leads to **Hereditary Angioedema** (characterized by low C4 levels) [2]. * **CH50 Assay:** The screening test of choice for suspected classical complement pathway deficiency [2]. * **Eculizumab:** A monoclonal antibody against C5 (used in PNH) increases the risk of *Neisseria* infection; patients must be vaccinated.

Question 182: A 67-year-old male presents with severe pain in the right foot and paleness of the right toe. He received unfractionated heparin 7 days prior. His hemogram shows: Hb – 13.2 g/dL, WBC – 10000/mm³, Platelet – 50000/mm³. Which of the following should be used to treat this condition?

A. High dose of Heparin
B. Platelet infusions
C. Argatroban (Correct Answer)
D. Warfarin

Explanation: **Explanation:** The clinical presentation of a patient developing thrombocytopenia and arterial thrombosis (the "white clot" syndrome causing foot pain and paleness) approximately 7 days after starting heparin is classic for **Heparin-Induced Thrombocytopenia (HIT) Type II**. **1. Why Argatroban is correct:** HIT is caused by IgG antibodies against the **Heparin-Platelet Factor 4 (PF4) complex**, leading to massive platelet activation and a paradoxical prothrombotic state. The first step in management is the immediate cessation of all heparin products. To maintain anticoagulation and prevent further thrombosis, a **Direct Thrombin Inhibitor (DTI)** like **Argatroban** (or Lepirudin/Danaparoid) must be started [1]. Argatroban is preferred in patients with renal impairment as it is hepatically cleared. **2. Why the other options are incorrect:** * **High dose Heparin:** This would be catastrophic, as it provides more substrate for the antibody-mediated reaction, worsening the thrombosis. * **Platelet infusions:** Generally contraindicated in HIT. Adding more platelets is like "adding fuel to the fire," potentially increasing the risk of thrombotic events. * **Warfarin:** Should **never** be used as monotherapy in the acute phase of HIT. It can cause a rapid drop in Protein C levels, leading to **venous limb gangrene** or skin necrosis. It should only be started once the platelet count has recovered to >150,000/mm³. **Clinical Pearls for NEET-PG:** * **The 4T Score:** Used clinically to assess the probability of HIT (Thrombocytopenia, Timing, Thrombosis, and oTher causes). * **Timing:** HIT typically occurs **5–10 days** after heparin exposure [1]. * **Diagnosis:** Initial screening with **ELISA (anti-PF4)**; Gold standard confirmatory test is the **Serotonin Release Assay (SRA)**. * **Management Rule:** Stop Heparin → Start DTI (Argatroban) → Delay Warfarin.

Question 183: Macrocytic anemia may be seen with all of the following conditions except:

A. Liver disease
B. Copper deficiency (Correct Answer)
C. Thiamine deficiency
D. Orotic aciduria

Explanation: The correct answer is **Copper deficiency** because it typically presents as a **microcytic or normocytic anemia**, often mimicking iron deficiency or myelodysplastic syndrome (sideroblastic anemia). Copper is a vital cofactor for *hephaestin* and *ceruloplasmin*, which are essential for iron transport and utilization. Its deficiency leads to impaired hemoglobin synthesis, resulting in small red cells, not macrocytes. **Analysis of other options:** * **Liver Disease:** This is a classic cause of non-megaloblastic macrocytosis. It occurs due to increased lipid deposition on the red cell membrane (target cells) and altered cholesterol metabolism. * **Thiamine (B1) Deficiency:** Specifically, **Thiamine-Responsive Megaloblastic Anemia (TRMA)** or Rogers Syndrome is a rare genetic triad of megaloblastic anemia, non-autoimmune diabetes, and sensorineural deafness. * **Orotic Aciduria:** This is an autosomal recessive disorder of pyrimidine synthesis. It presents with megaloblastic anemia that is **unresponsive** to B12 or folate, along with failure to thrive and orotic acid crystals in the urine. **NEET-PG High-Yield Pearls:** 1. **Copper Deficiency & Zinc:** Excessive zinc ingestion (e.g., denture creams) can induce copper deficiency because zinc competes for absorption via metallothionein. 2. **Megaloblastic vs. Non-Megaloblastic:** Megaloblastic macrocytosis (B12/Folate deficiency [1], Orotic aciduria) shows hypersegmented neutrophils; Non-megaloblastic (Liver disease, Alcohol, Hypothyroidism) does not. [1] 3. **Drug-induced Macrocytosis:** Always remember **Hydroxyurea, Methotrexate, and Zidovudine (AZT)** as common pharmacological causes tested in exams.

Question 184: Reduced platelet count is found in all the conditions except:

A. Disseminated intravascular coagulation
B. Aplastic anemia
C. Acute myelocytic leukemia
D. Von Willebrand disease (Correct Answer)

Explanation: **Explanation:** The correct answer is **Von Willebrand disease (vWD)** because it is primarily a **qualitative platelet disorder** (defect in platelet adhesion) rather than a quantitative one [1]. In most types of vWD (Type 1 and Type 2), the platelet count remains **normal**. The pathology lies in the deficiency or dysfunction of Von Willebrand Factor (vWF), which acts as a bridge between platelets and the subendothelial collagen [3]. **Analysis of Options:** * **Disseminated Intravascular Coagulation (DIC):** Characterized by widespread activation of the coagulation cascade, leading to the **consumption** of platelets and clotting factors [2]. Thrombocytopenia is a hallmark finding. * **Aplastic Anemia:** A bone marrow failure syndrome where there is peripheral pancytopenia due to marrow hypoplasia. Reduced production leads to a **low platelet count**. * **Acute Myelocytic Leukemia (AML):** Malignant proliferation of blast cells in the bone marrow "crowds out" normal hematopoiesis (myelophthisic effect), resulting in **decreased production** of mature platelets. **High-Yield Clinical Pearls for NEET-PG:** * **Exception in vWD:** **Type 2B vWD** is a unique variant where "gain-of-function" mutations cause increased binding of vWF to platelets, leading to their clearance and **mild thrombocytopenia** [2]. However, as a general rule for exams, vWD presents with a normal platelet count. * **Lab Findings in vWD:** Increased Bleeding Time (BT), normal or increased aPTT (due to low Factor VIII levels), and **abnormal Ristocetin cofactor assay** (the gold standard for diagnosis) [3]. * **Treatment of Choice:** Desmopressin (DDAVP) for Type 1; vWF concentrate for Type 3 [3].

Question 185: Erythropoietin is increased in all of the following conditions, except?

A. Hepatocellular carcinoma
B. Renal cell carcinoma
C. Cerebellar hemangioblastoma
D. Pancreatic carcinoma (Correct Answer)

Explanation: ### Explanation The correct answer is **Pancreatic carcinoma**. This question tests your knowledge of **Ectopic Erythropoietin (EPO) Production**, a classic paraneoplastic syndrome where non-renal tissues secrete EPO, leading to secondary polycythemia. **1. Why Pancreatic Carcinoma is the Correct Answer:** While pancreatic cancer is associated with various paraneoplastic syndromes (like Trousseau sign/migratory thrombophlebitis), it is **not** a recognized cause of ectopic EPO production. Therefore, EPO levels remain normal or are not characteristically elevated in this condition. **2. Analysis of Incorrect Options (Causes of Increased EPO):** Certain tumors are high-yield "classic" sources of ectopic EPO. These include: * **Renal Cell Carcinoma (RCC):** The most common tumor associated with ectopic EPO production. * **Hepatocellular Carcinoma (HCC):** Frequently secretes EPO, leading to erythrocytosis in up to 10% of patients. * **Cerebellar Hemangioblastoma:** A vascular tumor (often associated with Von Hippel-Lindau syndrome) that is a classic producer of EPO. **3. High-Yield Clinical Pearls for NEET-PG:** To remember the tumors that cause secondary polycythemia (increased EPO), use the mnemonic **"Potentially Really High Hematocrit"**: * **P:** **P**heochromocytoma * **R:** **R**enal Cell Carcinoma * **H:** **H**epatocellular Carcinoma * **H:** **H**emangioblastoma (Cerebellar) * **U:** **U**terine Fibroids (Leiomyoma) **Distinction Note:** In **Polycythemia Vera** (a primary myeloproliferative neoplasm), EPO levels are **decreased** due to feedback inhibition. In all the conditions listed in the options (except pancreatic cancer), EPO is **increased**, leading to secondary polycythemia.

Question 186: Which of the following is NOT true about Idiopathic Thrombocytopenic Purpura (ITP)?

A. Splenectomy is the treatment of choice in pediatric patients.
B. Splenectomy is not performed in all cases.
C. Splenomegaly is not essential for the diagnosis of ITP. (Correct Answer)
D. Intravenous immunoglobulin (IVIG) is not useful in adults.

Explanation: ### Explanation **Understanding the Correct Answer (Option C)** In Immune Thrombocytopenic Purpura (ITP), the pathophysiology involves the peripheral destruction of platelets by anti-platelet antibodies (IgG) [1]. While this destruction occurs primarily in the spleen, the spleen itself is **not typically enlarged**. In fact, the presence of significant splenomegaly should prompt a clinician to look for alternative diagnoses, such as leukemia, lymphoma, or portal hypertension. Therefore, the statement "Splenomegaly is not essential for the diagnosis" is medically accurate, making it the correct choice in the context of this question. **Analysis of Other Options** * **Option A:** This statement is **False**. In pediatric ITP, the majority of cases (approx. 80%) are acute and self-limiting, often following a viral infection. Conservative management or short-term steroids/IVIG are preferred; splenectomy is reserved only for chronic, refractory cases. * **Option B:** This statement is **True**. Splenectomy is a second-line treatment that produces complete remission in about 70% of patients [2]. Many patients respond well to corticosteroids (first-line), Rituximab, or TPO-receptor agonists (Eltrombopag/Romiplostim) [2]. * **Option D:** This statement is **False**. IVIG is highly effective in adults, especially when a rapid rise in platelet count is required (e.g., life-threatening bleed or emergency surgery). **NEET-PG High-Yield Pearls** * **First-line treatment:** Corticosteroids (Prednisolone or high-dose Dexamethasone). * **Bone Marrow Finding:** Increased or normal megakaryocytes (compensatory response to peripheral destruction). * **Diagnosis of Exclusion:** ITP is diagnosed only after ruling out other causes of thrombocytopenia [1]. * **Indication for treatment:** Generally started when platelets are <20,000–30,000/µL or if there is significant mucosal bleeding [1].

Question 187: A patient presents with renal failure and bone pain. X-rays show evidence of skeletal destruction. Laboratory evaluation reveals hypercalcemia. Serum electrophoresis shows a prominent M spike. Tissue biopsy shows plasmacytoma. Bone marrow shows plasmacytosis with 35 percent plasma cells. What is the most likely diagnosis?

A. Multiple Myeloma (Correct Answer)
B. Plasmacytoma
C. MGUS
D. Smoldering Myeloma

Explanation: The patient presents with the classic triad of **Multiple Myeloma (MM)**: bone destruction, renal insufficiency, and monoclonal protein proliferation. [1] **1. Why Multiple Myeloma is correct:** According to the International Myeloma Working Group (IMWG) criteria, a diagnosis of MM requires: * **Clonal bone marrow plasma cells ≥10%** (Patient has 35%) OR biopsy-proven extramedullary plasmacytoma. * **CRAB features** (Evidence of end-organ damage): **C**alcium elevation, **R**enal insufficiency, **A**nemia, or **B**one lesions. [1] This patient satisfies both criteria with hypercalcemia, renal failure, skeletal destruction, and 35% plasma cells. **2. Why other options are incorrect:** * **Plasmacytoma:** This refers to a solitary mass of neoplastic plasma cells. While the patient has a plasmacytoma, the presence of systemic involvement (bone marrow >10% and CRAB features) upgrades the diagnosis to Multiple Myeloma. * **MGUS (Monoclonal Gammopathy of Undetermined Significance):** Characterized by M-protein <3 g/dL, bone marrow plasma cells <10%, and **no** CRAB features. * **Smoldering Myeloma:** Characterized by M-protein ≥3 g/dL or bone marrow plasma cells 10–60%, but crucially, there is **no** end-organ damage (CRAB features). **Clinical Pearls for NEET-PG:** * **M-Spike:** Usually IgG (most common) or IgA. [1] * **Peripheral Smear:** Look for **Rouleaux formation** due to high protein levels. * **Bence-Jones Proteins:** Free light chains in urine (not detected by routine dipstick). * **Radiology:** "Punched-out" lytic lesions; Bone scans are often negative (as there is no osteoblastic activity). [1] * **Renal Failure:** Most commonly due to "Myeloma Kidney" (cast nephropathy).

Question 188: What is the best prognostic type of Hodgkin's lymphoma?

A. Lymphocytic predominant (Correct Answer)
B. Lymphocytic depletion
C. Mixed cellularity
D. Nodular sclerosis

Explanation: **Explanation:** The prognosis of Hodgkin’s Lymphoma (HL) is primarily determined by the ratio of reactive lymphocytes to Reed-Sternberg (RS) cells. [1] **1. Why Lymphocytic Predominant is correct:** Lymphocyte Predominant HL (LPHL) is characterized by an abundance of small B-lymphocytes and very few RS cells (specifically the "Popcorn cell" variant). Because lymphocytes represent the body’s effective immune response against the tumor, a high lymphocyte count correlates with an excellent prognosis, often presenting as localized (Stage I or II) disease with a high cure rate. [1] **2. Analysis of Incorrect Options:** * **Lymphocytic Depletion:** This is the **worst prognostic type**. It features sparse lymphocytes and numerous pleomorphic RS cells. It is often associated with advanced stage, systemic symptoms (B-symptoms), and HIV infection. * **Mixed Cellularity:** This type shows a diverse background of eosinophils, plasma cells, and histiocytes. It has an intermediate prognosis and is strongly associated with the **Epstein-Barr Virus (EBV)**. [1] * **Nodular Sclerosis:** This is the **most common type** of HL overall (especially in females and young adults). While it has a very good prognosis, it ranks slightly below Lymphocyte Predominant in terms of overall survival outcomes. **Clinical Pearls for NEET-PG:** * **Most Common Type:** Nodular Sclerosis (characterized by lacunar cells and collagen bands). * **Best Prognosis:** Lymphocyte Predominant. * **Worst Prognosis:** Lymphocyte Depletion. * **EBV Association:** Highest in Mixed Cellularity and Lymphocyte Depletion. * **Popcorn Cells (L&H cells):** Pathognomonic for Nodular Lymphocyte Predominant HL; these are CD20+ (unlike classic RS cells which are CD15+ and CD30+).

Question 189: Laboratory monitoring of which of the following is desirable with low molecular weight heparin therapy in a patient with renal failure?

A. aPTT
B. CT
C. PT
D. Anti-factor Xa activity (Correct Answer)

Explanation: ### Explanation **Correct Answer: D. Anti-factor Xa activity** **Mechanism and Rationale:** Low Molecular Weight Heparin (LMWH), such as Enoxaparin, primarily acts by inhibiting **Factor Xa** rather than Thrombin (Factor IIa) [1]. Unlike Unfractionated Heparin (UFH), LMWH has a predictable pharmacokinetic profile and is primarily excreted by the **kidneys**. In patients with **renal failure** (specifically CrCl <30 ml/min), LMWH can accumulate, significantly increasing the risk of major hemorrhage. Because LMWH does not significantly prolong the aPTT, standard coagulation tests are ineffective for monitoring. Therefore, **Anti-factor Xa activity** is the gold standard for monitoring LMWH when dosing safety is a concern (e.g., renal insufficiency, obesity, or pregnancy) [1]. **Why other options are incorrect:** * **A. aPTT (Activated Partial Thromboplastin Time):** This is used to monitor **Unfractionated Heparin (UFH)** [1]. LMWH has a high anti-Xa to anti-IIa ratio (approx. 3:1), meaning it does not prolong aPTT enough to be used for therapeutic monitoring. * **B. CT (Clotting Time):** This is an obsolete, non-specific bedside test (e.g., Lee-White method) with no role in monitoring modern anticoagulant therapy. * **C. PT (Prothrombin Time):** This measures the extrinsic pathway [3] and is used to monitor **Warfarin** (Vitamin K antagonists), not heparin products [2]. **NEET-PG High-Yield Pearls:** * **Monitoring LMWH:** Usually not required. Indications for monitoring Anti-Xa levels include **Renal failure**, **Pregnancy**, and **Extreme obesity** [1]. * **Antidote:** Protamine sulfate completely neutralizes UFH but only **partially** neutralizes LMWH (approx. 60-70%). * **Drug of Choice in Renal Failure:** If anticoagulation is needed in severe ESRD, **Unfractionated Heparin** is generally preferred over LMWH because it is cleared by the reticuloendothelial system, not the kidneys.

Question 190: A 19-year-old man presents with recurrent knee bleeding during contact sports. He has no history of spontaneous bleeding, but his brother has similar issues. He is diagnosed with "mild" hemophilia A. Which of the following factor abnormalities is consistent with this diagnosis?

A. Abnormal factor VIII function
B. Decreased levels of functional factor VIII (Correct Answer)
C. Decreased factor IX level
D. Decreased von Willebrand factor

Explanation: **Explanation:** **Hemophilia A** is an X-linked recessive bleeding disorder caused by a deficiency or dysfunction of **Clotting Factor VIII** [1]. The severity of the disease is directly correlated with the plasma levels of functional Factor VIII. 1. **Why Option B is correct:** In Hemophilia A, the primary pathology is a **quantitative or qualitative deficiency of Factor VIII**. "Mild" hemophilia is defined by Factor VIII levels between **5% and 40%** of normal. These patients typically do not bleed spontaneously but experience prolonged bleeding after significant trauma, surgery, or contact sports, as seen in this clinical vignette [1]. 2. **Why other options are incorrect:** * **Option A:** While abnormal function can occur, the standard diagnostic hallmark is the measurement of decreased *levels* of functional factor. Furthermore, "decreased levels" is a more encompassing term for the laboratory diagnosis. * **Option C:** Decreased Factor IX level is the hallmark of **Hemophilia B** (Christmas Disease). While clinically indistinguishable from Hemophilia A, it involves a different factor. * **Option D:** Decreased von Willebrand factor (vWF) characterizes **von Willebrand Disease (vWD)** [4]. While vWF stabilizes Factor VIII, vWD usually presents with mucosal bleeding (epistaxis, menorrhagia) rather than hemarthrosis (joint bleeding) [5]. **High-Yield Clinical Pearls for NEET-PG:** * **Severity Classification:** * Severe: <1% factor activity (Spontaneous joint bleeds) [3]. * Moderate: 1–5% factor activity (Bleeding with minor trauma). * Mild: >5–40% factor activity (Bleeding with major trauma/surgery) [1]. * **Lab Findings:** Prolonged **aPTT**, normal PT, and normal bleeding time. * **Treatment:** Recombinant Factor VIII concentrate. For mild cases, **Desmopressin (DDAVP)** can be used to release stored Factor VIII from endothelial cells [2].

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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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