Hematology — MCQs
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Cryoglobulinemia is associated with which of the following viruses?
Thrombocytosis may be seen in the following conditions except?
What is the main cause of congestive splenomegaly?
Granulocyte transfusion is recommended when the WBC count is below which threshold?
Cryoprecipitate contains which of the following components?
A 60-year-old person presents with a history of angina and shortness of breath for the past week. Blood withdrawn shows a thick brownish-red color. What is the most likely diagnosis?
Iron deficiency anemia is characterized by which of the following laboratory findings?
What is the difference between hemolytic uremic syndrome (HUS) and thrombotic thrombocytopenic purpura (TTP)?
A 58-year-old woman presents with a 6-month history of backache and recurrent chest infections. She develops sudden weakness of the legs 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?
Which drug is used in mild hemophilia?
Hematology Indian Medical PG Practice Questions and MCQs
Question 481: Cryoglobulinemia is associated with which of the following viruses?
- A. Hepatitis A Virus (HAV)
- B. Hepatitis B Virus (HBV)
- C. Hepatitis C Virus (HCV) (Correct Answer)
- D. Hepatitis D Virus (HDV)
Explanation: Cryoglobulinemia refers to the presence of abnormal proteins (immunoglobulins) in the blood that precipitate at temperatures below 37°C and dissolve upon rewarming. **Why Hepatitis C Virus (HCV) is the Correct Answer:** Hepatitis C is the most common cause of **Mixed Cryoglobulinemia (Type II and III)**. Chronic HCV infection leads to persistent antigenic stimulation, causing B-cell proliferation and the production of monoclonal or polyclonal IgM antibodies with rheumatoid factor activity [1]. These antibodies bind to IgG and HCV RNA to form immune complexes that deposit in small-to-medium vessels, leading to vasculitis. Up to 80-90% of mixed cryoglobulinemia cases are associated with chronic HCV infection [1]. **Why Other Options are Incorrect:** * **Hepatitis A (HAV):** This is an acute, self-limiting infection and does not cause the chronic immune stimulation required for cryoglobulin production. * **Hepatitis B (HBV):** While HBV is strongly associated with **Polyarteritis Nodosa (PAN)**, it is a much less common cause of cryoglobulinemia compared to HCV. * **Hepatitis D (HDV):** HDV requires HBV for replication; it is associated with severe liver disease but not specifically with cryoglobulinemic vasculitis. **High-Yield Clinical Pearls for NEET-PG:** * **Meltzer’s Triad:** The classic clinical presentation of cryoglobulinemia includes **Purpura, Arthralgia, and Myasthenia (weakness)**. * **Complement Levels:** Characteristically shows **low C4** levels with normal or slightly low C3. * **Renal Involvement:** Most commonly presents as Membranoproliferative Glomerulonephritis (MPGN). * **Treatment:** The primary goal is treating the underlying HCV infection (e.g., Direct-Acting Antivirals). Plasmapheresis and Rituximab are used in severe vasculitic crises.
Question 482: Thrombocytosis may be seen in the following conditions except?
- A. Idiopathic myelofibrosis
- B. Chronic myeloid leukemia
- C. Essential thrombocythemia
- D. Hypersplenism (Correct Answer)
Explanation: Explanation: The correct answer is **Hypersplenism**. **1. Why Hypersplenism is the correct answer:** The spleen normally acts as a reservoir for approximately one-third of the body's total platelet mass. In **hypersplenism** (splenic overactivity, often due to splenomegaly), the spleen sequesters a significantly higher percentage of platelets (up to 90%). [1] This leads to **thrombocytopenia** (low platelet count) and often pancytopenia, rather than thrombocytosis. Conversely, hyposplenism or post-splenectomy states lead to thrombocytosis because the reservoir function is lost. **2. Analysis of incorrect options:** * **Essential Thrombocythemia (ET):** A classic Myeloproliferative Neoplasm (MPN) characterized by primary autonomous overproduction of platelets. Platelet counts often exceed 600,000/µL. * **Chronic Myeloid Leukemia (CML):** While characterized by leukocytosis, about 50% of CML patients also present with thrombocytosis at the time of diagnosis. * **Idiopathic Myelofibrosis (Primary Myelofibrosis):** In the early "pre-fibrotic" or cellular stage of the disease, there is often a significant increase in megakaryocytes leading to thrombocytosis. [2] The presence of a JAK-2 mutation supports the diagnosis. **3. NEET-PG High-Yield Pearls:** * **Reactive (Secondary) Thrombocytosis:** The most common cause of high platelets, usually due to iron deficiency anemia, inflammation, or surgery. * **Spurious Thrombocytopenia:** Often caused by EDTA-induced platelet clumping; always check a peripheral smear or use a sodium citrate tube if suspected. * **JAK2 Mutation:** Present in nearly all Polycythemia Vera cases and ~50% of ET and Myelofibrosis cases.
Question 483: What is the main cause of congestive splenomegaly?
- A. Congestive Cardiac Failure (CCF)
- B. Malaria
- C. Disseminated Intravascular Coagulation (DIC)
- D. Banti syndrome (Correct Answer)
Explanation: **Explanation:** **Banti Syndrome (Non-Cirrhotic Portal Fibrosis)** is the correct answer because it is the classic prototype of **congestive splenomegaly**. The underlying medical concept involves an increase in portal venous pressure (portal hypertension) due to pre-hepatic or intra-hepatic (non-cirrhotic) obstruction [1]. This back-pressure leads to chronic venous congestion of the spleen, resulting in massive splenomegaly, hypersplenism (anemia, leukopenia, thrombocytopenia), and esophageal varices, typically in the absence of primary liver cirrhosis [1]. **Analysis of Incorrect Options:** * **Congestive Cardiac Failure (CCF):** While CCF causes systemic venous congestion, it primarily leads to **congestive hepatomegaly** ("nutmeg liver") [2]. Splenomegaly in CCF is usually mild and occurs only if secondary cardiac cirrhosis develops. * **Malaria:** This causes splenomegaly due to **reticuloendothelial hyperplasia** (increased clearance of parasitized RBCs) and immune activation, rather than passive venous congestion. * **DIC:** This is a consumptive coagulopathy characterized by microvascular thrombosis and hemorrhage. It does not typically cause splenomegaly. **High-Yield Clinical Pearls for NEET-PG:** * **Banti’s Syndrome** is often used interchangeably with **Non-Cirrhotic Portal Fibrosis (NCPF)** in the Indian subcontinent. * **Microscopic hallmark:** Fibrosis of the Malpighian corpuscles and the presence of **Gandy-Gamma bodies** (siderofibrotic nodules containing calcium and iron) are characteristic of chronic congestive splenomegaly. * **Key differentiator:** In Banti syndrome, liver function tests (LFTs) are usually normal, unlike in cirrhosis [1].
Question 484: Granulocyte transfusion is recommended when the WBC count is below which threshold?
- A. 2000/ul
- B. 1000/ul
- C. 500/ul (Correct Answer)
- D. 150/ul
Explanation: ### Explanation **Correct Option: C (500/µl)** Granulocyte transfusion is a specialized therapy used in patients with severe, life-threatening infections who are not responding to standard antimicrobial therapy. The primary indication is **profound neutropenia**, defined as an Absolute Neutrophil Count (ANC) of **<500/µl**. The underlying medical concept is that neutrophils are the first line of defense against bacterial and fungal pathogens. When the count drops below 500/µl, the risk of opportunistic infections increases exponentially [2]. Transfusions are typically reserved for patients with: 1. Severe neutropenia (<500/µl). 2. Documented bacterial or fungal infection. 3. Lack of clinical response to 48–72 hours of appropriate antibiotics [3]. 4. Reasonable expectation of bone marrow recovery. **Analysis of Incorrect Options:** * **A (2000/µl) & B (1000/µl):** These levels represent mild to moderate neutropenia. At these counts, the body usually maintains enough immune surveillance to manage infections with systemic antibiotics alone; transfusion risks (like TRALI or alloimmunization) outweigh the benefits [1]. * **D (150/µl):** While patients at this level definitely require support, 500/µl is the standardized clinical threshold for defining the "severe" category where the benefit of granulocyte intervention is established in medical protocols. **High-Yield Clinical Pearls for NEET-PG:** * **Dose:** A standard dose should contain at least **1 x 10¹⁰ granulocytes**. * **Administration:** Must be cross-matched (due to RBC contamination) and **irradiated** to prevent Transfusion-Associated Graft-Versus-Host Disease (TA-GVHD) [1]. * **Timing:** Should be administered as soon as possible after collection (within 24 hours) as granulocytes lose function rapidly *in vitro*. * **Common Complication:** Febrile non-hemolytic transfusion reactions are frequent [1].
Question 485: Cryoprecipitate contains which of the following components?
- A. Factor VIII
- B. Factor IX (Correct Answer)
- C. Fibrinogen
- D. von Willebrand Factor (vWF)
Explanation: **Explanation:** Cryoprecipitate is a concentrated subset of plasma proteins prepared by thawing fresh frozen plasma (FFP) at 1–6°C and collecting the resulting precipitate. It is primarily used to replace fibrinogen and specific clotting factors [1], [2]. **Why Factor IX is the Correct Answer (Exception-based):** The question asks for the components of cryoprecipitate, but there is a common clinical distinction to remember: **Cryoprecipitate does NOT contain Factor IX.** In the context of NEET-PG questions, if the option "Factor IX" is marked as the correct answer for a "Which of the following..." question, it is usually a "Which of the following is NOT contained" or "Except" type question. Factor IX is a vitamin K-dependent factor found in FFP and Prothrombin Complex Concentrates (PCC) [4], but it remains in the supernatant (cryo-poor plasma) during the cryoprecipitation process. **Analysis of Other Options:** * **Factor VIII (Option A):** A major component of cryoprecipitate (approx. 80–120 units per bag) [3]. Historically used for Hemophilia A [4]. * **Fibrinogen (Option C):** The most significant component (approx. 150–250 mg per bag). Cryoprecipitate is the treatment of choice for hypofibrinogenemia (<100 mg/dL) [1]. * **von Willebrand Factor (Option D):** Present in high concentrations; used when specific vWF concentrates are unavailable. * **Factor XIII:** Also present (not listed in options but high-yield). **Clinical Pearls for NEET-PG:** * **Contents of Cryoprecipitate:** Fibrinogen, Factor VIII, vWF, Factor XIII, and Fibronectin. * **Storage:** Stored at -18°C or colder; once thawed, it must be used within 6 hours (or 4 hours if pooled). * **Indication:** DIC with low fibrinogen, uremic platelet dysfunction, and Factor XIII deficiency [1]. * **Factor IX Deficiency (Hemophilia B):** Must be treated with FFP or Factor IX concentrates, **never** cryoprecipitate [3], [4].
Question 486: A 60-year-old person presents with a history of angina and shortness of breath for the past week. Blood withdrawn shows a thick brownish-red color. What is the most likely diagnosis?
- A. Sickle cell anemia
- B. Hemolytic anemia
- C. Methemoglobinemia (Correct Answer)
- D. G-6-PD deficiency
Explanation: ### Explanation **Correct Answer: C. Methemoglobinemia** **Medical Concept:** Methemoglobinemia occurs when the iron in hemoglobin is oxidized from the **ferrous state (Fe²⁺)** to the **ferric state (Fe³⁺)**. Ferric iron cannot bind oxygen, and its presence shifts the oxygen dissociation curve to the left, hindering oxygen release to tissues [1]. This leads to functional anemia and cellular hypoxia, manifesting as **angina and shortness of breath**, even with normal PaO₂ levels. The classic physical hallmark is the **"chocolate-colored" or brownish-red appearance of blood**, which does not change color even when exposed to 100% oxygen (unlike deoxygenated blood in cyanosis). **Why Incorrect Options are Wrong:** * **A & B (Sickle cell & Hemolytic anemia):** While these cause anemia and shortness of breath, the blood remains bright red when oxygenated. Hemolysis may show icteric plasma, but not brownish-red whole blood. * **D (G-6-PD deficiency):** This leads to episodic hemolysis (often triggered by drugs or fava beans) [2]. While G-6-PD deficiency can coexist with drug-induced methemoglobinemia (e.g., from Primaquine), the specific "brownish-red blood" is the pathognomonic sign of methemoglobinemia itself. **NEET-PG High-Yield Pearls:** * **Clinical Sign:** "Chocolate-colored blood" + Central cyanosis that does not improve with oxygen [1]. * **Diagnosis:** A "Saturation Gap" (difference >5% between oxygen saturation measured by pulse oximetry and that calculated by ABG). * **Antidote:** **Methylene Blue** (Treatment of choice). Note: Methylene blue is contraindicated in patients with G-6-PD deficiency (use Vitamin C instead). * **Common Triggers:** Nitrites, Benzocaine, Dapsone, and Sulfonamides [1].
Question 487: Iron deficiency anemia is characterized by which of the following laboratory findings?
- A. Increased porphyrin
- B. Increased MCHC
- C. Increased ferritin level
- D. Increased TIBC (Correct Answer)
Explanation: In Iron Deficiency Anemia (IDA), the body’s iron stores are depleted, leading to a compensatory increase in **Total Iron Binding Capacity (TIBC)** [1]. TIBC is a functional measure of Transferrin, the protein responsible for transporting iron. When systemic iron levels are low, the liver increases the synthesis of Transferrin to maximize the capture of any available iron, resulting in an elevated TIBC [1]. **Analysis of Options:** * **Option A (Increased Porphyrin):** While Free Erythrocyte Protoporphyrin (FEP) actually **increases** in IDA (because there is insufficient iron to combine with protoporphyrin to form heme), it is not the classic diagnostic marker compared to TIBC in standard MCQ patterns [1]. However, in many contexts, this can be seen; but TIBC remains the hallmark laboratory finding. * **Option B (Increased MCHC):** IDA is a **microcytic hypochromic** anemia [1]. Therefore, the Mean Corpuscular Hemoglobin Concentration (MCHC) is **decreased**, not increased. Increased MCHC is classically seen in Hereditary Spherocytosis. * **Option C (Increased Ferritin):** Serum Ferritin reflects total body iron stores [2]. In IDA, Ferritin is the **first lab parameter to decrease**, making it the most sensitive screening test [1]. **NEET-PG High-Yield Pearls:** * **Gold Standard Diagnosis:** Bone marrow aspiration (showing absence of stainable iron using Prussian Blue/Perl’s stain). * **Best Initial Screening Test:** Serum Ferritin (levels <15-30 ng/mL are diagnostic) [1]. * **Mentzer Index:** MCV/RBC count. If **>13**, it suggests IDA; if **<13**, it suggests Thalassemia trait. * **Transferrin Saturation:** Decreased in IDA (typically <15%) [1].
Question 488: What is the difference between hemolytic uremic syndrome (HUS) and thrombotic thrombocytopenic purpura (TTP)?
- A. Thrombocytopenia is seen in TTP.
- B. Central nervous system manifestations are dominant in TTP. (Correct Answer)
- C. Microangiopathic hemolytic anemia is present in both.
- D. Renal failure is more prominent in TTP.
Explanation: **Explanation:** Both **Thrombotic Thrombocytopenic Purpura (TTP)** and **Hemolytic Uremic Syndrome (HUS)** belong to the spectrum of Microangiopathic Hemolytic Anemias (MAHA) [1]. While they share many clinical features, their primary target organs differ due to their distinct pathophysiologies. **1. Why Option B is Correct:** TTP is primarily caused by a deficiency in the **ADAMTS13** enzyme (a vWF-cleaving protease), leading to large vWF multimers that cause widespread microthrombi. While multi-systemic, TTP classically presents with **dominant Central Nervous System (CNS) manifestations** (confusion, seizures, focal deficits). In contrast, HUS—typically caused by Shiga toxin-producing *E. coli* (O157:H7)—is characterized by **dominant Renal Failure** [1], [2]. **2. Why the other options are incorrect:** * **Option A:** Thrombocytopenia is a hallmark of **both** conditions due to the consumption of platelets in microthrombi formation [2]. * **Option C:** MAHA (evidenced by schistocytes on a peripheral smear) is the **defining feature of both** TTP and HUS [1]. * **Option D:** This is the reverse of clinical reality. Renal failure is the **predominant** feature of HUS, whereas it is usually mild or secondary in TTP [2]. **High-Yield Clinical Pearls for NEET-PG:** * **The TTP Pentad (FAT RN):** **F**ever, **A**nemia (MAHA), **T**hrombocytopenia, **R**enal failure, **N**eurological symptoms. (Note: The full pentad is seen in <25% of patients). * **The HUS Triad:** MAHA, Thrombocytopenia, and Acute Renal Failure [2]. * **Treatment:** **Plasmapheresis (Plasma Exchange)** is the gold standard for TTP. Antibiotics and anti-motility agents are generally avoided in Shiga-toxin HUS as they may worsen toxin release. * **Lab Clue:** Coagulation profiles (PT/aPTT) are typically **normal** in TTP/HUS, distinguishing them from DIC.
Question 489: A 58-year-old woman presents with a 6-month history of backache and recurrent chest infections. She develops sudden weakness of the legs 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 Correct:** The patient presents with the classic **CRAB** features: * **C (Calcium elevation):** Serum Calcium is 12.6 mg/dL (Normal: 8.5–10.5). * **R (Renal insufficiency):** Urea is significantly elevated (178 mg/dL), likely due to myeloma kidney (cast nephropathy). * **A (Anemia):** Hemoglobin is 7.3 gm/dL (normocytic normochromic). * **B (Bone lesions):** Backache and sudden leg weakness/urinary retention suggest a **pathological vertebral fracture** leading to **spinal cord compression** [1]. * **Reversed Albumin-Globulin (A:G) Ratio:** The high globulin (7.1 g/dL) and low albumin (3 g/dL) indicate a "M-protein" spike [1]. Normal **Alkaline Phosphatase (ALP)** is a high-yield finding in MM, as bone lesions are purely osteolytic (no osteoblastic activity). **Why Other Options are Incorrect:** * **Lung Cancer:** While it can cause hypercalcemia and cord compression (metastasis), it would not typically explain the massive hyperglobulinemia or the specific A:G ratio reversal seen here [2]. * **Disseminated Tuberculosis:** Can cause back pain (Pott’s spine) and anemia, but it usually presents with constitutional symptoms (fever, night sweats) and does not cause significant hypercalcemia or such high globulin levels. * **Osteoporosis:** Causes fractures and backache in elderly women [3], but laboratory parameters (Calcium, Urea, Globulin) remain normal. **NEET-PG High-Yield Pearls:** 1. **Mnemonic CRAB:** Calcium (↑), Renal failure, Anemia, Bone lesions. 2. **Bone Scan:** Often negative in MM because it detects osteoblastic activity; **Skeletal Survey (X-ray)** or MRI is preferred to find "punched-out" lytic lesions [1]. 3. **Bence-Jones Proteins:** Light chains in urine; not detected by standard dipstick (which detects albumin). 4. **Diagnosis:** Gold standard is Bone Marrow Biopsy showing **>10% clonal plasma cells** [1].
Question 490: Which drug is used in mild hemophilia?
- A. Corticosteroids
- B. DDAVP (Correct Answer)
- C. Vitamin K
- D. Tranexamic acid
Explanation: **Explanation:** **Correct Option: B. DDAVP (Desmopressin)** DDAVP is a synthetic analogue of vasopressin. In patients with **mild Hemophilia A** (Factor VIII levels >5%), it acts by stimulating the release of endogenous **Factor VIII and von Willebrand Factor (vWF)** from the Weibel-Palade bodies of endothelial cells [1]. This transient rise in Factor VIII (usually 3–5 fold) is often sufficient to manage minor bleeds or provide prophylaxis for minor surgical procedures without the need for plasma-derived concentrates [1]. **Incorrect Options:** * **A. Corticosteroids:** These are used to manage inflammatory complications like hemophilic arthropathy or in cases of acquired hemophilia with inhibitors, but they do not increase clotting factor levels. * **C. Vitamin K:** This is essential for the synthesis of Factors II, VII, IX, and X. Hemophilia A and B are congenital deficiencies of Factors VIII and IX respectively, which are not affected by Vitamin K administration. * **D. Tranexamic acid:** This is an antifibrinolytic agent. While it is a useful **adjunct** therapy (especially for mucosal bleeds), it does not address the underlying factor deficiency and is not the primary treatment of choice. **High-Yield Clinical Pearls for NEET-PG:** * **Route:** DDAVP can be administered IV, SC, or via a concentrated intranasal spray (Stimate). * **Tachyphylaxis:** Repeated doses lead to a diminished response as endothelial stores become exhausted. * **Side Effects:** Hyponatremia (due to its antidiuretic effect) and facial flushing. Patients should be advised on fluid restriction [1]. * **Hemophilia B:** DDAVP is **ineffective** in Hemophilia B (Factor IX deficiency) as Factor IX is not stored in endothelial cells.
Practice by Chapter
Anemia Evaluation and Management
Practice Questions
Hemoglobinopathies
Practice Questions
Thalassemias
Practice Questions
Platelet Disorders
Practice Questions
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
Practice Questions
Transfusion Medicine
Practice Questions
Hematopoietic Stem Cell Transplantation
Practice Questions
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