Hematology Practice Questions

Q: A pregnant lady in her second trimester has a hemoglobin level of 6 mg%. The gynecologist suggests IV transfusion of packed red cells. What is the most common oral change due to nutritional anemia?

Atrophic glossitis. The patient presents with severe anemia (Hb 6 g/dL) during pregnancy, which is most commonly due to **Iron Deficiency Anemia (IDA)** [1] or megaloblastic anemia (folate/B12 deficiency) [2]. **Why Atrophic Glossitis is correct:** Nutritional anemias lead to a high turnover rate of the oral mucosal cells. In iron deficiency, there is a depletion of iron-dependent intracellular enzymes, leading to the atrophy of the **filiform papillae** (and later fungiform papillae) on the dorsum of the tongue. This results in **Atrophic Glossitis**, characterized by a smooth, red, and "glazed" appearance of the tongue. It is often accompanied by angular cheilitis and burning sensations (glossodynia). **Analysis of Incorrect Options:** * **A. Enlarged tongue (Macroglossia):** This is typically seen in conditions like amyloidosis, hypothyroidism (myxedema), or acromegaly, rather than nutritional anemia. * **C. Generalized osteolysis:** This refers to bone destruction, commonly seen in Multiple Myeloma or metastatic bone disease, not anemia. * **D. Focal marrow expansion:** While chronic hemolytic anemias (like Thalassemia) cause marrow hyperplasia leading to "crew-cut" appearance on X-ray, it is not a common *oral* mucosal change of nutritional anemia. **High-Yield Clinical Pearls for NEET-PG:** * **Plummer-Vinson Syndrome (Paterson-Kelly Syndrome):** A classic triad of Iron deficiency anemia, Atrophic glossitis, and Esophageal webs. It carries an increased risk of post-cricoid carcinoma. * **Pernicious Anemia:** Often presents with **Hunter’s glossitis** (beefy red tongue). * **Oral manifestations of IDA:** Atrophic glossitis, angular cheilitis, and oral candidiasis.

Q: Which of the following is NOT a recognized cause of neutropenia?

Corticosteroid therapy. **Explanation:** The correct answer is **A. Corticosteroid therapy**. **1. Why Corticosteroids cause Neutrophilia (not Neutropenia):** Corticosteroids are a classic cause of **neutrophilia** (increased neutrophil count). This occurs through three primary mechanisms: * **Demargination:** They decrease the expression of adhesion molecules (like L-selectin), causing neutrophils to move from the endothelial walls (marginal pool) into the circulating blood. * **Delayed Apoptosis:** They extend the lifespan of mature neutrophils. * **Marrow Release:** They stimulate the premature release of neutrophils from the bone marrow. * *Note:* While they increase neutrophils, corticosteroids simultaneously cause **lymphopenia** [1] and **eosinopenia**. **2. Analysis of Incorrect Options (Causes of Neutropenia):** * **Typhoid Fever:** Unlike most bacterial infections that cause leukocytosis, enteric fever (Salmonella typhi) is a classic cause of leukopenia and neutropenia due to bone marrow suppression and increased peripheral destruction. * **Aplastic Anemia:** This is characterized by pancytopenia (reduction in RBCs, WBCs, and platelets) due to bone marrow failure. Neutropenia is a core component. * **Viral Infections:** Many viruses (e.g., Hepatitis, HIV, EBV, Influenza) cause transient neutropenia through redistribution or direct marrow suppression [1]. **Clinical Pearls for NEET-PG:** * **Drug-induced Neutropenia:** Common culprits include Clozapine, Antithyroid drugs (Methimazole/PTU), and Chemotherapy [1]. * **Felty’s Syndrome:** A high-yield triad of Rheumatoid Arthritis, Splenomegaly, and **Neutropenia**. * **Kostmann Syndrome:** A severe congenital neutropenia (autosomal recessive). * **Left Shift:** Corticosteroid-induced neutrophilia usually does *not* show a significant "left shift" (immature bands), unlike an acute bacterial infection.

Q: A 70-year-old male has been experiencing intermittent epistaxis, fatigue, and pain in bones for the past 4 months. Laboratory investigations are as follows: Serum Ca++: 12 mg/dL. This patient is likely to develop which complication?

Amyloidosis. **Explanation:** The clinical presentation of a 70-year-old male with **bone pain, fatigue (anemia), epistaxis (bleeding diathesis), and hypercalcemia (12 mg/dL)** is a classic triad for **Multiple Myeloma (MM)**. In MM, the neoplastic proliferation of plasma cells leads to the overproduction of monoclonal light chains (paraproteins). **Why Amyloidosis is the Correct Answer:** In Multiple Myeloma, excess light chains (specifically Lambda or Kappa) can undergo misfolding and deposit in various tissues as insoluble fibrils. This condition is known as **AL (Light Chain) Amyloidosis**. Approximately 10–15% of patients with Multiple Myeloma develop clinical amyloidosis, which can lead to organ dysfunction (macroglossia, restrictive cardiomyopathy, or nephrotic syndrome). **Analysis of Incorrect Options:** * **A & D (Floppy Mitral Valve / Calcific Aortic Valve):** While hypercalcemia can theoretically lead to metastatic calcification, it does not typically manifest as isolated valvular disease in the context of plasma cell dyscrasias. These are degenerative or connective tissue disorders unrelated to MM. * **B (Autoimmune Hemolytic Anemia):** AIHA is more commonly associated with **Chronic Lymphocytic Leukemia (CLL)** or Non-Hodgkin Lymphoma, rather than Multiple Myeloma. Anemia in MM is usually normocytic normochromic due to marrow infiltration and renal failure. **High-Yield Clinical Pearls for NEET-PG:** * **CRAB Criteria for MM:** **C**alcium elevation, **R**enal insufficiency, **A**nemia, **B**one lesions [1]. * **Bleeding in MM:** Epistaxis occurs due to "Platelet Coating" by paraproteins, interfering with aggregation [1]. * **Diagnosis:** Look for "punched-out" lytic lesions on X-ray and M-spike on Serum Protein Electrophoresis (SPEP) [1]. * **Amyloid Staining:** Congo Red stain showing **apple-green birefringence** under polarized light.

Q: Which bleeding disorder is characterized by prolonged activated partial thromboplastin time (APTT) and prothrombin time (PT)?

Severe liver disease. To understand this question, one must recall the coagulation cascade: **PT** measures the extrinsic and common pathways, while **aPTT** measures the intrinsic and common pathways [1]. ### **Why Severe Liver Disease is Correct** The liver is the primary site for the synthesis of almost all coagulation factors (except Factor VIII and von Willebrand factor). In **severe liver disease**, there is a global deficiency of clotting factors. Since factors in the common pathway (Factors X, V, II, and I) are affected, both PT and aPTT will be prolonged [1]. PT is typically the first to rise because Factor VII (extrinsic pathway) has the shortest half-life. ### **Why Other Options are Incorrect** * **A. Factor XIII deficiency:** Factor XIII stabilizes the fibrin clot. Deficiency results in a normal PT, aPTT, and Bleeding Time, but a positive **Urea Solubility Test**. * **C. Immune Thrombocytopenic Purpura (ITP):** This is a platelet disorder. It presents with a prolonged Bleeding Time (BT) but **normal PT and aPTT**, as the coagulation cascade remains intact [1]. * **D. Leiden (Factor V) deficiency:** This is a distractor. Factor V Leiden is a **pro-thrombotic** (hypercoagulable) state caused by resistance to Protein C, not a deficiency that causes bleeding or prolonged PT/aPTT. ### **High-Yield Clinical Pearls for NEET-PG** * **Isolated prolonged PT:** Think Factor VII deficiency or early Vitamin K deficiency/Warfarin use. * **Isolated prolonged aPTT:** Think Hemophilia A (VIII), B (IX), or C (XI), and Heparin use. * **Prolonged PT + aPTT:** Think Common pathway deficiency (X, V, II, I), Vitamin K deficiency, Warfarin overdose, DIC, or Liver disease [1]. * **Mixing Study:** If a prolonged aPTT corrects with normal plasma, it indicates a **factor deficiency**; if it does not correct, it indicates the presence of an **inhibitor** (e.g., Lupus anticoagulant) [1].

Q: Which metabolic abnormality is seen in multiple myeloma?

Hypercalcemia. **Explanation:** **Correct Answer: C. Hypercalcemia** **Mechanism:** In Multiple Myeloma (MM), malignant plasma cells in the bone marrow produce **Osteoclast Activating Factors (OAFs)**, such as RANK-ligand (RANKL), IL-1 (Osteoclast Activating Factor), and TNF-alpha. These factors stimulate osteoclasts and inhibit osteoblasts, leading to extensive bone resorption. This process releases large amounts of calcium into the extracellular fluid, resulting in hypercalcemia. It is a hallmark feature of the **CRAB** criteria (Calcium elevation, Renal insufficiency, Anemia, and Bone lesions). **Analysis of Incorrect Options:** * **A. Hyponatremia:** While MM can cause "Pseudohyponatremia" (due to high serum protein levels interfering with older lab techniques), it is not a primary metabolic feature. True hyponatremia is not characteristic. * **B. Hypokalemia:** MM is more commonly associated with hyperkalemia if renal failure develops. Hypokalemia is not a standard feature. * **D. Hyperphosphatemia:** While renal failure in late-stage MM can lead to phosphate retention, hypercalcemia is the direct and classic metabolic hallmark resulting from primary bone destruction. **High-Yield Clinical Pearls for NEET-PG:** * **CRAB Criteria:** **C**alcium (>11 mg/dL), **R**enal insufficiency (Cr >2 mg/dL), **A**nemia (Hb <10 g/dL), **B**one lesions (Lytic lesions). * **M-Spike:** Found on Serum Protein Electrophoresis (SPEP), usually IgG (most common) or IgA. * **Bence-Jones Proteins:** Free light chains (kappa/lambda) found in urine; they are not detected by standard dipsticks (which detect albumin). * **Peripheral Smear:** Characterized by **Rouleaux formation** due to increased ESR/fibrinogen/globulins. * **Bone Scan:** Often **negative** because it detects osteoblastic activity; Skeletal Survey (X-ray) or MRI is preferred to find "punched-out" lytic lesions.

Q: A 35-year-old female presents with bilateral deep vein thrombosis in her legs. She has a past history of recurrent fetal loss and one episode of pulmonary embolism. Screening tests of coagulation reveal a prolonged aPTT. What is the likely diagnosis?

Antiphospholipid syndrome. The clinical presentation of recurrent venous thromboembolism (DVT and PE) combined with a history of recurrent fetal loss in a young female is a classic triad for **Antiphospholipid Syndrome (APS)** [2]. **1. Why Antiphospholipid Syndrome (APS) is correct:** APS is an autoimmune prothrombotic state. The "paradox" of APS is that while it causes **thrombosis in vivo** (inside the body), it causes **prolonged aPTT in vitro** (in the lab). This occurs because antiphospholipid antibodies (specifically Lupus Anticoagulant) interfere with the phospholipids used in the aPTT reagent, artificially delaying clot formation in the test tube [3]. **2. Why other options are incorrect:** * **Factor VIII deficiency (Hemophilia A):** This leads to a bleeding diathesis, not thrombosis. While aPTT is prolonged, the clinical history of DVT and fetal loss contradicts this. * **Protein C and S deficiency:** These are common causes of inherited thrombophilia, but they typically present with a **normal aPTT** [1]. * **Hereditary excess of Antithrombin III:** Antithrombin III is a natural anticoagulant. An *excess* would lead to a bleeding tendency, whereas a *deficiency* leads to thrombosis [1]. **3. High-Yield Clinical Pearls for NEET-PG:** * **Diagnostic Criteria (Sapporo):** At least one clinical criteria (vascular thrombosis or pregnancy morbidity) + one laboratory criteria (Lupus anticoagulant, Anti-cardiolipin, or Anti-β2 glycoprotein I antibodies). * **Mixing Study:** In APS, the prolonged aPTT **does not correct** upon mixing with normal plasma (indicating the presence of an inhibitor), whereas in factor deficiencies, it does correct [3]. * **False Positive VDRL:** Patients with APS may show a false positive test for Syphilis due to cross-reactivity with cardiolipin. * **Treatment:** Long-term anticoagulation with Warfarin (INR 2.0–3.0) [4]. Note: DOACs are currently not recommended for "triple-positive" APS.

Q: A 25-year-old pregnant lady presents with thrombocytopenia (Platelet count < 50,000) and fragmented RBCs in peripheral smear. Which of the following is the least likely differential diagnosis?

Evan's syndrome. **Explanation:** The clinical presentation of **thrombocytopenia** and **fragmented RBCs (schistocytes)** on a peripheral smear indicates **Microangiopathic Hemolytic Anemia (MAHA)**. In pregnancy, this triad is a critical diagnostic marker for several life-threatening conditions. **Why Evan’s Syndrome is the least likely (Correct Answer):** Evan’s syndrome is an autoimmune condition characterized by the simultaneous or sequential occurrence of Immune Thrombocytopenic Purpura (ITP) and **Autoimmune Hemolytic Anemia (AIHA)**. Crucially, AIHA is a warm-antibody mediated destruction where RBCs are seen as **spherocytes**, not fragments (schistocytes). Since the question specifies fragmented RBCs, Evan’s syndrome is excluded. **Analysis of Incorrect Options (MAHA causes):** * **HELLP Syndrome:** The most common cause of MAHA in pregnancy. It involves microvascular endothelial damage leading to platelet activation and mechanical shearing of RBCs. * **TTP (Thrombotic Thrombocytopenic Purpura):** Characterized by a deficiency in ADAMTS13, leading to large vWF multimers that cause microthrombi, resulting in severe thrombocytopenia and RBC fragmentation. * **DIC (Disseminated Intravascular Coagulation):** Often secondary to placental abruption or sepsis, it involves systemic activation of coagulation, consumption of factors, and fibrin strands that shear RBCs. **High-Yield Clinical Pearls for NEET-PG:** * **MAHA Triad:** Thrombocytopenia, Schistocytes, and elevated LDH. * **Differential Marker:** To distinguish HELLP from TTP/HUS, look at blood pressure and liver enzymes (elevated in HELLP) vs. neurological symptoms or ADAMTS13 levels (TTP). * **Evan’s Syndrome Diagnosis:** Requires a **Positive Direct Coombs Test (DCT)**, whereas MAHA conditions (HELLP, TTP, DIC) are Coombs-negative.

Question 1

A pregnant lady in her second trimester has a hemoglobin level of 6 mg%. The gynecologist suggests IV transfusion of packed red cells. What is the most common oral change due to nutritional anemia?

Accepted Answer

Atrophic glossitis

Answer

Enlarged tongue

Answer

Generalized osteolysis

Answer

Focal marrow expansion

Question 2

Which of the following is NOT a recognized cause of neutropenia?

Accepted Answer

Corticosteroid therapy

Answer

Typhoid fever

Answer

Aplastic anemia

Answer

Viral infection

Question 3

A 70-year-old male has been experiencing intermittent epistaxis, fatigue, and pain in bones for the past 4 months. Laboratory investigations are as follows: Serum Ca++: 12 mg/dL. This patient is likely to develop which complication?

Accepted Answer

Amyloidosis

Answer

Floppy mitral valve

Answer

Autoimmune hemolytic anemia

Answer

Calcific aortic valve disease

Question 4

Which bleeding disorder is characterized by prolonged activated partial thromboplastin time (APTT) and prothrombin time (PT)?

Accepted Answer

Severe liver disease

Answer

Factor 13 deficiency

Answer

Immune thrombocytopenic purpura

Answer

Leiden (Factor V) deficiency

Question 5

Which metabolic abnormality is seen in multiple myeloma?

Accepted Answer

Hypercalcemia

Answer

Hyponatremia

Answer

Hypokalemia

Answer

Hyperphosphatemia

Question 6

A patient presents with persistent fever and significant weight loss for two months. Examination reveals cervical and axillary lymphadenopathy. Biopsy of cervical nodes is positive for Hodgkin's Lymphoma. What is the clinical stage of the patient?

Accepted Answer

Stage II B

Answer

Stage II A

Answer

Stage III A

Answer

Stage IV B

Question 7

All of the following are good prognostic features of Hodgkin's disease except?

Accepted Answer

Absolute lymphocyte count < 600/µL

Answer

Hemoglobin > 10 gm/dL

Answer

WBC count < 15000/mm³

Answer

Age < 45 years

Question 8

Which of the following is a common feature in multiple myeloma?

Accepted Answer

Hypocalcemia

Answer

Body ache and pain

Answer

Elevated serum globulin

Answer

Renal failure

Question 9

A 35-year-old female presents with bilateral deep vein thrombosis in her legs. She has a past history of recurrent fetal loss and one episode of pulmonary embolism. Screening tests of coagulation reveal a prolonged aPTT. What is the likely diagnosis?

Accepted Answer

Antiphospholipid syndrome

Answer

Factor VIII deficiency

Answer

Inherited Protein C and S deficiency

Answer

Hereditary excess of Antithrombin III

Question 10

A 25-year-old pregnant lady presents with thrombocytopenia (Platelet count < 50,000) and fragmented RBCs in peripheral smear. Which of the following is the least likely differential diagnosis?

Accepted Answer

Evan's syndrome

Answer

Thrombotic Thrombocytopenic Purpura (TTP)

Answer

Disseminated Intravascular Coagulation (DIC)

Answer

HELLP syndrome

Hematology — MCQs

Hematology — MCQs

On this page

Practice by Chapter

Want unlimited practice?