Hematology Practice Questions

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.

Q: What is true about alpha-thalassemia trait?

Microcytosis. Explanation: Alpha-thalassemia trait (also known as $\alpha$-thalassemia minor) occurs when there is a deletion of two of the four $\alpha$-globin genes ($--/\alpha\alpha$ or $-\alpha/-\alpha$). **1. Why Microcytosis is correct:** In $\alpha$-thalassemia trait, the reduction in $\alpha\{0}-globin chain synthesis leads to a decrease in the total amount of hemoglobin produced per red cell. This results in **microcytosis** (low MCV) and **hypochromia** (low MCH). Characteristically, the MCV is very low (often <75 fL), while the red cell count (RBC count) remains normal or is slightly elevated, distinguishing it from iron deficiency anemia. **2. Why the other options are incorrect:** * **Increased HbF/HbA2:** Unlike $\beta$-thalassemia trait, where HbA2 and HbF increase to compensate for the lack of $\beta$-chains, $\alpha$-thalassemia involves a deficiency in the $\alpha$-chain, which is a component of **all** adult hemoglobins (HbA, HbA2, and HbF). Therefore, the ratios remain normal, and hemoglobin electrophoresis is typically **normal** in $\alpha$-thalassemia trait [1]. * **Severe Anemia:** $\alpha$-thalassemia trait usually presents with **mild anemia** or is asymptomatic. Severe anemia is characteristic of HbH disease (3-gene deletion) or Hydrops Fetalis (4-gene deletion). **High-Yield Clinical Pearls for NEET-PG:** * **Diagnosis:** $\alpha$-thalassemia trait is a "diagnosis of exclusion" because electrophoresis is normal [1]. Definitive diagnosis requires **Genetic Testing (PCR)**. * **Mentzer Index:** (MCV/RBC count) is typically ** 13). * **Hb Barts:** Composed of $\gamma_4$ tetramers; seen in neonates with $\alpha$-thalassemia. * **HbH:** Composed of $\beta_4$ tetramers; seen in 3-gene deletion (HbH disease), appearing as "golf ball cells" on supra-vital staining.

Q: All of the following are causes of eosinophilia except:

Corticosteroid therapy. The correct answer is **Corticosteroid therapy**. Corticosteroids are a classic cause of **eosinopenia** (a decrease in the number of circulating eosinophils). They act by inducing the sequestration of eosinophils in the bone marrow and lymphoid tissues, as well as promoting their apoptosis. **Why the other options are incorrect:** * **Allergic Rhinitis:** Allergic and atopic conditions (Type I hypersensitivity) are the most common causes of mild-to-moderate eosinophilia in developed countries [1], [2]. Eosinophils are recruited to the nasal mucosa in response to IL-5 and other Th2 cytokines. * **Trichinosis:** Helminthic parasitic infections (like *Trichinella spiralis*) are notorious for causing profound eosinophilia, especially during the tissue-invasion phase [2]. * **Rheumatoid Arthritis:** Eosinophilia can occur in systemic autoimmune and connective tissue diseases (CTDs). In RA, it is often a marker of severe disease or systemic vasculitis. **NEET-PG High-Yield Pearls:** 1. **Causes of Eosinopenia (The "S" Rule):** **S**teroids, **S**tress (due to endogenous cortisol), and **S**evere acute bacterial infections (sepsis). 2. **NAACP Mnemonic for Eosinophilia:** **N**eoplasia (Hodgkin’s, CTCL), **A**llergy (Asthma, Rhinitis), **A**ddison’s disease (low cortisol leads to high eosinophils), **C**onnective tissue diseases (Churg-Strauss/EGPA), and **P**arasites [2]. 3. **Drug Reaction:** DRESS syndrome (Drug Reaction with Eosinophilia and Systemic Symptoms) is a frequently tested cause of significant eosinophilia. 4. **Addison’s vs. Cushing’s:** Remember that **hypo**cortisolism (Addison’s) causes eosinophilia, while **hyper**cortisolism (Cushing’s or exogenous steroids) causes eosinopenia.

Q: What is the most common site for lytic lesions in multiple myeloma?

Vertebral column. Multiple myeloma is a plasma cell dyscrasia characterized by the neoplastic proliferation of a single clone of plasma cells [1]. These cells secrete osteoclast-activating factors (such as RANK-ligand and IL-6), leading to the classic "punched-out" lytic lesions. [1] **Why the Vertebral Column is Correct:** Lytic lesions in multiple myeloma primarily occur in areas of the **active (red) bone marrow**. The **vertebral column** is the most common site for these lesions (found in approximately 65-70% of patients), followed by the ribs, skull, pelvis, and femur [1]. The high concentration of axial bone marrow in the vertebrae makes it the most frequent location for plasma cell infiltration and subsequent bone destruction, often leading to pathological compression fractures. [1] **Analysis of Incorrect Options:** * **Femur (A):** While the proximal femur is a common site for pathological fractures in myeloma, it is less frequently involved than the axial skeleton (spine and ribs). * **Clavicle (B):** The clavicle is rarely the primary or most common site for lytic lesions compared to the central skeleton. * **Pelvis (C):** The pelvis is frequently involved (approx. 40%), but statistically, it ranks lower than the vertebral column. **High-Yield Clinical Pearls for NEET-PG:** * **Mnemonic for Myeloma (CRAB):** **C**alcium (elevated), **R**enal failure, **A**nemia, **B**one lesions [1]. * **Skull X-ray:** Classically shows "Raindrop" or "Punched-out" lytic lesions. * **Bone Scan Caution:** Technetium-99m bone scans are often **negative** in myeloma because they detect osteoblastic activity, whereas myeloma is purely **osteolytic** [1]. Skeletal surveys (X-rays) or MRI/CT are preferred. * **Bence-Jones Proteins:** These are free light chains found in urine; they do not show up on a standard dipstick (which detects albumin) [1].

Question 1

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 2

Which metabolic abnormality is seen in multiple myeloma?

Accepted Answer

Hypercalcemia

Answer

Hyponatremia

Answer

Hypokalemia

Answer

Hyperphosphatemia

Question 3

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 4

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 5

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 6

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 7

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

Question 8

What is true about alpha-thalassemia trait?

Accepted Answer

Microcytosis

Answer

Increased HbF

Answer

Increased HbA

Answer

Severe anemia

Question 9

All of the following are causes of eosinophilia except:

Accepted Answer

Corticosteroid therapy

Answer

Allergic Rhinitis

Answer

Trichinosis

Answer

Rheumatoid arthritis

Question 10

What is the most common site for lytic lesions in multiple myeloma?

Accepted Answer

Vertebral column

Answer

Femur

Answer

Clavicle

Answer

Pelvis

Hematology — MCQs

Hematology — MCQs

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