Hematology Practice Questions

Q: All are features of hemolytic anemia except?

Thrombocytopenia. Explanation: Hemolytic anemia is characterized by the premature destruction of red blood cells (RBCs) [1]. The hallmarks of this condition are related to the release of intracellular contents and the body’s compensatory response to anemia. Why Thrombocytopenia is the correct answer: Thrombocytopenia (low platelet count) is **not** a standard feature of hemolytic anemia. In most hemolytic processes, the pathology is specific to the erythrocyte lineage. While certain conditions like Evans Syndrome (AIHA + ITP) or Microangiopathic Hemolytic Anemias (TTP/HUS) involve both low RBCs and platelets, they are specific syndromes rather than general features of hemolysis [2]. Why the other options are incorrect: * **Decreased Haptoglobin:** Haptoglobin is a transport protein that binds to free hemoglobin. In intravascular hemolysis, haptoglobin is rapidly consumed as it clears hemoglobin, making it a highly sensitive marker for hemolysis. * **Raised Indirect Bilirubin:** When RBCs break down, heme is converted into unconjugated (indirect) bilirubin. The liver's conjugating capacity is overwhelmed, leading to unconjugated hyperbilirubinemia and clinical jaundice. * **Hemosiderinuria:** In chronic intravascular hemolysis, filtered hemoglobin is reabsorbed by renal tubular cells. When these cells slough off into the urine, they contain iron deposits (hemosiderin), which can be detected by Prussian blue staining. NEET-PG High-Yield Pearls: * **Best initial test for hemolysis:** Peripheral smear (look for schistocytes or spherocytes) and Reticulocyte count (will be elevated). * **Most specific marker for intravascular hemolysis:** Low serum Haptoglobin. * **Intravascular vs. Extravascular:** Hemoglobinuria and Hemosiderinuria are features of **intravascular** hemolysis only. Splenomegaly is more common in **extravascular** hemolysis [1]. * **LDH:** Serum Lactate Dehydrogenase is typically elevated due to release from ruptured RBCs.

Q: Which of the following is associated with Bence Jones myeloma?

kappa or lambda light chain disease. **Explanation:** **Bence Jones Myeloma** (also known as Light Chain Myeloma) is a variant of Multiple Myeloma where the malignant plasma cells produce only monoclonal free light chains (FLCs) rather than complete immunoglobulin molecules [1]. 1. **Why Option C is Correct:** In this condition, there is a failure to produce heavy chains. Instead, the plasma cells secrete either **kappa (κ) or lambda (λ) light chains**. Because of their low molecular weight (approx. 22-44 kDa), these light chains are easily filtered by the renal glomeruli and excreted in the urine, where they are known as **Bence Jones proteins** [2]. These proteins are unique because they precipitate when heated to 40–60°C and redissolve upon boiling (100°C). 2. **Why Other Options are Incorrect:** * **Options A, B, and D:** These refer to **Heavy Chain Diseases (HCDs)**, such as Franklin’s disease (gamma), Seligmann’s disease (alpha), and Mu-chain disease. In these rare B-cell proliferative disorders, the plasma cells produce truncated heavy chains without associated light chains. This is the exact opposite of Bence Jones Myeloma. **High-Yield Clinical Pearls for NEET-PG:** * **Diagnosis:** Bence Jones proteins are **not detected by standard urine dipsticks** (which primarily sense albumin) [2]. They require **Sulphosalicylic acid (SSA) test** or Urine Protein Electrophoresis (UPEP) [1]. * **Renal Impact:** The filtration of these light chains can lead to "Myeloma Kidney" (Cast Nephropathy), where light chains precipitate with Tamm-Horsfall protein in the distal tubules. * **Frequency:** Light chain myeloma accounts for approximately 15–20% of all Multiple Myeloma cases. * **CRAB Criteria:** Remember the classic presentation of Multiple Myeloma: **C**alcium elevation, **R**enal insufficiency, **A**nemia, and **B**one lesions [1].

Q: Anti-phospholipid antibody syndrome is characterized by all the following features except?

Thrombocytosis. **Explanation:** Antiphospholipid Antibody Syndrome (APS) is an autoimmune hypercoagulable state characterized by the presence of antiphospholipid antibodies (Lupus anticoagulant, Anti-cardiolipin, and Anti-β2 glycoprotein I). **Why Thrombocytosis is the correct answer:** APS is typically associated with **Thrombocytopenia** (low platelet count), not thrombocytosis [1]. The reduction in platelets occurs because they are consumed during the formation of thrombi or cleared by the reticuloendothelial system due to antibody coating. Thrombocytosis is not a feature of APS and often suggests an alternative diagnosis like a myeloproliferative neoplasm. **Analysis of other options:** * **Arterial and venous thrombosis:** This is the hallmark of APS. It can affect any vessel size, leading to Deep Vein Thrombosis (DVT), pulmonary embolism, or strokes. * **Recurrent abortions:** APS causes placental insufficiency and placental infarctions, leading to recurrent pregnancy loss (typically >10 weeks), premature births, or pre-eclampsia. * **Livedo reticularis:** This is the most common cutaneous manifestation of APS, presenting as a mottled, purplish, net-like pattern on the skin caused by swelling of the venules due to obstruction of capillaries by small blood clots [2]. **High-Yield Clinical Pearls for NEET-PG:** * **The Paradox:** APS causes a **prolonged aPTT** *in vitro* (due to antibody interference with phospholipids in the test), but it causes **thrombosis** *in vivo*. * **Catastrophic APS (Asherson’s Syndrome):** Rapidly progressive multiorgan failure due to small vessel occlusion. * **Treatment:** Long-term anticoagulation with Warfarin (Target INR 2.0–3.0). Note: DOACs are generally avoided in triple-positive APS patients.

Q: Which of the following is NOT a component of POEMS syndrome?

Multiple osteolytic lesions. **Explanation:** POEMS syndrome is a rare multisystemic disorder caused by an underlying plasma cell dyscrasia. The diagnosis is based on the acronym itself, which represents its core clinical features. **Why "Multiple osteolytic lesions" is the correct answer:** In POEMS syndrome, the characteristic bone involvement is **osteosclerotic lesions** (bone-forming), not osteolytic (bone-destroying). This is a critical distinction from Multiple Myeloma, where punched-out osteolytic lesions are the hallmark [1]. In POEMS, the plasma cell proliferative disorder is typically associated with high levels of Vascular Endothelial Growth Factor (VEGF), which contributes to the unique sclerotic bone changes. **Analysis of other options:** * **A. Polyneuropathy:** This is a mandatory major criterion. It is typically a chronic, symmetric, sensorimotor polyradiculoneuropathy. * **B. Organomegaly:** Commonly involves hepatomegaly, splenomegaly, or lymphadenopathy (often associated with Castleman disease). * **C. Endocrinopathy:** Frequent manifestations include hypothyroidism, hypogonadism, adrenal insufficiency, and diabetes mellitus. **High-Yield Clinical Pearls for NEET-PG:** * **The Acronym:** **P**olyneuropathy, **O**rganomegaly, **E**ndocrinopathy, **M**onoclonal protein (M-spike), and **S**kin changes (e.g., hyperpigmentation, hypertrichosis). * **Key Biomarker:** Elevated serum **VEGF** levels are highly sensitive and specific for monitoring disease activity. * **Mandatory Criteria for Diagnosis:** 1. Polyneuropathy AND 2. Monoclonal plasma cell proliferative disorder (usually Lambda light chain). * **Association:** Frequently associated with **Castleman disease**. * **Treatment:** Targeted at the underlying plasma cell clone (e.g., radiation for localized lesions, systemic chemotherapy, or autologous stem cell transplant).

Q: Which of the following is NOT an example of massive splenomegaly?

Acute lymphoblastic leukemia. The classification of splenomegaly is a high-yield topic for NEET-PG. Splenomegaly is categorized by the distance the spleen extends below the left costal margin: **Mild** ( 8 cm or weight >1000g). **Why Acute Lymphoblastic Leukemia (ALL) is the correct answer:** In **Acute Lymphoblastic Leukemia**, the disease progression is rapid. The spleen does not have sufficient time to undergo the massive compensatory hypertrophy or extensive infiltration seen in chronic conditions. Splenomegaly in ALL is typically **mild to moderate**. Massive splenomegaly is almost exclusively a feature of chronic myeloproliferative disorders or chronic infections [1]. **Analysis of Incorrect Options:** * **Chronic Myeloid Leukemia (CML):** This is the classic cause of massive splenomegaly. * **Chronic Malaria:** Repeated infections lead to persistent congestion and hyperplasia of the reticuloendothelial system. * **Tropical Splenomegaly (Hyperreactive Malarial Splenomegaly):** This is an exaggerated immune response to malaria characterized by massive IgM production and huge splenic enlargement. **Clinical Pearls for NEET-PG:** * **Mnemonic for Massive Splenomegaly (The "3 C's and 3 M's"):** 1. **C**ML (Most common) 2. **C**LL (Less common than CML) [3] 3. **C**irrhosis (with portal hypertension - though usually moderate) 4. **M**yelofibrosis [2] 5. **M**alaria (Chronic/Tropical) 6. **M**ala-azar (Visceral Leishmaniasis) 7. *Bonus:* **G**aucher’s disease (Storage disorder) * **Note:** In **Polycythemia Vera**, splenomegaly is common, but it is rarely "massive" unless it transforms into myelofibrosis.

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.

Question 1

All are features of hemolytic anemia except?

Accepted Answer

Thrombocytopenia

Answer

Hemosiderinuria

Answer

Decreased haptoglobin

Answer

Raised indirect bilirubin

Question 2

Which of the following is NOT a feature of chronic leukemia?

Accepted Answer

Leukocytosis with circulating blasts and cytopenias are common

Answer

Often diagnosed incidentally

Answer

Splenomegaly is common

Answer

Lymphadenopathy is common

Question 3

Which of the following is associated with Bence Jones myeloma?

Accepted Answer

kappa or lambda light chain disease

Answer

gamma chain disease

Answer

alpha chain disease

Answer

heavy chain disease

Question 4

In Von Willebrand disease, what is the primary defect?

Accepted Answer

Defects in von Willebrand factor

Answer

Factor VII deficiency

Answer

Factor VIII C deficiency

Answer

Factor X deficiency

Question 5

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 6

Anti-phospholipid antibody syndrome is characterized by all the following features except?

Accepted Answer

Thrombocytosis

Answer

Arterial and venous thrombosis

Answer

Recurrent abortions

Answer

Livedo reticularis

Question 7

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 8

Which of the following is NOT a component of POEMS syndrome?

Accepted Answer

Multiple osteolytic lesions

Answer

Polyneuropathy

Answer

Organomegaly

Answer

Endocrinopathy

Question 9

Which of the following is NOT an example of massive splenomegaly?

Accepted Answer

Acute lymphoblastic leukemia

Answer

Chronic myeloid leukemia

Answer

Chronic malaria

Answer

Tropical splenomegaly

Question 10

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

Hematology — MCQs

Hematology — MCQs

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