Hematology Practice Questions

Q: Polycythemia is not caused by which of the following?

Lung carcinoma. **Explanation:** The question tests the concept of **Secondary Polycythemia** caused by inappropriate **Erythropoietin (EPO)** production. **Why Lung Carcinoma is the correct answer:** While lung carcinoma (specifically Small Cell Lung Cancer) is notorious for paraneoplastic syndromes like SIADH or ectopic ACTH production [1], [3], it is **not** typically associated with ectopic EPO production. Therefore, it does not cause polycythemia. In fact, chronic malignancy often leads to the "anemia of chronic disease." **Analysis of Incorrect Options (Causes of Polycythemia):** Certain tumors are classic "EPO-producers," leading to an absolute increase in red cell mass: * **Renal Cell Carcinoma (RCC):** The most common tumor associated with ectopic EPO production [1]. * **Hepatocellular Carcinoma (Liver):** A well-recognized cause of paraneoplastic polycythemia [1]. * **Cerebellar Hemangioblastoma:** A classic association, often seen in Von Hippel-Ludlau (VHL) syndrome [1]. **Clinical Pearls for NEET-PG:** To remember the common tumors causing ectopic EPO production, use the mnemonic **"Potentially Really High Hematocrit"** [1]: 1. **P**heochromocytoma 2. **R**enal Cell Carcinoma 3. **H**epatocellular Carcinoma 4. **H**emangioblastoma (Cerebellar) 5. **U**terine Fibroids (Leiomyoma) **Distinction:** * **Primary Polycythemia (Polycythemia Vera):** Low EPO levels due to JAK2 mutation [2]. * **Secondary Polycythemia:** High EPO levels due to hypoxia or ectopic tumor production [2].

Q: Hemophilia manifests clinically as a rise in which of the following parameters?

APTT. Hemophilia (A and B) is a X-linked recessive bleeding disorder caused by a deficiency in **Factor VIII** (Hemophilia A) or **Factor IX** (Hemophilia B). Both of these factors are integral components of the **Intrinsic Pathway** of the coagulation cascade. **1. Why APTT is the correct answer:** The **Activated Partial Thromboplastin Time (APTT)** is the screening test used to evaluate the integrity of the intrinsic and common pathways [1]. Since Hemophilia involves a deficiency in intrinsic pathway factors (VIII or IX), the APTT will be characteristically **prolonged (increased)**. **2. Why the other options are incorrect:** * **PT (Prothrombin Time):** This tests the **Extrinsic Pathway** (Factor VII) and the common pathway [1]. Since Factor VII levels are normal in Hemophilia, the PT remains normal. * **CT (Clotting Time):** While CT can be prolonged in severe hemophilia, it is a non-specific, insensitive, and outdated bedside test. APTT is the definitive laboratory parameter for diagnosis. * **FDP (Fibrin Degradation Products):** These are elevated in conditions involving excessive fibrinolysis or clot breakdown, such as **DIC (Disseminated Intravascular Coagulation)**, not in primary factor deficiencies like Hemophilia [1]. **Clinical Pearls for NEET-PG:** * **Mixing Study:** If APTT is prolonged, a mixing study is performed [1]. If the APTT **corrects** after adding normal plasma, it indicates a factor deficiency (Hemophilia). If it does **not correct**, it indicates the presence of an inhibitor (e.g., Lupus anticoagulant). * **Bleeding Profile in Hemophilia:** Prolonged APTT; Normal PT, Normal Bleeding Time (BT), and Normal Platelet Count. * **Clinical Presentation:** Characterized by deep tissue bleeding, **hemarthrosis** (bleeding into joints), and delayed surgical bleeding.

Q: Low iron and low TIBC is seen in which condition?

Anaemia of chronic disease. ### Explanation **Correct Answer: A. Anaemia of chronic disease (ACD)** The hallmark of **Anaemia of Chronic Disease** is the body's inability to utilize iron despite adequate stores [1]. This is primarily mediated by **Hepcidin**, an acute-phase reactant [2]. * **Mechanism:** Inflammatory cytokines (like IL-6) increase Hepcidin levels [1]. Hepcidin degrades ferroportin (the iron exporter), leading to iron sequestration in macrophages and decreased intestinal absorption [2]. * **Lab Findings:** Because iron is "locked away," **Serum Iron is low**. Simultaneously, the body downregulates the synthesis of Transferrin (the protein measured by TIBC) as part of the acute-phase response. Therefore, **TIBC is low**. Ferritin (stored iron) is typically normal or high [4]. --- ### Why the other options are incorrect: * **B. Sideroblastic Anaemia:** Characterized by a defect in heme synthesis. Iron is not utilized, leading to **High Serum Iron** and high Ferritin. TIBC is usually normal or low. * **C. Iron Deficiency Anaemia (IDA):** This is the most important differential. In IDA, the body is starved of iron, so **Serum Iron is low**, but the liver compensates by producing more Transferrin to "scout" for iron, resulting in **High TIBC** [3]. * **D. Aplastic Anaemia:** This is a bone marrow failure syndrome. Since the marrow cannot produce RBCs, iron is not consumed, leading to **High Serum Iron** and high Ferritin levels. --- ### NEET-PG High-Yield Pearls: * **TIBC (Total Iron Binding Capacity)** is an indirect measure of **Transferrin**. * **Serum Ferritin** is the most sensitive and specific lab test to differentiate IDA (Low Ferritin) from ACD (Normal/High Ferritin) [4]. * **Transferrin Saturation (TSAT):** Low in both IDA and ACD, but usually much lower in IDA (<15%). * **Soluble Transferrin Receptor (sTfR):** Elevated in IDA but **Normal** in ACD; this is a key marker to differentiate the two when they coexist.

Q: A patient with A-negative blood group can receive blood from which of the following donor blood groups?

A negative. ### Explanation The fundamental principle of blood transfusion is that the recipient must not have antibodies against the donor’s red cell antigens [1]. **1. Why A negative is correct:** A patient with **A-negative** blood has: * **Antigens:** A antigen on the RBC surface [2]. * **Antibodies:** Naturally occurring anti-B antibodies in the plasma [1]. * **Rh status:** Absence of the D antigen (Rh-negative). These individuals will develop anti-D antibodies if exposed to Rh-positive blood. Therefore, an A-negative patient can safely receive blood that lacks the B antigen and lacks the Rh (D) antigen. **A-negative** and **O-negative** are the only compatible groups [1]. **2. Why the other options are incorrect:** * **O positive:** While O is the "universal donor" for ABO, the **positive** Rh status means it contains the D antigen. This would trigger a transfusion reaction (isoimmunization) in an Rh-negative recipient. * **B negative:** This blood contains the B antigen. The recipient’s naturally occurring **anti-B antibodies** would cause immediate hemolytic transfusion reaction [1]. * **AB positive:** This blood contains both the B antigen and the Rh (D) antigen, both of which are incompatible with an A-negative recipient [1]. **3. Clinical Pearls for NEET-PG:** * **Universal Donor (RBCs):** O negative (lacks A, B, and D antigens) [1]. * **Universal Recipient (RBCs):** AB positive (lacks anti-A, anti-B, and anti-D antibodies). * **Universal Donor (Plasma):** AB (lacks anti-A and anti-B antibodies). * **Rh Incompatibility:** In emergencies, Rh-negative females of childbearing age **must** receive Rh-negative blood to prevent Rh isoimmunization and future Hemolytic Disease of the Newborn (HDN).

Q: A patient presented with painless proptosis. What is the next investigation to diagnose it as chloroma?

Peripheral smear. **Explanation:** **Chloroma**, also known as **Myeloid Sarcoma** or Granulocytic Sarcoma, is an extramedullary collection of immature myeloid cells. In the pediatric population, it classically presents as **painless proptosis** due to orbital involvement. **Why Peripheral Smear is the Correct Next Step:** Chloroma is most commonly associated with **Acute Myeloid Leukemia (AML)**, particularly the **M2 (AML with maturation)** and **M4/M5** subtypes [1]. When a patient presents with a clinical suspicion of chloroma, the immediate priority is to look for systemic involvement of leukemia. A **Peripheral Smear** is the most rapid, cost-effective, and non-invasive "next step" to identify circulating myeloblasts, Auer rods, or abnormal cell counts that point toward a primary hematologic malignancy [1]. **Analysis of Incorrect Options:** * **A & C (Hemoglobin/Platelets):** While these may show cytopenias (anemia or thrombocytopenia) in leukemia, they are non-specific and do not provide a definitive morphological diagnosis of the underlying disease. * **D (Bone Marrow Biopsy):** While this is the *gold standard* for confirming and subtyping leukemia, it is a more invasive procedure [1]. In the diagnostic algorithm, a peripheral smear always precedes a bone marrow biopsy. **High-Yield Clinical Pearls for NEET-PG:** * **Color:** The name "Chloroma" comes from the Greek *chloros* (green), due to the presence of the enzyme **Myeloperoxidase (MPO)**, which gives the tumor a greenish hue upon exposure to light. * **Common Site:** The orbit is a classic site in children; other sites include the skin (leukemia cutis), lymph nodes, and gingiva [2]. * **Cytogenetics:** Frequently associated with **t(8;21)** [1]. * **Management:** Treatment involves systemic chemotherapy (as for AML), even if the bone marrow appears uninvolved at presentation.

Q: What is the most appropriate investigation for a 40-year-old female presenting with anemia, jaundice, and spherocytosis?

Coomb's test. ### Explanation The clinical triad of **anemia, jaundice, and spherocytosis** in a 40-year-old female strongly suggests a diagnosis of **Autoimmune Hemolytic Anemia (AIHA)**. **1. Why Coomb's Test is the Correct Answer:** In clinical practice, the most common cause of acquired spherocytosis is AIHA. The **Direct Antiglobulin Test (Coomb’s test)** is the gold standard investigation to confirm this [1]. It detects antibodies (IgG) or complement (C3) bound to the surface of red blood cells. In AIHA, splenic macrophages partially "nibble" the antibody-coated RBC membrane, reducing the surface-area-to-volume ratio and transforming the cells into **spherocytes** [1]. **2. Why Other Options are Incorrect:** * **Osmotic Fragility (A):** While increased in both Hereditary Spherocytosis (HS) and AIHA, it is a non-specific test. In a 40-year-old presenting acutely, AIHA must be ruled out first before considering a congenital condition like HS [1]. * **Electrophoresis (C):** This is used to diagnose hemoglobinopathies (e.g., Thalassemia, Sickle Cell Anemia), which typically present with microcytic or sickle cells, not primary spherocytosis. * **RBC Enzyme Analysis (D):** Used for G6PD deficiency or Pyruvate Kinase deficiency. These conditions present with bite cells or echinocytes, respectively, rather than predominant spherocytosis [2]. **Clinical Pearls for NEET-PG:** * **Hereditary Spherocytosis (HS) vs. AIHA:** Both show spherocytes. However, HS usually presents in childhood with a positive family history and a **negative** Coomb’s test. AIHA is usually acquired in adulthood and is **Coomb’s positive** [1]. * **MCHC:** Spherocytosis is the only condition where the Mean Corpuscular Hemoglobin Concentration (MCHC) is typically **increased** (>36 g/dL). * **Confirmatory Test for HS:** The Eosin-5-maleimide (EMA) binding test via flow cytometry is now preferred over osmotic fragility.

Q: What is the commonest mode of inheritance of Von Willebrand's disease?

Autosomal dominant. **Explanation:** **1. Why Autosomal Dominant is Correct:** Von Willebrand Disease (vWD) is the most common inherited bleeding disorder worldwide. It is primarily caused by quantitative or qualitative defects in Von Willebrand Factor (vWF) [3]. The gene for vWF is located on **Chromosome 12**. The vast majority of clinical cases (approximately 70-80%) fall under **Type 1** (quantitative deficiency) and **Type 2** (qualitative defect), both of which are inherited in an **Autosomal Dominant** fashion. Because it is autosomal, it affects males and females equally, distinguishing it from Hemophilia. **2. Why the Other Options are Incorrect:** * **Codominant:** While some blood group systems (like ABO) exhibit codominance, vWD does not follow this pattern. * **Autosomal Recessive:** This is the mode of inheritance for **Type 3 vWD** (the most severe form with near-total absence of vWF) and certain rare subtypes of Type 2 (like 2N). However, these represent a very small percentage of total cases. * **X-linked Recessive:** This is the classic inheritance pattern for **Hemophilia A (Factor VIII deficiency) and Hemophilia B (Factor IX deficiency)**. vWD is specifically known for being the "autosomal" alternative to Hemophilia [2]. **3. NEET-PG High-Yield Pearls:** * **Most Common Type:** Type 1 (Autosomal Dominant). * **Clinical Presentation:** Mucocutaneous bleeding (epistaxis, menorrhagia, gingival bleeding) [4]. * **Lab Findings:** Prolonged Bleeding Time (BT) and often a prolonged aPTT (since vWF stabilizes Factor VIII). Platelet count is usually normal (except in Type 2B). * **Screening Test:** Ristocetin Cofactor Activity (decreased) [3]. * **Treatment of Choice:** Desmopressin (DDAVP) for Type 1 [1]; Factor VIII concentrates containing vWF for severe cases.

Q: Which one of the following findings is NOT consistent with the diagnosis of aplastic anemia?

Splenomegaly. **Explanation:** Aplastic anemia is a bone marrow failure syndrome characterized by **pancytopenia** and a **hypocellular bone marrow**. **Why Splenomegaly is the Correct Answer:** The hallmark of aplastic anemia is the replacement of hematopoietic tissue with fat. Because the primary pathology is a failure of production (stem cell depletion) rather than peripheral destruction or infiltration, **splenomegaly is characteristically absent**. If a patient presents with pancytopenia and an enlarged spleen, clinicians should instead suspect conditions like portal hypertension (cirrhosis), hypersplenism, hairy cell leukemia, or myelofibrosis [1]. **Analysis of Other Options:** * **Option A:** According to the **Camitta Criteria** for severe aplastic anemia, the bone marrow must show cellularity <25% (or <50% if less than 30% of remaining cells are hematopoietic). * **Option B:** In true aplastic anemia, the few remaining hematopoietic cells should appear **morphologically normal**. The presence of significant dysplasia (abnormal morphology) would point toward Myelodysplastic Syndrome (MDS) rather than aplastic anemia. * **Option C:** The anemia is typically **normocytic normochromic**, though a mild macrocytosis (increased MCV) is sometimes seen due to stressed erythropoiesis. **NEET-PG High-Yield Pearls:** * **Most common cause:** Idiopathic (Autoimmune T-cell mediated destruction of stem cells). * **Drug triggers:** Chloramphenicol (most famous), Carbamazepine, Sulfonamides, and Gold salts. * **Viral triggers:** Hepatitis (Non-A, Non-B, Non-C, Non-G), Parvovirus B19 (usually causes pure red cell aplasia or aplastic crisis in hemolytic states). * **Treatment of choice:** Allogeneic Bone Marrow Transplant (for young patients) or Immunosuppressive Therapy (Antithymocyte globulin + Cyclosporine).

Question 1

Polycythemia is not caused by which of the following?

Accepted Answer

Lung carcinoma

Answer

Renal carcinoma

Answer

Liver carcinoma

Answer

Cerebellar hemangioma

Question 2

Hemophilia manifests clinically as a rise in which of the following parameters?

Accepted Answer

APTT

Answer

PT

Answer

CT

Answer

FDP

Question 3

Low iron and low TIBC is seen in which condition?

Accepted Answer

Anaemia of chronic disease

Answer

Sideroblastic anaemia

Answer

Iron deficiency anaemia

Answer

Aplastic anemia

Question 4

A patient with A-negative blood group can receive blood from which of the following donor blood groups?

Accepted Answer

A negative

Answer

O positive

Answer

B negative

Answer

AB positive

Question 5

A patient presented with painless proptosis. What is the next investigation to diagnose it as chloroma?

Accepted Answer

Peripheral smear

Answer

Blood haemoglobin

Answer

Platelets

Answer

Bone marrow biopsy

Question 6

Which of the following is used to irradiate blood products?

Accepted Answer

Gamma rays

Answer

Alpha rays

Answer

Beta rays

Answer

X-rays

Question 7

Pancytopenia with massive/moderate splenomegaly is seen in which of the following conditions?

Accepted Answer

Thalassemia

Answer

Myelofibrosis

Answer

Polycythemia Rubra Vera (PRV)

Answer

Hairy cell leukemia

Question 8

What is the most appropriate investigation for a 40-year-old female presenting with anemia, jaundice, and spherocytosis?

Accepted Answer

Coomb's test

Answer

Osmotic fragility

Answer

Electrophoresis

Answer

RBC Enzyme analysis

Question 9

What is the commonest mode of inheritance of Von Willebrand's disease?

Accepted Answer

Autosomal dominant

Answer

Codominant

Answer

Autosomal recessive

Answer

X-linked recessive

Question 10

Which one of the following findings is NOT consistent with the diagnosis of aplastic anemia?

Accepted Answer

Splenomegaly

Answer

Hematopoietic cells occupying less than 25% of marrow space

Answer

Hematopoietic cells morphology should be normal

Answer

Normocytic normochromic anemia

Hematology — MCQs

Hematology — MCQs

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