Hematology Practice Questions

Q: Which of the following factors can differentiate primary polycythemia from secondary polycythemia?

Alveolar oxygen tension <90% on room air. The fundamental difference between primary and secondary polycythemia lies in the **erythropoietin (EPO) drive**. **Primary Polycythemia (Polycythemia Vera)** is a myeloproliferative neoplasm (usually due to a JAK2 mutation) where the bone marrow produces excess red cells autonomously, independent of EPO levels [1]. In fact, EPO levels are typically low. **Secondary Polycythemia** is a physiological or pathological response to **hypoxia**. When arterial oxygen saturation drops (e.g., chronic lung disease, high altitude, or cyanotic heart disease), the kidneys sense the hypoxia and increase EPO production to stimulate erythropoiesis [1]. Therefore, **Alveolar oxygen tension (SaO2) <92% (or <90% in some clinical contexts)** is a hallmark of secondary polycythemia caused by hypoxemia. **Analysis of Incorrect Options:** * **A. Increased red cell mass:** This is the definition of absolute polycythemia and is present in **both** primary and secondary forms; hence, it cannot differentiate them [1]. * **C. Pneumonitis:** While lung inflammation can lead to hypoxia, it is a specific clinical condition rather than a diagnostic parameter used to classify polycythemia. * **D. Hypertension:** Hypertension is a common finding in Polycythemia Vera (due to hyperviscosity) but can also be seen in patients with secondary causes like Obstructive Sleep Apnea (OSA) or renal artery stenosis [1]. It is not a specific differentiating factor. **NEET-PG High-Yield Pearls:** * **JAK2 V617F mutation:** Present in >95% of Polycythemia Vera cases [1]. * **EPO Levels:** Low in Primary; High in Secondary polycythemia. * **Splenomegaly:** Highly suggestive of Primary Polycythemia (PV) [1]. * **Gaisbock Syndrome:** "Stress polycythemia" where red cell mass is normal but plasma volume is decreased (Relative Polycythemia) [1].

Q: What is the most likely subtype of leukemia associated with the provided finding?

AML-M3. ***AML-M3*** - The finding shows **faggot cells** (promyelocytes with multiple bundled **Auer rods**), which is **pathognomonic** for AML-M3 (Acute Promyelocytic Leukemia). - Associated with **t(15;17) chromosomal translocation** and **PML-RARA fusion gene**, making it highly responsive to **all-trans retinoic acid (ATRA)** therapy. *B cell ALL* - Characterized by **lymphoblasts** with high nuclear-to-cytoplasmic ratio and **absent Auer rods**. - Typically affects **children** and presents with **lymphadenopathy** and **hepatosplenomegaly**. *AML-M4* - Shows **myeloblasts** and **monoblasts** with single Auer rods, not the characteristic **bundled Auer rods** seen in faggot cells. - Associated with **inv(16)** or **t(16;16)** chromosomal abnormalities and **eosinophilia**. *AML-M5* - Predominantly contains **monoblasts** and **promonocytes** with **folded nuclei** and abundant cytoplasm. - Auer rods are **rare or absent**, and cells lack the distinctive **faggot cell** morphology of AML-M3.

Q: Plasmapheresis is recommended in all of the following conditions except?

Chronic active hepatitis. Plasmapheresis (Therapeutic Plasma Exchange) is a procedure used to remove high-molecular-weight substances, such as autoantibodies, immune complexes, or paraproteins, from the plasma. **Why Chronic Active Hepatitis is the correct answer:** Chronic active hepatitis is primarily an inflammatory and fibrotic liver disease managed with immunosuppressants (like corticosteroids) [1] or antiviral therapy [2]. Plasmapheresis has no established therapeutic role in its management as the pathology is not driven by circulating macromolecules that require mechanical removal. **Analysis of other options:** * **Hyperviscosity Syndrome:** This is a classic indication. Plasmapheresis rapidly reduces blood viscosity by removing excess proteins (usually IgM), preventing complications like stroke or retinal hemorrhage. * **Macroglobulinaemia (Waldenström’s):** This condition involves high levels of monoclonal IgM. Because IgM is large and mostly intravascular (80%), plasmapheresis is highly effective at removing it to treat associated hyperviscosity. * **Immune Complex Glomerulonephritis:** Conditions like Goodpasture’s syndrome or rapidly progressive glomerulonephritis (RPGN) utilize plasmapheresis to physically remove circulating nephrotoxic autoantibodies or immune complexes to prevent irreversible renal damage. **NEET-PG High-Yield Pearls:** * **ASFA Category I Indications (First-line):** Guillain-Barré Syndrome (GBS), Myasthenia Gravis (crisis), TTP (Thrombotic Thrombocytopenic Purpura), and Goodpasture’s Syndrome. * **TTP Fact:** Plasmapheresis is the treatment of choice for TTP; it removes ADAMTS13 inhibitors and replenishes the enzyme. * **IgM vs. IgG:** Plasmapheresis is more efficient for IgM-mediated diseases (like Waldenström’s) because IgM is primarily intravascular, whereas IgG is distributed in the extravascular space.

Q: A 60-year-old man presents with a 6-month history of increasing fatigue. Physical examination reveals marked pallor, and a CBC shows a macrocytic anemia. Which of the following is the most likely cause of anemia in this patient?

Alcoholism. ### Explanation **Correct Option: A. Alcoholism** The key to this question lies in the **MCV (Mean Corpuscular Volume)**. The patient presents with **macrocytic anemia** (MCV >100 fL). Alcoholism is one of the most common causes of non-megaloblastic macrocytosis [1]. Alcohol has a direct toxic effect on the bone marrow (interfering with erythrocyte maturation) and is often associated with poor nutrition, leading to secondary **folate deficiency** [1]. In chronic alcoholics, macrocytosis can occur even in the absence of anemia or liver disease [3]. **Why Incorrect Options are Wrong:** * **B. Chronic Disease:** Anemia of Chronic Disease (ACD) is typically **normocytic, normochromic**, though it can become microcytic in long-standing cases [2], [4]. It is never macrocytic. * **C. Iron Deficiency:** This is the most common cause of **microcytic, hypochromic** anemia (MCV <80 fL) due to impaired hemoglobin synthesis [2]. * **D. Renal Disease:** Anemia in chronic kidney disease (CKD) is primarily due to decreased erythropoietin production [2]. It is characteristically **normocytic and normochromic**. **NEET-PG High-Yield Pearls:** 1. **Macrocytic Anemia Classification:** * **Megaloblastic:** (Hypersegmented neutrophils present) – Vitamin B12 and Folate deficiency [1], [5]. * **Non-megaloblastic:** Alcoholism, Liver disease, Hypothyroidism, and Myelodysplastic Syndrome (MDS). 2. **Alcohol & MCV:** An unexplained increase in MCV is often an early biochemical marker of occult alcohol abuse. 3. **Round vs. Oval:** Macrocytes in alcoholism/liver disease are usually **round**, whereas in B12/Folate deficiency, they are **oval** (macro-ovalocytes).

Q: What is the commonest acute presentation of sickle cell anemia?

Bone pain. **Explanation:** **Correct Answer: B. Bone pain** **Why Bone Pain is Correct:** The hallmark of Sickle Cell Anemia (SCA) is the **Vaso-occlusive Crisis (VOC)**. Under conditions of hypoxia, acidosis, or dehydration, HbS polymerizes, causing RBCs to become sickle-shaped [2]. These rigid cells obstruct microvasculature, leading to tissue ischemia and infarction [2]. The **most common** site for these crises is the bone marrow, manifesting as severe, acute bone pain [1]. In infants, this often presents as **Dactylitis** (Hand-foot syndrome), while in older children and adults, it typically affects long bones, ribs, and the spine. **Analysis of Incorrect Options:** * **A. Priapism:** While a well-known and serious complication of SCA due to venous stasis in the corpora cavernosa, it is far less frequent than bone pain. * **C. Fever:** Fever is a common *trigger* or associated symptom of a crisis (often due to underlying infection), but it is not the primary presentation of the sickle cell process itself [2, 3]. * **D. Splenomegaly:** In early childhood, the spleen may be enlarged. However, due to repeated infarctions, the spleen eventually undergoes fibrosis and shrinkage, a process known as **Autosplenectomy**. This is a chronic sequela rather than a common acute presentation. **High-Yield Clinical Pearls for NEET-PG:** * **Most common cause of death (Adults):** Acute Chest Syndrome [1]. * **Most common cause of death (Children):** *Streptococcus pneumoniae* sepsis (due to functional asplenia). * **Osteomyelitis in SCA:** While *Staphylococcus aureus* is the most common cause of osteomyelitis generally, **Salmonella** is uniquely associated with SCA. * **Radiology:** "Hair-on-end" appearance on skull X-ray and "H-shaped" vertebrae (Codfish vertebrae) due to central endplate infarction.

Q: Iron overload occurs in all of the following conditions except?

Polycythemia vera. **Explanation:** The core concept behind iron overload in hematological disorders is **ineffective erythropoiesis** and **chronic transfusion requirements**. **Why Polycythemia Vera (PV) is the correct answer:** Polycythemia Vera is a myeloproliferative neoplasm characterized by the autonomous overproduction of red blood cells. Unlike the other conditions listed, PV is actually associated with **iron deficiency**, not overload [1]. This occurs because the massive expansion of the red cell mass consumes the body's iron stores. In fact, therapeutic phlebotomy (the mainstay of treatment for PV) further depletes iron to help control the hematocrit levels. **Analysis of Incorrect Options:** * **Thalassemia:** Iron overload occurs due to two mechanisms: chronic blood transfusions and increased intestinal iron absorption triggered by suppressed hepcidin (due to ineffective erythropoiesis) [1]. * **Myelodysplastic Syndrome (MDS):** Patients often become transfusion-dependent. Additionally, ineffective erythropoiesis leads to the suppression of hepcidin, increasing dietary iron absorption [1]. * **Sideroblastic Anemia:** This is a classic cause of iron overload. It involves a defect in heme synthesis, leading to iron accumulation in the mitochondria of erythroblasts (forming "ringed sideroblasts"). **Clinical Pearls for NEET-PG:** * **Hepcidin Connection:** Ineffective erythropoiesis releases "Erythroferrone," which inhibits Hepcidin. Low Hepcidin levels lead to increased ferroportin activity, causing excessive iron absorption even without transfusions [1]. * **Hereditary Hemochromatosis:** The most common genetic cause of primary iron overload (HFE gene mutation). * **Diagnostic Gold Standard:** While serum ferritin is a screening tool, **MRI T2*** is the non-invasive gold standard for quantifying cardiac and hepatic iron overload.

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: A 23-year-old asymptomatic female pilot presents with MCV of 70 fL, ferritin of 100 g/L, and Hb of 10 g/dL. What is the most likely cause?

Thalassemia trait. **Explanation:** The clinical presentation describes a patient with **microcytic anemia** (MCV 70 fL, Hb 10 g/dL) but with **normal iron stores** (Ferritin 100 g/L) [2]. This dissociation is the hallmark of Thalassemia trait. **1. Why Thalassemia Trait is correct:** In Thalassemia trait (minor), there is a genetic defect in globin chain synthesis [1]. This leads to a high number of small (microcytic), pale (hypochromic) red blood cells. Crucially, because the pathology is globin-related and not iron-related, the **Serum Ferritin remains normal or slightly elevated**. Additionally, patients are often asymptomatic and the anemia is typically mild [1][2]. **2. Why the other options are incorrect:** * **Iron Deficiency Anemia (IDA):** While IDA also presents with low MCV, it is characterized by **low Ferritin** (usually 100 fL; macrocytosis), not a low MCV. **3. NEET-PG High-Yield Pearls:** * **Mentzer Index:** Calculated as **MCV / RBC count**. A value ** 13** suggests Iron Deficiency Anemia. * **RBC Count:** In Thalassemia trait, the RBC count is often paradoxically high (polycythemia) despite low Hb, whereas in IDA, the RBC count is low. * **Confirmatory Test:** Hb Electrophoresis (showing increased HbA2 >3.5% in Beta-Thalassemia trait) is the gold standard for diagnosis.

Question 1

Which of the following factors can differentiate primary polycythemia from secondary polycythemia?

Accepted Answer

Alveolar oxygen tension <90% on room air

Answer

Increased red cell mass

Answer

Pneumonitis

Answer

Hypertension

Question 2

What is the most likely subtype of leukemia associated with the provided finding?

Accepted Answer

AML-M3

Answer

B cell ALL

Answer

AML-M4

Answer

AML-M5

Question 3

Plasmapheresis is recommended in all of the following conditions except?

Accepted Answer

Chronic active hepatitis

Answer

Hyperviscosity syndrome

Answer

Macroglobulinaemia

Answer

Immune complex glomerulonephritis

Question 4

A 60-year-old man presents with a 6-month history of increasing fatigue. Physical examination reveals marked pallor, and a CBC shows a macrocytic anemia. Which of the following is the most likely cause of anemia in this patient?

Accepted Answer

Alcoholism

Answer

Chronic disease

Answer

Iron deficiency

Answer

Renal disease

Question 5

What is the commonest acute presentation of sickle cell anemia?

Accepted Answer

Bone pain

Answer

Priapism

Answer

Fever

Answer

Splenomegaly

Question 6

Which of the following conditions has the least impact on life expectancy since the point of diagnosis?

Accepted Answer

Chronic lymphoid leukemia

Answer

Chronic myeloid leukemia

Answer

Acute myeloid leukemia

Answer

Acute lymphoid leukemia

Question 7

A 48-year-old woman presents with a 3-week history of fatigue, yellow skin, and yellow sclerae. Physical examination reveals mild jaundice. Her serum bilirubin level is 3.7 mg/dL, predominantly unconjugated. Liver function tests, including serum AST, ALT, and alkaline phosphatase, are normal. Hemoglobin level is 6.0 g/dL. Jaundice resolves after corticosteroid administration. What is the most likely cause of hyperbilirubinemia in this patient?

Accepted Answer

Autoimmune hemolytic anemia

Answer

Acute hepatitis B infection

Answer

Gallstone in the common bile duct

Answer

Primary biliary cirrhosis

Question 8

Iron overload occurs in all of the following conditions except?

Accepted Answer

Polycythemia vera

Answer

Thalassemia

Answer

Myelodysplastic syndrome

Answer

Sideroblastic anemia

Question 9

Polycythemia is not caused by which of the following?

Accepted Answer

Lung carcinoma

Answer

Renal carcinoma

Answer

Liver carcinoma

Answer

Cerebellar hemangioma

Question 10

A 23-year-old asymptomatic female pilot presents with MCV of 70 fL, ferritin of 100 g/L, and Hb of 10 g/dL. What is the most likely cause?

Accepted Answer

Thalassemia trait

Answer

Vitamin B12 deficiency

Answer

Folate deficiency

Answer

Iron deficiency

Hematology — MCQs

Hematology — MCQs

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