Hematology Practice Questions

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].

Q: Which of the following is NOT a cause of iron deficiency anemia?

Chronic renal failure (CRF). The correct answer is **A. Chronic renal failure (CRF)**. In Chronic Renal Failure, the primary cause of anemia is a **deficiency of Erythropoietin (EPO)**, which is produced by the peritubular interstitial cells of the kidney. This results in a **normocytic normochromic anemia**, not iron deficiency anemia (IDA). While patients on dialysis may develop IDA due to blood loss or frequent sampling, the hallmark of CRF-related anemia is "Anemia of Chronic Disease" (ACD), characterized by poor iron utilization rather than a lack of iron stores [2]. **Analysis of Incorrect Options:** * **Young female:** This is a classic cause of IDA due to physiological blood loss during **menstruation** [1, 2] and increased iron demands during pregnancy [3]. * **Celiac sprue:** This condition causes malabsorption [2]. Since iron is primarily absorbed in the **duodenum and upper jejunum**, the villous atrophy seen in Celiac disease directly impairs iron absorption. * **Hookworm infestation:** (*Ancylostoma duodenale* and *Necator americanus*) is a leading cause of IDA in developing countries [2]. The worms attach to the intestinal mucosa and suck blood, leading to chronic occult GI blood loss [1]. **NEET-PG High-Yield Pearls:** * **Most common cause of IDA worldwide:** Nutritional deficiency/Hookworm [1, 2]. * **Most common cause of IDA in adult males/post-menopausal females:** Occult GI bleed (must rule out malignancy) [1]. * **Absorption Site:** Iron is absorbed in the **Duodenum** (Ferrous form, $Fe^{2+}$) [4]. * **CRF Anemia Treatment:** Recombinant Human Erythropoietin (target Hb: 10–11 g/dL). Always ensure adequate iron stores before starting EPO.

Q: What is the drug of choice for Heparin-induced thrombocytopenia?

Argatroban. **Explanation:** **Heparin-induced thrombocytopenia (HIT)** is a life-threatening prothrombotic condition caused by IgG antibodies against the Heparin-Platelet Factor 4 (PF4) complex. The primary goal of management is the immediate cessation of all heparin products and the initiation of a non-heparin anticoagulant. **Why Argatroban is the Correct Answer:** Argatroban is a parenteral **Direct Thrombin Inhibitor (DTI)**. It is the drug of choice because it does not cross-react with HIT antibodies. It directly binds to the active site of both free and clot-bound thrombin. It is particularly preferred in patients with renal impairment as it is **metabolized by the liver**, though it requires monitoring via aPTT. **Why Other Options are Incorrect:** * **Warfarin:** It is **contraindicated** in the acute phase of HIT. Starting warfarin alone can lead to a rapid depletion of Protein C, creating a hypercoagulable state that results in **venous limb gangrene** or skin necrosis. * **Low Molecular Weight Heparin (LMWH):** These are strictly contraindicated because they show high cross-reactivity with HIT antibodies and will worsen the condition. * **Dabigatran:** While it is an oral DTI, it is not the standard of care for the *acute* management of HIT, which typically requires titratable parenteral anticoagulation. **High-Yield NEET-PG Pearls:** 1. **Alternative in Renal Failure:** Use Argatroban (Hepaticaly cleared). 2. **Alternative in Hepatic Failure:** Use **Danaparoid** or **Bivalirudin** (Renally cleared). 3. **Diagnosis:** Suspect HIT if platelet count drops by >50% after 5–10 days of heparin therapy. Use the **4T Score** for clinical probability. 4. **Transition:** Only start Warfarin once the platelet count has recovered to >150,000/µL, overlapping with a DTI for at least 5 days.

Q: Which marker differentiates Chronic Lymphocytic Leukemia (CLL) from Mantle Cell Lymphoma?

CD 23. **Explanation:** Chronic Lymphocytic Leukemia (CLL) and Mantle Cell Lymphoma (MCL) are both mature B-cell neoplasms that share several immunophenotypic markers, most notably **CD5** and **CD19/20**. Differentiating between them is crucial for prognosis and treatment. **Why CD23 is the correct answer:** **CD23** (the low-affinity IgE receptor) is the classic marker used to distinguish these two entities. * **CLL/SLL:** Characteristically **CD23 positive**. * **Mantle Cell Lymphoma:** Characteristically **CD23 negative**. In clinical practice, the Matutes scoring system utilizes CD23 positivity as a key parameter to diagnose CLL. **Analysis of Incorrect Options:** * **A. CD5:** This is a T-cell marker aberrantly expressed in both CLL and MCL. Therefore, it cannot be used to differentiate the two. * **B. CD17:** This is a glycosphingolipid marker (lactosylceramide) found on granulocytes and monocytes; it has no diagnostic utility in differentiating B-cell lymphomas. * **C. CD22:** This is a pan-B-cell marker present in most B-cell malignancies, including both CLL and MCL (though expression is often "dim" in CLL). **High-Yield Clinical Pearls for NEET-PG:** * **FMC-7:** Another differentiating marker; it is typically **negative** in CLL and **positive** in MCL. * **Cyclin D1:** MCL is characterized by the **t(11;14)** translocation, leading to overexpression of Cyclin D1. CLL is Cyclin D1 negative. * **SOX11:** A highly specific nuclear marker for Mantle Cell Lymphoma, especially useful in Cyclin D1-negative cases. * **Smudge Cells:** Classically seen on the peripheral smear of CLL patients due to the fragility of the lymphocytes.

Q: Sudden abdominal pain in polycythemia vera is most commonly due to which of the following complications?

Hepatic vein thrombosis. Explanation: 1. Why Hepatic Vein Thrombosis is Correct: Polycythemia Vera (PV) is a chronic myeloproliferative neoplasm characterized by an absolute increase in red cell mass. This leads to a prothrombotic state due to both increased blood viscosity and qualitative platelet abnormalities. A classic and high-yield complication of PV is Budd-Chiari Syndrome (BCS), which is the obstruction of hepatic venous outflow. Sudden abdominal pain, hepatomegaly, and ascites in a PV patient are hallmark signs of hepatic vein thrombosis. PV is, in fact, the most common underlying primary myeloproliferative cause of BCS. The presence of a JAK-2 mutation supports the diagnosis of such myeloproliferative disorders [1]. 2. Why the Other Options are Incorrect: * B. Hyperviscosity: While PV causes hyperviscosity, it typically presents with neurological symptoms (headache, dizziness, visual disturbances) or mucosal bleeding rather than sudden, localized abdominal pain. * C. Pancreatitis: While patients with PV may have an increased risk of gallstones (due to high cell turnover), pancreatitis is not a direct or "most common" vascular complication of the disease itself. * D. Small bowel obstruction: This is usually a mechanical issue (adhesions, hernias). While mesenteric ischemia can occur in PV due to thrombosis, hepatic vein involvement is more classically associated with the sudden presentation of the "abdominal triad" in this specific pathology. Clinical Pearls for NEET-PG: * JAK2 V617F Mutation: Present in >95% of PV cases [1]. * Aquagenic Pruritus: Itching after a warm bath is a pathognomonic symptom. * Spent Phase: PV can evolve into secondary myelofibrosis or Acute Myeloid Leukemia (AML). * Treatment: Phlebotomy (target Hct <45%) and low-dose aspirin are first-line. Hydroxyurea is used for high-risk patients.

Question 1

What is true about alpha-thalassemia trait?

Accepted Answer

Microcytosis

Answer

Increased HbF

Answer

Increased HbA

Answer

Severe anemia

Question 2

All of the following are causes of eosinophilia except:

Accepted Answer

Corticosteroid therapy

Answer

Allergic Rhinitis

Answer

Trichinosis

Answer

Rheumatoid arthritis

Question 3

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

Accepted Answer

Vertebral column

Answer

Femur

Answer

Clavicle

Answer

Pelvis

Question 4

A 32-year-old woman with systemic lupus erythematosus (SLE) and chronic renal failure manifests rapidly progressive weakness. On physical examination, she appears pale and has slightly yellow sclerae and an enlarged spleen. Blood tests reveal severe anemia and mild, mostly unconjugated, hyperbilirubinemia. Coombs test is positive at 37 C but negative at 0-4 C. This patient developed anemia because of?

Accepted Answer

IgG directed against red blood cells

Answer

Bone marrow aplasia

Answer

IgM directed against red blood cells

Answer

Renal failure

Question 5

Which of the following is NOT a cause of iron deficiency anemia?

Accepted Answer

Chronic renal failure (CRF)

Answer

Young female

Answer

Celiac sprue

Answer

Hookworm infestation

Question 6

What is the drug of choice for Heparin-induced thrombocytopenia?

Accepted Answer

Argatroban

Answer

Warfarin

Answer

Low molecular weight heparin

Answer

Dabigatran

Question 7

A 72-year-old woman has an elevated WBC count on routine testing, with a manual differential noting an increased number of mature lymphocytes. She reports no recent illnesses or infectious symptoms, and her past medical history is significant for hypertension, osteoarthritis, chronic stable angina, and dyslipidemia. She is taking appropriate medications for these conditions and has no change in symptoms or medications. Her physical examination is normal. Which of the following features best characterizes chronic lymphocytic leukemia (CLL)?

Accepted Answer

Is frequently asymptomatic

Answer

Is usually a T-cell disorder

Answer

Is a disease of children

Answer

Is responsive to splenectomy

Question 8

Which marker differentiates Chronic Lymphocytic Leukemia (CLL) from Mantle Cell Lymphoma?

Accepted Answer

CD 23

Answer

CD 5

Answer

CD 17

Answer

CD 22

Question 9

Which of the following is true regarding anemia of chronic disease?

Accepted Answer

Decreased serum ferritin level

Answer

Decreased TIBC

Answer

Increased macrophage iron in marrow

Answer

Decreased serum iron levels

Question 10

Sudden abdominal pain in polycythemia vera is most commonly due to which of the following complications?

Accepted Answer

Hepatic vein thrombosis

Answer

Hyperviscosity

Answer

Pancreatitis

Answer

Small bowel obstruction

Hematology — MCQs

Hematology — MCQs

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