Hematopathology Practice Questions

Q: Megaloblastic anemia may be caused by all of the following except?

Long term aspirin intake. Megaloblastic anemia is characterized by impaired DNA synthesis, leading to the presence of large, nucleated red blood cell precursors (megaloblasts) in the bone marrow [1]. **Why Long-term Aspirin is the Correct Answer:** Aspirin (Acetylsalicylic acid) is a non-steroidal anti-inflammatory drug (NSAID) that inhibits cyclooxygenase (COX) enzymes. While chronic aspirin use is associated with **Iron Deficiency Anemia** (due to occult gastrointestinal bleeding), it does not interfere with DNA synthesis or folate/B12 metabolism. Therefore, it does not cause megaloblastic anemia. **Analysis of Incorrect Options:** * **Vitamin B12 & Folic Acid Deficiency:** These are the most common causes [3]. B12 and Folate are essential co-factors for DNA synthesis [2]. Deficiency leads to "nuclear-cytoplasmic asynchrony," where the nucleus matures slower than the cytoplasm. * **Dilantin (Phenytoin) Toxicity:** Phenytoin is a notorious cause of drug-induced megaloblastic anemia. It interferes with folate metabolism by inhibiting the intestinal enzyme (folate conjugase) required for folate absorption and by increasing folate catabolism. **NEET-PG High-Yield Pearls:** * **Drug-Induced Megaloblastic Anemia (Mnemonic: "M-P-S-T"):** * **M**ethotrexate (Dihydrofolate reductase inhibitor) * **P**henytoin/Pyrimethamine * **S**ulfa drugs (Trimethoprim) * **T**rimethoprim * **Zidovudine (AZT):** A common cause of macrocytosis (increased MCV) without necessarily causing full megaloblastic changes. * **Nitrous Oxide:** Can cause acute megaloblastic anemia by oxidizing the cobalt atom in Vitamin B12, rendering it inactive.

Q: Which of the following is NOT a classical feature of primary myelofibrosis?

Biconcave RBCs. **Explanation:** Primary Myelofibrosis (PMF) is a chronic myeloproliferative neoplasm characterized by clonal proliferation of megakaryocytes and granulocytes, leading to reactive bone marrow fibrosis [1]. **Why "Biconcave RBCs" is the correct answer:** Normal, healthy red blood cells are biconcave discs. In PMF, the bone marrow is replaced by dense collagen (fibrosis). As RBCs attempt to squeeze through the narrowed, fibrotic marrow spaces and the distorted vasculature of the spleen (extramedullary hematopoiesis), they undergo mechanical trauma. This results in the formation of **Dacrocytes (Tear-drop RBCs)**, not the maintenance of normal biconcave morphology [1]. **Analysis of Incorrect Options:** * **Tear drop RBCs (Dacrocytes):** These are the hallmark peripheral smear finding in PMF [1]. They occur due to the "stretching" of RBCs as they exit the fibrotic marrow. * **Leucoerythroblastosis:** This refers to the presence of immature white cells (myelocytes, metamyelocytes) and nucleated red cells in the peripheral blood [1]. It occurs because the fibrotic marrow cannot hold onto developing cells, and extramedullary sites (liver/spleen) lack the "blood-marrow barrier." * **Abnormal Megakaryocytes:** PMF is characterized by "cloud-like" or "balloon-like" clusters of atypical megakaryocytes with bulbous, hyperchromatic nuclei. **High-Yield Clinical Pearls for NEET-PG:** * **Mutation:** JAK2 V617F (approx. 50%), CALR, or MPL mutations. * **Clinical Sign:** Massive splenomegaly (due to extramedullary hematopoiesis) [1]. * **Bone Marrow:** Often results in a **"Dry Tap"** on aspiration; diagnosis requires a trephine biopsy showing silver-stained reticulin fibers. * **Laboratory:** Increased serum uric acid and LDH are common. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Diseases of White Blood Cells, Lymph Nodes, Spleen, and Thymus, pp. 628-629.

Q: Which of the following is true for von Willebrand disease?

Normal prothrombin time. Von Willebrand Disease (vWD) is the most common inherited bleeding disorder, characterized by a deficiency or dysfunction of von Willebrand Factor (vWF) [2]. vWF has two primary roles: mediating platelet adhesion to subendothelial collagen (primary hemostasis) and acting as a carrier protein to stabilize Factor VIII (secondary hemostasis) [2]. **Why Option C is correct:** The **Prothrombin Time (PT)** measures the extrinsic and common pathways (Factors VII, X, V, II, and I) [3]. Since vWD only affects vWF and potentially Factor VIII (intrinsic pathway), the PT remains **normal** [3]. **Why other options are incorrect:** * **A. Normal PTT:** This is incorrect because vWF stabilizes Factor VIII. In many cases of vWD (especially Type 1 and 2N), Factor VIII levels are low, leading to a **prolonged Activated Partial Thromboplastin Time (aPTT)** [2]. * **B. Decreased platelets:** Platelet count is typically **normal** in most types of vWD [2]. The exception is Type 2B vWD (gain-of-function mutation), where increased binding to platelets leads to mild thrombocytopenia, but this is not the general rule. * **D. Normal bleeding time:** Bleeding time (BT) measures primary hemostasis. Since vWF is essential for platelet-vessel wall adhesion, the **BT is characteristically prolonged**. **High-Yield Clinical Pearls for NEET-PG:** * **Inheritance:** Most types are Autosomal Dominant (Type 3 is Autosomal Recessive) [2]. * **Screening Tests:** Prolonged BT, normal/prolonged aPTT, and normal PT/Platelet count [2], [3]. * **Confirmatory Test:** Ristocetin Cofactor Assay (measures vWF activity) [2]. * **Treatment:** **Desmopressin (DDAVP)** is the drug of choice for Type 1 as it releases stored vWF from Weibel-Palade bodies [1], [2]. For Type 3 or severe cases, vWF-containing concentrates are used [2].

Q: Pseudothrombocytopenia is due to platelet agglutination antibodies when the calcium content is decreased by blood EDTA. The antibody responsible for this effect is mainly:

IgG. **Explanation:** **Pseudothrombocytopenia (PTCP)** is an *in vitro* laboratory artifact where the automated platelet count is falsely low. This occurs due to platelet clumping (agglutination) in blood samples collected in **EDTA-anticoagulated tubes**. **1. Why IgG is the correct answer:** The phenomenon is mediated by **naturally occurring autoantibodies**, which are almost always of the **IgG class** (though IgM is rarely implicated). These antibodies are "cryptic," meaning they only recognize and bind to the **GP IIb/IIIa receptor** on the platelet surface when its conformation is altered. EDTA acts as a chelating agent that decreases ionized calcium; this reduction in calcium causes a structural change in the GP IIb/IIIa complex, exposing the hidden epitopes. The IgG antibodies then bind to these sites, causing platelets to agglutinate, which the automated counter misidentifies as single large particles or leukocytes. **2. Why other options are incorrect:** * **IgA and IgD:** These immunoglobulins are not associated with the cold-reacting autoantibody mechanism involved in EDTA-induced clumping. * **IgM:** While IgM can occasionally be involved in cold agglutinin diseases, the specific EDTA-dependent mechanism that targets the GP IIb/IIIa complex is predominantly mediated by IgG. **Clinical Pearls for NEET-PG:** * **Diagnosis:** Suspect PTCP if the patient has a low platelet count but **no clinical signs of bleeding** (petechiae/purpura). * **Confirmation:** Examine a **peripheral blood smear** to visualize platelet clumps. * **Management:** Repeat the test using a different anticoagulant, such as **Sodium Citrate (blue top)** or Heparin, or perform a manual count immediately after collection. * **Key Association:** It is a purely *in vitro* phenomenon with no clinical significance for the patient's actual hemostatic status.

Question 1

Howell-Jolly bodies may be seen after which procedure?

Accepted Answer

Splenectomy

Answer

Hepatectomy

Answer

Pancreatectomy

Answer

Cholecystectomy

Question 2

Thymic hyperplasia is seen in which condition?

Accepted Answer

Myasthenia gravis

Answer

Thymoma

Answer

Thymic lymphoma

Answer

Scleroderma

Question 3

Megaloblastic anemia may be caused by all of the following except?

Accepted Answer

Long term aspirin intake

Answer

Dilantin toxicity

Answer

Vitamin B12 deficiency

Answer

Folic acid deficiency

Question 4

Which of the following is NOT a cause of pancytopenia with hypocellular marrow?

Accepted Answer

Aleukemic leukemia

Answer

Acquired aplastic anemia

Answer

Fanconi's anaemia

Answer

Some myelodysplasia

Question 5

All of the following acute myeloid leukemias are diagnosed regardless of blast count, except?

Accepted Answer

AML with t(1;9)

Answer

AML with t(8;21)

Answer

AML with t(15;17)

Answer

AML with t(16;16)

Question 6

Which of the following is associated with an adverse prognosis in Acute Myeloid Leukemia (AML)?

Accepted Answer

Del 7q

Answer

t(8;21)

Answer

t(15;17)

Answer

Normal cytogenetics

Question 7

Which of the following is NOT a classical feature of primary myelofibrosis?

Accepted Answer

Biconcave RBCs

Answer

Tear drop RBCs

Answer

Leucoerythroblastosis

Answer

Abnormal megakaryocytes

Question 8

Which of the following is true for von Willebrand disease?

Accepted Answer

Normal prothrombin time

Answer

Normal partial thromboplastin time

Answer

Decreased platelets

Answer

Normal bleeding time

Question 9

Prothrombin time is useful for which of the following?

Accepted Answer

Evaluation of a patient taking anticoagulant drugs

Answer

Detection of clot retraction

Answer

Platelet count

Answer

Diagnosis of hemophilia

Question 10

Pseudothrombocytopenia is due to platelet agglutination antibodies when the calcium content is decreased by blood EDTA. The antibody responsible for this effect is mainly:

Accepted Answer

IgG

Answer

IgA

Answer

IgM

Answer

IgD

Hematopathology — MCQs

Hematopathology — MCQs

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