Hematopathology — MCQs
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Hilar lymphadenopathy is seen in which type of Hodgkin's disease?
A 42-year-old man presents with a 2-week history of fever, weakness, and bleeding gums. Peripheral smear shows pancytopenia. Bone marrow examination revealed 26% blasts, frequently exhibiting Auer rods and mature myeloid cells. An occasional neutrophil with pseudo Pelger-Huet anomaly was also noted. Which of the following cytochemical stains is most likely to be positive?
What is the main inflammatory mediator in anemia of chronic disease?
Which of the following is a hemolytic anemia?
In acute myeloid leukemia, Auer rods are numerous in which subtype?
"Chicken-wire" appearance of enlarged bone marrow spaces is seen in which of the following conditions?
Lysis of RBCs are seen in all of the following except?
Which of the following laboratory parameters is increased in hemophilia A?
A 76-year-old man presents with a lytic lesion in the vertebrae. X-ray skull showed multiple punched-out lesions. What is the most likely diagnosis?
Pelger-Huët anomaly is characterized by the presence of which of the following in neutrophils?
Hematopathology Indian Medical PG Practice Questions and MCQs
Question 921: Hilar lymphadenopathy is seen in which type of Hodgkin's disease?
- A. Lymphocyte predominant
- B. Mixed type
- C. Lymphocyte depleted
- D. Nodular sclerosis (Correct Answer)
Explanation: **Explanation:** **Nodular Sclerosis (NSHL)** is the most common subtype of Hodgkin Lymphoma (HL), accounting for approximately 60-70% of cases. It has a unique clinical predilection for **young adults (especially females)** and characteristically involves the **mediastinal and hilar lymph nodes** in over 80% of patients [1], [2]. Pathologically, it is defined by broad bands of collagen fibrosis encircling nodules of lymphoid tissue and the presence of **Lacunar cells** (a variant of Reed-Sternberg cells). **Why other options are incorrect:** * **Lymphocyte Predominant (NLPHL):** Typically presents with isolated peripheral lymphadenopathy (cervical or axillary). Mediastinal/hilar involvement is extremely rare [2]. It features "Popcorn cells" (L&H cells) and has the best prognosis. * **Mixed Cellularity:** This is the second most common type, often associated with EBV infection and older age groups [2]. It usually presents with peripheral nodes and systemic "B" symptoms rather than primary hilar involvement [3]. * **Lymphocyte Depleted:** The rarest and most aggressive form, often seen in HIV-positive patients. It typically presents with advanced-stage disease involving the bone marrow and abdominal viscera rather than isolated hilar nodes [3]. **High-Yield Pearls for NEET-PG:** * **Most common subtype overall:** Nodular Sclerosis. * **Subtype with the best prognosis:** Lymphocyte Predominant. * **Subtype with the worst prognosis:** Lymphocyte Depleted. * **Subtype most associated with EBV:** Mixed Cellularity (and Lymphocyte Depleted) [2]. * **Bimodal age distribution:** HL shows peaks at 15–35 years and >55 years. * **RS Cell Markers:** CD15+ and CD30+ (except in Lymphocyte Predominant, which is CD20+ and CD45+). **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 558-559. [2] 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. 616-618. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 559-560.
Question 922: A 42-year-old man presents with a 2-week history of fever, weakness, and bleeding gums. Peripheral smear shows pancytopenia. Bone marrow examination revealed 26% blasts, frequently exhibiting Auer rods and mature myeloid cells. An occasional neutrophil with pseudo Pelger-Huet anomaly was also noted. Which of the following cytochemical stains is most likely to be positive?
- A. Acid phosphatase
- B. Nonspecific esterase
- C. Myeloperoxidase (Correct Answer)
- D. Toluidine blue
Explanation: **Explanation:** The clinical presentation of fever, weakness, and bleeding gums combined with pancytopenia and 26% blasts in the bone marrow confirms a diagnosis of **Acute Myeloid Leukemia (AML)** (WHO criteria requires >20% blasts) [1]. The presence of **Auer rods** is a pathognomonic finding for the myeloid lineage. Auer rods are composed of fused primary granules (lysosomes) that contain high concentrations of the enzyme **Myeloperoxidase (MPO)** [1]. Therefore, MPO is the most specific cytochemical stain to confirm the myeloid nature of the blasts [1]. The mention of pseudo Pelger-Huet anomalies and mature myeloid cells suggests a background of dysplastic changes, often seen in AML with myelodysplasia-related changes, but the lineage remains myeloid [2]. **Analysis of Incorrect Options:** * **A. Acid Phosphatase:** Primarily used to identify T-cell Acute Lymphoblastic Leukemia (T-ALL), where it shows a characteristic focal "block-like" or "polar" positivity in the Golgi region. * **B. Nonspecific Esterase (NSE):** This stain is a marker for the **monocytic lineage**. It would be strongly positive in AML-M4 (Myelomonocytic) or AML-M5 (Monocytic), but MPO is more characteristic for general myeloid blasts with Auer rods [1]. * **C. Toluidine Blue:** This is a metachromatic stain used specifically to identify **mast cells and basophils**, as it binds to heparin and histamine in their granules. **High-Yield Pearls for NEET-PG:** * **Auer Rods:** Found in AML M1, M2, M3, and M4. They are never seen in Lymphoblastic Leukemia (ALL) [1]. * **MPO vs. SBB:** Sudan Black B (SBB) stains phospholipids in granules and is generally more sensitive but less specific than MPO for myeloid cells. * **M3 (APL):** Characterized by "Faggot cells" (bundles of Auer rods) and a strong MPO positivity [1]. * **NSE:** Inhibited by sodium fluoride in monocytic cells, a key diagnostic differentiator. **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. 620-622. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 613-614.
Question 923: What is the main inflammatory mediator in anemia of chronic disease?
- A. Interleukin-1 (IL-1)
- B. Interleukin-2 (IL-2)
- C. Interleukin-6 (IL-6) (Correct Answer)
- D. Interferon-gamma (IFN-γ)
Explanation: **Explanation:** The correct answer is **Interleukin-6 (IL-6)**. **1. Why IL-6 is correct:** Anemia of Chronic Disease (ACD), also known as Anemia of Inflammation, is primarily mediated by the liver-produced hormone **Hepcidin**. During chronic inflammation, inflammatory cytokines—most notably **IL-6**—stimulate the hepatocytes to increase the synthesis and secretion of Hepcidin [1]. * **Mechanism:** Hepcidin binds to and induces the degradation of **ferroportin** (the only iron efflux channel) on enterocytes and macrophages [1]. * **Result:** This traps iron inside macrophages and prevents dietary iron absorption, leading to low serum iron despite adequate total body iron stores (high ferritin) [1]. **2. Why other options are incorrect:** * **IL-1 & TNF-̑:** While these are pro-inflammatory cytokines present in chronic disease, they primarily contribute to ACD by suppressing erythropoietin (EPO) production and inhibiting erythroid proliferation, but they are not the primary triggers for Hepcidin synthesis [1]. * **IL-2:** This is a T-cell growth factor involved in the adaptive immune response and has no direct role in iron metabolism or ACD. * **IFN-̴:** This cytokine is involved in the sequestration of iron within macrophages, but it is not the "main" mediator compared to the central role of the IL-6-Hepcidin axis. **3. NEET-PG High-Yield Pearls:** * **Hallmark of ACD:** Low serum iron + Low TIBC + **High/Normal Ferritin**. * **Hepcidin:** Known as the "Negative Regulator" of iron absorption [1]. * **Morphology:** Initially Normocytic Normochromic; can become Microcytic Hypochromic in long-standing cases. * **Treatment:** Treat the underlying cause; EPO may be used in specific cases (e.g., CKD) [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 658-662. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 586-587.
Question 924: Which of the following is a hemolytic anemia?
- A. Sickle cell anemia
- B. Thalassemia
- C. Hereditary spherocytosis
- D. All of the above (Correct Answer)
Explanation: **Explanation:** Hemolytic anemias are a group of disorders characterized by the **premature destruction of red blood cells (RBCs)**, where the lifespan of the RBC is reduced from the normal 120 days [1]. This leads to a compensatory increase in erythropoiesis within the bone marrow. * **Sickle Cell Anemia (Option A):** This is a qualitative hemoglobinopathy caused by a point mutation in the β-globin gene. The resulting HbS polymerizes under deoxygenated conditions, causing the RBCs to "sickle" [1]. These rigid cells are destroyed prematurely in the spleen (extravascular hemolysis) and within vessels (intravascular hemolysis) [2]. * **Thalassemia (Option B):** This is a quantitative hemoglobinopathy where there is reduced synthesis of α or β globin chains. The imbalance of globin chains leads to the formation of unstable aggregates that damage the RBC membrane, resulting in ineffective erythropoiesis and extravascular hemolysis. * **Hereditary Spherocytosis (Option C):** This is a red cell membrane defect (most commonly involving **Ankyrin**). The loss of membrane surface area forces the cells to become spherical. These spherocytes are inflexible and are trapped and destroyed by splenic macrophages (extravascular hemolysis) [3]. Since all three conditions involve the premature destruction of RBCs, **Option D (All of the above)** is the correct answer. **High-Yield Clinical Pearls for NEET-PG:** * **Hallmark Lab Findings:** Increased unconjugated bilirubin, increased LDH, and increased reticulocyte count (indicating marrow compensation) [3]. * **Haptoglobin:** Decreased in both types, but significantly lower in intravascular hemolysis. * **Splenomegaly:** A common feature in chronic extravascular hemolysis (like HS and Thalassemia) [2]. * **Peripheral Smear:** Look for **Howell-Jolly bodies** in sickle cell (autosplenectomy) [2] and **Target cells** in Thalassemia. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 598-599. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 644-645. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 597-598.
Question 925: In acute myeloid leukemia, Auer rods are numerous in which subtype?
- A. M2
- B. M3 (Correct Answer)
- C. M4
- D. M5
Explanation: **Explanation:** Auer rods are needle-like, azurophilic cytoplasmic inclusions formed by the fusion of primary granules (lysosomes) containing peroxidase. They are pathognomonic for **Acute Myeloid Leukemia (AML)**. **Why M3 is the correct answer:** In the FAB classification, **AML-M3 (Acute Promyelocytic Leukemia)** is characterized by a proliferation of abnormal promyelocytes. These cells contain an abundance of primary granules, leading to the formation of **numerous Auer rods** [1]. A classic finding in M3 is the presence of **"Faggot cells,"** which are blasts containing bundles or clusters of multiple Auer rods [1]. This subtype is associated with the **t(15;17)** translocation and carries a high risk of Disseminated Intravascular Coagulation (DIC) due to the release of procoagulant material from these granules [1]. **Analysis of incorrect options:** * **M2 (AML with maturation):** Auer rods are frequently present but are usually solitary or few in number, not "numerous" as seen in M3 [1]. * **M4 (Acute Myelomonocytic Leukemia):** Blasts show both myeloid and monocytic differentiation. Auer rods may be present in the myeloid component but are not a hallmark feature [1]. * **M5 (Acute Monocytic Leukemia):** Auer rods are typically **absent** in pure monocytic leukemias (M5a/M5b) [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Auer Rods Composition:** Crystalline aggregates of **Myeloperoxidase (MPO)**. * **M3 Treatment:** All-trans retinoic acid (ATRA) and Arsenic trioxide. * **M4eo Subtype:** Associated with **inv(16)** and characterized by abnormal eosinophils with large basophilic granules [1]. * **M5 Association:** Often presents with **gum hypertrophy** and skin involvement (leukemia cutis). **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. 620-622.
Question 926: "Chicken-wire" appearance of enlarged bone marrow spaces is seen in which of the following conditions?
- A. Fetal alcohol syndrome
- B. Sickle cell anaemia
- C. Haemophilia A
- D. Beta thalassemia major (Correct Answer)
Explanation: The **"chicken-wire" appearance** in Beta-thalassemia major refers to the radiographic and pathological appearance of the bone marrow. In this condition, severe chronic anemia leads to a massive compensatory increase in erythropoietin, causing **extreme erythroid hyperplasia**. This expansion of the marrow cavity results in the thinning of the cortical bone and the rarefaction of the trabeculae [1]. On imaging or gross examination, the remaining prominent trabeculae intersect to form a lattice-like or "chicken-wire" pattern. **Analysis of Options:** * **Beta-thalassemia major (Correct):** The massive expansion of the marrow causes the classic "chicken-wire" appearance, "crew-cut" or "hair-on-end" appearance on skull X-rays, and "chipmunk facies" due to maxillary marrow expansion [1]. * **Sickle cell anemia:** While it also features erythroid hyperplasia and "hair-on-end" appearance, the "chicken-wire" terminology is classically associated with the severe trabecular remodeling seen in Thalassemia major. * **Haemophilia A:** This is a coagulation disorder. It does not involve marrow hyperplasia; its primary skeletal manifestation is hemarthrosis (joint bleeding) leading to joint destruction. * **Fetal alcohol syndrome:** This is a congenital developmental disorder characterized by facial dysmorphism and CNS impairment, with no specific bone marrow remodeling patterns. **NEET-PG High-Yield Pearls:** * **Skull X-ray:** "Hair-on-end" appearance is seen in both Thalassemia [1] and Sickle Cell Anemia. * **Facial features:** "Chipmunk facies" (prominent cheekbones) is due to extramedullary hematopoiesis and marrow expansion in the facial bones. * **Diagnosis:** Gold standard is **Hb Electrophoresis** (showing increased HbF and HbA2, with absence/reduction of HbA). * **Peripheral Smear:** Characterized by microcytic hypochromic RBCs, **target cells**, and nucleated RBCs (normoblasts). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 648-649.
Question 927: Lysis of RBCs are seen in all of the following except?
- A. Thalassemia
- B. Methotrexate therapy
- C. Obstructive jaundice (Correct Answer)
- D. Sickle cell anemia
Explanation: **Explanation:** The core concept of this question lies in understanding the difference between **hemolysis** (premature destruction of RBCs) and **morphological changes** that increase RBC surface area without causing lysis. **Why Obstructive Jaundice is the correct answer:** In obstructive jaundice, there is an accumulation of bile salts and cholesterol in the plasma. These lipids are deposited onto the RBC membrane, increasing the surface area-to-volume ratio. This results in the formation of **Target Cells (Codocytes)**. Importantly, these cells are more resistant to osmotic lysis because the redundant membrane allows them to swell more than a normal RBC before bursting. Therefore, obstructive jaundice is associated with **decreased osmotic fragility**, not lysis. **Analysis of Incorrect Options:** * **Thalassemia:** This is a classic hemolytic anemia. The globin chain imbalance leads to the precipitation of unpaired chains (Heinz-like bodies), causing oxidative damage and splenic sequestration/lysis of RBCs [1]. * **Methotrexate therapy:** Methotrexate is a folate antagonist that causes **Megaloblastic Anemia**. While primarily a defect in DNA synthesis, it leads to "ineffective erythropoiesis," where fragile macro-ovalocytes are destroyed within the bone marrow or shortly after entering circulation (intramedullary and extramedullary hemolysis) [1]. * **Sickle cell anemia:** Polymerization of HbS causes the RBCs to become rigid and "sickle." These cells undergo both extravascular hemolysis (trapped in splenic sinusoids) and intravascular lysis due to membrane damage [2]. **NEET-PG High-Yield Pearls:** * **Target Cells** are seen in: **H**bC disease, **A**splenia, **L**iver disease (Obstructive Jaundice), and **T**halassemia (Mnemonic: **HALT**). * **Osmotic Fragility Test (OFT):** Increased in Hereditary Spherocytosis; Decreased in Thalassemia and Iron Deficiency Anemia. * **Methotrexate** toxicity is managed with **Leucovorin (Folinic acid) rescue**. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 596-597. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 639-640.
Question 928: Which of the following laboratory parameters is increased in hemophilia A?
- A. Prothrombin time (PT)
- B. Activated partial thromboplastin time (aPTT) (Correct Answer)
- C. Prothrombin time (PT) and activated partial thromboplastin time (aPTT)
- D. None of the above
Explanation: **Explanation:** Hemophilia A is an X-linked recessive bleeding disorder characterized by a deficiency of **Coagulation Factor VIII** [1]. To understand the lab findings, one must recall the coagulation cascade: 1. **Why aPTT is increased:** The **Activated Partial Thromboplastin Time (aPTT)** measures the integrity of the **Intrinsic** and Common pathways (Factors XII, XI, IX, VIII, X, V, II, and I). Since Factor VIII is a critical component of the intrinsic pathway, its deficiency leads to a prolonged (increased) aPTT. 2. **Why PT is normal:** The **Prothrombin Time (PT)** measures the **Extrinsic** and Common pathways (Factors VII, X, V, II, and I). Factor VIII is not involved in the extrinsic pathway; therefore, the PT remains normal in Hemophilia A. 3. **Why Option C is wrong:** As explained above, the defect is localized to the intrinsic pathway [3]. A simultaneous increase in both PT and aPTT would suggest a defect in the Common pathway (e.g., Factor X deficiency) or multiple factor deficiencies (e.g., Vitamin K deficiency or Liver disease) [3]. **High-Yield Clinical Pearls for NEET-PG:** * **Bleeding Time (BT):** Remains **normal** in Hemophilia A because BT assesses primary hemostasis (platelet function), which is unaffected. * **Mixing Study:** If aPTT is prolonged, a mixing study is performed. If the aPTT **corrects** after adding normal plasma, it confirms a factor deficiency (like Hemophilia). If it does not correct, it indicates the presence of an inhibitor. * **Clinical Presentation:** Characterized by deep tissue bleeding, **hemarthrosis** (bleeding into joints), and delayed postsurgical bleeding [2]. * **Treatment:** Recombinant Factor VIII concentrate or Cryoprecipitate (though the latter is less preferred now). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 670-671. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 623-624. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 624-625.
Question 929: A 76-year-old man presents with a lytic lesion in the vertebrae. X-ray skull showed multiple punched-out lesions. What is the most likely diagnosis?
- A. Metastasis
- B. Multiple myeloma (Correct Answer)
- C. Osteomalacia
- D. Hyperparathyroidism
Explanation: **Explanation:** The clinical presentation of an elderly patient with vertebral lytic lesions and classic **"punched-out" lesions** on the skull X-ray is the hallmark of **Multiple Myeloma (MM)** [1][2]. **Why Multiple Myeloma is correct:** Multiple Myeloma is a plasma cell dyscrasia characterized by the neoplastic proliferation of a single clone of plasma cells [3]. These cells secrete cytokines, most notably **RANKL**, which activates osteoclasts. This leads to extensive bone resorption, resulting in hypercalcemia and the characteristic radiolucent, "punched-out" lytic lesions (without reactive new bone formation) typically seen in the skull, vertebrae, and ribs [1][4]. **Why the other options are incorrect:** * **Metastasis:** While common in the elderly, most bony metastases (like from prostate cancer) are osteoblastic (sclerotic). While some (like lung or breast) can be lytic, they rarely present with the classic, discrete "punched-out" appearance seen in MM. * **Osteomalacia:** This involves defective mineralization of the osteoid matrix, usually due to Vitamin D deficiency. It presents with diffuse bone pain and "Looser’s zones" (pseudofractures), not focal lytic lesions. * **Hyperparathyroidism:** This leads to generalized bone resorption. Classic radiographic findings include subperiosteal resorption (especially in phalanges) and "Brown tumors," but not the discrete punched-out lesions of the skull. **High-Yield Clinical Pearls for NEET-PG:** * **CRAB Criteria:** **C**alcium (elevated), **R**enal insufficiency, **A**nemia, **B**one lesions [1]. * **Diagnosis:** Bone marrow biopsy showing >10% clonal plasma cells [4]; M-spike on serum protein electrophoresis (SPEP) [3]. * **Peripheral Smear:** **Rouleaux formation** (due to increased globulins) [4][5]. * **Urinalysis:** Bence-Jones proteins (light chains) may be present [2]; notably, these are **not** detected by standard dipstick tests. **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, p. 608. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 616-617. [3] 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. 606-607. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 617-618. [5] 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. 607-608.
Question 930: Pelger-Huët anomaly is characterized by the presence of which of the following in neutrophils?
- A. Hyposegmented neutrophils (Correct Answer)
- B. Hypersegmented neutrophils
- C. Unsegmented neutrophils
- D. None of the above
Explanation: **Explanation:** **Pelger-Huët Anomaly (PHA)** is an autosomal dominant inherited condition characterized by a failure of normal nuclear segmentation in neutrophils. This occurs due to a mutation in the **Lamin B receptor (LBR) gene**, which is essential for maintaining the nuclear envelope's structure. 1. **Why Option A is correct:** In PHA, the neutrophil nuclei are **hyposegmented**. They typically present with only two lobes connected by a thin filament of chromatin, giving them a characteristic **"pince-nez" appearance** (like a pair of spectacles). Despite the abnormal shape, the chromatin is mature and coarse, and the cells function normally. 2. **Why Option B is incorrect:** **Hypersegmented neutrophils** (defined as >5% of neutrophils having 5 lobes or any having ≥6 lobes) are the hallmark of **Megaloblastic anemia** (Vitamin B12 or Folate deficiency) [1]. 3. **Why Option C is incorrect:** While some neutrophils in PHA may appear unsegmented (round or oval nuclei), the defining diagnostic feature is the consistent pattern of hyposegmentation across the majority of the granulocyte population. **High-Yield Clinical Pearls for NEET-PG:** * **Pseudo-Pelger-Huët Anomaly:** This is an *acquired* form of hyposegmentation seen in **Myelodysplastic Syndromes (MDS)**, Acute Myeloid Leukemia (AML), or certain drug therapies (e.g., Tacrolimus). * **Differentiation:** In the inherited form, nearly 100% of neutrophils are affected. In the acquired (pseudo) form, only a fraction of cells are affected, and they often show "hypogranularity." * **Key Morphological Clue:** Look for the **"Pince-nez"** description in clinical vignettes to identify PHA. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, p. 654.
Practice by Chapter
Anemias: Classification and Approach
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Hemolytic Anemias
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Myeloproliferative Neoplasms
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Myelodysplastic Syndromes
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Acute Leukemias
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Chronic Leukemias
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Lymphomas and Lymphoid Neoplasms
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Plasma Cell Disorders
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Bleeding Disorders
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Thrombotic Disorders
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