Hematopathology — MCQs

Hematopathology Indian Medical PG Practice Questions and MCQs

Question 671: Popcorn cells are characteristic of which type of Hodgkin's lymphoma?

A. Nodular sclerosis
B. Mixed cellularity
C. Lymphocyte predominance (Correct Answer)
D. Lymphocyte depletion

Explanation: **Explanation:** **Popcorn cells** (also known as **L&H cells** – Lymphocytic and Histiocytic variants) are the hallmark diagnostic feature of **Nodular Lymphocyte Predominant Hodgkin Lymphoma (NLPHL)** [1]. Unlike the classic Reed-Sternberg (RS) cells, these cells have a multi-lobed, folded nucleus resembling a kernel of popped corn, with inconspicuous nucleoli and a B-cell phenotype (CD20+, CD45+, but CD15- and CD30-) [1][2]. **Analysis of Options:** * **Nodular Sclerosis (Option A):** Characterized by **Lacunar cells** (RS cells sitting in empty spaces due to formalin fixation) and broad bands of collagen fibrosis [2]. It is the most common subtype. * **Mixed Cellularity (Option B):** Characterized by **classic "Owl-eye" RS cells** (CD15+, CD30+) in a polymorphic background of eosinophils, plasma cells, and histiocytes [2]. Often associated with EBV. * **Lymphocyte Depletion (Option D):** The rarest and most aggressive form, showing numerous **pleomorphic/anaplastic RS cells** with very few background lymphocytes. **High-Yield Pearls for NEET-PG:** 1. **Immunophenotype:** Popcorn cells are **CD20+ and CD45+**, whereas Classic Hodgkin Lymphoma (CHL) cells are **CD15+ and CD30+**. 2. **Clinical Course:** NLPHL usually presents as localized peripheral lymphadenopathy (cervical/axillary) and has an excellent prognosis, though it can transform into Diffuse Large B-Cell Lymphoma (DLBCL) [1]. 3. **Background:** In NLPHL, the background consists predominantly of small B-lymphocytes arranged in a nodular pattern, unlike the T-cell rich background of CHL [1]. **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. 618. [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, p. 616.

Question 672: What is a cause of Vitamin B12 deficiency megaloblastic anemia?

A. Fish tapeworm infestation (Correct Answer)
B. Dilantin therapy
C. Gastrectomy
D. Ileal resection

Explanation: **Explanation:** Megaloblastic anemia results from impaired DNA synthesis, most commonly due to a deficiency in Vitamin B12 (Cobalamin) or Folic Acid [1]. **Why Option A is Correct:** **Fish tapeworm infestation** (*Diphyllobothrium latum*) is a classic cause of Vitamin B12 deficiency. This parasite, typically acquired by consuming undercooked freshwater fish, competes with the host for dietary Vitamin B12 in the proximal small intestine. It can absorb up to 80-100% of the host's intake, leading to a profound deficiency. **Analysis of Other Options:** * **Option B: Dilantin (Phenytoin) therapy** is a well-known cause of **Folic Acid deficiency**, not B12 deficiency. It interferes with folate absorption and metabolism. * **Option C: Gastrectomy** leads to B12 deficiency because the stomach's parietal cells are removed, eliminating the production of **Intrinsic Factor (IF)**, which is essential for B12 absorption [1], [2]. * **Option D: Ileal resection** causes B12 deficiency because the **terminal ileum** is the specific anatomical site where the B12-IF complex is absorbed [1], [3]. *Note: While C and D also cause B12 deficiency, in the context of standard medical examinations, if a single "most specific" or "classic" parasitic cause is asked, D. latum is the intended answer. However, clinically, all three (A, C, and D) are valid causes.* **High-Yield NEET-PG Pearls:** * **Neurological symptoms:** B12 deficiency presents with **Subacute Combined Degeneration (SCD)** of the spinal cord (affecting posterior and lateral columns), whereas Folate deficiency does not [1]. * **Peripheral Smear:** Look for macro-ovalocytes and **hypersegmented neutrophils** (>5 lobes) [3]. * **Biochemical markers:** Both B12 and Folate deficiency show elevated **Homocysteine**, but only B12 deficiency shows elevated **Methylmalonic Acid (MMA)**. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 130-131. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 592-593. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, p. 654.

Question 673: Which of the following conditions is characterized by a deficiency in Gp?

A. Glanzmann's thrombasthenia (Correct Answer)
B. Bernard-Soulier syndrome
C. Platelet storage pool disorders
D. Glycoprotein IIb/IIIa deficiency

Explanation: **Explanation:** **Glanzmann’s Thrombasthenia (GT)** is an autosomal recessive bleeding disorder characterized by a deficiency or dysfunction of the **Glycoprotein IIb/IIIa (GpIIb/IIIa)** complex [1]. This complex is the primary receptor for **fibrinogen**; its absence prevents platelet-to-platelet aggregation, leading to a failure in forming a primary hemostatic plug [2], [3]. **Analysis of Options:** * **Option A & D (Correct):** Glanzmann’s Thrombasthenia is defined by the deficiency of GpIIb/IIIa [1]. (Note: In many exam formats, Option A and D might be synonymous; however, GT is the clinical name of the syndrome). * **Option B (Incorrect):** **Bernard-Soulier Syndrome (BSS)** is characterized by a deficiency of the **GpIb-IX-V** complex [1]. This complex is the receptor for von Willebrand factor (vWF), meaning BSS is a disorder of platelet **adhesion**, not aggregation [2]. * **Option C (Incorrect):** **Storage Pool Disorders** involve deficiencies in platelet granules (Alpha or Delta granules), such as Gray Platelet Syndrome or Hermansky-Pudlak Syndrome, rather than surface glycoproteins. **High-Yield Clinical Pearls for NEET-PG:** * **Peripheral Smear:** In GT, platelets appear normal in size and morphology but are **isolated** (no clumping). In BSS, platelets are **large (Giant Platelets)** and reduced in number. * **Platelet Aggregation Studies:** In GT, aggregation is **absent with ADP, Epinephrine, and Collagen**, but **normal with Ristocetin** [1]. (The opposite is true for BSS and vWD). * **Flow Cytometry:** This is the gold standard for diagnosis, showing decreased expression of CD41 (GpIIb) and CD61 (GpIIIa). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 668-669. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, p. 128. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 669-670.

Question 674: Oral anticoagulants are monitored by which laboratory test?

A. Bleeding time (BT)
B. Coagulation time (CT)
C. Prothrombin time (PT) (Correct Answer)
D. Partial thromboplastin time (PTT)

Explanation: **Explanation:** Oral anticoagulants, primarily **Warfarin**, function as Vitamin K antagonists [1]. They inhibit the enzyme Vitamin K epoxide reductase, thereby preventing the gamma-carboxylation of Vitamin K-dependent clotting factors: **II, VII, IX, and X**, as well as proteins C and S [1]. **Why Prothrombin Time (PT) is the correct answer:** The PT test measures the **Extrinsic and Common pathways** of the coagulation cascade. Factor VII (part of the extrinsic pathway) has the shortest half-life (~6 hours) among all clotting factors. Therefore, PT is the most sensitive and earliest indicator of the anticoagulant effect of Warfarin. In clinical practice, PT is standardized as the **International Normalized Ratio (INR)** to ensure consistency across laboratories. **Analysis of Incorrect Options:** * **Bleeding Time (BT):** Measures **platelet function** and vascular integrity. It is used to screen for disorders like Von Willebrand Disease or platelet dysfunction, not the coagulation cascade. * **Coagulation Time (CT):** An obsolete, non-specific test for the overall clotting process; it lacks the sensitivity required for drug monitoring. * **Partial Thromboplastin Time (PTT/aPTT):** Measures the **Intrinsic and Common pathways**. It is primarily used to monitor **Unfractionated Heparin** therapy, which affects factors XII, XI, IX, and VIII. **High-Yield Clinical Pearls for NEET-PG:** * **Warfarin Monitoring:** PT/INR (Target INR usually 2.0–3.0). * **Heparin Monitoring:** aPTT. * **LMWH Monitoring:** Anti-Factor Xa assay (though routine monitoring is usually unnecessary). * **Warfarin Overdose Antidote:** Vitamin K (slow) or Fresh Frozen Plasma/Prothrombin Complex Concentrate (rapid). * **Early Warfarin Therapy:** Can cause a transient prothrombotic state due to the rapid depletion of Protein C; hence, "heparin bridging" is required. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 582-583.

Question 675: Which of the following statements regarding Leukocyte Alkaline Phosphatase (LAP) is true?

A. It is a screening test used to distinguish Chronic Myeloid Leukemia (CML) from other Myeloproliferative Disorders.
B. LAP levels increase in all Myeloproliferative Disorders except CML.
C. LAP levels increase in Polycythemia Vera.
D. All of the above. (Correct Answer)

Explanation: **Explanation:** The **Leukocyte Alkaline Phosphatase (LAP) score**, also known as the Neutrophil Alkaline Phosphatase (NAP) score, is a cytochemical stain used to assess the enzyme activity within the secondary granules of mature neutrophils. 1. **Why Option D is Correct:** * **Distinguishing CML (Option A):** In Chronic Myeloid Leukemia (CML), the LAP score is characteristically **low or zero** due to the presence of immature, functionally defective neutrophils [1]. This makes it an excellent screening tool to differentiate CML from a **Leukemoid Reaction** or other Myeloproliferative Neoplasms (MPNs) where the score is typically elevated [1]. * **MPNs vs. CML (Option B):** While CML shows a decreased score, other MPNs like Polycythemia Vera (PV), Essential Thrombocythemia (ET), and Primary Myelofibrosis (PMF) generally show **increased** LAP levels [1], [2]. * **Polycythemia Vera (Option C):** An elevated LAP score is a classic finding in PV, helping distinguish it from secondary polycythemia (where the score is usually normal) [3]. **Clinical Pearls for NEET-PG:** * **Decreased LAP Score (<20):** CML (most common), Paroxysmal Nocturnal Hemoglobinuria (PNH), Hypophosphatasia, and Aplastic Anemia. * **Increased LAP Score (>100):** Leukemoid Reaction, Polycythemia Vera, Pregnancy (due to estrogen), and Stress/Infection. * **Normal Range:** 20–100. * **Modern Context:** While the LAP score is a classic exam favorite, it has largely been replaced in clinical practice by molecular testing for the **BCR-ABL1** fusion gene (for CML) [1] and **JAK2** mutations (for other MPNs) [2]. **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. 624-625. [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, p. 624. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 614-615.

Question 676: What is the most common tumor of the spleen?

A. Lymphoma (Correct Answer)
B. Sarcoma
C. Hemangioma
D. Metastasis

Explanation: **Explanation:** The spleen is a secondary lymphoid organ, making it a frequent site for both primary and secondary involvement of hematological malignancies [1]. **Why Lymphoma is Correct:** **Lymphoma** is considered the **most common tumor of the spleen** overall. While primary splenic lymphoma (originating solely in the spleen) is rare, secondary involvement of the spleen by systemic non-Hodgkin lymphoma (NHL) or Hodgkin lymphoma is extremely common [1]. Since the spleen is essentially a large lymph node, it is the most frequently involved organ in systemic lymphomas [2]. **Analysis of Incorrect Options:** * **Hemangioma:** This is the most common **benign** primary tumor of the spleen. It is usually an incidental finding and asymptomatic. * **Sarcoma:** Primary splenic sarcomas (like angiosarcoma) are the most common primary **malignant** non-lymphoid tumors of the spleen, but they are exceptionally rare compared to lymphoma. * **Metastasis:** While the spleen is highly vascular, metastases from solid visceral tumors (e.g., lung, breast, melanoma) are relatively **uncommon**. This is thought to be due to the spleen's high concentration of immune cells and the rhythmic contraction of its capsule, which prevents "seeding." **High-Yield NEET-PG Pearls:** * **Most common benign tumor:** Hemangioma. * **Most common primary malignancy:** Lymphoma (specifically Splenic Marginal Zone Lymphoma is a classic primary type) [1]. * **Most common non-lymphoid primary malignancy:** Angiosarcoma (highly aggressive). * **Gaucher Disease:** The most common cause of massive splenomegaly (non-neoplastic). * **Gamna-Gandy Bodies:** Siderofibrotic nodules (calcium and iron deposits) seen in the spleen in portal hypertension. **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. 569-570. [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. 609-610.

Question 677: Acid phosphatase cytochemical staining is used in the diagnosis of which of the following hematological neoplasms?

A. Chronic myeloid leukemia
B. Acute myeloid leukemia
C. B-cell acute lymphoblastic leukemia
D. T-cell acute lymphoblastic leukemia (Correct Answer)

Explanation: **Explanation:** **Acid Phosphatase (AP)** is a cytochemical stain primarily used to differentiate subtypes of Acute Lymphoblastic Leukemia (ALL). 1. **Why T-cell ALL is correct:** In **T-cell ALL**, the acid phosphatase reaction shows a characteristic **focal, intense, "block-like" positivity** specifically in the **paranuclear (Golgi) region** of the lymphoblasts. This is a classic diagnostic marker used to distinguish T-ALL from B-ALL. 2. **Why other options are incorrect:** * **Chronic Myeloid Leukemia (CML):** The hallmark cytochemical stain for CML is **Leukocyte Alkaline Phosphatase (LAP)**. In CML, the LAP score is characteristically **decreased**, which helps differentiate it from a Leukemoid Reaction (where the score is increased). * **Acute Myeloid Leukemia (AML):** The primary stains for AML are **Myeloperoxidase (MPO)** and **Sudan Black B (SBB)**. While some monocytic leukemias (AML-M4/M5) show diffuse acid phosphatase positivity, it is not the diagnostic standard compared to Non-specific Esterase (NSE). * **B-cell ALL:** Lymphoblasts in B-ALL are typically **negative** or show only weak, diffuse activity for acid phosphatase, unlike the focal polar positivity seen in T-cells. **High-Yield Clinical Pearls for NEET-PG:** * **TRAP (Tartrate-Resistant Acid Phosphatase):** A specialized version of this stain is the gold standard for diagnosing **Hairy Cell Leukemia**. * **MPO:** The most sensitive stain for the myeloid lineage; it is always negative in ALL. * **PAS (Periodic Acid-Schiff):** Shows "block-like" positivity in both B-ALL and T-ALL, representing glycogen deposits. * **T-ALL Presentation:** Often presents as a **mediastinal mass** in adolescent males (the "Terrible T's": T-cell, Thymus, Teenager) [1]. **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. 599-600.

Question 678: Chronic granulocytic leukemia is due to which of the following chromosomal abnormalities?

A. Chromosomal deletion
B. Chromosomal mutation
C. Chromosomal translocation (Correct Answer)
D. None of the above

Explanation: **Explanation:** **Chronic Granulocytic Leukemia (CGL)**, now more commonly known as **Chronic Myeloid Leukemia (CML)**, is the classic example of a malignancy caused by a specific **chromosomal translocation** [4]. 1. **Why Translocation is Correct:** The hallmark of CML is the **Philadelphia chromosome (Ph)** [3]. This is a result of a reciprocal translocation between chromosomes 9 and 22, denoted as **t(9;22)(q34;q11)**. This event moves the *ABL1* proto-oncogene from chromosome 9 to the *BCR* gene on chromosome 22. The resulting **BCR-ABL1 fusion gene** encodes a chimeric protein with constitutive (always active) **tyrosine kinase activity**, which drives uncontrolled proliferation of the myeloid lineage [1], [2]. 2. **Why Other Options are Incorrect:** * **Chromosomal Deletion:** While deletions (like 5q- or 7q-) are common in Myelodysplastic Syndromes (MDS) or AML, they are not the primary driver of CML. * **Chromosomal Mutation:** This is a vague term. While point mutations (like *JAK2 V617F* in Polycythemia Vera) drive other myeloproliferative neoplasms, CML is specifically defined by the large-scale structural rearrangement of a translocation. **High-Yield Clinical Pearls for NEET-PG:** * **Cytogenetics:** The Philadelphia chromosome is found in >95% of CML cases. * **Diagnosis:** The most sensitive test to detect the BCR-ABL1 fusion is **RT-PCR** (qualitative for diagnosis, quantitative for monitoring). * **LAP Score:** Leukocyte Alkaline Phosphatase (LAP) score is characteristically **decreased** in CML (helps differentiate it from a Leukemoid reaction where LAP is high). * **Treatment:** The first-line treatment is **Imatinib** (Gleevec), a selective tyrosine kinase inhibitor (TKI) that targets the BCR-ABL protein [2]. **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. 624. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 295-296. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. (Basic Pathology) introduces the student to key general principles of pathology, both as a medical science and as a clinical activity with a vital role in patient care. Part 2 (Disease Mechanisms) provides fundamental knowledge about the cellular and molecular processes involved in diseases, providing the rationale for their treatment. Part 3 (Systematic Pathology) deals in detail with specific diseases, with emphasis on the clinically important aspects., pp. 225-226. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 605-607.

Question 679: Which of the following is pathognomonic of thalassemia major?

A. Conjugated hyperbilirubinemia
B. Raised HbA2
C. Raised HbF (Correct Answer)
D. Severe anemia

Explanation: ### Explanation **Correct Answer: C. Raised HbF** In **Thalassemia Major** (Cooley’s Anemia), there is a near-total or total absence of $\beta$-globin chain synthesis ($\beta^0/\beta^0$). To compensate for the lack of Adult Hemoglobin (HbA, $\alpha_2\beta_2$), the body continues to produce $\gamma$-chains, which combine with $\alpha$-chains to form **Fetal Hemoglobin (HbF, $\alpha_2\gamma_2$)**. In these patients, HbF levels are characteristically markedly elevated, often exceeding **90%** of total hemoglobin [1]. This is the diagnostic hallmark (pathognomonic feature) used to confirm the condition via Hemoglobin Electrophoresis or HPLC. **Analysis of Incorrect Options:** * **A. Conjugated hyperbilirubinemia:** Thalassemia involves extravascular hemolysis (ineffective erythropoiesis). This leads to **unconjugated (indirect) hyperbilirubinemia**, not conjugated. * **B. Raised HbA2:** While HbA2 ($\alpha_2\delta_2$) is elevated in **Thalassemia Minor** (Trait), it is variable or absent in Thalassemia Major because $\delta$-chain synthesis cannot compensate for the massive $\beta$-chain deficit. * **D. Severe anemia:** While Thalassemia Major presents with severe microcytic hypochromic anemia [2], this is a **non-specific** finding seen in various conditions like severe Iron Deficiency Anemia or Sideroblastic Anemia. **NEET-PG High-Yield Pearls:** * **Target Cells:** Common peripheral smear finding in Thalassemia. * **X-ray Findings:** "Hair-on-end" appearance of the skull and "Crew-cut" sign due to compensatory extramedullary hematopoiesis [3]. * **Mentzer Index:** (MCV/RBC count) < 13 suggests Thalassemia; > 13 suggests Iron Deficiency Anemia. * **Complication:** Iron overload (hemosiderosis) due to chronic transfusions is the leading cause of mortality (cardiac failure) [3]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, p. 648. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 600-601. [3] 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 680: All of the following statements regarding Sickle Cell Anemia are true EXCEPT:

A. The shift from HbF to HbS occurs due to point mutation.
B. Microvascular occlusion is a severe complication of Sickle Cell Anemia.
C. Deoxygenation of RBCs can lead to extensive membrane damage.
D. Adults, but not children, with sickle cell disease are functionally asplenic, making them susceptible to infections caused by encapsulated bacteria, such as pneumococci. (Correct Answer)

Explanation: **Explanation** The correct answer is **D** because the statement "Adults, but not children" is incorrect. In Sickle Cell Anemia (SCA), functional asplenia begins in **early childhood** (often by 6 months to 1 year of age) due to repeated splenic infarcts caused by microvascular occlusion [1]. By adulthood, the spleen is typically reduced to a small fibrous remnant, a process known as **autosplenectomy** [2]. Both children and adults are at high risk for life-threatening infections from encapsulated organisms (e.g., *Streptococcus pneumoniae*, *Haemophilus influenzae*) [1]. **Analysis of other options:** * **Option A:** True. SCA is caused by a **point mutation** (GAG → GTG) in the 6th codon of the β-globin gene, resulting in the substitution of Valine for Glutamic acid. * **Option B:** True. Polymerized HbS causes RBCs to sickle, leading to **vaso-occlusive crises**. This results in tissue ischemia, pain, and organ damage (e.g., Acute Chest Syndrome) [2]. * **Option C:** True. Repeated cycles of deoxygenation and sickling cause **membrane damage**, leading to calcium influx and potassium loss. Eventually, the RBCs become "irreversibly sickled" and are removed by the spleen (extravascular hemolysis) [1]. **High-Yield NEET-PG Pearls:** * **Protective Factor:** HbF inhibits the polymerization of HbS; hence, symptoms appear only after 6 months when HbF levels drop. Hydroxyurea is used therapeutically to increase HbF. * **Infection Risk:** The most common cause of osteomyelitis in SCA patients is *Salmonella*. * **Blood Film:** Look for **Sickle cells** and **Howell-Jolly bodies** (indicative of asplenia) [1]. * **Metaplastic change:** "Crew-cut" appearance on skull X-ray due to compensatory erythroid hyperplasia [1]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 644-645. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 645-646.

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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