Hematopathology — MCQs
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A 50-year-old woman presents with easy fatigability, a smooth sore tongue, numbness and tingling of the feet, and weakness of the legs. A complete blood count shows a megaloblastic anemia that is not reversed by folate therapy. Hemoglobin is 5.6 g/dL, WBC count is 5,100/mL, and platelets are 240,000/mL. This patient most likely has a deficiency of which of the following vitamins?
Which of the following agents is of value in the postoperative care of the hemophilic patient?
Which is the most common lymphoma in adults?
Birbeck’s granules in the cytoplasm are seen in:
Which of the following statements regarding Fanconi anemia is incorrect?
Osmotic fragility is increased in which of the following conditions?
What is the characteristic shape of Birbeck granules?
What causes hemolysis in G6-PD deficiency?
In which of the following conditions are Auer rods seen?
Thrombocytopenia is caused by which of the following conditions?
Hematopathology Indian Medical PG Practice Questions and MCQs
Question 1221: A 50-year-old woman presents with easy fatigability, a smooth sore tongue, numbness and tingling of the feet, and weakness of the legs. A complete blood count shows a megaloblastic anemia that is not reversed by folate therapy. Hemoglobin is 5.6 g/dL, WBC count is 5,100/mL, and platelets are 240,000/mL. This patient most likely has a deficiency of which of the following vitamins?
- A. Vitamin B1 (thiamine)
- B. Vitamin B2 (riboflavin)
- C. Vitamin B12 (Correct Answer)
- D. Vitamin K
Explanation: ### Explanation **Correct Option: C. Vitamin B12 (Cobalamin)** The clinical presentation of **megaloblastic anemia** (fatigue, low Hb) combined with **neurological symptoms** (numbness, tingling, weakness) is a classic hallmark of Vitamin B12 deficiency [1]. * **Pathophysiology:** Vitamin B12 is essential for DNA synthesis and the maintenance of myelin in the nervous system [1]. A deficiency leads to ineffective erythropoiesis (megaloblastic changes). Crucially, while folate can bypass the "methyl-folate trap" to correct the anemia, it **cannot** correct the neurological damage (Subacute Combined Degeneration of the spinal cord) [1]. The fact that the anemia was not reversed by folate therapy strongly points toward B12 deficiency. * **Clinical Signs:** The "smooth sore tongue" (atrophic glossitis) is common in both B12 and folate deficiency, but the neurological involvement is specific to B12 [1]. **Why Incorrect Options are Wrong:** * **Vitamin B1 (Thiamine):** Deficiency causes Beriberi (dry/wet) or Wernicke-Korsakoff syndrome. It does not cause megaloblastic anemia. * **Vitamin B2 (Riboflavin):** Deficiency leads to cheilosis, corneal vascularization, and glossitis, but not megaloblastic anemia or dorsal column spinal cord symptoms. * **Vitamin K:** Essential for the gamma-carboxylation of clotting factors (II, VII, IX, X). Deficiency leads to bleeding diathesis (increased PT/aPTT), not anemia. **NEET-PG High-Yield Pearls:** * **Schilling Test:** Historically used to determine the cause of B12 malabsorption (e.g., Pernicious Anemia). * **Biochemical Markers:** In B12 deficiency, both **Homocysteine** and **Methylmalonic Acid (MMA)** levels are elevated. In folate deficiency, only Homocysteine is elevated. * **Peripheral Smear:** Look for **hypersegmented neutrophils** (>5 lobes) and macro-ovalocytes [3]. * **Pernicious Anemia:** The most common cause of B12 deficiency, caused by autoimmune destruction of gastric parietal cells (leading to lack of Intrinsic Factor) [2]. **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, pp. 654-655.
Question 1222: Which of the following agents is of value in the postoperative care of the hemophilic patient?
- A. Vitamin K
- B. Monsel's solution
- C. Aminocaproic acid (Correct Answer)
- D. Factor 8 cryoprecipitate
Explanation: ### Explanation **Correct Answer: C. Aminocaproic acid** **Mechanism and Rationale:** In hemophilic patients, post-operative bleeding is often exacerbated by **fibrinolysis**. While factor replacement therapy helps form a clot, the clot is inherently unstable due to the underlying deficiency. **Aminocaproic acid (EACA)** and Tranexamic acid are **antifibrinolytic agents** that competitively inhibit plasminogen activation [1]. By preventing the breakdown of the newly formed fibrin clot, these agents are invaluable in the postoperative period, particularly after dental extractions or mucosal surgeries, to reduce the requirement for factor replacement and prevent delayed secondary hemorrhage. **Analysis of Incorrect Options:** * **A. Vitamin K:** This is essential for the synthesis of Factors II, VII, IX, and X. Hemophilia A and B are hereditary deficiencies of Factors VIII and IX, respectively, and are not caused by Vitamin K deficiency. Supplementation will not correct the genetic defect. * **B. Monsel’s solution (Ferric subsulfate):** This is a topical hemostatic agent used for superficial capillary bleeding (e.g., after a skin biopsy). It is not a systemic postoperative management strategy for the complex coagulation defect in hemophilia. * **D. Factor 8 cryoprecipitate:** While cryoprecipitate contains Factor VIII, it is no longer the preferred treatment due to the risk of transfusion-transmitted infections. Modern management utilizes **recombinant Factor VIII concentrates**. Furthermore, the question asks for an "agent of value" in postoperative care; antifibrinolytics are specific adjunctive therapies used to maintain clot stability once factor levels are stabilized. **NEET-PG High-Yield Pearls:** * **Antifibrinolytics** are specifically contraindicated in patients with **hematuria** (risk of unresolvable obstructive clots in the ureter). * **Desmopressin (dDAVP)** is the treatment of choice for **Mild Hemophilia A** as it releases endogenous Factor VIII and vWF from Weibel-Palade bodies. * **Cryoprecipitate** contains: Factor VIII, XIII, Fibrinogen, vWF, and Fibronectin. It does **not** contain Factor IX. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, pp. 130-132.
Question 1223: Which is the most common lymphoma in adults?
- A. Adult T-cell leukemia/lymphoma (ATLL)
- B. Hodgkin lymphoma
- C. Diffuse large B-cell lymphoma (DLBCL) (Correct Answer)
- D. Follicular lymphoma
Explanation: **Explanation:** **Diffuse Large B-cell Lymphoma (DLBCL)** is the most common histological subtype of Non-Hodgkin Lymphoma (NHL) worldwide, accounting for approximately **30–40% of all adult cases**. It is an aggressive (high-grade) B-cell neoplasm characterized by large lymphoid cells with a diffuse growth pattern that obliterates the lymph node architecture [1]. It typically presents as a rapidly enlarging mass [2] and can occur both de novo or as a transformation from low-grade lymphomas (e.g., Richter transformation) [1]. **Analysis of Incorrect Options:** * **Adult T-cell leukemia/lymphoma (ATLL):** This is a rare peripheral T-cell neoplasm caused by the **HTLV-1 virus**. It is endemic in specific regions like Japan and the Caribbean but is not the most common lymphoma globally. * **Hodgkin Lymphoma:** While common in young adults (bimodal age distribution), it is significantly less frequent than the collective group of Non-Hodgkin Lymphomas. * **Follicular Lymphoma:** This is the **second most common** NHL in adults and the most common "indolent" (low-grade) lymphoma [3]. It is characterized by a $t(14;18)$ translocation involving the *BCL2* gene [4]. **High-Yield Clinical Pearls for NEET-PG:** * **Most common NHL in children:** Burkitt Lymphoma or Lymphoblastic Lymphoma [5]. * **Most common site of extranodal lymphoma:** Stomach (usually MALToma or DLBCL). * **DLBCL Markers:** CD19, CD20, CD22, and CD79a (Pan-B cell markers). * **Prognostic Index:** The International Prognostic Index (IPI) is used to predict outcomes in DLBCL based on Age, Stage, LDH levels, Performance status, and Extranodal involvement. **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. 563-564. [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. 604-605. [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. 602-604. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 561-562. [5] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 560-561.
Question 1224: Birbeck’s granules in the cytoplasm are seen in:
- A. Langerhans cells (Correct Answer)
- B. Mast cells
- C. Myelocytes
- D. Thrombocytes
Explanation: **Explanation:** **Langerhans cells (Option A)** are specialized dendritic cells found primarily in the skin (stratum spinosum) and other squamous epithelia [1]. The pathognomonic ultrastructural feature of these cells is the **Birbeck granule** [1]. Under electron microscopy, these are rod-shaped, pentalaminar cytoplasmic organelles with a central striated line and a bulbous end, giving them a characteristic **"tennis racket" appearance** [1]. They contain the protein **langerin (CD207)**, which is involved in the endocytosis and degradation of viruses [1]. **Why other options are incorrect:** * **Mast cells (Option B):** These are characterized by dense, membrane-bound cytoplasmic granules containing histamine, heparin, and tryptase. They do not contain Birbeck granules. * **Myelocytes (Option C):** These are precursors in the granulocytic series. They contain primary (azurophilic) and secondary (specific) granules, but lack Birbeck granules. * **Thrombocytes (Option D):** Platelets contain alpha-granules (fibrinogen, vWF) and dense granules (ADP, ATP, serotonin, calcium), but no Birbeck granules. **High-Yield Clinical Pearls for NEET-PG:** * **Langerhans Cell Histiocytosis (LCH):** A group of disorders (e.g., Letterer-Siwe disease, Hand-Schüller-Christian disease) characterized by the proliferation of these cells [1]. * **Immunohistochemistry (IHC) Markers:** LCH cells are characteristically positive for **S-100**, **CD1a**, and **CD207 (Langerin)** [1]. * **Radiology:** Often presents with "punched-out" lytic bone lesions, especially in the skull. **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. 629-630.
Question 1225: Which of the following statements regarding Fanconi anemia is incorrect?
- A. It is an autosomal dominant disorder. (Correct Answer)
- B. Bone marrow examination typically shows pancytopenia.
- C. It commonly presents as aplastic anemia.
- D. It results from a defect in DNA repair.
Explanation: **Explanation** **1. Why Option A is the Correct (Incorrect Statement):** Fanconi Anemia (FA) is primarily an **autosomal recessive** disorder. While rare cases of X-linked inheritance (FANCB gene) exist, it is **not** an autosomal dominant condition. This is a common trap in NEET-PG; most inherited bone marrow failure syndromes are recessive. **2. Analysis of Other Options:** * **Option B & C:** FA is the most common cause of **inherited aplastic anemia** [1]. The defect leads to progressive bone marrow failure, which manifests as **pancytopenia** (reduction in RBCs, WBCs, and platelets). Bone marrow examination typically reveals hypocellularity with increased fat replacement [2]. * **Option D:** The fundamental pathogenesis involves mutations in the **FANC gene family**, which are responsible for the **DNA interstrand cross-link repair** pathway. This defect leads to genomic instability and hypersensitivity to DNA-damaging agents. **3. Clinical Pearls & High-Yield Facts for NEET-PG:** * **Physical Findings:** Look for "Thumb and Radius" defects (absent/hypoplastic), short stature, microcephaly, and **Café-au-lait spots**. * **Diagnostic Test:** The gold standard is the **Chromosomal Breakage Analysis** using Clastogenic agents like **Diepoxybutane (DEB)** or Mitomycin C. * **Malignancy Risk:** Patients have a significantly high risk of developing **AML** (Acute Myeloid Leukemia) and squamous cell carcinomas (head, neck, and anogenital). * **Treatment:** Hematopoietic stem cell transplant (HSCT) is the definitive treatment for hematologic manifestations. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 595-596. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 662-663.
Question 1226: Osmotic fragility is increased in which of the following conditions?
- A. Sickle cell anaemia
- B. Thalassemia
- C. Hereditary spherocytosis (Correct Answer)
- D. Chronic lead poisoning
Explanation: ### Explanation **Correct Answer: C. Hereditary spherocytosis** **Mechanism:** Osmotic fragility (OF) measures the resistance of red blood cells (RBCs) to hemolysis when exposed to varying concentrations of hypotonic saline [1]. The primary determinant of OF is the **surface area-to-volume ratio**. In **Hereditary Spherocytosis (HS)**, molecular defects in membrane proteins (like Ankyrin, Spectrin, or Band 3) lead to a loss of membrane fragments [2]. This forces the cell to assume a spherical shape—the smallest possible surface area for a given volume. Because spherocytes have no "spare" membrane to expand when water enters via osmosis, they rupture at higher saline concentrations than normal biconcave cells, resulting in **increased osmotic fragility** [1]. **Analysis of Incorrect Options:** * **A. Sickle cell anaemia & B. Thalassemia:** These conditions are characterized by **target cells** (codocytes) [3]. Target cells have an excess of membrane relative to their hemoglobin content (increased surface area-to-volume ratio). They can withstand more swelling before bursting, thus showing **decreased osmotic fragility**. * **D. Chronic lead poisoning:** This typically presents with microcytic anemia and basophilic stippling. It does not characteristically increase osmotic fragility; in fact, any condition producing target cells or iron deficiency may decrease it. **High-Yield Pearls for NEET-PG:** * **Confirmatory Test for HS:** The **Eosin-5-maleimide (EMA) binding test** (via flow cytometry) is now the gold standard, though the Osmotic Fragility Test remains a classic exam favorite. * **Incubated OFT:** Sensitivity of the OF test increases if the blood is incubated at 37°C for 24 hours. * **MCHC:** Hereditary Spherocytosis is one of the few conditions where the **Mean Corpuscular Hemoglobin Concentration (MCHC) is increased** (>36 g/dL). **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 597-598. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 640-641. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, p. 638.
Question 1227: What is the characteristic shape of Birbeck granules?
- A. Tennis racket (Correct Answer)
- B. Hockey stick
- C. Bat
- D. Ball
Explanation: **Explanation:** **Birbeck granules** are the pathognomonic ultrastructural hallmark of **Langerhans Cell Histiocytosis (LCH)** [1]. Under an electron microscope, these cytoplasmic organelles appear as elongated, rod-shaped structures with a central striated line and a terminal bulbous expansion, giving them a classic **tennis racket** appearance [1]. * **Why Option A is correct:** Birbeck granules are composed of **Langerin (CD207)**, a protein involved in endocytocis and the transport of antigens [1]. The "handle" of the racket is formed by the pentalaminar fusion of membranes, while the "head" represents a vesicular dilation [1]. * **Why Options B, C, and D are incorrect:** These shapes do not correspond to any recognized ultrastructural organelles in hematopathology. While "hockey stick" or "drumstick" appearances are used to describe other medical findings (e.g., mitral stenosis on imaging or Barr bodies in neutrophils), they are not associated with Birbeck granules. **High-Yield Clinical Pearls for NEET-PG:** 1. **Immunohistochemistry (IHC):** Langerhans cells are characteristically positive for **S100, CD1a, and Langerin (CD207)** [1]. Langerin is the most specific marker. 2. **Morphology:** On light microscopy, the cells show characteristic **"coffee-bean" nuclei** (grooved nuclei) [1]. 3. **Clinical Presentation:** LCH can range from a single bone lesion (Eosinophilic granuloma) to multisystem involvement (Letterer-Siwe disease). 4. **Key Association:** Always look for the "tennis racket" description when an electron microscopy (EM) finding is mentioned in a case of suspected histiocytosis [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. 630.
Question 1228: What causes hemolysis in G6-PD deficiency?
- A. Hemoglobin defect
- B. Oxidative stress (Correct Answer)
- C. Membrane defect
- D. Vitamin B12 deficiency
Explanation: ### Explanation **Correct Answer: B. Oxidative Stress** Glucose-6-Phosphate Dehydrogenase (G6PD) is the rate-limiting enzyme in the **Hexose Monophosphate (HMP) Shunt**. This pathway is the sole source of **NADPH** in red blood cells [1]. NADPH is essential for maintaining a pool of **reduced glutathione**, which acts as a primary antioxidant to neutralize reactive oxygen species (ROS) like hydrogen peroxide. In G6PD deficiency, the cell cannot regenerate reduced glutathione. When exposed to **oxidative stress** (triggered by infections, fava beans, or drugs like Primaquine and Sulphonamides), ROS accumulate and denature hemoglobin [1]. This denatured hemoglobin precipitates into **Heinz bodies**, which damage the RBC membrane and lead to hemolysis [1]. **Why other options are incorrect:** * **A. Hemoglobin defect:** While hemoglobin denatures in G6PD deficiency, the primary pathology is an enzyme deficiency, not a structural or quantitative defect in globin chains (like Sickle Cell Anemia or Thalassemia) [1]. * **C. Membrane defect:** Although the membrane is damaged during the process, "Membrane defect" typically refers to primary cytoskeletal protein abnormalities, such as Hereditary Spherocytosis [1]. * **D. Vitamin B12 deficiency:** This causes megaloblastic anemia due to impaired DNA synthesis, not oxidative hemolysis. **High-Yield Clinical Pearls for NEET-PG:** * **Inheritance:** X-linked recessive (more common in males) [1]. * **Morphology:** Look for **Heinz bodies** (supravital stains like Crystal Violet) and **Bite cells** (formed by splenic macrophages plucking out Heinz bodies) [1]. * **Diagnosis:** Quantitative enzyme assay is the gold standard, but it must **not** be performed during an acute hemolytic episode (as young reticulocytes have higher enzyme levels, leading to a false-normal result) [1]. * **Common Triggers:** Infections (most common), Fava beans (Favism), and drugs (Primaquine, Dapsone, Nitrofurantoin) [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. 638-654.
Question 1229: In which of the following conditions are Auer rods seen?
- A. Myelodysplastic syndrome
- B. Multiple myeloma
- C. Granulocytic sarcoma (Correct Answer)
- D. Leukemia cutis
Explanation: **Explanation:** **Auer rods** are pathognomonic markers of the myeloid lineage. They are elongated, needle-like pink/red inclusions in the cytoplasm of blasts, formed by the fusion of azurophilic granules (containing peroxidase) [2]. 1. **Why Granulocytic Sarcoma is correct:** Also known as **Chloroma** or Myeloid Sarcoma, this is an extramedullary tumor mass consisting of myeloid blasts. Since it is essentially a localized collection of leukemic myeloblasts (often associated with AML), Auer rods can be identified within these cells upon biopsy, confirming the myeloid origin of the tumor. 2. **Analysis of Incorrect Options:** * **Myelodysplastic Syndrome (MDS):** While Auer rods can occasionally be seen in specific subtypes (like MDS with excess blasts-2), their presence automatically upgrades the diagnosis to a higher grade or suggests transformation to AML. However, they are not a defining or consistent feature of MDS as a whole compared to the definitive myeloid nature of a granulocytic sarcoma. * **Multiple Myeloma:** This is a plasma cell dyscrasia. Plasma cells do not contain Auer rods; they may contain Russell bodies or Mott cells, but never Auer rods. * **Leukemia Cutis:** This refers to the infiltration of the skin by leukemic cells. While it can occur in AML, it is more frequently associated with monocytic lineages (AMoL) where Auer rods are much rarer or absent. **High-Yield Clinical Pearls for NEET-PG:** * **Composition:** Auer rods are rich in **Myeloperoxidase (MPO)**. * **Faggot Cells:** Cells containing bundles of Auer rods; these are the hallmark of **Acute Promyelocytic Leukemia (AML-M3)** [1]. * **Translocation:** AML-M3 is associated with **t(15;17)** [1]. * **Diagnostic Rule:** Auer rods are **never** seen in Lymphoblasts (ALL). Their presence always rules out a lymphoid lineage. **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. 620. [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. 621-622.
Question 1230: Thrombocytopenia is caused by which of the following conditions?
- A. Aspirin
- B. Acyclovir
- C. Disseminated Intravascular Coagulation (DIC) (Correct Answer)
- D. Henoch-Schonlein Purpura (HSP)
Explanation: ### Explanation **Correct Answer: C. Disseminated Intravascular Coagulation (DIC)** **Mechanism of Thrombocytopenia in DIC:** Disseminated Intravascular Coagulation (DIC) is a thrombohemorrhagic disorder characterized by the systemic activation of the coagulation cascade [2]. This leads to the widespread formation of microthrombi throughout the microvasculature. Thrombocytopenia occurs due to the **consumptive coagulopathy**—platelets and clotting factors are rapidly "used up" or consumed during the formation of these extensive clots, leaving an insufficient supply in the systemic circulation [1]. **Analysis of Incorrect Options:** * **A. Aspirin:** Aspirin causes **qualitative platelet dysfunction** by irreversibly inhibiting the enzyme Cyclooxygenase-1 (COX-1), which prevents the synthesis of Thromboxane A2. It affects platelet *aggregation*, but the total platelet *count* remains normal. * **B. Acyclovir:** This is an antiviral medication. While many drugs can cause idiosyncratic bone marrow suppression, Acyclovir is not a classic or high-yield cause of thrombocytopenia [3]. * **D. Henoch-Schonlein Purpura (HSP):** HSP is an IgA-mediated small-vessel **vasculitis**. A hallmark diagnostic feature of HSP is "non-thrombocytopenic purpura," meaning the skin lesions occur due to vessel wall inflammation, while the platelet count remains characteristically **normal**. **High-Yield Clinical Pearls for NEET-PG:** * **DIC Lab Profile:** Decreased platelets, prolonged PT/aPTT, decreased Fibrinogen, and **elevated D-dimer** (most specific) or FDPs [1]. * **Peripheral Smear in DIC:** Look for **Schistocytes** (fragmented RBCs), indicating microangiopathic hemolytic anemia (MAHA) [1]. * **HSP Tetrad:** Palpable purpura (lower extremities), arthralgia, abdominal pain, and renal involvement (IgA nephropathy). Always remember: Platelet count is normal in HSP. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 667-668. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 671-672. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 665-666.
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Anemias: Classification and Approach
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Hemolytic Anemias
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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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