Hematopathology — MCQs

Hematopathology Indian Medical PG Practice Questions and MCQs

Question 301: Synthesis of which of the following clotting factors is not affected in liver disease?

A. Factor II
B. Factor V
C. Factor VIII (Correct Answer)
D. Factor IX

Explanation: **Explanation:** The liver is the primary site for the synthesis of almost all coagulation factors [1]. However, **Factor VIII (Anti-hemophilic factor)** is the notable exception. While the liver (specifically sinusoidal endothelial cells) does produce some Factor VIII, the majority is synthesized by **extrahepatic endothelial cells** throughout the body, particularly in the lungs and kidneys. * **Why Factor VIII is the correct answer:** In patients with end-stage liver disease, levels of Factor VIII are typically **normal or even elevated**. This occurs because Factor VIII is an acute-phase reactant and its carrier protein, **von Willebrand Factor (vWF)**, is produced by endothelial cells and megakaryocytes, not hepatocytes. Therefore, Factor VIII levels do not decline even when hepatic synthetic function is severely compromised. * **Why other options are incorrect:** * **Factor II (Prothrombin), Factor IX, and Factor X:** These are Vitamin K-dependent clotting factors synthesized exclusively by hepatocytes [1]. Their levels drop significantly in liver disease [1]. * **Factor V:** This is a non-Vitamin K-dependent factor synthesized by the liver. Because it is not affected by Vitamin K deficiency but *is* affected by liver cell failure, it is often used as a specific marker to distinguish between liver disease and Vitamin K deficiency. **High-Yield Clinical Pearls for NEET-PG:** 1. **Factor VII** has the shortest half-life (4–6 hours) and is the first to decrease in liver disease [1], making **Prothrombin Time (PT)** the best early indicator of hepatic synthetic dysfunction. 2. **Factor VIII** is the only clotting factor not synthesized by hepatocytes. 3. **Factor V** levels are used to assess the severity of fulminant hepatic failure; a decrease indicates poor prognosis. 4. In liver disease, PT is prolonged, but Factor VIII levels remain high. In **DIC**, both PT is prolonged and Factor VIII levels are decreased due to consumption [2]. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 582-583. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 625-626.

Question 302: Megaloblasts are precursors of which of the following cell types?

A. Megakaryocytes
B. Normoblasts (Correct Answer)
C. Myelocytes
D. Macrocytes

Explanation: **Explanation:** The correct answer is **B. Normoblasts**. [1] **Understanding the Concept:** Megaloblasts are abnormal, large erythroid precursors found in the bone marrow of patients with **Megaloblastic Anemia** (typically due to Vitamin B12 or Folate deficiency). [1] These deficiencies impair DNA synthesis, leading to "nuclear-cytoplasmic asynchrony," where the nucleus remains immature (fine, lacy chromatin) while the cytoplasm matures and hemoglobinizes normally. [1] In the normal erythropoietic sequence, the precursors are called **Normoblasts**. Therefore, megaloblasts are the pathological counterparts/precursors that replace or precede the normal normoblastic stages in these deficiency states. **Analysis of Incorrect Options:** * **A. Megakaryocytes:** These are the large bone marrow cells responsible for producing platelets. While megaloblastic anemia can show giant metamyelocytes or multisegmented neutrophils, megakaryocytes are a different lineage entirely. * **C. Myelocytes:** These are precursors in the granulocytic (white blood cell) series. The erythroid equivalent is the normoblast/megaloblast. * **D. Macrocytes:** These are the large, mature red blood cells found in the **peripheral blood**. Megaloblasts are the **nucleated precursors** found in the bone marrow; they do not circulate. [1] **High-Yield Clinical Pearls for NEET-PG:** * **Nuclear-Cytoplasmic Asynchrony:** The hallmark of megaloblastic maturation. [1] * **Peripheral Smear:** Look for **Macro-ovalocytes** and **Hypersegmented neutrophils** (more than 5 lobes in one cell or 5% cells with 5 lobes). [1] * **Bone Marrow:** Characterized by hypercellularity and the presence of **Giant Metamyelocytes** (the most sensitive indicator of megaloblastic change in the marrow). * **Ineffective Erythropoiesis:** Megaloblasts often undergo intramedullary hemolysis, leading to increased LDH and indirect bilirubin. **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 592-595.

Question 303: Massive splenomegaly is not seen in which of the following conditions?

A. Malaria
B. Chronic myelogenous leukemia
C. Syphilis
D. Sickle cell anemia (Correct Answer)

Explanation: The correct answer is **Sickle Cell Anemia (SCA)**. In adult patients with SCA, the spleen is typically small and fibrotic rather than enlarged [1]. This occurs due to repeated episodes of vaso-occlusion and splenic infarction caused by the sickling of red blood cells in the hypoxic environment of the splenic sinusoids [2]. Over time, this leads to progressive shrinkage and scarring, a process known as **autosplenectomy** [2]. **Analysis of Options:** * **Malaria (Option A):** Chronic or repeated infections with *Plasmodium vivax* or *falciparum* can lead to "Tropical Splenomegaly Syndrome" (Hyperreactive Malarial Splenomegaly), where the spleen can reach massive proportions due to chronic immune stimulation [4]. * **Chronic Myelogenous Leukemia (Option B):** CML is a classic cause of massive splenomegaly [3]. The spleen becomes an organ of extramedullary hematopoiesis and is infiltrated by a massive proliferation of granulocytic cells [3]. * **Syphilis (Option C):** While less common today, congenital syphilis is a recognized cause of significant splenomegaly in neonates and infants due to diffuse inflammation and extramedullary hematopoiesis. * **Sickle Cell Anemia (Option D):** While children with SCA may initially have splenomegaly, by adulthood, the spleen is usually non-palpable due to autosplenectomy. **High-Yield Clinical Pearls for NEET-PG:** * **Massive Splenomegaly Definition:** Spleen crossing the midline or extending into the pelvis (>1000g or >20cm) [3]. * **Common Causes:** CML, Myelofibrosis, Visceral Leishmaniasis (Kala-azar), Malaria, and Gaucher’s disease [3][4]. * **Autosplenectomy:** Associated with Howell-Jolly bodies on peripheral smear (nuclear remnants in RBCs normally cleared by a functional spleen). * **SCA Exception:** Splenomegaly *can* occur in SCA during a **Sequestration Crisis** (a life-threatening emergency in children) or in **Sickle-Thalassemia** variants. **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. 631-632. [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. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 611-612. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Diseases Of The Urinary And Male Genital Tracts, pp. 568-569.

Question 304: Burkitt's lymphoma is associated with which chromosomal translocation?

A. t(8;14) (Correct Answer)
B. t(9;22)
C. t(15;17)
D. Deletion of chromosome 5

Explanation: The original text with citations added follows: **Explanation:** **1. Why Option A is Correct:** Burkitt’s Lymphoma is a highly aggressive B-cell non-Hodgkin lymphoma characterized by the overexpression of the **c-MYC proto-oncogene** [1]. The hallmark genetic feature is the **t(8;14)** translocation, which occurs in approximately 85% of cases [1]. In this translocation, the *c-MYC* gene on chromosome 8 is moved adjacent to the **Immunoglobulin Heavy chain (IgH)** locus on chromosome 14 [1]. Since the IgH promoter is highly active in B-cells, it leads to the constitutive expression of c-MYC, a transcription factor that drives rapid cellular proliferation [1]. (Note: Variant translocations include t(2;8) and t(8;22) involving light chains). **2. Why Other Options are Incorrect:** * **Option B: t(9;22)** – Known as the **Philadelphia chromosome**, this is the hallmark of **Chronic Myeloid Leukemia (CML)** and a subset of ALL [2]. It creates the *BCR-ABL1* fusion protein with tyrosine kinase activity [2]. * **Option C: t(15;17)** – This is diagnostic for **Acute Promyelocytic Leukemia (APL - AML M3)**, involving the *PML-RARA* fusion gene. It is clinically significant due to its responsiveness to All-Trans Retinoic Acid (ATRA). * **Option D: Deletion of chromosome 5 (5q-)** – This is commonly associated with **Myelodysplastic Syndromes (MDS)** and carries a specific prognosis and treatment profile (Lenalidomide). **3. High-Yield Clinical Pearls for NEET-PG:** * **Morphology:** "Starry-sky" appearance (tingible body macrophages against a sea of neoplastic B-cells). * **Association:** Strongly linked with **Epstein-Barr Virus (EBV)**, especially the endemic (African) variety involving the jaw. * **Immunophenotype:** CD19+, CD20+, CD10+, and **BCL-6+**; notably **BCL-2 negative**. * **Ki-67 index:** Typically near **100%**, reflecting the highest proliferation rate among human tumors. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Neoplasia, pp. 324-325. [2] 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.

Question 305: What is true about Burkitt's lymphoma?

A. CD34 positive and surface immunoglobulin positive
B. CD34 positive and surface immunoglobulin negative
C. CD34 negative and surface immunoglobulin negative
D. CD34 negative and surface immunoglobulin positive (Correct Answer)

Explanation: **Explanation:** Burkitt’s Lymphoma (BL) is a highly aggressive B-cell non-Hodgkin lymphoma derived from **germinal center B-cells**. Understanding its immunophenotype is crucial for distinguishing it from other hematological malignancies like Acute Lymphoblastic Leukemia (ALL) [1]. 1. **Why Option D is correct:** * **CD34 Negative:** CD34 is a marker of hematopoietic stem cells and early precursors (blasts) [3]. Since Burkitt’s lymphoma consists of **mature** B-cells that have passed the blast stage, it is consistently **CD34 negative**. * **Surface Immunoglobulin (sIg) Positive:** As a mature B-cell neoplasm, BL cells express surface IgM (with either kappa or lambda light chains). This confirms their differentiation beyond the pre-B cell stage. 2. **Why other options are incorrect:** * **Options A & B (CD34 positive):** These are incorrect because CD34 positivity is a hallmark of **B-lymphoblastic leukemia/lymphoma (B-ALL)**, not mature B-cell lymphomas like Burkitt’s [3]. * **Option C (sIg negative):** This is incorrect because the absence of surface Ig is typical of immature precursor B-cells (blasts). Mature B-cell lymphomas are defined by the presence of sIg. **High-Yield Facts for NEET-PG:** * **Immunophenotype:** Positive for CD19, CD20, CD10, and **BCL-6** (germinal center markers). Crucially, it is **BCL-2 negative** (unlike Follicular Lymphoma). * **Genetics:** Characterized by **t(8;14)** involving the **MYC gene** and IGH locus. * **Morphology:** Classic **"Starry-sky appearance"** (tingible body macrophages against a sea of cohesive tumor cells) [1]. * **Proliferation:** Extremely high Ki-67 index (approaching **100%**). * **Variants:** Endemic (African/Jaw), Sporadic (Abdominal), and Immunodeficiency-associated [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. 606. [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. 605-606. [3] 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 306: Leiden mutation is associated with which of the following?

A. Factor V (Correct Answer)
B. Factor VI
C. Protein C
D. Protein S

Explanation: **Explanation:** **Factor V Leiden** is the most common inherited cause of hypercoagulability (thrombophilia) among Caucasians [1]. The mutation involves a specific single nucleotide polymorphism (G to A substitution at nucleotide 1691) in the Factor V gene, which leads to the replacement of **Arginine by Glutamine at position 506** [1]. 1. **Why Factor V is correct:** Normally, Activated Protein C (APC) inactivates Factor Va to prevent excessive clotting. The mutation at the Arg506 cleavage site renders Factor V resistant to degradation by Protein C [1]. This phenomenon is known as **Activated Protein C Resistance (APCR)**, leading to a prothrombotic state and increased risk of Venous Thromboembolism (VTE) [1]. 2. **Why other options are incorrect:** * **Factor VI:** This factor does not exist in the modern coagulation cascade (it was historically assigned to activated Factor V). * **Protein C and Protein S:** These are natural anticoagulants [2]. While deficiencies in Protein C or S also cause thrombophilia, they are distinct genetic defects and are not referred to as the "Leiden mutation." In Factor V Leiden, Protein C levels are normal, but the *substrate* (Factor V) is resistant to its action [1]. **High-Yield Clinical Pearls for NEET-PG:** * **Inheritance:** Autosomal Dominant. * **Clinical Presentation:** Recurrent Deep Vein Thrombosis (DVT) and Pulmonary Embolism [1]. It is also associated with recurrent pregnancy loss. * **Diagnosis:** Screening is done via the **APCR ratio** (functional assay); confirmation is via **PCR** for the G1691A mutation. * **Key Association:** Heterozygotes have a 5–10 fold increased risk of thrombosis, while homozygotes have an 80-fold increased risk. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, pp. 133-134. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 582-583.

Question 307: A 65-year-old man presents with anemia and back pain. A panoramic radiograph reveals multiple radiolucencies. What is the most likely diagnosis?

A. Multiple myeloma (Correct Answer)
B. Osteosarcoma
C. Giant cell granuloma
D. Eosinophilic granuloma

Explanation: ### Explanation **Correct Answer: A. Multiple Myeloma** Multiple myeloma is a plasma cell dyscrasia characterized by the neoplastic proliferation of a single clone of plasma cells [1]. The classic clinical triad includes **anemia, bone pain (often back pain), and renal insufficiency** [4]. The pathophysiology involves the secretion of Osteoclast Activating Factors (OAFs), such as IL-6 and RANK-L, which stimulate osteoclasts to resorb bone. This leads to the characteristic **"punched-out" lytic lesions** (radiolucencies) seen on skeletal surveys, particularly in the skull, vertebrae, and jaws [2], [3]. **Incorrect Options:** * **B. Osteosarcoma:** Typically presents in adolescents (bimodal distribution) as a solitary, painful mass near the knee. Radiographically, it shows bone formation (osteoid) with a "sunburst" appearance or Codman’s triangle, rather than multiple punched-out radiolucencies. * **C. Giant cell granuloma:** Usually presents as a solitary, localized expansile lesion of the jaw. It does not typically cause systemic anemia or generalized back pain in an elderly patient. * **D. Eosinophilic granuloma:** A form of Langerhans Cell Histiocytosis (LCH). While it can cause lytic bone lesions, it is primarily a disease of children and young adults and is less likely to present with the systemic features seen in this 65-year-old patient. **High-Yield Clinical Pearls for NEET-PG:** * **CRAB Criteria:** **C**alcium (hypercalcemia), **R**enal failure, **A**nemia, **B**one lesions [2]. * **Diagnosis:** Bone marrow biopsy shows >10% clonal plasma cells; Serum Protein Electrophoresis (SPEP) shows an **M-spike** [1]. * **Peripheral Smear:** **Rouleaux formation** due to increased serum proteins [3]. * **Urine:** Bence-Jones proteins (free light chains) may be present (detected by heat coagulation test, not dipstick) [1], [4]. * **Radiology:** Skeletal survey is preferred over bone scans (bone scans are often negative as there is no osteoblastic activity). **References:** [1] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 616-617. [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. 608. [3] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 617-618. [4] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 618-619.

Question 308: All of the following are hypercoagulable conditions EXCEPT?

A. Antithrombin III deficiency
B. Protein C deficiency
C. Protein S deficiency
D. Antiphospholipid antibody syndrome (associated with lupus anticoagulant) (Correct Answer)

Explanation: **Explanation:** The question asks to identify the condition that is **not** a primary hypercoagulable state in the same category as the others. While all four options are clinically associated with thrombosis, the distinction lies in the **nature of the defect** (Inherited vs. Acquired) [3]. **Why Option D is the correct answer:** Antiphospholipid Antibody Syndrome (APS) is an **acquired** thrombophilia [1]. The "Lupus Anticoagulant" (LA) is a laboratory paradox; although it causes thrombosis *in vivo*, it causes a **prolonged Activated Partial Threshold Time (aPTT)** *in vitro* because the antibodies interfere with the phospholipids used in the lab assay [1], [2]. In the context of standard NEET-PG classification, Options A, B, and C are classic **Inherited (Primary) Thrombophilias**, making Option D the outlier. **Analysis of Incorrect Options:** * **A. Antithrombin III Deficiency:** An inherited deficiency where the body cannot neutralize thrombin and Factor Xa. It is high-yield because patients are **resistant to Heparin** therapy. * **B & C. Protein C and S Deficiency:** These are inherited vitamin K-dependent anticoagulant deficiencies. Protein C inactivates Factors Va and VIIIa (with Protein S as a cofactor) [3]. A key clinical pearl is **Warfarin-induced skin necrosis**, which occurs if these patients are started on Warfarin without Heparin bridging. **High-Yield NEET-PG Pearls:** * **Most common inherited cause of hypercoagulability:** Factor V Leiden (Resistance to Activated Protein C) [3]. * **Most common acquired cause:** Surgery/Immobilization; among autoimmune causes, it is APS. * **APS Triad:** Venous/Arterial thrombosis, recurrent fetal loss, and thrombocytopenia [2]. * **Mixing Study:** In APS, the prolonged aPTT **does not correct** when mixed with normal plasma (unlike factor deficiencies). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, pp. 134-135. [2] Cross SS. Underwood's Pathology: A Clinical Approach. 6th ed. Common Clinical Problems From Blood And Bone Marrow Disease, pp. 626-627. [3] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, pp. 133-134.

Question 309: Which clotting factor deficiency is asymptomatic?

A. II
B. V
C. XII (Correct Answer)
D. XI

Explanation: **Explanation:** The correct answer is **Factor XII (Hageman factor)**. **1. Why Factor XII is the correct answer:** Factor XII is the first factor in the **intrinsic pathway** of the coagulation cascade [1]. While its deficiency leads to a **markedly prolonged Activated Partial Thromboplastin Time (aPTT)** in vitro, it does not cause clinical bleeding in vivo [1]. This is because Factor XII is more involved in the activation of the fibrinolytic system, kinin generation (bradykinin), and inflammation rather than primary clot formation [1]. In the human body, Factor XI can be activated directly by thrombin, bypassing the need for Factor XII for hemostasis [1]. **2. Why the other options are incorrect:** * **Factor II (Prothrombin):** Deficiency is extremely rare and usually incompatible with life. Partial deficiency causes severe bleeding diathesis. * **Factor V (Parahemophilia):** Deficiency leads to mild to severe bleeding manifestations, including epistaxis, mucosal bleeding, and menorrhagia. * **Factor XI (Plasma Thromboplastin Antecedent):** Deficiency causes **Hemophilia C**. Unlike Factor XII, it is associated with a mild and unpredictable bleeding tendency, particularly after surgery or trauma (common in Ashkenazi Jews). **3. High-Yield Clinical Pearls for NEET-PG:** * **The Paradox:** Factor XII deficiency is the classic "laboratory-only" abnormality—**prolonged aPTT but zero bleeding symptoms.** * **Thrombosis Risk:** Interestingly, some patients with Factor XII deficiency may actually have an increased risk of **thromboembolism** due to impaired fibrinolysis [1]. * **Other Asymptomatic Deficiencies:** Deficiency of **Prekallikrein (Fletcher factor)** and **High Molecular Weight Kininogen (Fitzgerald factor)** also present with a prolonged aPTT without clinical bleeding. * **Factor XIII Deficiency:** This is the opposite—it presents with severe bleeding (e.g., umbilical cord stump bleeding) but shows **normal PT and aPTT** (diagnosed by the Urea Solubility Test). **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Hemodynamic Disorders, Thromboembolic Disease, and Shock, pp. 128-132.

Question 310: Downey cells are characteristic findings in which of the following conditions?

A. Multiple Myeloma
B. Chronic Myeloid Leukemia
C. Hairy Cell Leukemia
D. Infectious Mononucleosis (Correct Answer)

Explanation: **Explanation:** **Downey cells** are **atypical lymphocytes** (specifically activated CD8+ T-cells) that appear in the peripheral blood in response to B-cells infected by the **Epstein-Barr Virus (EBV)** [1]. In **Infectious Mononucleosis**, these cells exhibit characteristic morphology: they are larger than normal lymphocytes, possess abundant pale blue cytoplasm that appears to "hug" or indent around adjacent red blood cells (ball-handing appearance), and have a less condensed nuclear chromatin [1]. **Analysis of Options:** * **A. Multiple Myeloma:** Characterized by the malignant proliferation of **plasma cells** in the bone marrow. Key findings include "M-spike" on electrophoresis and "Rouleaux formation" on peripheral smear, not atypical T-cells. * **B. Chronic Myeloid Leukemia (CML):** A myeloproliferative neoplasm characterized by a "spectrum of myeloid cells" (neutrophils, myelocytes, metamyelocytes) and the presence of the **Philadelphia chromosome** t(9;22). * **C. Hairy Cell Leukemia:** A B-cell lymphoproliferative disorder where cells show fine, hair-like cytoplasmic projections [2]. These cells are positive for **TRAP** (Tartrate-Resistant Acid Phosphatase) stain. **High-Yield Clinical Pearls for NEET-PG:** * **Triad of Infectious Mononucleosis:** Fever, Pharyngitis, and Lymphadenopathy (typically posterior cervical) [1]. * **Paul Bunnell Test / Monospot Test:** Detects heterophile antibodies (IgM) produced during EBV infection. * **Morphology Tip:** Downey cells are "T-cells" reacting against "B-cells." * **Complication:** Avoid contact sports due to the risk of **splenic rupture**. * **Diagnostic Clue:** If a patient with pharyngitis is given Ampicillin/Amoxicillin and develops a maculopapular rash, suspect Infectious Mononucleosis. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Infectious Diseases, pp. 368-370. [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. 612.

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