A 10-year-old girl develops fever, epistaxis, and oliguria 5 days after attending a picnic at which hamburgers and hot

dogs are served. Physical examination shows scattered petechiae and ecchymoses on the arms, chest, and back. Laboratory studies show: Hemoglobin 9 g/dL WBC count 8000/mm3 Platelet count 30,000/mm3 Prothrombin time (PT) 12 sec Activated partial thromboplastin time (aPTT)35 sec Serum blood urea nitrogen (BUN) 40 mg/dL Serum creatinine 4 mg/dL A peripheral smear shows fragmented RBCs. What is the most likely diagnosis?The patient has HUS, which most commonly occurs in children. HUS is due to a toxin (Verotoxin) produced by the 0157:H7 strain of Escherichia coli, causing widespread endothelial cell damage at the arteriolecapillary junction. E. coli often contaminates improperly cooked beef (e.g., hamburgers). Platelet thrombi develop at all the injury sites, causing consumption of platelets and thrombocytopenia (epistaxis, petechiae, ecchymoses, easy bruising) as well as renal failure (increased serum BUN and serum creatinine). RBCs that collide with the platelet thrombi are damaged (fragmented RBCs or schistocytes), causing a hemolytic anemia (microangiopathic hemolytic anemia; see Fig. 11-35 in Rapid Review Pathology, 3rd edition). Option A (Aplastic anemia) is incorrect. Aplastic anemia is characterized by decreased production of WBCs, RBCs, and platelets. Aplastic anemia is excluded in this patient, because the WBC count is normal. Option B (Disseminated intravascular coagulation (DIC)) is incorrect. In DIC, fibrin clots are produced in the microcirculation that obstruct blood flow and consume coagulation factors. Factors that are consumed in a fibrin clot are fibrinogen (factor I), prothrombin (factor II), and factors V and VIII. Since coagulating factors present in the final common pathway are consumed (fibrinogen, prothrombin, factor V), there is prolongation of the PT and aPTT (not present in this patient). Platelets are trapped in the fibrin clots leading to thrombocytopenia. Fragmented RBCs (schistocytes) are present in the peripheral blood, due to damage to RBCs by the fibrin clots. There are many overlapping features of DIC with HUS; however, in the former disorder coagulation factors are consumed causing prolongation of the PT and aPTT, while in the latter, platelets are consumed in the formation of platelet thrombi and coagulation studies are normal. Option D (Idiopathic thrombocytopenic purpura (ITP)) is incorrect. ITP is autoimmune destruction of platelets, where IgG antibodies are directed against the GpIIb:IIIa fibrinogen receptors on platelets. ITP is excluded in this patient because it is not associated with anemia and renal failure. Option E (Thrombotic thrombocytopenic purpura (TTP)) is incorrect. TTP occurs in women and is uncommon in children. The pathophysiology of TTP and HUS is similar. TTP is a disorder characterized by endothelial injury with the formation of platelet thrombi that consume platelets, not coagulation factors; therefore, the PT and PTT are normal (not prolonged).

The photograph shows characteristic leukocyte alterations in peripheral blood obtained from a 23-year-old man with fever. Which of the following conditions is the most compatible with these change

Streptococcal tonsillitis) is correct. The peripheral blood smear shows leukocyte alterations that characterize acute bacterial infections, such as streptococcal tonsillitis. These changes include the presence of band neutrophils (without segmentation) and of multilobed neutrophils that show toxic granulation (prominent azurophilic granules) and cytoplasmic vacuolization (phagolysosomes). When band neutrophils exceed 10% of the total leukocytes, the term left shift is used, indicating that more immature cells in the neutrophil series are being released from the bone marrow. These cells are released from the post-mitotic neutrophil pool in the bone marrow due to the presence of interleukin-1 and tumor necrosis factor-. Option A (Acute myeloblastic leukemia) is incorrect. A peripheral blood smear from a patient with acute myeloblastic leukemia would show myeloblasts containing rodlike structures (Auer rods) in the cytoplasm and other immature myeloid elements. Option B (Infectious mononucleosis) is incorrect. A peripheral blood smear from a patient with infectious mononucleosis would show atypical lymphocytes, which have abundant cytoplasm and enlarged nuclei with prominent nucleoli. Option C (Invasive helminth infection) is incorrect. A peripheral blood smear from a patient with invasive helminths (e.g., Strongyloides stercoralis) would show eosinophils, which contain bright red granules in the cytoplasm that are larger than the azurophilic granules seen in neutrophils. Option E (Viral gastroenteritis) is incorrect. A peripheral blood smear from a patient with viral gastroenteritis would show absolute lymphocytosis (increased total lymphocyte count), the leukocyte alteration that characterizes viral infections. Lymphocytes have round nuclei and are usually surrounded by a thin rim of cytoplasm.

In which of the following clinical scenarios would the patient most likely have an increase in the leukocyte shown in the photograph?

Option D (A 45-year-old woman has severe rheumatoid arthritis.) is correct. Monocytosis is the primary leukocyte alteration in chronic inflammation (e.g., rheumatoid arthritis). The photograph shows a monocyte with grayish-blue cytoplasm that contains many fine azurophilic granules and nucleus that is horse-shoe shaped (this monocyte), round, or kidney shaped. Option A (A 4-year-old child has whooping cough.) is incorrect. Bordetella pertussis is the cause of whooping cough. The lymphotoxin in this bacteria inhibits signal transduction by chemokine receptors which prevents lymphocytes from entering lymph nodes leading to lymphocytosis. Lymphocyte counts are often >50,000/mm3 (lymphoid leukemoid reaction). The photograph shows a small lymphocyte with scant cytoplasm surrounding a dark nucleus. Option B (A 24-year-old man, who raises hogs, has a habit of eating raw bacon.) is incorrect. This patient would most likely develop trichinosis, due to Trichinella spiralis. It is contracted by eating raw or undercooked pork. The larvae penetrate muscle producing muscle pain and tenderness. Invasive helminths produce eosinophilia (type I hypersensitivity). The photograph shows an eosinophil with cytoplasm packed with reddishorange granules that do not cover the nucleus. Option C (A 28-year-old man has a perforated acute appendicitis.) is incorrect. A perforated acute appendicitis produces neutrophilic leukocytosis with left shift (e.g., band neutrophils) and toxic granulation (prominent azurophilic granules). Option E (A 56-year-old man with polycythemia vera has flushing of his face.) is incorrect. In polycythemia, all cell lines except lymphocytes are increased. An increase in basophils and mast cells causes the release of histamine, which produces flushing of the face (called plethora), headaches, and pruritus after bathing. All of the myeloproliferative diseases have basophilia. A febrile 65-year-old man with prostate hyperplasia and urinary retention develops endotoxic shock. Within 24 hours, he has oozing of blood from all needle puncture sites, extensive ecchymoses and petechiae, and gastrointestinal bleeding. Laboratory studies show a hemoglobin of 9 g/dL, platelet count 75,000/mm3, prothrombin time (PT) 20 seconds, partial thromboplastin time, activated partial thromboplastin time (aPTT) 50 sec, and a positive ddimer assay. What is the most likely diagnosis Option C (Disseminated intravascular coagulation (DIC)) is correct. The endotoxins in endotoxic shock (most often due to Escherichia coli sepsis) damage tissue, causing the release of tissue thromboplastin. This activates the extrinsic coagulation system, causing DIC. Septic

shock is the most common cause of DIC. In DIC, fibrin clots are produced in the microcirculation that obstruct blood flow and consume coagulation factors, causing bleeding from needle puncture sites and the gastrointestinal tract. Factors that are normally consumed in a fibrin clot are fibrinogen (factor I), prothrombin (factor II), and factors V and VIII. Since coagulating factors present in the final common pathway are consumed (fibrinogen, prothrombin, factor V), there is prolongation of the PT and aPTT. Platelets are trapped in the fibrin clots leading to thrombocytopenia, which produces petechiae and ecchymoses. The fibrinolytic system is activated (secondary fibrinolysis), and plasmin cleaves the fibrin strands holding the fibrin clots together. Fibrin strands are held together by cross-links, and cleaved fragments with cross-links are detected in the d-dimer assay, which is the most sensitive test for diagnosing DIC. Option A (Autoimmune thrombocytopenia) is incorrect. DIC is associated with fibrin clots, multiple coagulation factor deficiencies, activation of the fibrinolytic system, and thrombocytopenia. Therefore, conditions that produce thrombocytopenia, such as autoimmune thrombocytopenia, do not explain all of the clinical and laboratory findings that are present in DIC. Option B (Circulating anticoagulant) is incorrect. Circulating anticoagulants are antibodies that destroy coagulation factors (e.g., factor VIII), causing prolongation of the aPTT and/or PT. However, these antibodies do not destroy platelets or produce fibrin clots that obstruct the microcirculation as in DIC. Option D (Primary fibrinolysis) is incorrect. Primary fibrinolysis is uncommon. It is usually seen in the setting of radical prostatectomy and open heart surgery. Only the fibrinolytic system is activated. Therefore, clinical findings are primarily those related to coagulation factor deficiencies (e.g., fibrinogen, factor V, factor VIII). The platelet count is normal and ddimers are not present, because there are no fibrin clots. Option E (Thrombotic thrombocytopenic purpura (TTP)) is incorrect. DIC is associated with fibrin clots, multiple coagulation factor deficiencies, activation of the fibrinolytic system, and thrombocytopenia. TTP is a disorder characterized by endothelial injury with the formation of platelet thrombi that consume platelets, not coagulation factors; therefore, the PT and PTT are normal (not prolonged). A 22-year-old man has fever, fatigue, and a sore throat. Findings on physical examination include exudative pharyngitis, hepatosplenomegaly, and painful generalized lymphadenopathy. Laboratory findings show an increased WBC count, normal hemoglobin concentration, and normal platelet count. The photograph shows one of many similar WBCs in the peripheral blood of the patient. Which of the following laboratory studies would be most useful in confirming the diagnosis in this patient?

In which of the following clinical scenarios would the patient most likely have an increase in the leukocyte shown in the photograph?

Option E (A 56-year-old man with polycythemia vera has flushing of his face.) is correct. In polycythemia, all cell lines except lymphocytes are increased. An increase in basophils and mast cells causes the release of histamine, which produces flushing of the face (called plethora), headaches, and pruritus after bathing. All of the myeloproliferative diseases have basophilia. The basophil in the photograph shows the cytoplasm packed with large purpleblack granules that cover the nucleus. Option A (A 4-year-old child has whooping cough.) is incorrect. Bordetella pertussis is the cause of whooping cough. The lymphotoxin in this bacteria inhibits signal transduction by chemokine receptors which prevents lymphocytes from entering lymph nodes leading to lymphocytosis. Lymphocyte counts are often >50,000/mm3 (lymphoid leukemoid reaction). Option B (A 24-year-old man, who raises hogs, has a habit of eating raw bacon.) is incorrect. This patient would most likely develop trichinosis, due to Trichinella spiralis. It is contracted by eating raw or undercooked pork. The larvae penetrate muscle producing muscle pain and tenderness. Invasive helminths produce eosinophilia (type I hypersensitivity). The photograph shows an eosinophil with cytoplasm packed with reddishorange granules that do not cover the nucleus. Option C (A 28-year-old man has a perforated acute appendicitis.) is incorrect. A perforated acute appendicitis produces neutrophilic leukocytosis with left shift (e.g., band neutrophils) and toxic granulation (prominent azurophilic granules). Option E (A 45-year-old woman has severe rheumatoid arthritis.) is incorrect. Monocytosis is the primary leukocyte alteration in chronic inflammation (e.g., rheumatoid arthritis).

Option B (Heterophil antibody test) is correct. This patient has infectious mononucleosis, which is caused by the Epstein-Barr virus (EBV). Infectious mononucleosis is usually transmitted by saliva (kissing disease). The photograph shows atypical lymphocytes with dark chromatin and abundant blue-gray cytoplasm. In mononucleosis, these are antigenically stimulated T cells that are responding to B cells infected by the virus. Recall that EBV has CD21 receptors on B cells and causes them to produce plasma cells that generate IgM heterophile antibodies that are used to screen for the infection (87% sensitivity). The heterophil antibodies that are specific for mononucleosis are IgM antibodies against horse, sheep, or bovine RBCs. Antibodies that are also useful diagnosing mono, particularly if the heterophile antibody test is negative, are anti-viral capsid antigen antibodies and antibodies against early antigen, both of which have >90% sensitivity and specificity. Hepatosplenomegaly and painful generalized lymphadenopathy are invariably present in mononucleosis. Option A (Bone marrow aspiration) is incorrect. Bone marrow aspiration biopsies are most often performed to rule out leukemias or primary disorders of the bone marrow (e.g., aplastic anemia, myelofibrosis). Option C (Lymph node biopsy) is incorrect. A lymph node biopsy is usually performed when a neoplastic process (e.g., malignant lymphoma, metastatic disease) is suspected. A neoplastic process produces painless enlargement of lymph nodes, which is not present in this case. This patient's painful lymphadenopathy indicates a benign, reactive process. Option D (Serum antibody screening) is incorrect. Standard serum antibody screening (indirect Coombs test) detects antibodies directed against Rh and other antigens that occur normally on the surface of human RBCs. It does not detect the antibodies that are present in infectious mononucleosis. Option E (Serum transaminase tests) is incorrect. Tests for serum transaminases (e.g., alanine aminotransferase) are useful in the diagnosis of hepatitis, which is invariably present in patients with infectious mononucleosis. Thus, markedly increased levels of serum transaminases would be expected in this patient, but they would not help diagnose the cause of the hepatitis. The hepatitis in mononucleosis is self-limited and does not progress into chronic hepatitis. An Rh-positive 25-year-old woman with blood group O delivers an Rh-negative infant with blood group A. The infant develops jaundice 8 hours after birth. An antibody screen of the mother is negative. Laboratory studies show that the infant has a mild normocytic anemia and an unconjugated hyperbilirubinemia. A direct Coombs test of the cord blood is positive. A peripheral blood smear shows spherocytes. Which of the following is the most likely diagnosis? Option A (ABO hemolytic disease of the newborn) is correct. The most common cause of jaundice within the first 24 hours after birth is ABO hemolytic disease of the newborn. Individuals with blood group O normally have anti-A and anti-B antibodies of the IgM type as well as anti-A,B antibodies of the IgG type. Therefore, ABO incompatibility occurs in pregnant women who are blood group O and carrying fetuses with blood group A or blood group B. Maternal anti-A,B-IgG antibodies cross the placenta and attach to the A or B antigens of the fetal RBCs. Fetal macrophages in the spleen phagocytose and destroy the IgG-coated fetal

RBCs, causing the release of unconjugated bilirubin (macrophage end-produce of bilirubin degradation) into the fetal blood and a mild hemolytic anemia. The unconjugated bilirubin is removed by the mothers liver. In this neonate, the liver is unable to metabolize the increased unconjugated bilirubin, causing jaundice within the first 24 hours. A direct Coombs test of the RBCs is positive, because IgG antibodies coat the surface of the RBCs. The peripheral blood contains numerous spherocytes, which are produced when splenic macrophages remove part of the RBC membrane coated by the IgG antibodies rather than the entire RBC. In most cases, an exchange transfusion is unnecessary in treating ABO hemolytic disease of the newborn, because the degree of anemia is not very severe and the level of unconjugated bilirubin is not high enough to produce kernicterus. Option B (Glucose-6-phosphate dehydrogenase (G6PD) deficiency) is incorrect. G6PD deficiency is an X-linked recessive disorder that produces an intravascular hemolysis caused by hydrogen peroxideinduced damage of RBC membranes and hemoglobin. G6PD deficiency is not an antibody-mediated hemolysis; therefore, the direct Coombs test is negative, not positive. Option C (Hereditary spherocytosis) is incorrect. Hereditary spherocytosis is an autosomal dominant disorder caused by a defect in ankyrin in the cell membrane. Hereditary spherocytosis is not an antibody-mediated hemolysis; therefore, the direct Coombs test is negative, not positive. Option D (Pyruvate kinase deficiency) is incorrect. Pyruvate kinase deficiency is an autosomal recessive hemolytic anemia. In pyruvate kinase deficiency, RBCs have no adenosine triphosphate, causing dehydration of the RBCs due to damage to the RBC membrane. The RBCs have spiny protuberances from the surface. Splenic macrophages remove the damaged RBCs causing a hemolytic anemia with jaundice. Pyruvate kinase deficiency is not an antibody-mediated hemolysis; therefore, the direct Coombs test is negative, not positive. Option E (Rh hemolytic disease of the newborn) is incorrect. Rh hemolytic disease of the newborn occurs when Rh-positive infants are born to Rh-negative (D-antigen negative) mothers. The neonate, in this case, is Rh negative. In which of the following clinical scenarios would the patient most likely have an increase in the leukocyte shown in the photograph?

Option A (A 4-year-old child has whooping cough.) is correct. Bordetella pertussis is the cause of whooping cough. The lymphotoxin in this bacteria inhibits signal transduction by chemokine receptors which prevents lymphocytes from entering lymph nodes leading to lymphocytosis. Lymphocyte counts are often >50,000/mm3 (lymphoid leukemoid reaction).

The photograph shows a small lymphocyte with scant cytoplasm surrounding a dark nucleus. Option B (A 24-year-old man, who raises hogs, has a habit of eating raw bacon.) is incorrect. This patient would most likely develop trichinosis, due to Trichinella spiralis. It is contracted by eating raw or undercooked pork. The larvae penetrate muscle producing muscle pain and tenderness. Invasive helminths produce eosinophilia (type I hypersensitivity). The photograph shows an eosinophil with cytoplasm packed with reddishorange granules that do not cover the nucleus. Option C (A 28-year-old man has a perforated acute appendicitis.) is incorrect. A perforated acute appendicitis produces neutrophilic leukocytosis with left shift (e.g., band neutrophils) and toxic granulation (prominent azurophilic granules). Option D (A 45-year-old woman has severe rheumatoid arthritis.) is incorrect. Monocytosis is the primary leukocyte alteration in chronic inflammation (e.g., rheumatoid arthritis). Option E (A 56-year-old man with polycythemia vera has flushing of his face.) is incorrect. In polycythemia, all cell lines except lymphocytes are increased. An increase in basophils and mast cells causes the release of histamine, which produces flushing of the face (called plethora), headaches, and pruritus after bathing. All of the myeloproliferative diseases have basophilia. A few weeks after an upper respiratory infection, a 10-year-old boy has several bouts of epistaxis associated with nonpruritic lesions on the skin (see photograph). The skin lesions are nonpalpable and do not blanch under digital pressure. There is no evidence of lymphadenopathy or hepatosplenomegaly on physical examination. Hemoglobin and WBC counts are normal. WBC morphology is normal. The platelet count is 25,000/mm3. Which of the following is the most likely cause of the platelet abnormality?

Option A (Antibodies directed against a platelet receptor) is correct. The patient has idiopathic thrombocytopenic purpura (ITP), which is caused by IgG antibodies that are directed against glycoprotein IIb/IIIa fibrinogen receptors on the surface of platelets (type II hypersensitivity reaction). Splenic macrophages with receptors for IgG phagocytose destroy the platelets leading to thrombocytopenia. The lesions shown in the photograph are petechiae, which are defined as pinpoint areas of hemorrhage into the subcutaneous tissue. Petechiae and epistaxis are common signs of a platelet disorder. ITP is the most common cause of thrombocytopenia in children and is treated with corticosteroids. The prognosis is

excellent. Option B (Deficiency of von Willebrand factorcleaving protease) is incorrect. A deficiency of von Willebrand factorcleaving protease in endothelial cells is found in thrombotic thrombocytopenic purpura (TTP), an uncommon cause of thrombocytopenia in women. It is characterized by endothelial damage at the arteriole-capillary junctions throughout the body. This exposes von Willebrand factor (vWF), which is a platelet adhesion factor that is normally synthesized by endothelial cells. Platelets have GpIb receptors that adhere to the exposed vWF. Following adhesion, there is platelet aggregation and the formation of platelet thrombi at all of these injury sites. Consumption of platelets in these thrombi is sufficient enough to produce thrombocytopenia. TTP produces a classic pentad of fever, thrombocytopenia, microangiopathic hemolytic anemia with schistocytes (platelet thrombi damage RBCs), central nervous system dysfunction, and renal failure. Option C (Immunocomplex vasculitis involving small vessels) is incorrect. Immunocomplex vasculitis involving small vessels damages the vessels and causes multifocal areas of subcutaneous hemorrhage (purpura or ecchymoses). The acute inflammatory reaction causes the affected tissue to swell causing the lesions to be palpable; hence, the term palpable purpura as an identifying feature of small vessel vasculitis. Option D (Infiltrative bone marrow disease with destruction of megakaryocytes) is incorrect. Infiltrative bone marrow disease with destruction of megakaryocytes commonly occurs in leukemia, myelofibrosis, and metastatic disease to the bone marrow. In all these conditions, immature WBCs and nucleated RBCs are present in the peripheral blood. Option E (Vessel damage due to a toxin produced by Escherichia coli) is incorrect. The O157:H7 strain of E. coli produces a toxin that damages small vessels causing hemolytic uremic syndrome. It is usually contracted by eating undercooked beef products (e.g., steak, hamburgers). Findings are very similar to what has been described for TTP; except, the toxin is responsible for injury at the arteriole-capillary junctions that initiates platelet thrombus formation and consumption of platelets. An afebrile blood group O, Rh negative (O) 75-year-old man has a massive lower gastrointestinal bleed from sigmoid diverticulosis. He has to be transfused with blood group O, Rh positive (O+) blood, because no group O, Rh negative (O) blood is currently available in the blood banks in the area. He states that he has been transfused once in the past without any problems. In the pretransfusion workup, the patient has a negative antibody screen and a compatible major crossmatch with 4 units of group O, Rh positive (O+) blood. Midway through infusion of the third unit of blood he develops fever, headache, and tachycardia. The transfusion is stopped and a transfusion workup in the blood bank exhibits the following on a posttransfusion specimen of patient blood: Patient temperature: 103o F (39.4 C) Patient blood pressure: 130/86 mm Hg Patient pulse: 130 beats/minute Patient plasma: clear Patient antibody screen:negative Patient direct Coombs: negative Patient urine: negative dipstick for blood

Which of the following best explains the mechanism for the transfusion reaction? Option E (Patient anti-HLA antibodies are directed against donor leukocytes) is correct. The patient has a febrile transfusion reaction. In these reactions, the recipient has anti-human leukocyte antigen (HLA) antibodies directed against foreign HLA antigens on donor leukocytes (type II hypersensitivity reaction). Destruction of the donor leukocytes releases pyrogens causing fever as well as other findings such as chills, headache, and flushing. Option A (Delayed hemolytic transfusion reaction) is incorrect. The antibody screen and direct Coombs test are both negative. This excludes the presence of IgG antibodies in the serum attaching to foreign antigens on donor RBCs. This would lead to phagocytosis and destruction of the RBCs by splenic macrophages (extravascular hemolysis) and unconjugated hyperbilirubinemia, with a possibility of developing jaundice. Option B (Error in the major crossmatch) is incorrect. Although errors in crossmatching blood do occur, they are extremely rare. Furthermore, an error would not explain the correlation of fever with infusion of the blood. Option C (Hemolytic transfusion reaction related to receiving Rh positive blood) is incorrect. The patient had a negative antibody screen prior to his transfusions, which excludes the presence of preexisting anti-D antibodies. Receiving D antigen positive blood would not result in the immediate development of antibodies leading to a hemolytic anemia. However, it is likely, that in the future, he would have to receive D antigen negative blood, because of anti-D antibodies from D antigen positive transfusions. Option D (Histamine-related transfusion reaction) is incorrect. The patient does not have an allergic type of transfusion reaction, which involves the release of histamine from mast cells leading to itching, flushing, and hives (type I hypersensitivity reaction). In which of the following clinical scenarios would the patient most likely have an increase in the leukocyte shown in the photograph?

Option B (A 24-year-old man, who raises hogs, has a habit of eating raw bacon.) is correct. This patient would most likely develop trichinosis, due to Trichinella spiralis. It is contracted by eating raw or undercooked pork. The larvae penetrate muscle producing muscle pain and tenderness. Invasive helminths produce eosinophilia (type I hypersensitivity). The photograph shows an eosinophil with cytoplasm packed with reddishorange granules that do not cover the nucleus.

Option A (A 4-year-old child has whooping cough.) is incorrect. Bordetella pertussis is the cause of whooping cough. The lymphotoxin in this bacteria inhibits signal transduction by chemokine receptors which prevents lymphocytes from entering lymph nodes leading to lymphocytosis. Lymphocyte counts are often >50,000/mm3 (lymphoid leukemoid reaction). Option C (A 28-year-old man has a perforated acute appendicitis.) is incorrect. A perforated acute appendicitis produces neutrophilic leukocytosis with left shift (e.g., band neutrophils) and toxic granulation (prominent azurophilic granules). Option D (A 45-year-old woman has severe rheumatoid arthritis.) is incorrect. Monocytosis is the primary leukocyte alteration in chronic inflammation (e.g., rheumatoid arthritis). Option E (A 56-year-old man with polycythemia vera has flushing of his face.) is incorrect. In polycythemia, all cell lines except lymphocytes are increased. An increase in basophils and mast cells causes the release of histamine, which produces flushing of the face (called plethora), headaches, and pruritus after bathing. All of the myeloproliferative diseases have basophilia.