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Causes of anemias? increased red cell destruction, decreased red cell production, bleeding; secondary to a systemic disease
What are the hypochromic microcytic anemias? iron deficiency anemia, thalassemia, sickle-cell anemia, long-standing anemia of chronic disease
In microcytic anemias with an MCV < 70 fL, the cause is either ______ _________ or __________. iron deficiency, thalassemia
Macrocytic anemias with an MCV > 125 fL almost always are ________, except for those associated with ____________ ________. megaloblastic, myelodysplastic syndromes
What laboratory studies are typically used to evaluate anemias? CBC (Hgb, Hct, red cell indices, red cell distribution width), peripheral smear, corrected reticulocyte count
What is the most common cause of anemia in the world? iron deficiency anemia (inadequate supply of iron for synthesis of hemoglobin)
What is usually the cause of iron deficiency in adults? bleeding from the GI tract; chronic ASA or NSAID use may contribute to the cause
What are other typical causes of iron deficiency anemia? low dietary intake of Fe (children and pregnant women), menstrual blood loss
Clinical features of iron deficiency anemia? general complaints (Hct < 25%) include pallor, easy fatigability, irritability, anorexia, tachycardia, DOE, poor weight gain in infants
What is a hallmark of iron deficiency? pica
What are clinical features of severe iron deficiency anemia? brittle nails, cheliosis, smooth tongue, formation of esophageal webs (Plummer-Vinson syndrome)
Laboratory findings in iron deficiency anemia? H&H decreased; eventually peripheral smear shows hypochromic microcytic RBC's, anisocytosis, and poikilocytosis; plasma ferritin and serum Fe both decrease to < 30 ug/dL; TIBC ELEVATED; transferrin sats < 15%
Tx of iron deficiency anemia? 1. ID bleeding source 2. ferrous sulfate, 325 mg tid, given in a slow, escalating dose (best absorbed on empty stomach, but frequently given w/ meals to avoid AE's) 3. parenteral Fe appropriate for certain pt's
After starting tx of Fe deficiency anemia, how long will it take for Hct to reach normal levels? How long should supplementation continue? should reach normal levels within 2 months, but supplementation should continue for up to 6 mo or longer to replenish tissue stores
Which patients need iron supplementation? during pregnancy and lactation
hereditary anemias in which synthesis of alpha or beta-globin chains is reduced, resulting in defective hemoglobinization of RBC's thalassemia syndromes
caused by gene deletion; most commonly seen in ppl of Southeast Asian or Chinese origin alpha-thalassemia
caused by point mutations; most commonly seen in Mediterranean populations beta-thalassemia
What is the most common feature of the thalassemias? microcytosis out of proportion to the degree of anemia
Who should thalassemia be suspected in? in a person w/ positive family hx or a personal hx of lifelong microcytic anemia, esp. if unresponsive to iron therapy
Clinical features of alpha-thalassemias? (keep in mind that deficits range from silent carriers to profound anemia) may have mild sx or none (thal trait; carriers). Pt's often dx'ed after a nonresponse to tx for a prescribed Fe deficiency.
Patients with only one alpha-globin chain have ___________ _________, which is variably symptomatic. When all 4 chains are deleted, what occurs? hemoglobin H disease; stillbirth occurs from hydrops fetalis
When do problems begin with beta thalassemia major? problems begin at 4-6 mo's, when the switch from fetal hemoglobin (hemoglobin F) to adult hemoglobin occurs
Clinical features of beta thalassemia major? severe anemia, growth retardation, abnormal faical structure, pathologic fractures, osteopenia, bone deformities, hepatosplenomegaly, jaundice
Labs to obtain if thalassemia is suspected? CBC, retic count, peripheral smear, HEMOGLOBIN ELECTROPHORESIS CONFIRMS DIAGNOSIS
What will peripheral smear show with thalassemias? marked microcytosis for degree of anemia
Hct 28-40%, normal Hgb electrophoresis, normal retic count, peripheral smear showing target cells and acanthocytes alpha-thalassemia minor (trait)
Hct 22-32%, increased retic count, peripheral smear shows target cells and poikilocytes, electrophoresis shows hemoglobin H alpha-thalassemia H
Hct 28-40%, normal or increased retic count, peripheral smear shows target cells and basophilic stippling; electrophoresis shows Hemoglobin A2 and hemoglobin F B-thalassemia minor
Hct as low as 10%, increased retic count, peripheral smear shows target cells, poikilocytes, basophilic stippling, nucleated RBC's; electrophoresis shows hgb F and A2 B-thalassemia major
Treatment of alpha-thalassemia (hgb H) disease? folic acid supplements and AVOID iron supplements and oxidative drugs (i.e. dapsone, quinidine, sulfonamides) --> risk of iron overload
Treatment of B-thalassemia major? transfusions to keep hgb concentrations at least 12 g/dL; may also be tx'ed w/ allogenic bone marrow transplantation and iron chelation or splenectomy
Patients w/ b-thalassemia major used to die fm cardiac failure by age 30 (before effective Fe chelation and allogenic stem cell transplants). What does iron overload cause? hemosiderosis, heart failure, cirrhosis, endocrinopathies (use deferoxamine to avoid or postpone hemosiderosis)
Treatment of mild alpha or beta thalassemia? do not give Fe d/t risks associated with Fe overload
acquired d/o's with reduced Hgb synthesis causing iron accumulation, especially in the mitochondria sideroblastic anemia
Causes of sideroblastic anemia? myelodysplais, chronic alcoholism, lead poisoning
Laboratory findings associated with sideroblastic anemia? peripheral smear shows NL and hypochromic cells; Prussian blue staining of bone marrow cells shows ringed sideroblasts (BONE MARROW EVAL NECESS FOR DX); Hct 20-30%
Treatment of sideroblastic anemia? tx underlying cause, transfusion may be required
anemias caused by organ failure or impaired marrow function resulting from systemic disease; MCV 80-100 fL normochromic normocytic anemias
Significant anemia in pt's with chronic disease usually indicates what kind of anemia? folate or iron deficiency
anemia that arises from injury or abnormal expression of the pluripotent hematopoietic stem cell aplastic anemia
Clinical features of aplastic anemia? weakness, fatigue, vulnerability to infection, pallor, purpura, petechiae
Laboratory studies-hallmark of aplastic anemia? pancytopenia; bone marrow is hypocellular
Treatment of aplastic anemia? mild-supportive tx with transfusion of RBC's and paltelets; severe-bone marrow transplantation or immunosuppression
What causes macrocytic anemias (MCV > 100 fL)? acute hemorrhage, hemolysis, deficiences leading to megaloblastic states
What is the most common cause of folic acid deficiency? poor dietary intake
Other causes of folic acid deficiency? pregnancy, hemolytic anemia, alcohol abuse, consumption of folic acid antagonists
Clinical features of folic acid deficiency? sore tongue (glossitis), vague GI symptoms; no neuro sx (in contrast to vitamin B12 deficiency)
Lab findings of folic acid deficiency? MACRO-OVALOCYTES AND HYPERSEGMENTED PMNS ARE PATHOGNOMONIC; Howell-Jolly bodies are typical; RBC folate < 150 ng/mL is diagnostic; vit. B12 is NL
Treatment of folic acid deficiency? folic acid 1 mg/day=first line tx DISCONTINUE ALCOHOL AND FOLIC ACID ANTAGONISTS
Causes of vitamin B12 (cobalamin) deficiency? pernicious anemia (most common cause) --> leads to atrophic gastritis and increased risk of gastric carcinoma; strict vegan diet, gastric surgery, Crohn's disease
Where does absorption and storage of B12 occur? absorption in terminal ileum and storage in liver
What foods supply vitamin B12? foods of animal origin
What is the most concerning effect of uncorrected B12 deficiency? irresversible neuro damage can be caused by uncorrected deficiency
What can mask, but not correct, vitamin B12 deficiency? folate supplementation
Clinical features of vitamin B12? glossitis and vague GI symptoms; neuro findings include stocking-glove paresthesias, loss of position, fine touch and vibratory sensation, clumsiness, dementia, and ataxia
Laboratory studies for diagnosis of vitamin B12? anemia may be severe, MCV usually markedly elevated; anisocytosis, poikilocytosis, macro-ovalocytosis, hypersegmented neutrophils; retic count reduced; B12 LOW!
Treatment of vitamin B12 deficiency? lifelong supplemental vitamin B12 usually given IM for pernicious anemia; daily oral cobalamin may be used; neuro signs/sx reversible if treated w/in 6 months
What causes hemolytic anemias? characterized by episodic or continuous RBC destruction; based on intrinsic red cell defects or extracellular causes
What are intrinsic causes of hemolytic anemia? hereditary spherocytosis and elliptocytosis, paroxysmal noctural hemoglobinuria, G6PD deficiency, methemoglobinemia, sickle-cell sydnromes
What are external causes of hemolytic anemia? autoimmune and lymphoproliferative diseases, drug toxicity, thrombotic thrombocytopenic purpura, hemolytic-uremic syndrome, DIC, valvular hemolysis, metastatic adenocarcinoma, vasculitides, infxns, hypersplenism, burns
Clinical features of hemolytic anemias? may present with jaundice, gallstones, pallor, and sx related to decreased O2 delivery to tissues; infection w/ parvovirus B19 can lead to a transient aplastic crisis
Lab findings in hemolytic anemia? elevated retic count, peripheral smear may show immature RBC's, nucleated RBC's, or morphologic changes; indirect bili and total bili slightly elevated
Treatment of hemolytic anemias? treat underlying disorder
autosomal recessive hemolytic anemia sickle cell anemia
Pathophysiology of sickle cell anemia? RBC's containing primarily hemoglobin S sickle under deoxygenated conditions
Clinical features of sickle cell anemia? problems beginin infancy when hemoglobin F levels fall; by childhood or adolescence, vascular occlusions produce painful crises, lasting for hrs to days, with organ swelling and dysfunction and infarction
What causes sickling to increase? dehydration, acidosis, hypoxemia
What problems are sickle cell patients at increased risk for? cholelithiasis, splenomegaly, poorly healing ulcers, infection with encapsulated organisms (ie. strep pneumoniae), strokes, priapism, retinopathies, osteomyelitis, avascular necrosis of femoral head; aplastic crises (life-threatening)
Diagnosis of sickle cell anemia? Hgb electrophoresis shows hemoglobin S in RBC's, peripheral smear reveals sickled cells, target cells, nucleated RBC's, Howell-Jolly bodies, elevated retic count
Treatment of sickle cell anemia? 1. Symptomatic tx includes administration of analgesics, fluids, oxygen. 2. Folic acid supplementation. 3. Hydroxyurea for severe cases. 4. Pneumococcal vaccine 5. Vaso-occlusive may require transfusion
X-linked recessive d/o commonly seen in American black males and Mediterranean populations G6PD deficiency
Pathophysiology of G6PD deficiency? characterised by abnormally low levels of glucose-6-phosphate dehydrogenase, a metabolic enzyme involved in the pentose phosphate pathway, especially important in RBC metabolism
What may cause episodic hemolysis in patients with G6PD deficiency? infection and oxidant drugs (i.e. dapsone, quinidine, nitrofurantoin, sulfonamides) may cause episodic hemolysis
Clinical features of patients with G6PD deficiency? female carriers rarely affected; patients w/ episodic hemolysis usually healthy and w/o splenomegaly
Lab findings in patient with G6PD deficiency? G6PD levels low in between hemolytic episodes (if severe, G6PD levels always low); peripheral smear reveals bite cells and Heinz bodies; during hemolytic episodes, retics and indirect bili increase
Treatment of G6PD deficiency? AVOID oxidative drugs; hemolytic episodes are self-limited as RBC's are replaced
diseases characterized by unrestrained growth of leukocytes and leukocyte precursors in the tissues leukemias
How are leukemias classified? lymphoid and myeloid, acute and chronic
Risk factors for leukemia? positive family history, exposures to ionizing radiation, benzene, certain alkylating agents
Who does acute lymphocytic leukemia tend to affect most? children, ages 3-7 (80%)
Who does acute myelogenous leukemia tend to affect most? median onset is 60 years old
Clinical features of acute leukemias? findings related to replacement of normal bone marrow with malignant cells; gingival bleeding, epistaxis, menorrhagia; infxns fm neutropenia commonly caused by gm-neg bacteria or fungi (common presentations-cellulitis, pneumonia, perirectal infxn)
How do children and young adults tend to present with acute leukemias? fatigue, abrupt onset of fever, lethargy, H/A bone or joint pain
How do older adults tend to present with acute leukemias? slow, progressive onset with lethargy, anorexia, dyspnea
Lymphadenopathy and splenomegaly are more common with ____ than ____. ALL, AML
Laboratory findings with acute leukemias? HALLMARK=pancytopenia w/ circulating blasts (blasts make up at least 20% of nucleated cells in bone marrow); WBC counts usually high, hyperuricemia
What confirms the diagnosis of acute leukemias? bone marrow biopsy
What findings are seen specifically with AML? auer rods (rod-shaped structures in cell cytoplasm)
What findings are seen specifically with ALL? mediastinal mass on CXR, terminal deoxynucleotidyl transferase (present in 95% cases), presence of Philadelphia chromosome unfavorable in ALL
Treatment of ALL? >50% children with ALL can be cured with chemotherapy (induction chemo plus consolidation therapy)
Prognosis of ALL related to what factors? related to age and WBC count at diagnosis
Treatment of AML? greater than 70% of adults younger than 60 years achieve complete remission w/ tx for AML; further chemo leads to cure in 30-40% patients
Possible treatments available for AML and ALL? 1. induction (remission-inducing) chemotherapy targeted toward eradication of most of leukemic cells 2. consolidation therapy destroys remainder of leukemic cells 3. allogeneic bone marrow transplantation used in pt's w/ poor response to tx
clonal malignancy of B lymphocytes; most prevalent of all leukemias; 2x common in men as women; median presenting age is 65 y.o. chronic lymphocytic leukemia (CLL)
Normal course of CLL? usually has indolent course, w/ a median survival time of 6 yrs; often harmless but resistant to cure (a variant, polylymphocytic leukemia, is more aggressive)
Clinical manifestations of CLL? peripheral lymphocytosis and lymphocytic invasion of bone marrow, liver, spleen, and lymph nodes; recurrent infxns, splenomegaly, LA common
What syndrome occurs in 5% cases of CLL? Richter's syndrome --> an isolated node transforms into aggressive, large-cell lymphoma
Laboratory findings associated with CLL? HALLMARK=isolated lymphocytosis, w/ leukocytosis of > 20,000 cells/mL; peripheral smear shows increased mature small lymphocytes and SMUDGE CELLS ARE PATHOGNOMONIC; bone marrow is hypercellular and w/ a left shift
Treatment of CLL? usually palliative once disease is symptomatic
myeloproliferative disorder; presents in young to middle-aged adults (median age 55 y.o.); occurs in 3 phases (chronic, accelerated, acute) but inevitably transforms into acute disease chronic myelogenous leukemia (CML)
Symptoms of CML? fatigue, anorexia, weight loss, low-grade fever, excessive sweating, abdominal fullness (caused by splenomegaly); may have respiratory distress, blurred vision
Laboratory findings associated with CML? HALLMARK=leukocytosis (median WBC of 150,000 cells/mL); Philadelphia chromosome identified in 95% cases; may show anemia and thrombocytosis; bone marrow hypercellular with left shift
Treatment of CML? STI571 (imitanib mesylate) has replaced former standard therapy - effective during chronic phase(hydroxyurea used for iminitab intolerance); allogeneic bone marrow transplantation may be initial tx and only therapy that is curative!
Group of CA's characterized by enlargement of lymphoid tissue, spleen, and liver and presence of Reed-Sternberg cells Hodgkin's disease
Demographics of Hodgkin's disease? common between ages 15-45, more common in males; EVB can be found in 40-50% cases
Typical presentation of Hodgkin's disease? painless cervical, supraclavicular, and mediastinal LA; pain in affected node after ingestion of alcohol may occur
What are the two stages of symptoms and what are they? Stage A (lack of constitutional sx); Stage B (fever, night sweats, weight loss, pruritis, fatigue)
What are the various sub-types of Hodgkin's disease? nodular sclerosis subtype (more common in women); lymphocyte predominant, mixed cellularity, lymphocyte depletion
Laboratory studies to diagnose Hodgkin's and non-Hodgkin's lymphoma? REED-STERNBERG CELLS CONFIRM DIAGNOSIS. Basic staging includes CT of neck, chest, abdomen, and pelvis, as well as bx of bone marrow. Ann Arbor system used to stage Hodgkin's and non-Hodgkin's
Treatment of Hodgkin's lymphoma for patients with low-risk stage IA and IIA disease? radiation therapy is initial tx choice if low risk; good prognosis
Treatment of Hodgkin's lymphoma if higher risk or even those with advanced-stage disease? combination chemotherapy cures > 50% patients
malignancies that arise from lymphocytes, 90% cases dervied from B lymphocytes; peak incidence 20-40 y.o. non-Hodgkin's lymphoma
Most common presentation of non-Hodgkin's lymphoma? diffuse or isolated, painless, persistent LA; bone marrow involvement is frequent
Common extralymphatic sites where non-Hodgkin's lymphoma may present include? GI tract, skin, bone, bone marrow (Burkitt's lymphoma likely to present w/ abdominal fullness)
Fever, night sweats, weight loss, puritus, and fatigue are _____ ________ than with Hodgkin's disease. less likely (but do occur w/ intermediate and high-grade disease)
Laboratory studies to evaluate non-Hodgkin's lymphoma? biopsy persistent, unexplained, enlarged lymph nodes; CT of abdomen, pelvis, chest (for staging); bone marrow bx
Treatment of non-Hodgkin's lymphoma? spontaneous remission may occur; aggressive lymphomas may require aggressive combo chemo or autologous stem cell transplantation
single LNR or single ELS stage I hodgkins: ann arbor criteria
two or more LNRs on same side of diaphragm or one solitary ELS and one or more LNRs on same side of diaphragm stage II hodgkins: ann arbor criteria
LNR on both sides of diaphragm; w/ spleen involvement or solitary involvement of an ELS or both stage III hodgkins: ann arbor criteria
diffuse involvement of ELS w/ or w/o node involvement stage IV hodgkins: ann arbor criteria
malignancy of plasma cells, possibly caused by a herpes virus multiple myeloma
replacement of bone marrow leads to failure; bone destruction leads to pain, osteoporosis, lytic lesions, and pathologic fractures; plasmacytomas may cause spinal cord compression multiple myeloma
Most common presentation of multiple myeloma? median age of dx=65 y.o.; anemia, bone pain (low back, ribs), infection (more prone to recurrent infxn)
Less common presentation of multiple myeloma? renal failure, spinal cord compression, hyperviscosity syndrome; some cases found thru abnormal labs --> hypercalcemia, proteinuria, elevated ESR; f/u electrophoresis abnormal
Laboratory studies with multiple myeloma? anemia (rouleau formation common), lytic lesions or osteoporosis on radiography of axial skeleton (bone scan NOT helpful)
Hallmark of multiple myeloma? monoclonal spike (M-spike) on serum electrophoresis
Treatment of multiple myeloma? options changing rapidly and include thalidomide derivative; bisphosphonates are important adjuncts
Initial assessment of a patient with a suspected bleeding disorder should include what? platelet count, peripheral smear, bleeding time (PT/PTT/INR), thrombin clotting time measures the rate of conversion of fibrinogen to fibrin in the presence of thrombin
abnormal decrease in the # of platelets in the blood; most common cause of abnormal bleeding! thrombocytopenia
Causes of thrombocytopenia? impaired production, increased destruction, splenic sequestration, or dilution
self-limited autoimmune (IgG) disorder found most commonly in children of both sexes and is associated with a preceding viral URI idiopathic thrombocytopenic purpura (ITP)
d/o of bleeding that may occur at any age and is more common in women; often coexists w/ other autoimmune diseases chronic ITP
Clinical features of acute ITP? abrupt appearance of petechiae, purpura, and hemorrhagic bullae on the skin and mucous membranes; possibly epistaxis, oral bleeding, menorrhagia
Clinical features of chronic ITP? develop petechiae on skin and mucous membranes; may also have epistaxis, oral bleeding, and menorrhagia
What drug most commonly causes an ITP-like reaction in hospitalized patients? heparin!! other causes may include sulfonamides, thiazides, cimetidine, gold
What are other causes of secondary thrombocytopenia? SLE and CLL
Laboratory findings associated with acute ITP? decreased platelets (10,000-20,000), eosinophilia, mild lymphocytosis
Laboratory findings associated with chronic ITP? platelet count of 25,000-75,000
Treatment of acute ITP? usually resolves spontaneously; some patients require steroids or splenectomy
Treatment of chronic ITP? initial tx=high-dose prednisone; splenectomy is definitive and often required; may need platelet transfusion
rare but often fatal disorder; found in previously healthy people (20-50 y.o.); characterized by severe thrombocytopenia with purpura, petechiae, pallor, abdominal pain, microangiopathic hemolytic anemia, fever, abnml neuro signs, renal failure thrombotic thrombocytopenic purpura (TTP)
What may precipitate TTP? More common in women or men? estrogen use, pregnancy, drugs such as quinine and ticlopidine; more common in women
disorder similar to TTP but found primarily in children and does not include neurological symptoms hemolytic-uremic syndrome
disorder that causes generalized hemorrhage in pt's w/ severe underlying systemic illness, such as sepsis, tissue injury, obstetric complications, CA, and in severe transfusion reactions DIC
Laboratory findings associated with TTP and HUS? anemia, red cell fragmentation, NL leukocytes, reticulocytosis, thrombocytopenia, polychromatophilia; ADAMTS 13 (metalloprotease enzyme) is low; LDH markedly elevated; indirect bili increases
Treatment of TTP? large-volume plasmapheresis; prednisone and antiplatelet agents also ahve been used
What are the most common causes of acquired platelet dysfunction? ASA and other NSAIDS
What clinical findings may be seen in pt's on ASA and other NSAIDS? prolonged bleeding time, skin and mucosal bleeding; labs indicate nl number of platelets, but platelet function study results are abnml
autosomal dominant, congenital bleeding disorder; most common congenital coagulopathy von Willebrand's disease
reduced levels of factor VIII antigen or ristocetin cofactor von Willebrand's disease
How many types of von Willebrand's disease exist? 6 major types, all characterized by deficient or defective vWF; Type I accounts for 75-80% cases
Clinical features of von Willebrand's disease? bleeding occurs in nasal, sinus, vaginal, and GI mucous membranes; spontaneous hemarthrosis and soft-tissue bleeds uncommon but can occur
What exacerbates bleeding in von Willebrand's disease? What decreases bleeding? ASA exacerbates it; pregnancy or use of estrogen decreases it
Lab findings in von Willebrands? bleeding time usually prolonged, vWF is low
Treatment of von Willebrand disease? varies according to type of disease; desmopressin acetate useful in type I; Factor VIII concentrates preferred if factor replacement necessary
x-linked recessive disease (affecting males) characterized by excessively prolonged coagulation; most severe bleeding disorder and 2nd most common congenital coagulopathy hemophilia A (factor VIII deficiency or classic hemophilia)
Other general characteristics of hemophilia A? many pt's seropositive for HIV b/c of infected factor VIII transfusions; recent genetic mutation causes 1/3 of all cases of hemophilia A
Clinical features of patients severely affected by hemophilia A? repeated spontaneous hemorrhagic episodes w/ hemarthroses, epistaxis, intracranial bleeding, hematemesis, melena, microscopic hematuria, bleedings into soft tissue and gingiva
Clinical features of patients mildly affected by hemophilia A? excessive bleeding following trauma or surgery
Laboratory findings associated with hemophilia A? PTT is prolonged, factor assay shows reduced factor VIII:C levels (vWF NL)
Standard treatment of hemophilia A? infusion of heat-treated or recombinant factor VIII concentrates; desmopressin may also help elevated factor VIII; AVOID ASA!
x-linked recessive d/o (affecting males) similar to hemophilia A but occurs less frequently factor IX deficiency, Christmas disease
mild, autosomal recessive d/o seen primarily in Ashkenazi Jews factor XI deficiency (rare hemophilia C)
Tx of factor XI deficiency? fresh-frozen plasma
Clinical features of factor XI deficiency? little spontaneous bleeding, but may hemorrhage with surgical procedures and ppx is required
Congenital d/o's associated with thrombotic states typically are _______ _______. autosomal dominant
Acquired hypercoaguable states are associated with? malignancy, pregnancy, OCP's, nephrotic syndrome, immobilization, UC and Crohn's, myeloproliferative disease, anticardiolipin antibodies, DIC, TTP-HUS, antiphospholipid syndrome
Congenital causes of hypercoaguable states include? antithrombin III deficiency, factor V Leiden, protein C deficiency, protein S deficiency, abnormal plasminogen, dysfibrogenemia
Created by: rad548



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