دسترسی نامحدود
برای کاربرانی که ثبت نام کرده اند
برای ارتباط با ما می توانید از طریق شماره موبایل زیر از طریق تماس و پیامک با ما در ارتباط باشید
در صورت عدم پاسخ گویی از طریق پیامک با پشتیبان در ارتباط باشید
برای کاربرانی که ثبت نام کرده اند
درصورت عدم همخوانی توضیحات با کتاب
از ساعت 7 صبح تا 10 شب
ویرایش: سری: ISBN (شابک) : 9783031758096, 3031758099 ناشر: Springer سال نشر: 2025 تعداد صفحات: 322 زبان: English فرمت فایل : PDF (درصورت درخواست کاربر به PDF، EPUB یا AZW3 تبدیل می شود) حجم فایل: 11 مگابایت
در صورت تبدیل فایل کتاب Consulting Hematology and Oncology Handbook (Jan 11, 2025)_(3031758099)_(Springer) به فرمت های PDF، EPUB، AZW3، MOBI و یا DJVU می توانید به پشتیبان اطلاع دهید تا فایل مورد نظر را تبدیل نمایند.
توجه داشته باشید کتاب دفترچه راهنمای خون شناسی و آنکولوژی (11 ژانویه ، 2025) _ (3031758099) _ (اسپرینگر) نسخه زبان اصلی می باشد و کتاب ترجمه شده به فارسی نمی باشد. وبسایت اینترنشنال لایبرری ارائه دهنده کتاب های زبان اصلی می باشد و هیچ گونه کتاب ترجمه شده یا نوشته شده به فارسی را ارائه نمی دهد.
Preface Contents Contributors Part I: Malignant Hematology Chapter 1: What Should We Quickly Know About Hemopoietic Malignancies? Acute Leukemia Acute Myelogenous Leukemia Definitions Classification Etiology Germline Predisposition Aging Associated Risk Drug-Induced Genotoxic Effect Clinical Context Laboratory Investigation Acute Lymphoblastic Leukemia Definitions Classification Etiology Germline Predisposition Chromosomic Abnormalities Clinical Context Laboratory Investigation What Are the Basic Principles for Initial Evaluation of Myeloproliferative Neoplasms? Chronic Myeloid Leukemia Definitions Clinical Context Risk Stratification Risk of TKIs Toxicity Laboratory Investigation Useful Tools References Chapter 2: Acute Myeloid Leukemia Risk Stratification Acute Myelogenous Leukemia Risk Stratification Case Demonstration Definitions Clinical Context Laboratory Investigation Useful Tools European LeukemiaNet (ELN) Risk Stratification of Adult AML AML Relapse Risk References Chapter 3: How to Diagnose Acute Myelogenous Leukemia Clinical Manifestations Tests to Establish a Diagnosis Genetic Analyses Morphology Additional Tests or Procedures at Diagnosis Differential Diagnoses to Consider References Chapter 4: Preparing Your Patient for Chemotherapy Leukostasis Case Demonstration Definitions Leukostasis Clinical Context Laboratory Investigation Other Investigation Management Case Demonstration (Continued) Disseminated Intravascular Coagulation Definition Clinical Context Laboratory Investigation Management Supportive Care Caveats Case Demonstration (Continued) Neutropenic Fever Definition Clinical Context Important Timelines After Chemotherapy Exposure Laboratory Investigation Other Diagnostic Tools Caveats Tumor Lysis Syndrome Case Demonstration Definition Clinical Context Clinical Manifestations Laboratory Investigation Risk Stratification Management Caveats Specific Considerations References Chapter 5: Acute Chemotherapy Administration and Complications Management of Adult AML Acute Promyelocytic Leukemia Case Demonstration APL Risk Stratification Treatment of APL Low-Risk Induction High-Risk Induction Caveats Management of DS Minimal Residual Disease (MRD) Monitoring after Induction Consolidation Management After Consolidation Management of Non-APL Acute Myeloid Leukemia Case Demonstration Hyperleukocytosis in Newly Diagnosed AML Leukapheresis Caveats Hydroxyurea (HU) Cytarabine Infusion Caveats Pretreatment Evaluation “7 + 3” Induction Therapy for Medically Fit Patients Acute Chemotherapy Complications Additional Therapies to Backbone 7 + 3 Liposomal Daunorubicin Plus Cytarabine Treatment Options for Medically Unfit Patients Case Demonstration Low-Intensity Therapy Options Hypomethylating Agents (Monotherapy) Caveats BCL-2 Inhibitor Combination Therapies Caveats Targeted Therapies Relapsed/Refractory Disease References Chapter 6: Acute Differentiation Syndrome Case 1 Acute APL Differentiation Syndrome (DS) Definition Pathogenesis Incidence and Timing of Onset Clinical Manifestations Grading of DS Laboratory and Radiologic Investigation Case 1 Continued Pulmonary Manifestations of Acute DS Cardiovascular Manifestations of Acute DS Management Steroids Interruption in ATRA or ATO Therapy Cytoreductive Strategies Hydroxyurea Chemotherapy Gemtuzumab Ozogamicin DS Prophylaxis Caveats Predictors of DS Case 2 Targeted Therapy-Associated DS Clinical Manifestations Management References Chapter 7: Cardiovascular Complications After Chemotherapy and Targeted Agents Case 1 Definition Pathogenesis Investigation in Patients with Suspected Impaired Heart Failure Additional Investigation in Patients with Suspected Impaired EF Case 1 Cont’d Clinical Context Dexrazoxane Dosing Case 2 Cardiovascular Side Effects Initiated by TKI Patient Management Risk Factors Management References Chapter 8: Neutropenic Sepsis: Antibiotic Prophylaxis Case Demonstration Part 1 Clinical Context Neutrophils and the Immune System Definitions of Neutropenia Etiologies of Neutropenia Neutropenic Fever Risk of Febrile Neutropenia Development Environmental Considerations in Reducing Opportunistic Infection in Neutropenic Hosts Case 1 (Continued) Clinical Context Febrile Neutropenia Evaluation/Investigation Risk Calculations Prophylaxis for Febrile Neutropenia Antibacterial Prophylaxis Recommendations Antifungal Prophylaxis Recommendations Additional Microorganism to Consider Antiviral Prophylaxis Treatment of Neutropenic Fever Case 1 (Continued) Clinical Context Empiric Antibiotic Treatment Case 1 (Continued) Clinical Context Persistent Fevers in Neutropenic Patient Caveats Antifungal Treatment Antiviral Treatment Therapeutic Drug Monitoring References Chapter 9: Diagnosis and Management of Diffuse Large B-Cell Lymphoma Case Demonstration Definition Clinical Context Investigation/Workup Morphology Immunophenotyping Cytogenetics/FISH Others Next-Generation Sequencing [1] Classification: DLBCL NOS Cell of Origin Molecular (Fig. 9.2) Genetic Prognostic Index Pretreatment Evaluation Laboratory Studies Other CNS Prophylaxis Management (Fig. 9.3) Upfront Therapy Limited Stage DLBCL Advanced Stage DLBCL Standard NOS DLBCL Double Expressor Lymphoma High Grade Lymphoma with MYC, BCL-2, BCL-6 Rearrangements (Double Hit/Triple Hit) Relapsed/Refractory Disease Chimeric Antigen Receptor T-Cell Therapy Agents Available for Relapsed/Refractory Disease Antibody Drug Conjugates (ADCs) Small Molecules BiTEs (Bispecific Antibodies) Specific Considerations Useful Tools References Chapter 10: Supportive Care for Treatment of Hematologic Malignancies Case Demonstration Definition [1–4] Clinical Context [1, 2, 4, 5] Etiology Pathophysiology Risk Factors Clinical Manifestation [1–4, 6] Assessment [1, 2, 5, 6] Laboratory Investigation [1, 2, 6] Management [2–6] Specific Considerations [3, 5, 6] Useful Tools References Chapter 11: Plasma Cell Disorders Case 1 Demonstration Definitions Clinical Context Clinical Manifestations Case 1 (Cont) Tests to Establish Diagnosis Identification of Bone Lesions Risk Stratification High Risk Disease Standard Risk Myeloma Case (Cont) Treatment Supportive Care Case 1 (Cont) Case 2 Demonstration Definitions Testing Follow-Up Case 3 Demonstration Definitions Diagnostic Testing Treatment Useful Tools How to Read SPEP/UPEP [50] References Part II: Benign Hematology Chapter 12: Primer to Bleeding Disorders Case Clinical Context Table 12.1 Approach to the clinical history and physical exam Malignancy Associated Acquired von Willebrand Syndrome Alcohol Use Disorder Liver Disease Systemic Lupus Erythematosus Hypothyroidism Clinical Manifestations Laboratory Investigation Tests to Assess Secondary Hemostasis Coagulation studies, PT, APTT Fig. 12.1 The clotting cascade responsible for secondary hemostasis Table 12.2 Interpretation of prolonged coagulation studies Table 12.3 Types of Hemophilia [22–24] Fig. 12.2 Diagram representation of VWD subtypes and differences in quantitative/qualitativedefects Table 12.4 Types of von Willebrand disease and their features [25–27] Thrombin and Reptilase Time Table 12.5 Disorders of fibrinogen [19, 20] Mixing Studies Table 12.6 Rare inherited bleeding disorders [28] Table 12.7 Interpretation of aggregometry in platelet disorders Table 12.8 Platelet disorders Table 12.9 Disorders of hyperfibrinolysis The Bethesda Assay Specific Clotting Factor Assays Tests to Assess Primary Hemostasis Management Fig. 12.3 Formation of the fibrin degradation product, D-dimer Management of VWD Table 12.11 Treatment modalities for VWD and aVWS DDAVP VWF Concentrates Other Agents Treatment of Hemophilia Table 12.12 Summary of FVIII replacement products for hemophilia A Table 12.13 Summary of FIX replacement products for hemophilia B Table 12.14 Recommendations for factor replacement in hemophilia patients Table 12.15 Bypassing agents and their clinical applications Treatment of Acquired and Congenital Platelet Disorders Treatment of Acquired and Congenital Fibrinogen Disorders Table 12.16 Fibrinogen replacement therapy [57] Useful Tools References Chapter 13: Interpretation of Blood Clotting Studies Case Demonstration Definitions Fig. 13.1 Coagulation pathways. FVa activated factor V, FVIIIa activated factor VIII, PL phospholipid,TF tissue factor Clinical Context Complete Correction in a Mixing Study Uncorrected Results Fig. 13.2 Possible etiologies for an uncorrected mixing study. DOACs direct oral anticoagulants,PT prothrombin time, aPTT activated partial thromboplastin time, WRR within reference range Fig. 13.3 Algorithm for evaluation of abnormal coagulation test and interpretation of mixing studies.DIC: disseminated intravascular coagulation; FII: factor II; FV: factor V; FVII: factor VII;FVIII: factor VIII; FIX: factor IX; FX: factor X; FXI: factor XI; PT: prothrombin time; aPTT:activated partial thromboplastin time; RT: reptilase time; TT: thrombin time; vWD: von Willebranddisease Special Considerations Case Demonstration, Continued Achieving Hemostasis in Active, Clinically Significant Bleeding First-line treatment options include the following: Inhibitor Eradication Monitoring References Chapter 14: Venous Thromboembolism Case Demonstration 1 Definitions Clinical Context Clinical Manifestations Laboratory and Radiologic Investigation Management of Provoked DVT Table 14.1 Anticoagulants for venous thromboembolism (VTE) [5, 6] Caveats Case Demonstration 2 Definitions [7] Clinical Context Fig. 14.1 First VTE diagnosis approach. Laboratory Investigation Table 14.2 Venousthrombophilia screening Case Demonstration 2 (Continued) Definitions Clinical Manifestations Fig. 14.2 Diagnosis and treatment of PE. Diagnosis Laboratory Investigation Management of PE [4] Submassive PE Useful Tools Table 14.3 The PulmonaryEmbolism Severity Index(PESI) and simplified PESI References Chapter 15: Consultation for Thrombocytopenia Thrombotic Thrombocytopenic Purpura (TTP) Case Presentation Definition Clinical Context Table 15.1 TMA syndromes and systemic disorders Clinical Manifestations Fig. 15.1 Diagnostic and initial treatment for TTP. *While awaiting ADAMTS13 activity, startplasma exchange. Treatment can be changed once results are obtained. **In settings without reasonableaccess to ADAMTS13 activity testing, the use of caplacizumab is not recommended,regardless of the pretest probability of TTP Fig. 15.2 Pathophysiology of acquired TTP. In biologic normal condition, very large vWF multimersare cleaved by ADAMTS13 to avoid pathologic platelet aggregability. ADAMTS13 depletionresults in uncleaved large vWF allowing widespread platelet aggregability and adhesion Laboratory Investigations Table 15.2 Laboratoryinvestigations in TTP Management Table 15.3 TTP treatment paradigm [2, 6] Table 15.4 Plasmic Diagnostic Score Fig. 15.3 TTP treatment algorithm. *While awaiting ADAMTS13 activity, start plasma exchange.Treatment can be changed once results are obtained. **In settings without reasonable access toADAMTS13 activity testing, the use of caplacizumab is not recommended, regardless of the pretestprobability of TTP Monitoring Specific Considerations Useful Tools Heparin-Induced Thrombocytopenia Case Definition Fig. 15.4 Pathophysiology of HIT. Auto-antibody IGG against platelet factor 4 (PF4)-heparincomplex avidly bind platelets and monocytes inducing activation. Platelet aggregability and procoagulantparticle release leads to thrombosis Table 15.5 Characteristics of type I and type II HIT Table 15.6 HIT variants Clinical Context Fig. 15.5 Diagnostic and initial treatment for HIT Table 15.7 4Ts score for heparin-induced thrombocytopenia Clinical Manifestations Table 15.7 4Ts score for heparin-induced thrombocytopenia Laboratory Investigations Management Special Considerations Other Tools Immune Thrombocytopenia Purpura Case Definition Table 15.10 Common causes of thrombocytopenia Table 15.11 Clinical manifestations of ITP Clinical Context Clinical Manifestations Laboratory Investigations Management Fig. 15.7 Initial treatment for ITP Table 15.12 First-line therapies [29, 30] Fig. 15.8 Urgenttreatment for ITP Fig. 15.9 Second line treatment options for ITP Table 15.13 Second-line therapies for ITP [29] Special Considerations Disseminated Intravascular Coagulation Case Definition Clinical Context Clinical Manifestations Table 15.14 Clinical manifestations of DIC Table 15.14 Clinical manifestations of DIC Laboratory Investigations Table 15.15 Laboratory abnormalities in acute and chronic DIC Management Table 15.16 Blood products administered as supportive care in DIC Table 15.17 Algorithm for diagnosis of DIC Useful Tools Table 15.17 Algorithm for diagnosis of DIC References Chapter 16: Erythrocytosis Case Demonstration Definitions Fig. 16.1 The regulation pathway of erythropoiesis Fig. 16.2 Classification of erythrocytosis. Clinical Context and Manifestations Laboratory Investigation Initial Table 16.1 2016 World Health Organization criteria for Polycythemia vera [6] Fig. 16.3 Diagnosis approach of erythrocytosis. Management Fig. 16.4 Treatment PV. Fig. 16.5 Treatment approach for JAK2 unmutated erythrocytosis. Specific Considerations References Chapter 17: Anemia Case Clinical Context Low MCV < 80 fL Normal MCV (80–100) fL Acquired Hemolytic Anemia Congenital Hemolytic Anemias High MCV > 100 fL Table 17.6 Laboratory signs of hemolysis (not including peripheral blood smear) Clinical Manifestations Laboratory Investigation Table 17.9 Mean corpuscular volume Table 17.10 Peripheral blood smear and anemia Table 17.11 Special laboratory tests may help to identify anemia subtypes Management Table 17.12 Treatment of B12 and folate deficiencies [30] Table 17.13 Oral iron preparations Table 17.14 Parental iron preparations Table 17.15 Treatment of warm autoimmune hemolytic anemia Table 17.16 Treatment of cold agglutinin disease Fig. 17.4 Treatment options for PNH Fig. 17.3 Antiglobulin (Coombs) test [13] Special Considerations Useful Tools References Chapter 18: Bone Marrow Failure Syndromes Case 1 (Hypercellular MDS) Definition of Bone Marrow Failure Fig. 18.1 Myelodysplastic syndrome with ring sideroblasts and single lineage dysplasi Clinical Evaluation of Bone Marrow Failure Table 18.1 Diagnosticevaluation of suspected bonemarrow failure Acquired Causes of Bone Marrow Failure Myelodysplastic Syndrome Definition Diagnosis Treatment Fig. 18.4 Management of higher-risk MDS. HCT hematopoietic stem cell transplant, MDSmyelodysplastic syndrome. aHigher-risk defined as intermediate, high or very-high-riskMDS. bHMA includes azacitidine or decitabine or oral decitabine and cedazuridine Case 2 (Hypocellular MDS) Aplastic Anemia Definition Table 18.3 Aplastic anemia vs. hypoplastic MDS Diagnosis Treatment Fig. 18.5 Management of severe aplastic anemia Case 3 Inherited Causes of Bone Marrow Failure Fanconi Anemia Shwachman-Diamond Syndrome Diamond-Blackfan Anemia Dyskeratosis Congenita Congenital Amegakaryocytic Thrombocytopenia Severe Congenital Neutropenia Important Tools References Chapter 19: Sickle Cell Disease Case Clinical Context Clinical Manifestations Laboratory Investigation Management Management of Acute Pain Crisis Transfusion Therapy Chronic Management of SCA Prophylaxis Specific Considerations Stroke Retinopathy Acute Chest Syndrome Pulmonary Hypertension Hepatic Crisis Cholelithiasis Autosplenectomy Splenic Sequestration Renal Disease Aplastic Crisis Priapism Sickle Ulcers Useful Tools References Chapter 20: Transfusion Medicine Consultation General Principles in Transfusion Medicine ABO Blood Group Fig. 20.1 ABO blood types Rh Blood Group System Testing Prior to Transfusion Fig. 20.2 Forward typing Fig. 20.3 Reverse typing Transfusion of Blood Components RBCs (RBCs) Platelets Plasma Products Case Demonstration Part 1 Clinical Context Laboratory Investigation Case Demonstration Part 2 Clinical Context Fig. 20.4 Pathophysiology of acute hemolytic transfusion reactions Laboratory Investigation Case Demonstration Part 3 Part 3 Discussion Fig. 20.5 Pathophysiology of delayed hemolytic transfusion reactions Laboratory Investigation Treatment Case Demonstration Part 4 Transfusion Reactions Table 20.2 Blood transfusion complications Part 4 Discussion References Chapter 21: Hematologic Consultation During Pregnancy Pregnancy Considerations Anemia During Pregnancy Case Clinical Context Clinical Manifestations Laboratory Investigations Management Specific Considerations Thrombocytopenia During Pregnancy Case Clinical Context Etiologies of Thrombocytopenia in Pregnancy Clinical Manifestations Management Specific Considerations VTE in Pregnancy Case Clinical Context Clinical Manifestations Laboratory Investigations Management Specific Considerations References Index