Download Free Medical Acute Leukemia PowerPoint Presentation

Acute Leukemia PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : for medical students

Tags : Acute lymphocytic leukemia,Acute Leukemia,type of cancer,cancer,blood cancer,acute

Published on : Apr 28, 2023 | Views : 1693 | Downloads : 22

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

ACUTE MYELOGENOUS LEUKEMIA-AML ACUTE LYMPHOBLASTIC LEUKEMIA –ALL Mulugeta A.(INTERNIST) ACUTE LEUKEMIAS
Slide 2-

outline Introduction Epidemiology Classification Etiology Pathogenesis Clinical Presentation General Treatment Approach AML ALL
Slide 3-

Introduction Acute Leukemia (AL) is a clonal neoplastic disorder characterized by the proliferation & accumulation of immature and malignantly transformed cells in the BM and PB. The abnormal cells replace the normal BM tissue. The result is abnormal /insufficient hematopoiesis. Anemia Thrombocytopenia Leukocytosis/leukopenia Infiltrate other organ tissues
Slide 4-

Introduction... AL is basically one of the two types Acute Myelogenous Leukemia(AML) Acute Lymphoblastic Leukemia(ALL) Other very rare variants of AL Biphenotypic Leukemia Bilineage Leukemia Other rare variant in WHO classification AL can be De novo Secondary/ transformed Distinction b/n AML & ALL should be the first step in the diagnosis and management.
Slide 5-

Epidemiology Rare disease but has huge impact on cancer survival statistics The annual incidence of AML( in Western pop) 3.6 cases/100,000 80% of AL The annual incidence of ALL 1.4 cases/100,000 20% of AL The incidence of AML Increases with age Median age at presentation 60-65yrs
Slide 6-

Epidemiology... The peak incidence of ALL 3-4yrs of age Incidence decreases after 9yrs of age Rare after 40 Sex distribution M:F in AML = 1.3:1 M:F in ALL = 1.5:1 The relative frequency of the 4 leukemias ALL (11%) AML (46%) CLL (29%) CML (14%)
Slide 7-

Classification of AL The classification is based on biological features Clinical feature Morphology based on Wright or Giemsa stain Cytochemical studies Electron Microscope Flowcytometry Cytoplasmic markers Cytogenetic or molecular study Microarray analysis
Slide 8-

Classification of AL... French-American and British(FAB) Based on morphology & cytochemical studies ALL into L1-L3 AML into M0-M7 Immunological classification Specially for ALL into the different stages of B-Cell & T-Cell groups WHO classification For all hematological malignancies Cytogenetic studies included Comprehensive but not applicable in all setting
Slide 9-

ppt slide no 9 content not found
Slide 10-

ppt slide no 10 content not found
Slide 11-

ppt slide no 11 content not found
Slide 12-

ppt slide no 12 content not found
Slide 13-

Etiology in Acute Leukemias(AL) Most AL sporadic Acquisition of somatic mutation in hematopioetic progenitors Usually not possible to identify a cause Valuable clues from Rare heritable leukemias Cases related to specific environmental exposure Variable latency following exposure to causative agent Genetic Polymorphism
Slide 14-

Etiology in AL... Chemical exposure Benzene Other petroleum products & others Ionizing Radiation Virus HTLV-1 EBV Therapy Related (chemotherapy) Alkylating agents DNA topoisomerase inhibitors Anthracyclins( doxorubicin) Epipodophyllotoxins( etoposide) Autologous stem cell transplantation ? Hematopoietic growth factors
Slide 15-

Etiology in AL... Antecedent Hematological Disorders Myeloproliferative Disorders Myelodysplastic Syndromes(MDS) Paroxysmal Nocturnal Hemoglobinuria (PNH) Familial Leukemias Down’s Syndrome ( trisomy 21) Trisomy 8
Slide 16-

Etiology in AL... Familial Disorders leading to Leukemias Defective DNA repair syndromes Bloom’s Syndrome Fanconi’s Anemia Neurofibromatosis Li-Fraumeni Syndrome Wiskott-Aldrich Syndrome Blackfan-Diamond Syndrome Kostmann’s Syndrome ( Infantile Agranulocytosis)
Slide 17-

Pathogenesis Single cell of origin of AL Leukemic Stem Cell Clonality Like other human malignancies, in AL one or more of the following somatic mutation and genetic abnormalities are involved Oncogene mutations (Proto-oncogenes) Tumor Suppressor gene mutation General Genomic instability Multistep and multicausal
Slide 18-

Pathogenesis... Two –hit hypothesis Mutations giving proliferative& survival advantage The next impairing differentiation The two models for the explanation of heterogeneous groups in AL Transformation at one of the several developmental stages Transformation within the primitive multipotent progenitor cells Specific or recurrent genetic abnormalities leading to certain leukemia types
Slide 19-

Clinical Features of AL AL presents acutely Exception- transformed/secondary AL In general patients manifest signs & symptoms related to Abnormalities of the 3 blood cell lines Infiltration of organs & tissues Certain features are specific to the AL type Family history of malignancy and history of predisposing factors should be looked for.
Slide 20-

Symptoms of AL Sxs of anemia Sxs of thrombocytopenia Fever High grade due to infections Low grade with systemic sxs due to the AL Sxs due to CNS involvement Seizure, headache, cranial nerves dysfunction Vomiting, blurring of vision, altered mentation Abdominal fullness & other GI sxs due to organomegaly and electrolyte disturbance Oliguria
Slide 21-

Signs of AL Pallor Bleeding Mucocutaneous DIC Fever and other signs of infection accordingly
Slide 22-

Signs ... Signs of tissue or organ infiltration Gingival hyperplasia LAP Hepatosplenomegaly Bone(sternal tenderness) Chloromas Leukemic cutis Cranial nerve palsies Mengeal irritation signs Extramedullary disease Prominent LAP & signs of mediastinal LAP
Slide 23-

ppt slide no 23 content not found
Slide 24-

Investigation in AL Complete history and physical examination CBC, differential, platelets, ESR, Blood group Serological screening ( HIV, HBV, HCV, CMV...) Examination of peripheral smear BM aspiration & biopsy Morphology Flowcytometry Cytochemical studies Cytogenetic study
Slide 25-

Investigation in AL... CXR Coagulation profile Biochemical tests Liver & renal functions Serum electrolytes Uric acid Serum LDH Serum lysozymes Blood and other specimen for culture
Slide 26-

Investigation in AL... LP CT Scan HLA TYPING Cardiac function ( ECG, ECHO)
Slide 27-

Treatment Requires comprehensive team & good setup Starts with the confirmation of specific AL dx & prognostication. In general has 2 important components Supportive Specific/ Definitive Certain parameters/ goals related to specific therapy Remission ( CR, PR) Survival (leukemia free, overall survival, relapse ) Cure
Slide 28-

Supportive Care Fluid & electrolyte management Blood component therapy Packed red cells transfusion Platelet transfusion Treatment of infection Broad spectrum IV antibiotics( empiric/emergency) culture and other studies Prevention of uric acid nephropathy & tumor lysis syndrome hydration Allopurinol & other agents
Slide 29-

Supportive Care Recombinant growth factors (GM-CSF, G-CSF, EPO, IL-11, Thrombopoietin) Hyperleukocytosis/hyperviscosity, leukostasis Associated with various complications Leukopheresis Emergency irradiation of whole-brain Adminstration of drugs for cytoreduction Hydroxyurea, steriods Early dx & Rx of coagulation abnormality Reverse-barrier ( reverse – isolation)
Slide 30-

Supportive Care Vascular access Birth control and fertility advice Treatment of comorbid conditions Psychosocial support
Slide 31-

Specific Treatment Chemotherapy Specific regimen of the AL types Phases Remission Induction Postremission Hematopoietic Stem Cell Transplantation Allogeneic-SCT Syngeneic-SCT Autologous-SCT Investigational Therapy Clinical trails
Slide 32-

DDX MDS Aplastic Anemia Infectious Mononucleosis ( LAP & atypical lymphocytes) BM failure syndromes & infiltration Severe infection with leukocytosis & shift Aggressive & very aggressive NHL ITP
Slide 33-

GENERAL REMARKS CLASSIFICATION TREATMENT ACUTE MYELOGENOUS LEUKEMIA
Slide 34-

General remarks about AML A complex disease Heterogenous group Phenotypically Genotypically More than 100 recurrent cytogenetic abnormalities. Patients die of leukemia or Rx complication Still a challenge both clinically & in genetic study Certain groups with excellent prognosis
Slide 35-

Classification FAB Based on morphology & cytochemical studies Blast % in the BM for Dx Simple & still in wide clinical use but does not incorporate the recent advances in molecular study WHO Comprehensive Detail molecular and cytogenetic studies Currently not universally applicable
Slide 36-

ppt slide no 36 content not found
Slide 37-

ppt slide no 37 content not found
Slide 38-

ppt slide no 38 content not found
Slide 39-

ppt slide no 39 content not found
Slide 40-

ppt slide no 40 content not found
Slide 41-

ppt slide no 41 content not found
Slide 42-

ppt slide no 42 content not found
Slide 43-

ppt slide no 43 content not found
Slide 44-

ppt slide no 44 content not found
Slide 45-

ppt slide no 45 content not found
Slide 46-

ppt slide no 46 content not found
Slide 47-

Specific Rx for AML Chemotherapy Remission induction 7+3 regimen ( cytarabine + daunorubicin/doxorubicin) Alternative ( cytarabin + Idarubicin + etoposide) Elderly patients – modification Double induction Postremission therapy The best regimen not yet settled Consolidation/Intensification chemotherapy Allo-SCT Auto-SCT BM transplantation
Slide 48-

Specific Rx for AML... CNS prophylaxis or Rx M4 & M5 Relapsed and refractory AML Early vs late relapse Treatment of M3(APL) Special entity(t(15;17)) & Favourable outcome All- Trans-Retinoic Acid(ATRA) with other chemo Maintenance therapy Arsenic TriOxide(ATO) Treatment of secondary/ therapy related AML
Slide 49-

ppt slide no 49 content not found
Slide 50-

GENERAL REMARKS CLASSIFICATION TREATMENT ACUTE LYMPHOBLASTIC LEUKEMIA (ALL)
Slide 51-

General remarks about ALL ALL is a malignant d/s characterized by accumulation of lymphoblasts. Different treatment outcomes in children & adults. Cure rate Children 2/3 Adults 1/3 Reason for poor outcome in adults with ALL High rate of adverse prognosis(Ph-chromosome) high degree of toxicity with the drugs Different pharmacodynamics Much less heterogeneous in general and less common ( 20% of AL) in adults
Slide 52-

Stratification of patient into high- risk & low-risk is required to select therapy More intensive chemotherapy Stem cell transplantation CNS involvement and relapses are the features
Slide 53-

Classification of ALL FAB classification of ALL L1, L2, L3 Based on the morphology of lymphoblasts Less relevant in predicting outcome Immunological classification of ALL Based on cell marker and other studies B or T cell variant with their stage of development Comprehensive Relevant in predicting outcome
Slide 54-

FAB Classification for ALL L1 L2 L3
Slide 55-

ppt slide no 55 content not found
Slide 56-

ppt slide no 56 content not found
Slide 57-

ppt slide no 57 content not found
Slide 58-

ppt slide no 58 content not found
Slide 59-

Specific Treatment in ALL Chemotherapy Several phases Remission Induction CNS prophylaxis or Treatment Consolidation/Intensification Maintenance Upfront cytoreduction Cyclophosphamide and steriods 75-85% of adults achieve Complete Remission
Slide 60-

Specific Treatment in ALL Consolidation/ Intensification Difference b/n consolidation & intensification Early intensification Maintenance Continues for upto 22months Monthly pulse doses (Dexa + Vincristine) Methotrexate /wk + 6-mercaptopurine/d (orally)
Slide 61-

Specific Treatment in ALL Remission Induction 4-6 weekly cycles with the aim of CR Vincristine + Predinsolone + daunorubicin +/- L-Asparaginase CNS prophylaxis or Treatment Intrathecal(cytarabin,Methotrexate, hydrocortisol) High dose systemic chemo Cranial Irradiation
Slide 62-

ppt slide no 62 content not found
Slide 63-

Specific Treatment in ALL Stem Cell Transplantation Reserved for relapse or refractory ALL Types Allo-SCT Auto-SCT MUD & NMSCT
Slide 64-

Thank you!