Download Free Medical Leukemia PowerPoint Presentation

Leukemia PowerPoint Presentation

DOWNLOAD MEDICAL POWERPOINT PRESENTATION

About This Presentation

Description : Check out this medical presentation on Leukemia - Acute Lymphocytic, which is titled "Leukemia", to know about Leukemia, lymphoma and myeloma are cancers that originate in the bone marrow (leukemia & myeloma) or in lymphatic tissues (lymphoma).

Tags : Leukemia, Acute Lymphocytic, lymphoma, myeloma, cancers, bone marrow, lymphatic tissues

Published on : May 18, 2021 | Views : 10224 | Downloads : 91

Shareable Url :

Embed Code :

Comment

Transcript

Slide 1-

Leukemia
Slide 2-

Leukemia
Slide 3-

About the Disease Leukemia, lymphoma and myeloma are cancers that originate in the bone marrow (leukemia & myeloma) or in lymphatic tissues (lymphoma).
Slide 4-

Different Types of Blood Cancers Leukemia Non-Hodgkin Lymphoma Hodgkin Lymphoma Myeloma Myelodysplastic Syndromes
Slide 5-

What is Leukemia? Leukemia is cancer found in the blood cells There are many types of Leukemia They are classified by how quickly they progress and what type of cell they affect Leukemia is causes when there is an imbalance of healthy unhealthy blood cells in the body This occur when one cell awry and the body begins to produce large numbers of this cell
Slide 6-

What Is Leukemia? Cancer of the white blood cells Acute or Chronic Affects ability to produce normal blood cells Bone marrow makes abnormally large number of immature white blood cells called blasts
Slide 7-

What is Leukemia Greek word which means “white blood” Leukemia is when cells spread rapidly and destroy living tissue. It grows/invades the bone marrow which is the factory of blood and replaces normal blood elements with cancer cells. Cancer cells replace all bone marrow cells which causes infection and bleeding problems. Leukemia is basically white blood cells that don’t work well and cause trouble.
Slide 8-

Continued Millions of immature and useless white blood cells are produced which makes it harder to kill cancer cells and preserve the good/healthy ones. Leukemia causes change in cells, DNA, and gene. If the blood matches with donator then you are curried. Bone marrow is spongy tissue that fills in the center core of bone. There are 4 different types of Leukemia.
Slide 9-

Types of Leukemia Based on how quickly the disease develops it is classified as either acute or chronic In Acute Leukemia the white blood cells tend to develop more rapidly and very immature In Chronic Leukemia the cells tend to develop more slowly They are also classified by which type of white bloods cells are affected If the lymphoid cells are affected the disease is referred to as Lymphocytic Leukemia If the myeloid cells are affected it is called Myelongenous Leukemia
Slide 10-

Types of Leukemia Acute lymphoblastic Leukemia (ALL) Acute myeloblastic Leukemia (AML) Chronic lymphocyte Leukemia (CLL) Chronic myeloid Leukemia (CML)
Slide 11-

Demographics of Leukemia Patients (2001 Data) Total Reported Cases = 31,500 Sources from Leukemia, Lyphoma, Myeloma Facts 2001 CLL=Chronic Lymphocytic ALL=Acute Lymphocytic CML=Chronic Mylogenous AML=Acute Mylogenous
Slide 12-

Chronic and Acute Chronic Leukemia: Progress slowly (runs a slow course) Not immediately fatal. Acute Leukemia: Progress rapidly (runs a fast course) Life expectancy short without treatment.
Slide 13-

Lymphocyte and Myeloid Lymphocyte: Increase in white blood cells produced in lymph nodes and bone marrow. Strikes without any warning. Myeloid: Increase in white blood cells produced exclusively in the bone marrow. Strikes without any warning.
Slide 14-

Acute Myeloid Leukemia (AML): Mixed group of disease It means “marrow like” and in this context it simply means arising from developing blood cells. This type of leukemia runs a rapid course.
Slide 15-

Acute Lymphoblast Leukemia (ALL): Group of different diseases A complexity of which is still trying to be unraveled Reached a point where not all are being treated the same. This type of Leukemia runs a rapid course.
Slide 16-

Chronic Myeloid Leukemia (CML): Characterized by increased production of granulocytes in the bone marrow. Usually associated with a specific chromosomal abnormality called the Philadelphia chromosome Progresses slowly
Slide 17-

Chronic Lymphocyte Leukemia (CLL): This type of cancer is so rare it could be said not to arise at all in the first two decades of life. Starts of in the Bone marrow This type of cancer runs a slow course giving more time to live.
Slide 18-

Risk Factors As of now we do not know the exact cause of Leukemia Exposure to these have been identified as risk factors High energy radiation Some genetic syndromes People working with chemical benzene for a long period of time
Slide 19-

Causes High level radiation/toxin exposure Viruses Genes Chemicals Mostly unknown Can’t be caught
Slide 20-

Development of Leukemia in the Bloodstream Legend White Cell Red Cell Platelet Blast Germ Sources from Leukemia, by D. Newton and D. Siegel
Slide 21-

Effects On the Body Attacks the immune system Infections Anemia Weakness No more regular white blood cells, red blood cells, and platelets Blasts clog blood stream and bone marrow
Slide 22-

Symptoms When there are excessive white blood cells --> Infections When there are few red blood cells: Paleness --> Anemia When there are few platelets --> Excessive bleeding
Slide 23-

Signs Of Leukemia Most of the symptoms of leukemia are similar to those of a common illness such as the flu. The symptoms will vary according to the type of leukemia. Tired Frequent infections Easy bruising or bleeding Bone tenderness Headache Enlarged lymph nodes Low red blood count Pale skin Poor appetite
Slide 24-

Tests For Diagnosis Finger prick Blood sample Blood dye Bone marrow sample Spinal Tap/Lumbar Puncture
Slide 25-

Diagnosis As immature cells increase in the body leads to lower amounts of red blood cells and platelet cells The low amounts of red blood cells cause patient to be tired and pale Low amounts of platelet cells cause the patient to easily bruise or bleed During a physical exam the doctor detects swollen spleen, liver, or lymph nodes Then there is a blood test conducted to see if it is leukemia The type of Leukemia is determined after bone marrow is extracted and tested
Slide 26-

Diagnosis Most commonly leukemia is diagnosed by a blood test to count the number of red cells, white cells and platelets. A biopsy of the bone marrow may also be performed
Slide 27-

Pictures Of Blood Sources from Arginine.umdnj.edu Sources from beyond2000.com
Slide 28-

ppt slide no 28 content not found
Slide 29-

Diagnosis Requires all of the following diagnostic components: Documentation of bone marrow infiltration Myeloid origin of the leukemic cells FAB/WHO classification of the leukemia Karyotypic analysis
Slide 30-

Differential Diagnosis chronic myelogenous leukemia other myeloproliferative disorders reactive leukocytosis: leukemoid reaction acute leukemia
Slide 31-

Philadelphia Chromosome t(9;22)(q34;q11)
Slide 32-

BCR-ABL Gene Product
Slide 33-

BCR-ABL p210 Fusion Protein Activity Higher tyrosine kinase activity. Increases progenitor cells, reduces the pool of stem cells. Semin Hematol 1988;25:1-19. Defective cytoadherence. Hematol Oncol Clin North Am 1988;12:1-29. Suppression of apoptosis. Blood 1994;83:1575-85.
Slide 34-

BCR-ABL p210 Fusion Protein Evidence of its role in CML In vitro: cause factor-independent, leukemogenic cell growth in hematopoietic cell lines. In vivo: generate in mice CML-like syndrome. Science 1990;247:824-30.
Slide 35-

FAB Classifications M0: minimally differentiated M1: without maturation M2: with maturation. May have t(8;21) translocation. M3: promyelocytic. Good prognosis. Can be associated w/ t(15;17). M4: myelomonocytic; assoc. w/ t(16;16) or inv(16)(p13q22). M5: monoblastic M6: erythroleukemia M7: megakaryoblastic. Poor overall survival.
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-

Clinical Course Median survival: 3.5~8 yr. Chronic phase: 3~4 yr. Accelerated phase (15%): 3~6 mo, then enters acute phase. Acute phase (blast crisis), 25% in each year, findings: blasts > 30%, cytogenetic changes other than Ph chromosome, progression likes acute leukemia. 70% enters AML, 30% ALL.
Slide 46-

Prognosis “Good risk”: favorable karyotype, including t(8;21), t(15;17), inv(16)/t(16;16)/del(16q) or FAB subtype M3 “Poor risk”: adverse karyotype or resistant disease after first course of chemo (i.e. >15% blasts in post-tx bone marrow bx) 5-yr survival for good, standard, and poor risk patients 70, 48, and 15% respectively. Relapse rates are 33, 50, and 78% respectively.
Slide 47-

Treatment As of yet there is no cure for Leukemia Many advances have been made in the past couple years The survival rate of children with Acute Lymphocytic is around 82% Treatments include: Chemotherapy Radiotherapy Immunotherapy Bone marrow transplant
Slide 48-

Research New drugs Cord blood and planceta
Slide 49-

Treatment Depending on the type of cancer treatments may vary. Treatments of leukemia may include chemotherapy, radiation therapy, or bone marrow transplant. They also treat leukemia patients with the infusion of healthy blood cells and platelets. During and after the treatment blood counts are done to see if the patient is being controlled or in remission.
Slide 50-

Treatments Blood and marrow stem cell transplantation. Research. Development of new drugs. Immunotherapy. Vaccines. Reversal of multidrug resistance. Gene therapy.
Slide 51-

Management (1) Chronic phase Hydroxyurea or busulfan, relieves symptoms and control of disease. Interferon-a: 20% cytogenetic response, prolongation of survival. . It can gain 20 more months survival than C/T. This advantage must be weighed against its significant side effects.
Slide 52-

Management (2) BMT or PBSCT Allogeneic bone marrow transplantation in the chronic phase is the only therapy known to cure CML 5YS > 50%, relapse < 20%, 20~40% BMT related death in the first year. It should be done as soon as possible for patients Chronic phase. <50 years old. Has an HLA-identical sibling.
Slide 53-

Management (3) STI571 STI 571:Inhibitors of the BCR-ABL fusion proteins (tyrosine kinase) After six months of therapy with Glivec (STI571), preliminary findings showed that half of 290 patients tested were improving. They had what's known as a cytogenic remission -- a reduction in the 'Philadelphia Chromosome' which causes the disease. "In these patients we found a very high response rate, there was some response seen in 91 percent of the patients," said Dr. Talpaz of the M.D. Anderson Cancer Center. "Some of the patients returned to the chronic phase of the disease."
Slide 54-

Allogeneic Stem Cell Transplantation eradicates of the marrow cells (marrow-ablating C/T or R/T) implantation of allogeneic stem cells homing of the stem cells to the marrow cavity growth of the stem cells and recovery of the blood cells
Slide 55-

Complications of SCT rejection, graft failure graft-versus-host disease infection VOD obliterative bronchiolitis sepsis relapse of disease
Slide 56-

GVHD (Graft versus Host Disease) Immunologic reaction of donor lymphocytes to “foreign” antigens present on the surface of host cells “foreign” antigens: HLA antigens “minor” antigens not detected by current typing techniques
Slide 57-

Acute GVHD (1) incidence Within the first 3 months after BMT 20~50% of HLA-identical, 80% of HLA non-identical recipients incidence increases with patient age degree of HLA disparity
Slide 58-

Acute GVHD (2)manifestations Histology: lymphocytic infiltration of the epidermis and GI tract fever dermatitis: diffuse macular dermatitis, bullas, desquamation enteritis: cramping abdominal pain, watery to bloody diarrhea hepatitis: jaundice, cholestasis, hepatocellular necrosis infection: frequently related to mortality hyperacute GVHD (no prophylaxis): 7 days after BMT: exfoliative dermatitis, shock, hyperpyrexia
Slide 59-

Chronic GVHD (1) incidence develops > 3 months after BMT 20~50% of allografts, usually following acute GVHD 20~30% develops de novo, without prior acute GVHD
Slide 60-

Chronic GVHD (2) manifestations like collagen diseases skin: pigmentation, sclerosis mucosa: lichenoid oral plaque, esophagitis, polyserositis, oral and eye sicca syndrome liver: elevated ALP and GOT in 90% cases chronic wasting due to anorexia chronic pulmonary disease: 10~20% (diffuse interstitial pnuemonitis and obliterative bronchiloitis) death usually caused by infection, low mortality related to de novo onset & less tissue involvement.
Slide 61-

Blast Crisis 30% ALL, 70% AML Treatment likes de novo acute leukemia with poor success. Chance of achieving remission is possible in ALL, which may last 4~8 months, but low in AML. Survival is usually 2~4 months.
Slide 62-

CML in Blast Crisis