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ACUTE
LEUKAEMIAS
SCHOOL OF CLINICAL SCIENCES
INTRODUCTION
Definition
It is a group of malignant white cells, affecting the blood and blood –forming
tissue of the bone marrow, lymph system and spleen.
leukemias are a group of disorders characterized by the
accumulation of malignant white cells in the bone
marrow and blood.
The word Leukemia comes from the Greek leukos which
means "white" and aima which means "blood".
ETIOLOGY
Combination of predisposing factors including genetic and environmental
influences.
Chronic exposure to chemical such as benzene
Radiation exposure.
Congenital anomaly
 The presence of primary immunodeficiency and infection with the human
T –cell leukemia virus type-1
CLASSIFIFCATIONOFLEUKEMIA
Basically there are two types of leukemias :
ACUTE AND CHRONIC .
They are further divided into :MYELOID and LYMPHOID
ACUTELEUKEMIA
Acute leukemia is normally defined as the presence of
over 20% of blast cells in the bone marrow at clinical
presentation.
When these blast cell accumulate they affect normal
hemopoiesis.
It can be further divided base on the types of blast
present in the bone marrow.
myeloid lymphoid
LEUKEMIA
Is due to accumulation of myeloblast in the bone marrow.
Incidence
Acute myeloid leukaemia (AML) is the most common form of
acute leukaemia in adults and becomes increasingly common
with age, with a median onset of 65 years.
Bone marrow failure due to accumulation of myeloblast
which will result in decrease blood cells formation . This
will result in anemia, thrombocytopenia and neutropenia
etc.
Cont………
Accumulation of myelobast also will cause infiltration of
organs which will result in hepatomegaly spleenomegaly
lymphadenopathy.
The patient will also present with swollen gum which are
haemorrhagic.
OF AML
It is classified based on three headings:
Cytogenic abnormalities
Lineage of myloblast
Surface markers
CYTOGENIC: This classification is based on
genetic abnomalities as a result of translocation
eg
t(15:17)
t(8:21)
ACUTEPROMYLOCYTICLEUKEMIAt(15:17)
It occurs as a result of translocation between chromosome 15 and 17 this will
result in disruption of retionic acid receptors which will result in failure of the cell to
mature.
So promylocyte will accumulate since they contain auer rod there is a risk for DIC.
LEUKEMIA
It occurs as result of proliferation of monoblast and this blast will infiltrate the
gum.
It lacks myloperoxidase.
ACUTEMEGALOBLASTICLEUKEMIA
It occurs as a result of proliferation of megakaryoblast.
LEUKEMIA
Is the accumulation of lymphoblast in the bone marrow.
Due to cancerous transformation occurs in the type of marrow that makes
lymphocytes, the disease is called lymphocytic leukemia.
It is also called acute lymphoblastic leukemia and it is more common in
children.
Usually occurs before 14 years of age peak incidence is between 2-9 years
of age.
pathophysiology
It arising from a single lymphoid stem cell, with impaired maturation and
accumulation of the malignant cells in the bone marrow.
Signs and symptoms
• Clinical
manifestation
• Fever
• Pallor
• Bleeding
• Anorexia
• Fatigue
• Clinical
manifestation
• Weakness
• Bone, joint and
abdominal pain
• Increase intracranial
press.
AND AML
It is difficult to differentiate between the myloblast and lymphoblast however
there are certain makers :
Normochromic ,normocytic anea
Total WBC count may decreased or increased
Variable numbers of blast cells
LP increased pressure
Increased serum uric acid, lactate dehydrogenase or less comonly
hypercalcemia
Radiology : lytic bones and mediasternal mass
SUB- DIVISION OF ALL
It is sub-divided into:
B-ALL T-ALL
So this classification is based on surface markers.
B-ALL
It is the accumulation of B-lymphoblast in the bone marrow.
It is the most common type of ALL.
They express this classic makers CD10, CD19 and CD20.
T-ALL
It is the accumulation of T-lymphoblast in the bone marrow.
It expresses markers ranging from CD2-CD8 .
It present as thymic mass in the mediastinum and it occurs in teenagers.
However it is called acute lymphoblastic lymphoma
because it present as a mass.
Treatment
• GENAERAL
• Specific
• Remission induction
• Intensification
• CNS directed therapy
• Remission induction : Rapidly kills the tumour cells and it
defines less than 5% blast cells in the blood and marrow with
no other symptoms and signs of the disease.
• Drugs : prednisolone or dexamethasone (children) , vincristine
and asparaginase
• NOTE : remission is not cure
• Patients still harbour tumour cells and without further
chemotherapy virtually all patients may relapse
• But it a valuable step in the treament course
• Patients who fails to achieve remission have a poor prognosis.
• Intensification: uses high doses of multidrug chemotherapy in
other to completely reduce or elliminate the tumor burden to
very low levels . The doeses are near the level patients
tolerability .
Maintainance
• 2yrs in girls and adults and 3yrs for boys with daily
mercaptopurine and once weekly oral methotrexate
• i.v vincristine with short course (5days) of oral corticosteroids
added at monthly.
• Protocol :
• Vincristine , cyclophosphamide ,cytosine arabinoside,
daunorubicine etoposide ,thioguanine or mercaptorine given
as block in different combination .
• CNS directed therapy: high doses of i.v methottrexate ,
intrathecal methotrexate or cytosine arabinoside or cranial
irradiation

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ACUTE LEUKEMIA.pptxsalah.pptx111111111111111

  • 2. INTRODUCTION Definition It is a group of malignant white cells, affecting the blood and blood –forming tissue of the bone marrow, lymph system and spleen. leukemias are a group of disorders characterized by the accumulation of malignant white cells in the bone marrow and blood. The word Leukemia comes from the Greek leukos which means "white" and aima which means "blood".
  • 3. ETIOLOGY Combination of predisposing factors including genetic and environmental influences. Chronic exposure to chemical such as benzene Radiation exposure. Congenital anomaly  The presence of primary immunodeficiency and infection with the human T –cell leukemia virus type-1
  • 4. CLASSIFIFCATIONOFLEUKEMIA Basically there are two types of leukemias : ACUTE AND CHRONIC . They are further divided into :MYELOID and LYMPHOID
  • 5. ACUTELEUKEMIA Acute leukemia is normally defined as the presence of over 20% of blast cells in the bone marrow at clinical presentation. When these blast cell accumulate they affect normal hemopoiesis. It can be further divided base on the types of blast present in the bone marrow. myeloid lymphoid
  • 6. LEUKEMIA Is due to accumulation of myeloblast in the bone marrow. Incidence Acute myeloid leukaemia (AML) is the most common form of acute leukaemia in adults and becomes increasingly common with age, with a median onset of 65 years. Bone marrow failure due to accumulation of myeloblast which will result in decrease blood cells formation . This will result in anemia, thrombocytopenia and neutropenia etc.
  • 7. Cont……… Accumulation of myelobast also will cause infiltration of organs which will result in hepatomegaly spleenomegaly lymphadenopathy. The patient will also present with swollen gum which are haemorrhagic.
  • 8. OF AML It is classified based on three headings: Cytogenic abnormalities Lineage of myloblast Surface markers CYTOGENIC: This classification is based on genetic abnomalities as a result of translocation eg t(15:17) t(8:21)
  • 9. ACUTEPROMYLOCYTICLEUKEMIAt(15:17) It occurs as a result of translocation between chromosome 15 and 17 this will result in disruption of retionic acid receptors which will result in failure of the cell to mature. So promylocyte will accumulate since they contain auer rod there is a risk for DIC.
  • 10. LEUKEMIA It occurs as result of proliferation of monoblast and this blast will infiltrate the gum. It lacks myloperoxidase.
  • 11. ACUTEMEGALOBLASTICLEUKEMIA It occurs as a result of proliferation of megakaryoblast.
  • 12. LEUKEMIA Is the accumulation of lymphoblast in the bone marrow. Due to cancerous transformation occurs in the type of marrow that makes lymphocytes, the disease is called lymphocytic leukemia. It is also called acute lymphoblastic leukemia and it is more common in children. Usually occurs before 14 years of age peak incidence is between 2-9 years of age.
  • 13. pathophysiology It arising from a single lymphoid stem cell, with impaired maturation and accumulation of the malignant cells in the bone marrow.
  • 14. Signs and symptoms • Clinical manifestation • Fever • Pallor • Bleeding • Anorexia • Fatigue • Clinical manifestation • Weakness • Bone, joint and abdominal pain • Increase intracranial press.
  • 15. AND AML It is difficult to differentiate between the myloblast and lymphoblast however there are certain makers : Normochromic ,normocytic anea Total WBC count may decreased or increased Variable numbers of blast cells LP increased pressure Increased serum uric acid, lactate dehydrogenase or less comonly hypercalcemia Radiology : lytic bones and mediasternal mass
  • 16. SUB- DIVISION OF ALL It is sub-divided into: B-ALL T-ALL So this classification is based on surface markers.
  • 17. B-ALL It is the accumulation of B-lymphoblast in the bone marrow. It is the most common type of ALL. They express this classic makers CD10, CD19 and CD20.
  • 18. T-ALL It is the accumulation of T-lymphoblast in the bone marrow. It expresses markers ranging from CD2-CD8 . It present as thymic mass in the mediastinum and it occurs in teenagers. However it is called acute lymphoblastic lymphoma because it present as a mass.
  • 19. Treatment • GENAERAL • Specific • Remission induction • Intensification • CNS directed therapy
  • 20. • Remission induction : Rapidly kills the tumour cells and it defines less than 5% blast cells in the blood and marrow with no other symptoms and signs of the disease. • Drugs : prednisolone or dexamethasone (children) , vincristine and asparaginase • NOTE : remission is not cure • Patients still harbour tumour cells and without further chemotherapy virtually all patients may relapse
  • 21. • But it a valuable step in the treament course • Patients who fails to achieve remission have a poor prognosis. • Intensification: uses high doses of multidrug chemotherapy in other to completely reduce or elliminate the tumor burden to very low levels . The doeses are near the level patients tolerability .
  • 22. Maintainance • 2yrs in girls and adults and 3yrs for boys with daily mercaptopurine and once weekly oral methotrexate • i.v vincristine with short course (5days) of oral corticosteroids added at monthly.
  • 23. • Protocol : • Vincristine , cyclophosphamide ,cytosine arabinoside, daunorubicine etoposide ,thioguanine or mercaptorine given as block in different combination . • CNS directed therapy: high doses of i.v methottrexate , intrathecal methotrexate or cytosine arabinoside or cranial irradiation