aml ppt

MYELOID

Marc Delvin C Quero

ACU

TELEUKEMIA

Acute Myeloid Leukemia

• Cancer of blood and bone marrow cells.

• It affects myeloid cells.

• Blood cell production process is abnormal

• Large numbers of immature myeloid cells are produced.

• Acute myeloid leukemia is the most common form of acute

leukemia during the first few months of life.

CLINICAL OVERVIEW

Acute Myeloid Leukemia

• Fatigue

• Shortness of breath on exertion

• Easy bruising

• Petechiae

• Bleeding in the nose or from the gums

• Prolonged bleeding from minor cuts

• Recurrent minor infections or poor healing of minor cuts

• Loss of appetite or weight loss

• Mild fever

SIGNS AND SYMPTOMS

Acute Myeloid Leukemia

• Total WBC Count between 5x109/L and 30x109/L with myeloblasts in the peripheral blood smear

• Bone and joint pain are the first symptoms in 25% of patients. • Elevated serum lysozyme (especially in monocytic subtypes),

hyperuricemia (caused by increased cellular turnover), hyperkalemia (caused by cell breakdown),

hyperphosphatemia, and hypocalcemia.

• Renal failure, tetany, and lethal heart arrhythmias may develop.

SIGNS AND SYMPTOMS

Acute Myeloid Leukemia

•AgeOlder adults are more likely to develop AML

•Smoking20% of AML cases are linked to smokingDoubles the risk of disease in people older than 60

•Genetic disordersDown syndrome, Fanconi’s anemia

RISK FACTORS

Acute Myeloid Leukemia

•High doses of radiationLong-term survivors of atomic bombs

•Previous chemotherapy treatmentBreast cancer, ovarian cancer, lymphoma

•Exposure to industrial chemicalsBenzene

RISK FACTORS

Acute Myeloid Leukemia

CLINICAL OVERVIEW

Acute Myeloid Leukemia

CLINICAL OVERVIEW

Acute Myeloid Leukemia

WHO CLASSIFICATION•Acute myeloid leukemia with recurrent genetic abnormalities•Acute myeloid leukemia with t(8;21)(q22;q22), (AML1/ETO)•Acute myeloid leukemia with abnormal bone marrow eosinophils and inv(16)(p13q22) or t(16;16)(p13;q22), (CBFb/MYH11)•Acute promyelocytic leukemia with t(15;17)(q22;q12), (PML/RARa) and variants•Acute myeloid leukemia with 11q23 (MLL) abnormalities

•Acute myeloid leukemia with multilineage dysplasia•Following MDS or MDS/MPD•Without antecedent MDS or MDS/MPD, but with dysplasia in at least 50% of cells in two or more myeloid lineages•Acute myeloid leukemia and myelodysplastic syndromes, therapy-related•Alkylating agent, radiation-related type•Topoisomerase II inhibitor–related type (some may be lymphoid)•Others

•Acute myeloid leukemia, not otherwise categorized; classify as:•Acute myeloid leukemia, minimally differentiated•Acute myeloid leukemia without maturation•Acute myeloid leukemia with maturation•Acute myelomonocytic leukemia•Acute monoblastic, acute monocytic leukemia•Acute erythroid leukemia (erythroid-myeloid and pure erythroleukemia)•Acute megakaryoblastic leukemia•Acute basophilic leukemia•Acute panmyelosis with myelofibrosis•Myeloid sarcoma

Acute Myeloid Leukemia

DIAGNOSISMyeloblasts Monoblasts

Generally have central nuclei with fine, uncondensed chromatin and often prominent

nucleoli (usually three to five) but have variable cytoplasm and may have some cytoplasmic

granules.

Monoblasts are frequently large with abundant cytoplasm, diffuse chromatin and often prominent

nucleoli.

Primitive myeloblasts are identified by monoclonal antibodies against myeloid-associated antigens

(MPO, CD13, CD33, CD117).More mature myeloblasts can also be identified by cytochemical reactions with graulocyte-associated

enzymes using myeloperoxidase, Sudan Black B, and ASd-chloroacetate esterase (CAE) assays.

Monoblasts are characterized by strong reaction with alpha-naphthyl acetate esterase (ANA), which

is inhibited in monocytes by sodium fluoride as well as alpha-naphthyl butyrate esterase (ANB), or

antibodies including antilysozyme, CD68, CD64, and CD36.

AML requires 20% blasts in blood or marrow for diagnosis.

Acute Myeloid Leukemia

DIAGNOSIS

Acute Myeloid Leukemia

DIAGNOSIS

The presence of the following inclusions is helpful in the diagnosis of AML:

Auer rods, eosinophilic rod-like cytoplasmic inclusions derived from myeloperoxidase-positive primary granules.

Phi bodies, strings of eosinophilic bead-like granules from catalase-positive microperoxisomes.

Acute Myeloid Leukemia

DIAGNOSIS

Acute Myeloid Leukemia

DIAGNOSIS

Acute Myeloid Leukemia

DIAGNOSIS

MyelocytesMyelocytes

Acute Myeloid Leukemia

DIAGNOSIS

Myeloblasts

Acute Myeloid Leukemia

A number of chemotherapy medications are effective against AML.

Common remission induction regimens include cytarabine (IV) for 7 days, daunorubicin or idarubicin (IV), an anthracycline drug given in a single IV dose for the first three days of treatment. These drugs kill AML cells over the first 7 to 14 days; it then takes the normal bone marrow about 14 days to recover and produce normal blood cells again.

Post-remission therapy includes additional chemotherapy or a stem cell transplant.

TREATMENT

Acute Myeloid Leukemia

Rodak, B., Fritsma, G., and Doig, K. Hematology: Clinical Principles and Applications. 3rd Ed.

McPherson, R., and Pincus, M. Henry’s Clinical Diagnosis and Management by Laboratory Methods. 21st Ed.

Pollyea DA, Kohrt HE, Medeiros BC. Acute myeloid leukaemia in the elderly: a review. Br J Haematol 2011; 152:524.

Fernandez HF. New trends in the standard of care for initial therapy of acute myeloid leukemia. Hematology Am Soc

Hematol Educ Program 2010; 2010:56.

SOURCES

THANK YOUfo

rLISTENING