Thursday, November 15, 2018

aml meaning | Acute Myeloid Leukemia Referat






Acute Myeloid Leukemia Referat




INTRODUCTION
1.1. Background
       Leukemia is a situation in which growth occurs is irreversibel from stem cells from the blood. Growth starts from where it originated. The cells are, on various stadium will flood the bloodstream. In the case of Leukemia (blood cancer), white blood cells did not respond to a sign/signal is given. The production of excessive uncontrolled (abnormal) will come out from the bone marrow and are found in the peripheral blood or blood banks. The number of abnormal white blood cells this if overconsumption can disrupt the normal function of the cell to another, a person with this condition (Leukemia) will show some of the symptoms such as; easily exposed to infectious diseases, anaemia and bleeding. (Hematology Clinic 2,106 Ed.).
Acute myeloid leukaemia (AML), the leukemia that occurs in myeloid series, including (neutrophils, eosinophils, monocytes, basophils, megakariosit and others). In developed countries like United States, LMA represents 32% of all cases of leukemia. The disease is more commonly found in adults (85%) than in children (15%). (Textbook In Pathology Vol II, ed. IV. 1234).

1.2. Purpose and benefits
The purpose of this is to make the writing of referat writer or reader can understand about acute mieloblastik Leukemia (LMA) covers the causes, the dissemination, understanding, travel sickness, disease symptoms, complications and treatment of this disease. As well as the requirement to follow the final exams blocks.
  The benefits of this include referat students could better understand a disease due to directly create and craft a referat, as well as being able to explain about the case.

Chapter 2
DISCUSSION
ACUTE MIELOBLASTIK LEUKEMIA

2.1. the anatomy and physiology of the blood
A. Understanding
     Blood is the fluid in the blood vessels that functions transporting oxygen, carbohydrates and metabolites; set the balance of acids and bases; regulate body temperature by means of conduction (hantaran), carrying the body heat from the center of the production of heat (hepar and muscles) to distribute throughout the body; and setting the hormone with carry and delivers the gland to the target.
B. Functions Of Blood
·         Work of the transport system of the body, delivering all the chemicals, oxygen and chemicals needed for its normal function so that the body can run and get rid of carbon dioxide and other waste.
·         Red blood cells deliver oxygen to tissue and get rid of some of the carbon dioxide.
·         White blood cells provides a lot of baha protector and the arena from some cell phagocytosis movement then protects the body from bacterial attacks.
·         Plasma protein that is needed to split the establishment of networks; refreshing fluid network because through this fluid all body cells receive the food. And is a vehicle to transport waste material into various organs exkretorik to be discarded.
·         Hormones and enzymes are delivered from organ to organ by blood.


C. Blood Parts
·         Red blood cells
When viewed under a microscope, the blood red like the bikokaf channel has a reddish yellow colour, core, chewy nature so that the bias changed form in accordance with the blood vessels.
Red blood cells or erythrocytes in the form of a small channel, cebung on both sides so that it is seen from the side it looks like two Crescent mutually contradictory.
·         White blood cells
The shape is clear and colorless size is greater than pritosit, the larger 2 x shape of red blood cells, but also an assortment of cell nucleus, and many.
Polimorfonulitear cells and monocytes was formed only in normal bone marrow, plasma cells and lymphocytes instead generated in the various organs including the limfogen gland of the spleen, thymus glands, spleen and lymphoid forsit located in the gut and place another.
·         Platelets
Platelets are tiny cells roughly one-third the size of red blood cells. An important role in blood clotting.
       Platelets are small objects is dead. Shape and size varied, some are round and some are oval, white colour. Platelet cells but not the shape of chips that are the smallest parts of large cells. Platelets are made in the arrangement of bones, lungs and spleen with a size of approximately 2-4 miliron age sekitra 10 days of its release.

2.2. Definitions
   Acute mieloblastik leukemia (LMA) is a disease characterized by the transformation of anti-neoplastic activities and differentiation of progenitor cells from mieloid series. When left untreated, this disease will rapidly result in death within a few weeks to months after the diagnosis. Before the year 1960 the treatment of LMA terutam palliative in nature, but since about 40 years ago in the treatment of this disease develops rapidly and nowadays many patients LMA can be cured of his illness. Progress of treatment of LMA is achieved by better chemotherapy regimens, chemotherapy high doses bone marrow grafting with support and a better supportive therapy such as new generation antibiotics and transfusion of blood components to address the effects of treatment side. (Textbook In Pathology Vol II, ed. IV. 1234). 
2.3. The etiology
       In most cases, the etiology of the LMA is unknown. However there are some factors that are known to cause or at least be a factor prediposisi LMA on a particular population. Benzene, a chemical compound that is widely used on the incidence of tannery in developing countries, is the substance leukomogenik to LMA. In addition of ionic radiation also known to cause the LMA. It is known from research about the high incidence of cases of leukemia, including the LMA, on people who survived the atomic bomb in Hirosima and Nagasaki in 1945. Effect of leukomogenik from exposure to such radiation ions start to appear since 1.5 years after the bombing and reached its peak of 6 or 7 years after the bombing. Another factor is known as predisposing to LMA is Trisomy chromosome 21 which hereditary disease found in down syndrome. Down syndrome patients with trisommi of chromosome 21 have a risk of 10 to 18 times higher for suffering from leukemia, particularly LMA type M7. In addition a genetic syndrome in some patients such as Fanconi anemia, bloom syndrome and is also known to have a much higher risk than normal for a population suffering from LMA.
Other factors that can trigger the onset of LMA is treatment with cytotoxic chemotherapy on solid tumor patients. LMA due to therapy is a serious long-term complications from the treatment of lymphoma, multiple mieloma, ovarian cancer, breast cancer, and testicular cancer. This type of therapy that most commonly trigger onset LMA is the alkylating agents and topoisomerase II inhibitors.
2.4. Pathogenesis
       The primary pathogenesis of LMA is the maturity of the blockade is causing the process of differentiation of the cells series mieloid stalled in young cells (blast) with result occurs in the bone marrow blast accumulation. The accumulation of Blast in the bone marrow will cause a disruption in normal hematopoesis and in turn will lead to bone marrow failure syndrome (bone marrow failure syndrome) characterized by the presence of anemia (sitopenia, leukopeni, trombositopeni). The presence of anemia will cause the patient easily tired and in the case of more severe shortness of breath, will be the presence of thrombocytopenia will cause bleeding, signs are the presence of leukopenia will cause the patient vulnerable to infection, termausk infection the normal bacterial flora of the opportunists who are in the human body. In addition, the blast cells that form also have the ability to migrate out into the berinfiltrasi bone marrow and other organs such as the skin, bone, soft tissue and the central nervous system and damage to the organs with all its consequences.

Malignant cell in AML myeloblast. In normal hematopoiesis, the myeloblast is an immature precursor of myeloid white blood cells, a normal myeloblast will gradually grow into the mature white blood cells. However, in AML, a single myeloblast accumulates genetic changes which  "freeze " cells in the immature State and prevent differentiation. Such a mutation alone does not cause leukemia, but when like  "arrest differentiation " is combined with another gene mutation which disrupts control of proliferation, the result is uncontrolled growth of immature clones the cells, which leads to the clinical entity of AML.
Most of the diversity and heterogeneity of AML stems from the fact that the transformation of leukemia can occur in a number of different steps along the path of differentiation. Modern classification schemes for AML recognize that the characteristics and behavior of the leukaemia cells (and leukemia) may depend on the stage where differentiation is terminated.

Sitogenetika specific abnormalities can be found in many patients with AML, the type of chromosome abnormalities often have prognostic significance.
The chromosomal translocations encode abnormal fusion proteins, usually transcription factors which change the nature can cause the  "arrest differentiation. " as an example, acute promyelocytic leukemia, at t (15; 17) translocation produces a PML-RARα fusion protein which binds to the receptors retinoat acid elements in some specific genes myeloid promoter and inhibits myeloid differentiation. Clinical signs and symptoms of AML result from the fact that, as a clone of leukemia cells grow, it tends to displace or interfere with the development of normal blood cells in the bone marrow. This leads to neutropenia, anemia, and thrombocytopenia.

2.5. Clinical Symptoms
       In contrast to the general presumption during this time, in patients LMA were not always found to be leukositosis. Leukositosis occurs in about 50% of cases LMA, currently 15% of patients have a normal leukocytes figures and about 35% experienced netropenia. However, the blast cells in significant quantities in the blood banks will be found in 85% of cases LMA. It is therefore very important to check the details of the types of cells are leukocytes in blood banks as the initial examination, to avoid error diagnosis in people who allegedly suffered the LMA.
       The main signs and symptoms of LMA is a sense of tired, bleeding and infection caused by bone marrow failure syndrome as has already been mentioned above. Bleeding usually occurs in the form of purpura or petekia are often found in the form of epistaksis or lower extremities, bleeding gums and the retina. The heavier bleeding is rare except in the case of accompanied by DIC. The case of DIC is frequently encountered in the case of pling LMA type M3. Infections often occur in the throat, lungs, skin and the fairy rektl, so that the organs should be examined carefully in patients LMA with fever.
       Numbers of leukocytes in patients with very high (more than 100 000/mm3), common leukositosis, i.e. the leukocytes BLOB clog the flow of venous or arterial blood vessels. Leukositosis symptoms vary greatly, depending on the location of the sumbatannya. A common symptom is disturbance of consciousness, shortness of breath, chest pain and priapismus.
    Infiltration cells blast will cause the sign/symptom that varies depending on the organ infiltration. Infiltration of blast cells in the skin will cause leukemia kutis, namely in the form of lumps that are not pigmented and without pain, was infiltrating cells in soft tissue blast will cause the nodules under the skin (kloroma). Infiltration of blast cells in bone meninbulkan bone pain that will spontaneously or with mild stimulation. Pembengkakkan gums often encountered as a manifestation of blast cells infiltrating into the gums. Although rare, at the LMA also found infiltrating cells blast into the menings and for enforcement of the Cytopathology examination diagnosis required liquid cardiovascular procedures taken through spinal lumbar pungsi.
2.6. The Diagnosis
       Classically diagnosis LMA enforced based on physical examination, cell morphology and painting sitokimia. As already mentioned, since about two decades years ago developed two (2) the latest examination techniques: immunophenotyping and analysis sitogenik. Based on an examination of cell morphology and staining sitokimia combined Haematology, America, France and the United Kingdom in 1976 classification LMA consisting of 8 subtypes (M0 up to M7). This classification is known as the FAB classification (French American British). FAB classification to date is still the basic diagnosis of the LMA. Repainting sitokimia that are important to patients LMA is a Sudan Black B (SSB) and mieloperoksidase (MPO). The second painting that sitokimia will give positive results in patients LMA type M1, M2, M3, M4, and M6.

First, blood tests are performed to calculate the number of each type of different blood cells and see if they are in the normal range. In AML, the level of red blood cells may cause anemia, low levels of platelets may be low, leading to bleeding and bruising, and the level of white blood cells may be low, causing an infection.
      A bone marrow biopsy or aspiration (are siphoned off) from the bone marrow may be done if abnormal blood test results. During the biopsy, bone marrow, hollow needle is inserted into the hip bone to remove a small amount of bone marrow and for testing under the microscope. On a bone marrow aspiration, a small sample of bone marrow is withdrawn through a liquid injection.
     Pungsi lumbar, or press the spine, can be done to see if the disease has spread into the cerebrospinal fluid, which surrounds the central nervous system or the central nervous system (CNS)-the brain and marrow

spine. Diagnostic tests may include flow cytometry significant other (where the cells pass through a laser beam for analysis), immunohistochemical (using antibodies to differentiate between types of cancer cells), Sitogenetika (to determine changes in the chromosomes in the cell), and studies of molecular genetics (DNA and RNA from cells of cancer).
      The disease of Leukemia can be ensured with several checks, including; Biopsy, blood Examination {complete blood count (CBC)}, a CT or CAT scan, magnetic resonance imaging (MRI), x-ray, Ultrasound, Spinal tap/lumbar puncture.

Hematologis disorders
Ø the number of erythrocytes Anemia with decreased approximately 1-3 x 106/mm3.
Ø Leukositosis with the number of leukocytes between 50-100 x 103/mm3. Leukocytes that exist in the blood of most banks is myeloblas.
Ø the number of Platelet decline. Myeloblast-looking sometimes contain "auer agency" is a disorder that is pathogonomis for the LMA.
    
   Bone marrow hiperseluler because it contains a massive, were myeloblast megakariosit and pronormoblas is found very rarely. This bone marrow abnormalities will already be clear though myeloblas has yet to appear in blood banks. So sometimes found cases with pancytopenia but peripheral bone marrow was clear hiperseluler because of infiltration by myeloblas. Kadan-sometimes found "Auer body" in the myeloblast. Sometimes the first manifestation as eritroleukemia (ploriferasi eritroblas and myeloblast in bone marrow) that lasts a few months/years before the fambaran mieloblastiknya be obviously true.

2.7. Dignosis appeal
       Acute mieloblastik leukemia diagnosis should be made the appeal and all of the acute leukemia and anemia aplastik. If found "Auer body" then diagnosabandin g is not difficult, because of the enforced this disorder patogonomis for acute mieloblastik leukemia.
       If not found then it should done body Auer reaction which the myeloblast peroxidase pereksidase will be positive.
       Anemia aplastik with mieloblastik acute alekemik in distinguish on the basis of an examination of the bone marrow. Bakterialis endocarditis is clinically similar to leukemia mieloblastik akaut because of the febris, anemi, splenomegaly, and ptechiae. Certainly the existence of a history of heart disease, splenomegaly and absence of abnormality on the gums can distinguish both of these circumstances.
Pernicious anemia and splenomegaly are accompanied ptechiae may resemble acute mieloblastik leukemia.
       In pernicious anemia patients usually do not look sick, there are severe jaundice and no abnormalities on the gums.

2.8. Complications
      Two kinds of complications that are often fatal bleeding, namely serebelar and infections. A rare complication is due to complaints of pressure by a tumor leukemia.

2.9. Management
      Fix circumstances namely: anaemia blood tranfusi given with PCR (Packed red cell) or blood. Trombositopeni that konsetrat overcome by threatening transfusion of platelets. What if there is an infection given the antibiotic adekwat. Specific therapy such as leukemia therapy is generally started with the induction phase: Doxorubicin 40 mg/mm2 1-5 day weight. Fig C 100 assembled resumed mg IV every 12 hours the day of 1-7. For patients above 50 years of age-the dose is reduced by Adriamycin in just 3 days and 5 days C Fig. Substitute drug adriamycin is Farmorubicin. Clinical evaluation done and hematologis. Bone marrow examination at the end of the third mimggu. If it does not happen only a remission or remissions parsiil then the therapy should be replaced with other regimens.
       In case of complete remission (clinical and hematologis) then the starting stage of consolidation. At this stage given doxorubicin 40 mg/mm2 of the day 1-2 and Ara C 1-5. Refimen awarded 2 times with intervals of 4 weeks.
      If a State allows then a bone marrow graft is given in the event of complete remission. (Hematology Clinic 2,113 Ed.).
      Standard therapy was chemotherapy induction regimen with sitarabin and daunorubisin sitarabin Protocol with 100 mg/m2 given in continuous infusion for 7 days and daunorubisin 45-60 mg/m2/day iv for 3 days. About 30-40% of patients experienced a complete remission with sitarabin and dounorubisin therapy is given as a single drug, whereas if given as a drug combination of complete remission was achieved by more than 60% of patients. (Textbook In Pathology Vol II, ed. IV. 1238).
2.10. The Prognosis
        With aggressive therapy, 40-50% of sufferers achieve remission will live long (30-40% healing of the whole numbers). Penderit who are having chemotherapy or after obtaining relaps transplant autolog can be diterapi with CST allogenetik as rescue therapy. Some morphological or genetic subtypes of LMA has a better prognosis.
Chapter 3
COVER
3.1. Kesimpula
      Leukemia (blood cancer) is a type of cancer that attacks the white blood cells produced by the bone marrow (bone marrow). Bone marrow or bone marrow is in the human body produces three types of blood cells include white blood cells (functioned as endurance body fight infections), red blood cells (function bring oxygen into the body) and platelets (small part of blood cells that helps the process of blood clotting).
     Until recently the cause of disease of leukemia is not known for certain, but there are several factors that affect the frequency of the alleged occurrence of leukemia:
1. Radiation. This is supported by some reports from some of the research that deal with cases of Leukemia that employees often suffer leukemia more radiology, radiotherapy Penerita with more often suffer from leukemia, Leukemia was found in the victim's life the atomic bombs of Hiroshima and Nagasaki, Japan.
2. Leukemogenik. Some chemical substances are reported to have been identified could affect the frequency of leukemia, such as environmental toxins such as benzene, industrial chemicals such as insecticides, drugs used for chemotherapy.
3. Hereditary. Sufferers of Down Syndrom has the incidence of acute leukemia 20 times greater than normal people.
4. Virus. Some types of viruses can cause leukemia, such as retroviruses, feline leukemia virus, HTLV-1 in adults.
      Frequently used Therapy system in dealing with the sufferers of leukemia is the combination of Chemotherapy (chemotherapy) and the giving of drugs that focus on the dismissal of the production of abnormal white blood cells in the bone marrow. Next is the handling of some symptoms and signs which have been showed by the body of the sufferer with a komprehensive monitor.

3.2. Any suggestions
     Leukemia disease one of the harmful, so it must be controlled carefully, then it is very important to prevent this disease by means of avoiding risk factors and maintain healthy life patterns as early as possible.

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