scenario 3 anwar.docx

7/27/2019 Scenario 3 anwar.docx

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Scenario 3

Leukositosis in Chemical factory worker

Ms. Sarah, 34 years old, chemical factory worker, complaining of fever, weak, and

easily fatigue. She visits the doctor because often get fever. One month earlier her

stomach was cramping, her body was weak and fatigue. Two weeks before seeing the

doctor, sarah felt uncomfortable in her stomach, and lose appetite but no vommiting.

Patient also complaining of havingred spots under the skin and easily got bruise. In

physical examination, the liver palpable in about 4 fingers under arcus costae, hard, flat

surface, and no ache. Lien palpable in S-IV. Laboratory result shows hb 10 gr/dl,

leukosit 125.000/, platelet 100.000. what happened to this patient?

STEP 1

Leukoscytosis : increased the number of leukocyt/ white blood cell

STEP 2

1. Differential diagnosis

2. Criteria for diagnosis

3. Phatofishiology

4. what corelation chemical factory worker with organomegali

5. Treatment

STEP 3


Anemia aplastik

Acute lymphocytic leukemia (ALL)

Acute myelogenous leukemia (AML)

Chronic Lymphocytic Leukemia (CLL)

Chrinic myelogenous leukemia (CML)


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2. Criteria for diagnosis

anamnesis: History taking about signn and simptoms, history taking about riskfactor, others

Phyical examination Laboratory examination: anemia, Leukositosis, trombositopenia

3. Phatofishiology

In leukemias, a clone of malignant cells may arise at any stage of maturation, that is, in

the lymphoid, myeloid, or pluripotential stage. The cause for this clonal expansion is

poorly understood in most cases, but it appears to involve some rearrangement of the

DNA. External factors, such as alkylating drugs, ionizing radiation, and chemicals, and

internal factors, such as chromosomal abnormalities, lead to DNA changes.

4. what corelation chemical factory worker with organomegali

Leukemia results in the accumulation of cancer cells in the bone marrow and blood.

The presence of large numbers of abnormal cells in the bone marrow can inhibit the

marrow from producing normal healthy blood cells. Symptoms caused by bone marrow

failure include paleness, tiredness, shortness of breath, excessive bleeding, and

increased susceptibility to infections. Cancer cells can also infiltrate organs such as the

lymph nodes, spleen, and liver leading to swelling.

5. treatment

Step 4


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STEP 4


Acute leukemias are generally aggressive diseases in which cancerous transformation

occurs at early stages in the development of the affected blood cell. If untreated, these

diseases can berapidly fatal. Chronic leukemias are characterized by a slower

progression than acute leukemias. These leukemias are more difficult to cure, so the

approach to therapy is often conservative and aimed at controlling symptoms.

Acute Leukemia

Acute leukemias are caused by damage to stem cells or cells in the early stages of

development in the bone marrow. Mutations affecting control of cell division,differentiation, and cell death lead to the accumulation of early blood cell precursors

known as blast cells.

AcuteLymphoblasticLeukemia(ALL)

ALL is the most common form of leukemia diagnosed in children. The incidence of

ALL peaks between the ages of 3-7, falls by 10 years of age, and rises again after the

age of 40. Acute lymphocytic leukemia (ALL) occurs when the the body produces a

large number of immature white blood cells, called lymphocytes. The cancer cells

quickly grow and replace normal cells in the bone marrow. Bone marrow is the soft

tissue in the center of bones that helps form blood cells. ALL prevents healthy blood

cells from being made. Life-threatening symptoms can occur. This type of leukemia

usually affects children ages 3 - 7. It is the most common childhood acute leukemia.

However, the cancer may also occur in adults. Most of the time, there is no obvious

cause. However, the following may play a role in the development of leukemia in

general:

Certain chromosome problems Exposure to radiation, including x-rays before birth Past treatment with chemotherapy drugs Receiving a bone marrow transplant Toxins such as benzene
http://www.nlm.nih.gov/medlineplus/ency/article/002324.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/002331.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/002331.htmhttp://www.nlm.nih.gov/medlineplus/ency/article/002324.htm


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AcuteMyeloidLeukemia(AML)

AML represents 10-15% of leukemias diagnosed in childhood and is the most common

type of acute leukemia diagnosed in adults. Chronic lymphoid leukemias are diseases

characterized by the accumulation of fully developed B or T lymphocytes in the blood.

These diseases are closely related to lymphomas, in which lymphocytes accumulate in

lymph nodes and vessels. Acute myelogenous leukemia (AML), also known as acute

nonlymphocytic leukemia, represents a group of clonal hematopoietic stem cell

disorders in which both failure to differentiate and overproliferation into the stem cell

compartment result in the accumulation of myeloblasts. It is the most common

leukemia in adults.

There are a number of risk factors for the development of AML :

Genetic Predisposition

1. Chromosomal instability in several autosomal dominant conditions can lead toAML, including Fanconi's anemia, ataxia-telangiectasia, neurofibromatosis, and

Bloom's syndrome.

2. Germline mutations in theAML-1 gene are known to be associated with anincreased risk of the development of AML.

3. Additionally, congenital immunodeficiency disorders. including infantile X-linked agammaglobulinemia and Down syndrome, have also been associated

with an increased incidence of AML.

Environmental Exposure

Ionizing radiation and organic solvents such as benzene and other petroleum products

have been associated with a higher risk of developing AML. Both ras mutations and

polymorphisms resulting in the inactivation of nicotinamide adenine dinucleotide

phosphate, reduced (NADPH)quinone oxidoreductase have been found in patients

with these exposures.

Prior Therapy

Therapy-related AML typically develops after alkylating agent-induced damage at a

median of 5 to 7 years after therapy for the primary malignancy. It is usually associated

with an antecedent myelodysplastic disorder. DNA topoisomerase II agents may also

produce gene rearrangements leading to AML, with a short latency period of 12 to 18

months following treatment.


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Prior Bone Marrow Disorders

Secondary AML can develop in patients with various hematologic disorders, such as

aplastic anemia and severe congenital neutropenia. Other inherited hematologic

conditions have also been implicated, such as Bloom's syndrome and Fanconi's anemia.

Myelodysplastic and myeloproliferative syndromes, present for at least 3 months, can

also progress to AML.

Age

The incidence of AML increases with age. In the United States, the median age of

patients with AML is 68 years. The age-adjusted population incidence is 17.6 per

100,000 for people older than 65 years, compared with 1.8 per 100,000 for those

younger than 65 years. Similarly, chromosomal abnormalities occur with greater

frequency among this older population of patients.

The diagnosis of AML requires the identification of greater than 20% leukemic blasts in

the bone marrow (see later). Further analysis then must separate AML from acute

lymphoblastic leukemia by showing evidence for commitment to the myeloid lineage.

Immunohistochemical staining for myeloperoxidase is the best method for determining

which cells are committed to the myeloid lineage (fig.1). The leukemic clone giving

rise to AML can occur at any point in the differentiation of the myeloid cell, creating

heterogeneity among patients. Flow cytometry and cytogenetics are then used to

differentiate the various AML subtypes.

The subtypes of AML were previously described as M0 through M7 by the French-

American-British (FAB) system. In 1997, however, the World Health Organization

(WHO) reclassified AML into four categories (box 1) in an attempt to predict the

prognosis and biologic properties of AML subcategories more accurately and enhance

the clinical relevance of the system. This new classification reflected those entities with

similar biologic and clinical features. It also takes into account the morphologic,

genetic, and immunophenotypic features of the disease entities. The four categories

include AML with recurrent genetic abnormalities, AML with multilineage dysplasia,

therapy-related AML and myelodysplastic syndromes, and AML not otherwise

categorized, which roughly correlates with the FAB classification . The WHO

classification system differs from the FAB system in that the previous blast cell

threshold of 30% for the diagnosis of AML has been reduced to 20%, and patients with

recurring cytogenetic abnormalities are now classified as having AML regardless of

blast percentage.


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Box 1: WHO Classification of Acute Myelogenous Leukemia

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) andvariants

Acute myeloid leukemia with 11q23 (MLL) abnormalitiesAcute 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 inhibitorrelated 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

AML1, acute myelogenous leukemia 1; CBFb, core-binding factor b; ETO, eighttwenty-one; MDS, myelodysplastic syndromes; MYH11, myosin heavy chain, type 11;


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MLL, mixed lineage leukemia; MPD, myeloproliferative disease; PML, promyelocytic

leukemia; RARa, retinoic acid receptor.

The British Medical Research Council (MRC) AML 10 trial and a Cancer and

Leukemia Group B (CALGB) trial found that patients could then be categorized

prognostically based on their pretreatment cytogenetics. Patients could be separated into

three categories based on response to induction treatment, relapse risk, and overall

survivalfavorable, intermediate, and adverse cytogenetic groups. Typically, patients

with favorable-risk cytogenetics have abnormalities of the AML1-CBF DNA subunit.

This subunit is composed of two proteins, AML1 (also known as core-binding factor

2, CBF2) which heterodimerizes with another protein, CBF, to form a transcription

factor necessary for normal hematopoiesis. Adverse cytogenetics include complex

(three or more) abnormalities, deletion of 5q, abnormal 3q, and deletion of chromosome

7. Thus, it is crucial to test for cytogenetics and, when applicable, to use fluorescence in

situ hybridization (FISH), because these may help dictate therapy. More recently, gene

expression profiling has been shown to improve the molecular classification and

prediction of outcome in patients with AML.

Baseline evaluation involves routine blood work, including a complete blood count with

differential, complete metabolic profile, and coagulation studies. A bone marrow biopsy

should be evaluated by cytochemistry, immunophenotyping, flow cytometry, and

cytogenetics; this is necessary for determining diagnosis and prognosis. Additional

studies, including chest radiography and echocardiography are needed to determine a

patient's ability to undergo chemotherapy. A lumbar puncture may be needed if central

nervous system (CNS) symptoms are identified. Human leukocyte antigen (HLA)

typing and viral serologies are needed if bone marrow transplantation is necessary.

ChronicLymphocyticLeukemia(CLL)

This is a malignant monoclonal expansion of B lymphocytes with accumulation of

abnormal lymphocytes in the blood, bone marrow, spleen, lymph nodes and liver.

Morphologically these lymphocytes have a normal appearance but are immature and

nonreactive, resulting in immunological compromise. Chronic lymphocytic leukaemia

(CLL) represents about a quarter of all leukaemias seen in clinical practice and is

largely a disease of older people. The diagnosis of CLL is established by the following:


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The presence in the peripheral blood of 5,000 monoclonal B lymphocytes/mcLfor the duration of at least three months. The clonality of the circulating B

lymphocytes needs to be confirmed by flow cytometry.

The leukaemia cells found in the blood smear are characteristically small, maturelymphocytes with a narrow border of cytoplasm and a dense nucleus lacking

discernible nucleoli and having partially aggregated chromatin.

Epidemiology

CLL is the most common leukaemia in the Western world with an incidence of4.2/100,000/year.

The incidence increases to >30/100,000/year at an age of >80 years. The medianage at diagnosis is 72 years. About 10% of CLL patients are reported to be

younger than 55 years.

By far the most common type of chronic lymphoid leukemia, involves B lymphocytes.

CLL mainly affects elderly individuals, with a peak incidence between 60 and 80 years

of age.It is the most common form of leukemia in Western countries.CLL follows a

variable course, with survival ranging from months to decades.

Other types of chronic lymphoid leukemias include:

Prolymphocytic leukemia (PLL) Hairy cell leukemia (HCL) Plasma cell leukemia Large granular lymphocytic leukemia T-cell prolymphocytic leukemia (T-PLL)

ChronicMyeloid Leukemia(CML )

CML is a disorder of a hematopoietic stem cell. The disease, which accounts for

approximately 15% of leukemias, occurs most frequently between the ages of 40 and 60

years. Laboratory tests reveal increased numbers of cells belonging to the myeloid cell

line (monocytes, neutrophils, basophils, eosinophils) at various stages of development

circulating in the blood stream.


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Chronic myelogenous (or myeloid) leukemia (CML), also known as chronic

granulocytic leukemia (CGL), is a form of leukemia characterized by the increased and

unregulated growth of predominantly myeloid cells in the bone marow and the

accumulation of these cells in the blood. CML is a bone marrow stem cell disorder in

which proliferation of mature granulocytes (neutrophills, eosinophils, and basophils)

and their precursors is the main finding. It is a type of myeloproliferative disease

associated with a characteristic chromosomal translocation called the Philadephia

chromosome.

Laboratory diagnosis of CML is often suspected on the basis on the complete blood

count, which shows increased granulocytes of all types, typically including mature

myeloid cells. Basophils and eosinophils are almost universally increased; this feature

may help differentiate CML from a leukemoid reaction. A bone marrow biopsy is often

performed as part of the evaluation for CML, but bone marrow morphology alone is

insufficient to diagnose CML. Ultimately, CML is diagnosed by detecting

thePhiladephia chromosome. This characteristic chromosomal abnormality can be

detected by routine cytogenetics, by fluorescent in situ hybridization, or by PCR for the

bcr-abl fusion gene.

2. Criteria diagnosis

Performance status (prognostic factor) Ecchymosis and oozing from IV sites (DIC, possible acute promyelocytic

leukemia)

Fever and tachycardia (signs of infection) Papilledema, retinal infiltrates, cranial nerve abnormalities (CNS leukemia) Poor dentition, dental abscesses Gum hypertrophy (leukemic infiltration, most common in monocytic leukemia) Skin infiltration or nodules (leukemia infiltration, most common in monocytic

leukemia)

Lymphadenopathy, splenomegaly, hepatomegaly Back pain, lower extremity weakness [spinal granulocytic sarcoma, most likely

in t(8;21) patients]


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Laboratory examination:

Platelet counts 100,000/L (leukositosis)

3. Pathofhisiology

In leukemias, a clone of malignant cells may arise at any stage of maturation, that is, in

the lymphoid, myeloid, or pluripotential stage. The cause for this clonal expansion is

poorly understood in most cases, but it appears to involve some rearrangement of the

DNA. External factors, such as alkylating drugs, ionizing radiation, and chemicals, and

internal factors, such as chromosomal abnormalities, lead to DNA changes.

Chromosomal rearrangements may alter the structure or regulation of cellular

oncogenes. For instance, in the B-cell lymphocytic leukemias, chromosomal

translocations may put the genes that normally regulate heavy and light chain

immunoglobulin synthesis next to the genes that regulate normal cellular activation and

proliferation. This results in proliferation of lymphoblasts. As the population of cells

expands, the bone marrow starts to fail. Pancytopenia is typical and results in part from

the physical replacement of normal marrow elements by the immature cells. In addition,

the abnormal cells may secrete factors that inhibit normal hematopoiesis.

As the bone marrow becomes replaced, the abnormal cells spill into the circulation and

infiltrate other organs, such as the liver, the spleen, and the eye. The ocular

manifestations may be secondary to direct infiltration of the leukemic cells, as a result

of abnormal systemic hematological parameters, opportunistic infections, or iatrogenic

complications arising from chemotherapy.

4. What corelation chemical factory worker with organomegali

Leukemia results in the accumulation of cancer cells in the bone marrow and blood.

The presence of large numbers of abnormal cells in the bone marrow can inhibit the


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marrow from producing normal healthy blood cells. Symptoms caused by bone marrow

failure include paleness, tiredness, shortness of breath, excessive bleeding, and

increased susceptibility to infections. Cancer cells can also infiltrate organs such as the

lymph nodes, spleen, and liver leading to swelling. Many patients, however, experience

no symptoms at all throughout early stages of the disease.

Although the cause of leukemia in most patients is unknown, several factors are

associated with increased risk of developing the disease. Factors that influence risk of

developing leukemia include:

Age

Prior Chemotherapy Ethnicity/Gender Inherited Syndromes (such as Down Syndrome) Ionizing Radiation Infection by certain viruses Cigarette smoking

The relative effects of these and other risk factors in any given case of cancer is

variable.

Age

The risk of developing most types of leukemia increases steadily with age. The curve

for acute lymphoblastic leukemia (ALL) incidence, however, is U-shaped: highest

between the ages of 3-7 and rising again after the age of 40.(1) The reason for this peak

in early childhood ALL remains uncertain. More information about the relationship

between cancer and age can be found in the Mutation section.

Chemotherapy

There is a subset of acute myeloid leukemia (AML), known as "secondary AML" or

"therapy-related myeloid leukemia," which can develop following treatment with

chemotherapy. Although a causal relationship is implied by the name, the exact

mechanism remains unknown.Prognosis for secondary AML is generally unfavorable

compared to primary AML.

Ethnicity/Gender

With the exception of chronic myeloid leukemia (CML), which has a similar incidence

in whites and blacks, leukemia occurs more commonly in those of white ancestry
http://www.cancerquest.org/mutationhttp://www.cancerquest.org/mutation


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compared to those of Asian, Hispanic and black ancestry. Leukemia also occurs more

frequently in males than females.

InheritedSyndromes

Children with Down syndrome (DS) have a roughly 20-fold increased risk of

developing childhood leukemia compared to children without DS.Approximately 10%

of children with DS are born with a "transient leukemia" that resolves spontaneously

within months of birth. One to two percent, however, develop a malignant acute

leukemia requiring chemotherapy by the age of 4.While several hypotheses have been

proposed, the reason for this increased risk remains uncertain.

Other inherited syndromes that increase risk of leukemia include:

Ataxia-telangiectasia Bloom syndrome Fanconi syndrome Klinefelter syndrome Neurofibromatosis

Ionizing Radiation

An increase in leukemia has been observed in survivors of the atomic bombing of

Japanese cities. Although the risk associated with exposure to lower level radiation is

not clear, studies have shown an increase in leukemia following the use of radiotherapy

for ankylosing spondylitis (a form of arthritis) and exposure to diagnostic X-rays of the

fetus during pregnancy.

Viruses

Infection with Human T-cell Lymphotropic Virus-1 (HTLV-I) is linked to the

development of Adult T-cell Leukemia/Lymphoma (ATLL), a cancer of activated

mature T lymphocytes. Learn more about T lymphocytes

HTLV-I and ATLL are widespread in certain regions of the world, such as the

Caribbean basin, Japan, and parts of South America and Africa, while very rare in

others.Most people who are infected with HTLV-I do not develop leukemia.Data from

cancer registries in Japan suggest the lifetime risk of developing ATLL among those

infected is 2.1% for females and 6.6% for males.
http://www.cancerquest.org/acquired-immune-responsehttp://www.cancerquest.org/acquired-immune-response


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Although the exact mechanism by which HTLV-I infection induces cancer is not

known, laboratory studies have identified several mechanisms which may be involved.

Etiology

The etiology of the leukemias appears to be multifactorial. Genetic, viral, andenvironmental factors, such as ionizing radiation, drugs, and chemicals, have

been implicated in the pathogenesis of leukemia.

It is believed that the final common pathway is damage to the DNA. Thisdamage may rearrange the genetic material, thereby allowing previously silent

oncogenes to be expressed.

Patients with an abnormal number of chromosomes (eg, trisomy 21) andchromosomal translocations are at an increased risk of developing ALL.

Risk factors implicated in the development of AML include the following:o Myelotoxic agents (eg, ionizing radiation, benzene, alkylating agents)o Chromosomal abnormalities (eg, Down syndrome, chromosomal

instability syndromes)

o Predisposing hematological disorders (eg, aplastic anemia, chronicmyeloproliferative disorders, paroxysmal nocturnal hemoglobinuria)

Chromosomal abnormalities, especially trisomy 12, are common in patients withCLL. Familial case clusters have been reported in CLL. HTLV-1 infection has

also been implicated in CLL.

Damage to the bone marrow by agents, such as benzene and ionizing radiation,may cause CML.

Of patients with CML, 90% have an acquired chromosomal abnormality, thePhiladelphia chromosome, which is a translocation of half of the long arm of

chromosome 22 to another chromosome, usually chromosome 9.

5. Treatment

As our focus is on the biology of the cancers and their treatments, we do not give

detailed treatment guidelines. Instead, we link to organizations in the U.S. that generate

the treatment guidelines. The National cancer institute lists the following treatments for

leukemia:


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SurgeryThe treatment of breast cancer can be broken down into two categories: early

stage and advanced stage. Early stage treatment involves tumors that are

confined to the breast. Advanced stage treatment involves tumors that have

spread beyond the breast to other regions of the body. Treatment options are

dependent upon size of tumor, location, physical condition of patient, and stage

of cancer.

Radiation TherapyRadiation therapy is one of the many tools used to combat cancers. Radiation

treatments utilize high-energy waves such as x-rays to kill cancer cells.

Radiation can be used alone or in conjunction with other treatments (e.g.

chemotherapy and surgery) to cure or stabilize cancer.

Like other therapies, the choice to use radiation to treat a particular cancer

depends on a wide range of factors. These include, but are not limited to, the

type of cancer, the physical state of the patient, the stage of the cancer, and the

location of the tumor.

ChemotherapyThe term chemotherapy, or chemo., refers to a wide range of drugs used to treat

cancer. These drugs usually work by killing dividing cells. Since cancer cells

have lost many of the regulatory functions present in normal cells, they will

continue to attempt to divide when other cells do not. This trait makes cancer

cells susceptible to a wide range of cellular poisons.

The chemotherapy agents work to cause cell death in a variety of ways. Some of

the drugs are naturally occurring compounds that have been identified in various

plants and some are man-made chemicals. A few different types of

chemotherapy drugs are briefly described below. For more information on a

particular type of drug, choose from the list below.

Antimetabolites: Drugs that interfere with the formation of key bio-moleculeswithin the cell including nucleotides, the building blocks of DNA. These drugs

ultimately interfere with DNA replication and therefore cell division.

Genotoxic Drugs: Drugs that damage DNA. By causing DNA damage, theseagents interfere with DNA replication, and cell division.
http://www.cancerquest.org/breast-cancer-treatmenthttp://www.cancerquest.org/radiation-therapy-introductionhttp://www.cancerquest.org/chemotherapy-introductionhttp://www.cancerquest.org/chemotherapy-antimetaboliteshttp://www.cancerquest.org/genotoxic-chemotherapy-drugshttp://www.cancerquest.org/genotoxic-chemotherapy-drugshttp://www.cancerquest.org/chemotherapy-antimetaboliteshttp://www.cancerquest.org/chemotherapy-introductionhttp://www.cancerquest.org/radiation-therapy-introductionhttp://www.cancerquest.org/breast-cancer-treatment


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Spindle Inhibitors: These agents prevent proper cell division by interfering withthe cytoskeletal components that enable one cell to divide into two.

Other Chemotherapy Agents Glossary of Chemotherapy Agents: An easy to use table of chemotherapy drugs

including trade name, generic name, and type.

Normal cells are more resistant to the drugs because they often stop dividing

when conditions are not favorable. Not all normal dividing cells escape

however, a fact that contributes to the toxicity of these drugs. Cell types that are

normally rapidly dividing, such as those in the bone marrow and in the lining of

the intestine, tend to be hardest hit. Death of the normal cells produces some of

the common side-effects of chemotherapy.

Immunotherapythe purpose of cancer vaccines is to stimulate the body's defenses against cancer

by increasing the response of the immune system. Our immune system provides

a dynamic protective system against disease from foreign pathogens and from

abnormal body cells. Cancer cells are, in essence, normal body cells that have

sustained mutations and no longer function properly.

Tumor vaccines usually contain proteins found on or produced by cancer cells.

By administering forms of these proteins and other agents that affect the

immune system, the vaccine treatment aims to involve the patient's own

defenses in the fight to eliminate cancer cells. Immunotherapy is a new field in

cancer treatment and prevention, and many strategies are being examined in

clinical trials.

Stem Cell TransplantationBone marrow transplant is used to treat several types of cancer and is commonly

used for leukemias, lymphomas and other blood cell cancers.
http://www.cancerquest.org/mechanism-spindle-inhibitorshttp://www.cancerquest.org/additional-chemotherapy-agentshttp://www.cancerquest.org/chemotherapy-drug-tablehttp://www.cancerquest.org/tumor-vaccines-introductionhttp://www.cancerquest.org/bone-marrow-transplant-introductionhttp://www.cancerquest.org/bone-marrow-transplant-introductionhttp://www.cancerquest.org/tumor-vaccines-introductionhttp://www.cancerquest.org/chemotherapy-drug-tablehttp://www.cancerquest.org/additional-chemotherapy-agentshttp://www.cancerquest.org/mechanism-spindle-inhibitors


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STEP 5

1. Classification of leukemia2. Treatment of leukemia3. Leukositosis and leukopenia

STEP 6

(-)

STEP 7 :

1. Classification of leukemia

PATIENT GROUP AND

TYPE OF LEUKEMIA

SYMPTOMS SIGNS LABORATORY

FINDINGS

Children: acute

lymphocytic leukemia

Infection,

bleeding,

weakness

Enlarged liver,

spleen or lymph

nodes

Variable white

blood cell count,

anemia,

thrombocytopenia,

blast cells

Adults: acute

nonlymphocytic leukemia

(acute myeloid leukemia)

None, or malaise

and abdominal

discomfort

Enlarged spleen Leukocytosis

(myeloid

precursors), normal

or increased platelet

count

Adults: chronic

myelogenous leukemia

Older adults: chronic None, or Enlarged spleen Leukocytosis


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lymphocytic leukemia nonspecific

symptoms

or lymph nodes (lymphocytes)

A. ACUTE LEUKEMIASPatients with an acute leukemia often present with signs and symptoms of bone marrow

failure, such as fatigue and pallor, fever, infection and/or bleeding with purpura and

petechiae. In acute leukemias, the marrow is typically overpopulated with blast cells.

These cells are indistinguishable from stem cells by light microscopy, but the term

blast implies an acute leukemic clone. The maturing normal marrow cellular elements

are decreased or absent. Peripheral leukemic cell counts may range from leukocytosis to

leukopenia, but, as anticipated, anemia and thrombocytopenia are common.

The acute leukemias are broadly divided into two classes based on the cell of origin:

acute lymphocytic leukemia and acute non-lymphocytic leukemia. The previous

designation of acute myeloid leukemia has been replaced by acute nonlymphocytic

leukemia to appropriately encompass the full variety of possible abnormal cells

(undifferentiated, myeloid, monocytic and megakaryocytic).

Acute lymphocytic leukemia most commonly occurs in children less than 18 years of

age. Adults usually have acute nonlymphocytic leukemia. Occasionally, patients with

acute lymphocytic leukemia have a mediastinal mass or central nervous system

involvement at the onset of illness.

Blast cells are often seen in the peripheral blood smears of patients with acute leukemia.

Auer rods are a marker of acute nonlymphocytic leukemia. Because Auer rods do not

appear frequently, precise distinction between acute lymphocytic leukemia and acutenonlymphocytic leukemia usually cannot be accomplished based on the peripheral

smear alone; histochemistry, immunotyping and chromosome analysis are usually

required.

All patients with acute leukemia require prompt attention and therapy. White blood cell

counts in excess of 100,000 per mm3 (100 109 per L) constitute a medical emergency

because patients with this degree of leukocytosis are predisposed to brain infarction or

hemorrhage.


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B. CHRONIC LEUKEMIASPatients with a chronic leukemia typically present with much less severe illness than

those with an acute leukemia. Chronic leukemia is usually diagnosed incidentally based

on high white blood cell counts. The chronic leukemias are divided into two groupsaccording to the cell of origin: chronic lymphocytic leukemia and chronic myelogenous

leukemia.

Chronic lymphocytic leukemia results from the proliferation and persistence (lack of

apoptosis) of relatively mature-appearing lymphocytes. The spleen and lymph nodes are

enlarged because of the excessive accumulation of lymphocytes. Despite the increased

number of lymphocytes, this disease is associated with impaired immunity as a result of

the scarcity of normal lymphocytes.

Unless complications are present, patients with chronic lymphocytic leukemia do not

require urgent referral to a hematologist. In the absence of symptoms, such as fever,

sweats, weight loss, anemia, moderate thrombocytopenia or organ enlargement, the

leukocytosis usually does not require treatment.

Chronic myelogenous leukemia, which affects myeloid cells (polymorphonuclear cells

and less mature cell forms), is frequently diagnosed after the incidental finding of a

high white blood cell count. A peripheral blood smear from a patient with this form of

leukemia is shown in. In some situations, the smear can also show increases in

basophils or eosinophils.

Middle-aged adults more commonly develop chronic myelogenous leukemia. Some

patients describe fatigue, bleeding or weight loss. Splenomegaly is frequently present,

and the markedly enlarged spleen sometimes causes abdominal discomfort, indigestion

or early satiety. Lymphadenopathy is uncommon.

Platelet counts are usually normal to increased. In fact, chronic myelogenous leukemia

is the only leukemic process that is associated with thrombocytosis. Another laboratory

feature that distinguishes this disease from other leukemias and myeloproliferative

disorders is the presence of the Philadelphia chromosome, an abnormality of

translocation between chromosome 22 and chromosome 9.


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Chronic myelogenous leukemia eventually develops an accelerated phase and

subsequently transforms into acute leukemia. The accelerated phase is characterized by

fever, sweats, weight loss, bone pain, bruising and hepatosplenomegaly. During this

time, thrombocytopenia and anemia develop. The median time for transformation of

chronic myelogenous leukemia to acute leukemia is two to five years. After the

development of acute leukemia, median survival is short.

2. Treatment of LeukemiaThe goal of treatment for leukemia is to destroy the leukemia cells and allow normal

cells to form in your bone marrow. Treatment decisions are based on the kind of

leukemia you have, its stage, and your age and general health.

a. Treatment for acute leukemiaChemotherapy is the use of drugs to fight cancer. It is the usual treatment for acute

leukemia. For most people, that means receiving drugs in stages:

The goal of induction is to kill leukemia cells in the blood and bone marrow to induceremission. During remission, there are no signs or symptoms of leukemia.

The goal of consolidation is to kill any leukemia cells that may be present even thoughthey don't show up in tests. If these cells regrow, they could cause a relapse.

The goal of maintenance also is to prevent any remaining leukemia cells from growing.This may be done using lower doses of chemotherapy than those used during induction

or consolidation. This is only used in people with ALL and a few rare forms of AML.

Some types of acute leukemia spread to the brain and spinal cord. Regularchemotherapy cannot reach those areas, because your body puts up a special barrier to

protect them. A different way of giving chemotherapy, called intrathecal chemotherapy,

treats these areas by injecting the drugs directly into your spinal canal to attack any

leukemia cells there.

Radiation therapy uses high doses of radiation, such as X-rays, to destroy cancer cells.

Radiation is usually given from a machine outside the body that directs radiation to the

cancer (external radiation). Radiation is also used to treat acute leukemia that has spread

to the brain and spinal cord.


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Stem cell transplant may be part of the treatment plan for people who have high-risk

acute leukemia. Most stem cell transplants for leukemia are allogeneic, meaning the

stem cells are donated by someone else. The goal of a transplant is to destroy all the

cells in your bone marrow, including the leukemia cells, and replace them with new,

normal cells.

b. Treatment if acute leukemia gets worseSometimes leukemia gets worse in spite of treatments. Sometimes it gets better, or

"goes into remission." Sometimes it comes back, or "relapses." Even when that

happens, there are several treatments that may help to cure the leukemia or help you

live longer:

Stem cell transplant . Donated cells from a "matched" donor can rebuild your supply ofnormal blood cells and yourimmune system.

Chemotherapy. Sometimes medicines or doses that are different from those used duringyour initial chemotherapy can help.

A stem cell (blood or marrow) transplant is the infusion, or injection, of healthy stem

cells into your body to replace damaged or diseased stem cells. A stem cell transplant

may be necessary if your bone marrow stops working and doesn't produce enough

healthy stem cells. A stem cell transplant also may be performed if high-dose

chemotherapy or radiation therapy is given in the treatment of blood disorders such as

leukemia, lymphoma or multiple myeloma. A stem cell transplant can help your body

make enough healthy white blood cells, red blood cells or platelets, and reduce your

risk of life-threatening infections, anemia and bleeding.

Although the procedure to replenish your body's supply of healthy blood-forming cellsis generally called a stem cell transplant, it's also known as a bone marrow transplant,

peripheral blood stem cell transplant or an umbilical cord blood transplant, depending

on the source of the stem cells. Stem cell transplants can use cells from your own body

(autologous stem cell transplant), from a donor (allogeneic stem cell transplant) or from

an identical twin (syngeneic transplant).

Stem cell transplants are used to treat people whose stem cells have been damaged by

disease or the treatment of a disease, or as a way to have the donor's immune system
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fight a blood disorder such as leukemia. Stem cell transplants can benefit people with a

variety of both cancerous (malignant) and noncancerous (nonmalignant) diseases.

A stem cell transplant may help treat blood disorders by:

Killing cancer cells. In a stem cell transplant procedure, you'll first be given powerfuldrugs (chemotherapy) with or without radiation therapy to kill the cancer cells. Doctors

then infuse into your body healthy stem cells that previously have been collected from

you or a donor. The new stem cells migrate to your bone marrow and, over time,

produce healthy new cells. In addition, the donor cells also have the ability to kill some

types of cancer cells.

Helping you recover faster from high doses of chemotherapy and radiation. Thehealthy cells infused in a stem cell transplant also may allow you to recover faster from

chemotherapy and radiation, as these cells haven't been exposed to chemotherapy and

radiation.

An autologous transplant

This means that the stem cells used for the transplant come from your own body. They

are usually collected when you are free of any sign of disease (when you are in

remission) following conventional chemotherapy or other treatments. The stem cells

can be used soon after being collected. They can also be frozen, stored and used in the

future if needed. An autologous stem cell transplant is also called stem cell support, as

the stem cells come from your own body. So, strictly speaking, it is not

a transplantfrom a donor.

An allogenic transplant

This means the stem cells used for the transplant come from someone else - a donor.

This is often a close relative such as a brother or sister where there is a good chance of a

close match. Unrelated donors are sometimes matched to people needing a transplant.

Stem cells can be collected:

From the bone marrow. This involves a small operation to collect some marrowfrom the pelvic bone.

From the blood. Some stem cells occur in the blood (most are in the bone marrow).The stem cells in the blood can be collected (harvested) by a machine called a cellseparator. The blood flow is diverted from a vein in the arm to pass through the


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machine which separates out the stem cells. The procedure takes about 4-6 hours.

Drugs are given for a few days before this procedure to stimulate the body to make

more stem cells in the bone marrow which spill out into the blood.

From blood taken from the umbilical cord of a newborn baby.c. Treatment of chronic leukemia

Chronic lymphocytic leukemia (CLL)

Chronic lymphocytic leukemia is not always treated right away. It usually gets worse

more slowly than acute leukemia.

Treatment choices for CLL include:

Watchful waiting. CLL usually gets worse very slowly, and you may have nosymptoms for some time. You and your doctor may decide to hold off on treatment for

a while. During this time your doctor will watch you carefully.

Radiation therapy. Radiation may be used to destroy cancer cells. It also may be used toshrink swollen lymph nodes or a swollen spleen. Sometimes radiation is used on the

whole body to prepare for a bone marrow transplant.

Chemotherapy. Chemotherapy is the use of medicines that attack cancer cells. Manymedicines are available to fight leukemia and help you live longer.

Surgery. If the spleen starts destroying red blood cells and platelets, it may need to beremoved. This operation is called a splenectomy.

Targeted therapy with a monoclonal antibody. These antibodies can kill cancer cells,stop their growth, or keep them from spreading.

When you have CLL, your body is not able to fight infections very well. You and your

doctor need to watch for any signs of infections, such as pneumonia oryeast infections.

Early treatment of these and other infections will help you live longer. You can

sometimes prevent certain infections or keep from getting very sick by getting a flu shot

or a pneumonia vaccine. Your doctor also may give you antibiotics to prevent infection

while you are being treated for leukemia.

Chronic myelogenous leukemia (CML)

Chronic myelogenous leukemia is treated right away.

Treatment choices for CML include:
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Targeted therapy with a tyrosine kinase inhibitor, such as imatinib ordasatinib, is thefirst treatment used for CML.

Chemotherapy. Chemotherapy is the use of medicines that attack cancer cells. Manymedicines are available to fight leukemia and help you live longer.

Biological therapy. This is the use of special medicines that improve your body'snatural defenses against cancer.

High-dose chemotherapy with stem cell transplant. After chemotherapy is completed,stem cells that were previously donated and frozen are thawed and infused.

Donor lymphocyte infusion (DLI). This is a treatment that may be used after a stem celltransplant. With DLI, a person is given more of their donor's white blood cells

(lymphocytes).

Surgery. If the spleen starts destroying red blood cells and platelets, it may need to beremoved. This operation is called a splenectomy

d. Palliative careIf you have leukemia, you may want to consider having palliative care along with your

treatments. Palliative care is a kind of care for people who have serious illnesses. It can

help you manage symptoms from your treatment. Palliative care focuses on improving

your quality of life-not just in your body but also in your mind and spirit.

Palliative care may help you manage symptoms or side effects from treatment. It could

also help you cope with your feelings about living with a serious illness, make future

plans for your medical care, or help your family better understand your illness and how

to support you.

If you are interested in palliative care, talk to your doctor. He or she may be able to

manage your care or refer you to a doctor who specializes in this type of care.
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3. LeukocytosisThe investigation of leukocytosis begins with an understanding of its two basic causes:

(1) the appropriate response of normal bone marrow to external stimuli and (2) the

effect of a primary bone marrow disorder.

Leukocytosis with Normal Bone Marrow

In most instances, increased white blood cell counts are the result of normal bone

marrow reacting to inflammation or infection. Most of these cells are

polymorphonuclear leukocytes (PML). Circulating PML and less mature forms (e.g.,

band cells and metamyelocytes) move to a site of injury or infection. This is followed

by the release of stored leukocytes, commonly referred to as a left shift.

Inflammation-associated leukocytosis occurs in tissue necrosis, infarction, burns and

arthritis.

Leukocytosis may also occur as a result of physical and emotional stress.This is a

transient process that is not related to marrow production or the release of band cells or

other immature cells. Causes of stress leukocytosis include overexertion, seizures,

anxiety, anesthesia and epinephrine administration. Stress leukocytosis reverses within

hours of elimination of the inciting factor.

Other causes of leukocytosis include medications, splenectomy, hemolytic anemia and

malignancy. Medications commonly associated with leukocytosis include

corticosteroids, lithium and beta agonists. Splenectomy causes a transient leukocytosis

that lasts for weeks to months. In hemolytic anemia, non-specific increases in leukocyte

production and release occur in association with increased red blood cell production;

marrow growth factors are likely contributors. Malignancy is another recognized cause

of leukocytosis (and, occasionally, thrombocytosis); the tumor non-specifically

stimulates the marrow to produce leukocytosis.

An excessive white blood cell response (i.e., more than 50,000 white blood cells per

cm3 [50 109 per L]) associated with a cause outside the bone marrow is termed a

leukemoid reaction. Even this exaggerated white blood cell count is usually caused

by relatively benign processes (i.e., infection or inflammation). An underlying

malignancy is the most serious but least common cause of a leukemoid reaction.


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As mentioned previously, an increase in neutrophils is the most common cause of an

elevated white blood cell count, but other sub-populations of cells (eosinophils,

basophils, lymphocytes and monocytes) can also give rise to increased leukocyte

numbers.

A. EOSINOPHILIAEosinophils are white blood cells that participate in immunologic and allergic events.

The relative frequency of each cause usually relates to the clinical setting. For example,

parasitic infections are often responsible for eosinophilia in pediatric patients, and drug

reactions commonly cause an increased eosinophil count in hospitalized patients.

Dermatologists frequently find eosinophilia in patients with skin rashes, and

pulmonologists often see elevated numbers of eosinophils in conjunction with

pulmonary infiltrates and bronchoallergic reactions.

Other causes of eosinophilia include malignancies, especially those affecting the

immune system (Hodgkin's disease and non-Hodgkin's lymphoma), and immunologic

disorders such as rheumatoid arthritis and periarteritis. Eosinophilia-myalgia syndrome,

a recently described disorder associated with dietary supplements of tryptophan,

resembles a connective tissue disease with fibrosis of muscle fascial tissue and

peripheral eosinophilia.

B. BASOPHILIABasophilia is an uncommon cause of leukocytosis. Basophils are inflammatory

mediators of substances such as histamine. These cells, along with similar tissue-based

cells (mast cells), have receptors for IgE and participate in the degranulation of white

blood cells that occurs during allergic reactions, including anaphylaxis.

C.LYMPHOCYTOSISLymphocytes normally represent 20 to 40 percent of circulating white blood cells.

Hence, the occurrence of lymphocytosis often translates into an increase in the overall

white blood cell count. Increased numbers of lymphocytes occur with certain acute and

chronic infections. Malignancies of the lymphoid system may also cause

lymphocytosis.

Relative, rather than absolute, leukocytosis occurs in a number of clinical situations,such as infancy, viral infections, connective tissue diseases, thyrotoxicosis and


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Addison's disease. Splenomegaly causes relative lymphocytosis as a result of splenic

sequestration of granulocytes.

Leukocytosis with Primary Bone Marrow Disorders

Bone marrow disorders are generally grouped into leukemias and myeloproliferative

disorders.

Clinical Factors Increasing Suspicion of an Underl ying Bone Marrow Disorder

Leukocytosis: white blood cell count greater than 30,000 per mm (30 10 per L)*

Concurrent anemia or thrombocytopenia

Organ enlargement: liver, spleen or lymph nodes

Life-threatening infection or immunosuppression

Bleeding, bruising or petechiae

Lethargy or significant weight loss

Marrow abnormalities may occur with stem cells (acute leukemia) or more

differentiated cells (chronic leukemia). Delineating acute leukemias from chronic

leukemias is clinically important because the acute forms are more often associated

with rapidly life-threatening complications such as bleeding, brain infarction and

infection.

Treatment of leukocytosis

Your WBCs may return to normal with or without treatment. If you do have treatment,

your caregiver will usually treat the cause of your leukocytosis. If the cause is a

medicine, your caregiver may ask you to stop taking that medicine. Do not stop taking a

medicine unless your caregiver says it is okay. If the cause is an allergy, your caregiver

may ask you to avoid whatever is causing your allergy. Your treatment may also

include one or more of the following:


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Intravenous (IV) fluids: You may need extra fluid in your blood vessels. Theseliquids are given through an IV, which is a tube placed in your vein. This tube is

connected to tubing and liquid.

Medicine:o Antibiotics: Antibiotics may be given to help you treat or prevent the infection

that is causing your condition. It may also help stop you from getting sepsis,

which is a serious infection in your blood.

o Steroids: This medicine may be given to decrease inflammation. It may also helpdecrease the number of your WBCs.

o Antacids: These medicines help decrease the acid in your urine during yourtreatment for leukocytosis.

o Anti-uric acid medicine: This medicine may be given to decrease the amount ofuric acid in your body. Uric acid is a chemical found in your blood. It may also

help prevent more damage to your cells.

Leukocytoreduction: This procedure decreases the number of WBCs in your blood.It may also help stop leukostasis, which happens when your WBCs clump together

in your blood.

o Leukapheresis: During leukapheresis, blood is taken from your body through anIV. White blood cells (WBCs) are removed from the blood by a machine or a

caregiver. Your blood, without the WBCs, may be given back to you, or sent to a

lab for tests. It may also be stored and given to another person.

o Chemotherapy:o Chemotherapy is also called "chemo". It is a special medicine that is often

used to treat cancer, such as leukemia. It works by killing tumor cells. Your

caregiver will decide what kind and how much chemotherapy you may need.

Your caregiver may start you on one kind of chemotherapy and then switch to

another. Chemotherapy may be used to decrease the amount of WBCs in your

blood or treat your leukemia. Chemotherapy may also be used to shrink lymph

nodes that have cancer in them. Once the tumor is smaller, you may have

surgery to cut out the rest of the cancer.


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o Many different chemotherapy medicines are used to treat cancer. You mayneed blood tests often. These blood tests show how your body is doing and

how much chemotherapy is needed. Chemotherapy can have many side

effects. Caregivers will watch you closely and will work with you to decrease

side effects. Chemotherapy can cure some cancers. Even if the chemotherapy

does not cure your cancer, it may help you feel better or live longer.

Bone marrow transplant (BMT): This is when your diseased bone marrow is replaced

with healthy marrow. You are usually given bone marrow from someone else (a donor).

Sometimes your own marrow may be used if it is collected when your cancer is in

remission (not active). The bone marrow transplant is given to you in an IV while you

are in the hospital. A BMT may cure your illness, but it can cause other very serioushealth problems. You may be in the hospital for a month after your BMT.

Blood transfusion: You will get whole or parts of blood through an IV during a

transfusion. Blood is tested for diseases, such as hepatitis and HIV, to be sure it is safe.

LEUKOPENIA

Leukopenia is defined as a low white blood cell count that falls below 4,000 cells

per microliter. The most common causes of leukopenia include:

Viral infections that decrease the ability of the bone marrow to producewhite blood cells

Inherited disorders such as myelokathexis or Kostmann's syndrome thatprevent the white cells from entering the bloodstream

Cancer of the bone that damages the bone marrow Chemotherapy and other drugs (such as antibiotics and diuretics) that

disrupt the bone marrow or that destroy the white blood cells after they

are formed

Autoimmune disorders such as lupus Other disorders such as hypersplenism that can destroy blood cells as they

are produced

Massive infections that overwhelm the production of white blood cells sothey cannot be produced fast enough by the body


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Symptoms of Leukopenia

Your doctor will need to perform a blood test to determine if you have a low white

blood cell count. Other side effects can help you determine if this test is necessary, and

how severe your condition might be. Mild leukopenia is often temporary and will ceaseas your other symptoms lessen. If your symptoms are severe then you may need to seek

treatment for your leukopenia to prevent a potential life threatening condition from

developing.

a. Anemia is a common symptom of leukopenia. This is an indicator that the redblood cell count is dipping in addition to the white blood cell count. Patients

suffering from anemia may become tired easily, experience a pounding heartbeat

and shortness of breath after exercise. They may have difficulty concentrating and

become dizzy easily. Pale skin, leg cramps and insomnia are also common

indicators that the patient is suffering from anemia.

b. Menorrhagia. Women suffering from leukopenia may suffer from menorrhagia, oran abnormally heavy menstrual period. Their periods may last longer than they

usually would as well. Women may also experience metrorrhagia, or bleeding from

the uterus that is not caused by menstruation. Women suffering from metrorrhagia

should seek medical attention right away as this can be a sign that they have aserious infection or cancer.

c. Others. Patients with a low white blood cell account will commonly show signs offatigue which can be couples with irritability or hot flashes. They may frequently

develop headaches or mood swings as well. Because the immune system is

damaged the patient is more likely to develop inflammation in the mouth. This may

occur around the cheeks, lips, tongue cheeks, tonsils, etc. Patients may also develop

inflammation of the stomach lining as the natural bacteria in the system grows at an

unchecked rate. These conditions may cause the patient to crave hot beverages.

Patients must watch infections carefully as they are at a much higher rate to

develop ulcers or pneumonia during this dip in their infection.

Treatment of leukopenia

Because there are so many causes of leukopenia, the treatments for this disorder

are varied. All of these treatments must be supervised by your healthcare

provider.


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1.Try Prescribed Steroids. One of the effects of steroids is to increaseproduction of white blood cells in the bone marrow.

2.Consider Chinese Medication. Traditional Chinese medications andtreatments may help to increase white blood cell production. Be sure to

work with both your traditional medicine and Chinese providers to

ensure that the treatments being provided are complementary.

3.Remove Causative Agents. When possible, stop the medication or activitythat is causing the leukopenia. Although not always possible, this can be

a simple way to stop the problem.

4.Increase Essential Vitamin Intake. Be sure to get plenty of vitamins andminerals. Be sure to get plenty of Vitamin B12 and folate. These

vitamins cannot be produced or stored by the body so you must eat the

proper foods or take supplements to get them. Vitamin B12 is found in

fish, liver, milk and dairy products, eggs, kelp, yeast and tofu. Look for

breads with added Vitamin B12. Folate is readily available in beans,

grains, green vegetables, liver, pork, poultry, and citrus fruits.

5.Promote White Blood Cells Growth. Research published in 2006 in theAnnals of Oncology reports that using medication to promote white

blood cell growth is one of the most important parts of treatment. The

drugs Neupogen and Neulasta are the two most commonly prescribed

medications for this purpose. Side effects that should be reported when

using these drugs include shortness of breath, evidence of infection, and

abdominal pain.

6.Use Antibiotics to Prevent Infections. Your healthcare provider willprobably prescribe antibiotics to prevent or treat infections while your

white blood cell count is low. Be sure to let your provider know if you

have any signs of infection while you are leukopenic.


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Alwi, Idrus, et.al. 2009.Buku Ajar Ilmu Penyakit Dalam. Ed V. Jil II. Jakarta:

InternaPublishing

Fauci, Anthony, et.al. 2008.Harrisons Principles of Internal Medicine. 7th Ed. U.S:

Mc Graw Hill

Neil Abramson, M.D., And Becky Melton, M.D., Baptist Regional Cancer Institute,

Jacksonville, Florida.Am Fam Physician. 2000 Nov 1;62(9):2053-2060.

Price Sylvia, Wilson Lorrsine. 2005.Patofisiologi Konsep Klinis Proses-Proses

Penyakit. Ed 6. Vol 1. Jakarta: EGC

Robbin, Kumar, Cotran. 2007.Buku Ajar Patologi. Ed 7. Vol 2. Jakarta: EGC

Rodak, Bernadatte, et.al. 2007. Hematology: Cinical Principles and Applications. 3rdEd. U.S: Mc Graw Hill

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