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Acute Lymphoblastic Leukemia (ALL)
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Acute Lymphoblastic Leukemia (ALL)
- Wholesaling Blueprint - Steps to Wholesaling Real Estate Simple Systems
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- Western Front
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- THE SAMPLING PROCESS
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Acute Lymphoblastic Leukemia (ALL)
Infection and its relations toAcute Lymphoblastic Leukemia
The exact cause of Precursor B acutelymphoblastic leukemia (BCP-ALL) is stillunknown, but there has been a linkbetween BCP-ALL and Infection.
Researchers think that immune cells areactivated and expand, interacting withprecursor B cell that promote leukemia(Bürgler & Nadal 2017).
With T-helper cells present in thebone marrow, their role in theimmune system, and how receptivethe are to BCPALL cells, they wouldbe great for leukemia-supportiveimmune cells.
The interaction still remains unclear.
Treatments
Chemotherapy
Treatment of choice
Monitor for Toxicity
Supportive care
Blood tansfusion
Antibiotics
Antifungals
Antivirals
Allopurinol
Prevent uric acid production because uricacid levels could be increased with celldeath due to treatment
Bone Marrow transplantation
all-trans-Retinoic acid
Help with cell growth and development
Correct Metabolic Imbalances
Common Findings
Amemia
Fatigue
Thrombocytopenia
Bleeding
Petechiae
Ecchymosis
Gingival bleeding
Hematuria
Fever
Infection
Oral cavity
Throat
Respiratory tract
Lower colon
Urinary tract
Skin
EARLIEST SIGN
Weight loss
Anorexia
Muscle atrophy
Decrease in sense of taste
Swallowing difficulties
Organ enlargement
Hepatomegaly
Spleenomegaly
Lymphadenomathy
Pain
Bone pain
Abdominal pain and tenderness
Breast tenderness
Arthralgia
CNS abnormalities
Mediastinal Mass
Diagnostic Test
Immunotyping
Leukemic blast cells
Children
Transformed precursor B-cells
Adults
Mixture of transformed precursor B and Tcells
Blood Testing
Complete blood count
Elevated White blood count
Thrombocytopenia
Bone Marrow testing
Bone Marrow Biopsy
>25% bone marrow blast with or withoutmass lesion =Acute LymphoblasticLeukemia
Less than 25% bone marrow involvement,with mass lesion= Precursor B CellLymphoblastic Lymphoma
Staining of peripheral blood
Causes/Risk Factors
Specific causes are unknown
Prenatal exposure to radiation
Postnatal exposure to high dose radiation
Viral Infections
Higher incicences with genetic diseases
Prevention is almost impossible due tounknown cause
Pathophysiology
Progressive Neoplasm defined by thepresence of greater than 30% lymphoblastin the bone marrow or blood
Children
Most cases are found in children
median age of 13 year old
Adults
less prevalent, but higher mortality rate
Transfromed precursor B cells and or Tcells
Precursor B Cell ALL Different Phenotypes
Expresses CD19, Human leukocyte antigenDR
Other B-cell associated antigen in thecytoplasm
the most immature form of of precursorBcell ALL lack the expression of CD10
CD10 (Common ALL antigen)
Seen in 5% of patients
Most Common Precurssor B Cell ALLepressess CD10 antigen
Seen in 80% of patients
Have not undergone rearrangement ofImmunoglobulin genes
Strongly associated with aneuploidies
Philidelphia chromosome ALL carries theworst prognosis
seen more in adults
Seen More commonly in children
Precursor T Cell ALL
Most common lymphoid marker
CD3
Other lymphoid makers used
CD7
CD12
CD5
Most common genetic alteration in T-CellALL
T-cell Receptor (TCR)
More commonly seen in adults than inchildren