Acute Lymphoblastic Leukemia (ALL)

Get Started. It's Free
or sign up with your email address
Acute Lymphoblastic Leukemia (ALL) by Mind Map: Acute Lymphoblastic Leukemia (ALL)

1. Pathophysiology

1.1. Progressive Neoplasm defined by the presence of greater than 30% lymphoblast in the bone marrow or blood

1.1.1. Children Most cases are found in children median age of 13 year old

1.1.2. Adults less prevalent, but higher mortality rate

1.2. Transfromed precursor B cells and or T cells

1.2.1. Precursor B Cell ALL Different Phenotypes Expresses CD19, Human leukocyte antigen DR Other B-cell associated antigen in the cytoplasm the most immature form of of precursor B- cell ALL lack the expression of CD10 CD10 (Common ALL antigen) Seen in 5% of patients Most Common Precurssor B Cell ALL epressess CD10 antigen Seen in 80% of patients Have not undergone rearrangement of Immunoglobulin genes Strongly associated with aneuploidies Philidelphia chromosome ALL carries the worst prognosis Seen More commonly in children

1.2.2. Precursor T Cell ALL Most common lymphoid marker CD3 Other lymphoid makers used CD7 CD12 CD5 Most common genetic alteration in T-Cell ALL T-cell Receptor (TCR) More commonly seen in adults than in children

2. Diagnostic Test

2.1. Immunotyping

2.1.1. Leukemic blast cells Children Transformed precursor B-cells Adults Mixture of transformed precursor B and T cells

2.2. Blood Testing

2.2.1. Complete blood count Elevated White blood count Thrombocytopenia

2.3. Bone Marrow testing

2.3.1. Bone Marrow Biopsy >25% bone marrow blast with or without mass lesion =Acute Lymphoblastic Leukemia Less than 25% bone marrow involvement, with mass lesion= Precursor B Cell Lymphoblastic Lymphoma

2.4. Staining of peripheral blood

3. Treatments

3.1. Chemotherapy

3.1.1. Treatment of choice

3.1.2. Monitor for Toxicity

3.2. Supportive care

3.2.1. Blood tansfusion

3.2.2. Antibiotics

3.2.3. Antifungals

3.2.4. Antivirals

3.3. Allopurinol

3.3.1. Prevent uric acid production because uric acid levels could be increased with cell death due to treatment

3.4. Bone Marrow transplantation

3.5. all-trans-Retinoic acid

3.5.1. Help with cell growth and development

3.6. Correct Metabolic Imbalances

4. Causes/Risk Factors

4.1. Specific causes are unknown

4.2. Prenatal exposure to radiation

4.3. Postnatal exposure to high dose radiation

4.4. Viral Infections

4.5. Higher incicences with genetic diseases

4.6. Prevention is almost impossible due to unknown cause

5. Common Findings

5.1. Amemia

5.1.1. Fatigue

5.2. Thrombocytopenia

5.2.1. Bleeding Petechiae Ecchymosis Gingival bleeding Hematuria

5.3. Fever

5.3.1. Infection Oral cavity Throat Respiratory tract Lower colon Urinary tract Skin


5.4. Weight loss

5.4.1. Anorexia Muscle atrophy

5.4.2. Decrease in sense of taste

5.4.3. Swallowing difficulties

5.5. Organ enlargement

5.5.1. Hepatomegaly

5.5.2. Spleenomegaly

5.5.3. Lymphadenomathy

5.6. Pain

5.6.1. Bone pain

5.6.2. Abdominal pain and tenderness

5.6.3. Breast tenderness

5.6.4. Arthralgia

5.7. CNS abnormalities

5.8. Mediastinal Mass

6. Infection and its relations to Acute Lymphoblastic Leukemia

6.1. The exact cause of Precursor B acute lymphoblastic leukemia (BCP-ALL) is still unknown, but there has been a link between BCP-ALL and Infection.

6.2. Researchers think that immune cells are activated and expand, interacting with precursor B cell that promote leukemia (Bürgler & Nadal 2017).

6.3. With T-helper cells present in the bone marrow, their role in the immune system, and how receptive the are to BCP- ALL cells, they would be great for leukemia-supportive immune cells.

6.4. The interaction still remains unclear.