Childhood Leukemias Flashcards
What is leukemia
Malignant cell - blast
What blasts do in leukemia
Baby white blood cells that fail to mature
Crowd normal cells
Classification of leukemia
Acute : sudden onset; death in weeks to months of left untreated
Chronic: insidious (gradual) onset; death in years of left untreated
Types of childhood leukemia lineage, onset and type
Lymphoid; acute; ALL
Myeloid; acute; AML
Myeloid; chronic; CML
Children at increased risk for leukemia
Down’s syndrome
Neurofibromatosis type 1
Chromosomal breakage syndromes
Fanconi anemia
Bloom syndrome
Ataxia-telangiectasia
Incidence of ALL and age
2-5 years
75-80% childhood leukemia
25% of childhood cancer
Incidence of AML and age
2-5 years
15-20% childhood leukemia
5% all childhood cancers
Incidence of CML and age
Age none
<5% childhood leukemia
<1% of all childhood cancers
Survival rate ALL
91.8%
Survival rate AML
66.4%
Leukemia pathophysiology
Genetic damage to single bone marrow white blood cell
Uncontrolled proliferation of blasts
Decreased production of normal cells
Accumulation of blasts in body
organs/ tissues ( mostly liver and spleen)
Acute leukemia (ALL and AML) symptom onset and clinical appearance
1-6 weeks prior to diagnosis (days to several months)
Children with AML often “sicker” than those with ALL at diagnosis
Acute leukemia clinical presentation symptoms
Pallor
Fatigue
Anorexia
Fever/infection
Bruising/bleeding
Bone/joint abdominal pain
Headache
Vomiting
Visual disturbances
Acute leukemia clinical presentation: signs
Pallor
Tachycardia
Petechiae/purpura
Evidence of infection
Acute leukemia clinical presentation: signs- organs affected (blast accumulation)
Lymphadenopathy (swollen lymph nodes)
Hepatosplenomegaly
Cranial nerve palsies (paralysis and involuntary tremors)
Testicular enlargement
Acute leukemia clinical presentation: signs-
Chloromas
A rare type of cancer that is made up of myeloblasts (a type of immature white blood cell) and forms outside the bone marrow and blood
Leukemia cutis
the infiltration of neoplastic leukocytes or their precursors into the epidermis, the dermis, or the subcutis, resulting in clinically identifiable cutaneous lesions.
Gingival infiltration
represents a 5% frequency as the initial presenting complication of AML
Diagnostic work up: CBC
WBC: high, low, or normal
Platelets: low
Hgb: low
Differential: neutropenia and blasts
10% of patients have normal CBC
Can type of leukemia be diagnosed by CBC
NO
Diagnostic work up: chemistry panel
Potassium, phosphorus and iron acid may be high due to (cell tumor lysis)
Calcium: low (binds with phos)
Creatinine: high due to renal insufficiency due to tumor lysis
Lactate dehydrogenase (LDH)
High. Correlates to tumor burden
Diagnostic work up: coagulation studies
Presence of coagulopathy
Indicators:
High PTT and PT
Low fibrinogen
High fibrinogen degradation products (FDP)
High d-dimer
FDP (fibrin degradation products)
Clothing and bleeding at the same time
Diagnostic work up additional labs
Viral titers:
Varicella
Hepatitis
Cytomegalovirus
Herpes simplex virus
HIV
Quantitative immunoglobulins
used to detect abnormal levels of the three major classes (IgG, IgA and IgM)
Diagnostic work up : chest X-ray
Related to mediastinal mass
T-cell leukemia subtype — THORAX
present in 5-10% of ALL
Mass may cause respiratory arrest
**always obtain chest X-ray prior to sedating patient for procedure or surgery