Oncology Flashcards
Leading cause of death in 1-19 YO
pediatric cancer
Warning signs for childhood cancer
Continued, unexplained weightloss
Headaches - oftening w/ vomiting- early night/ early morning
Increased swelling or pain in bones, back, legs,
Lumps/mass
Development of excessive bruising, bleeding rash
Constant infections A whitish colour behind the pupil Nausea which persists of vomiting w/o nausea Constant tiredness or paleness Eye or vision changes Recurrent FUO
Most common malignancy in children
Acute lymphoblastic leukemia (ALL)
What causes ALL
uncontrolled proliferation of immature lymphocytes
B-precursor lineage (85%)
Peak incidence: 2-5 YO
Cause unknown; genetic factors (down syndrome); viral associations (viral infections, exposure to radiation)
Presentation of ALL
intermittent fever, fatigue, pallor bleeding (50%) - petechiae, purpura BONE PAIN! (pelvis, vertebral bodies, legs) hepatosplenomegaly LAD
Lab finding
anemia/thrombocytopenia w/ normal or depressed WBC
Neutropenia in differential (ANC <1000)
Peripheral smear: lymphoblasts
Dx of ALL
bone marrow bx (leukemic blasts replacing normal marrow)
Tx for ALL
may take 2-3 years to complete
Chemo (1st line)
Hematopoietic stem cell transplant (HSCT) - best form matched sibling
Prognosis for ALL
> 85% survival rate
tumor lysis syndrome
oncologic emergency!
Hyperkalemia, hyperuricemia, hyperphosphatemia
acute renal failure
Acute myeloid leukemia cause
myeloblasts cant differentiate into mature cells
Predisposing factors for AML
no risk factors often
congenital: down syndrome, NF1
Environmental: radiation, benzene (smoking) and previous chemo
Clinical findings for AML
fatigue, pallor, bleeding or infection (fever) CNS INVOLVEMENT (5-15%) - h/a, lethargy, mental status change, cranial nerve palsies
Lab findings for AML
anemia, thrombocytopenia, neutropenia (ANC <1000)
WBC >100,000! (2%)
Hyperleukocytosis (>75,000) may be associated w/ life-threatening complications- Medical emergency
Hyperleukocytosis
AML
Dx of AML
smear: myeloblasts >20% Auer rods (pathognomoic)
Dx requires both:
- bone marrow bx showing >20 blasts
- leukemic cells must be of myeloid origin
Tx for AML
chemo
HSCT
Prognosis
65-75% survival
CML
myeloproliferative disorder - uncontrolled proliferation of mature and maturing granulocytes
rare (5% of child canger)
Philadelphia chromosome
CML; translocation between chromosome 9 and 22
Presentation of CML
chronic phase –> accelerated phase –> blast phase
most asymptomatic bone pain fever, NIGHT SWEATS, fatigue (B sx) pallor, ecchymosis MASSIVE SPLENOMEGALY, variable hepatomegaly
Lab findings for CML
anema, thrombocytosis, and marked leukocytosis
smear: myeloid cells in all stages of maturation, increased basophils and blasts
blast cells >20% = blast crisis
Dx for CML
smear w/ myeloid cells in all stages
confirmation: philadelphia chromosome
Tx for CML
TKI*
HSCT
TKI
TK allows for dysregulation cellular proliferation
50% of childhood lymphomas
Hodgkin Lymphoma
Etiology of hodgkins
4:1 male predominance
familial, EBC association
arises in lymph nodes and spreads to contiguous nodal groups
Diagnostic for hdogkins
Reed-sternberg cells (germinal center B cells that have undergone malignant transformation)
Response to to hodgkinds
children have better response that adults
Presentation of hodgkin lymphoma
painless cervical or supraclavicular adenopathy
Mediastinal mass (75%)
B symptoms
complication w/ hodgkin lymphoma
SVC syndrome- dyspnea, cough, orthopnea, facial/upper extremity edema
Dx of hodgkin lymphoma
tissue bx w/ reed-sternberg cells
Auer rods
AML
Staging of hodgkin lymphoma
CXR
CT scan (chest, abdomen, and pelvis)
bone marrow bx
Tx for hodgkins
chemo
radiation
HSCT
Prognosis for hodgkins
90% 5-10 survival rate
NHL epidemiology
5th most common pediatric cancer
3:1 male predominance
arises in lymphoid tissue and spreads to distant nodes
NHL is associated w/
congenital and acquired immunodeficiency syndromes
EBV
NHL children
worse than in adults; rapidly proliferating, high-grade, diffuse malignancies