Oncology Flashcards
ALL
- Presentation/Sx
Ix:
- On FBE and film you have normochromic normocytic anaemia with BLASTS and reduced WCC and plt
Bone marrow failure
- Anaemia: pallor
- Thrombocytopaeani: purpura, bleeding
- Leukopaenia: recurrent fever or infection
Blastic infiltration
- Hepatosplenomegaly
- Lymphadenopathy
- Bone pain ++, limp
- Testicular swelling (common site for spread)
- Acute renal failure (TLS)
- CNS symptoms (signs of raised ICP, papilloedema, retinal haemmhorage)
- Mediastinal mass (T-ALL)

What is leukostasis
Which leukaemias is this associated this?
What organ systems are associated?
What is the main risk with this?
What is the mx?
High WBC (>300)
- > hyperviscosity, relatively low normal WCC, Hb, plt count to blast ratio
- > tissue hypoxia, DIC, risk of bleeding, risk of TLS
Associated with AML > ALL
Organs involved: CNS (alteration in conscious state) and lung (-> hypoxia)
Main risk: Haemmhoragic infarcts in brain
Mx:
- Platelet, PRBC transfusion
- Urgent cytoreductive tx with hydroxyurea
- TLS prophylaxis w allopurinol
- Hyperhydration
- Start induction chemo

Tumour lysis syndrome
- What is it?
- Which leukaemia/lymphomas is this associated with?
- Which blood cell is associated with leukaemia burden and cell death rate?
- What blood changes does it result in?
- Clinical consequences?
- Mx
- Monitoring?
Rapidly proliferating cancers: cell lysis and destruction -> releasing intracellular components into blood (K, Ph, Uric acid, H)
T-cell ALL > AML
-> HR is WCC >100 in acute leukaemias OR T/B cell lymphomas (Burkitt’s esp and bulky NHL)
LDH -> large tumour burden -> RF for TLS
Results in:
- Hyperuricemia (precipitates in kidneys)
- Hyperkalaemia
- Hyperphosphataemia
- Hypocalcaemia (Ca binds with Ph and deposits in renal tubules)
- Acidosis
=> End-result is ARF
Clinically can lead to
- AKI (uric acid nephropathy)
- Cardiac arrhythmia (hyperK)
- Seizure (hypoCa)
- Sudden death
MX
Intermediate/Low risk
- Allopurinol
- Alkalinisation (bicarb)
- Hyper-hydration
High risk
- Rasburicase
- Hyper-hydration
Serial Monitoring + electrolyte mx
- UEC, CMP, uric acid
Mediastinal compression
- what leukaemia is it associated with?
- what causes it and what sx result from this?
- What risk is associated?
- Crucial ix
- Major contra-indication?
Assoc w T cell ALL > AML + lymphoma (HL, BL, LL)
Results from vena cava compression and bronchtracheal compression
Results in facial oedema, dyspnoea, orthopnoea (don’t want to lie flat)
Assoc w sudden risk of sudden death (often assoc w pericardial effusion -> tamponade)
Ix - AP + lateral XR (?pericardial effusion)
Then needs urgent cardiac echo -> opportunistic pericardial tap for diagnosis and treatment (release of pressure)
Contra-indicated with GA due to cardiac and resp risk -> can make initial workup difficult
B ALL
1. NCI criteria (HR vs SR)
- addit Risk factors
NCI Criteria
- standard risk: age 1-9 and WCC <50
- high risk: age <1 or >10 OR WBC >50
Additional LR factors
• Rapid response to therapy
• cytogenetics
Additional HR factors
• T-cell immunophenotype
• Slow response to initial therapy
• CNS positive leukaemia
• Testicular disease
• cytogenetics
What cytogenetic abnormalities are considered favourable in B ALL?
Unfavourable?
Low risk:
- Hyperdiploidy (>50)
- Trisomies 4, 10, 17
- t(12:21) = TEL AML1 (ETV6-RUNX1)
High risk:
- t(9:22) = BCR ABL (Philadelphia chromosome, worst prognosis)
- t(4;11) = infant ALL = MLL AF4
- t(1:19)
- Hypodiploidy
- iAMP21 amplification
What is MRD in pre-B ALL and how does this impact prognosis?
MRD = ‘minimal residual disease’
How do the blasts respond to steroids (Intrathecal MTX) at various time points in treatments designates risk?
Induction: day 8 and day 29
End of consolidation
Risk stratification
- Low risk: negative for blasts at end of induction and end of consolidation
- Intermediate: positive for blasts and end of induction but negative at end of consolidation
- Very high risk - positive for blasts at end of induction AND consolidation -> predictive of failure of tx -> often go straight to HSCT
Pre T ALL
Risk stratification
- *MRD* is the main prognosticating tool (at day 8, end induction (D29) and end consolidation)
* Age and WCC NOT important - Poor steroid response is higher risk
- Early relapse (<18mo) is higher risk
ALL
Backbone of tx (list stages)
- ‘Induction’ (of remission) - 29 days long
+/- post induction intensification (tempo and intensity) - ‘Consolidation’ (of remission) - intensive multi-agent chemo + CNS prophylaxis (high dose IT mtx)
- Intensification - 2-3 blocks of intensive multi agent chemo aimed at clearing submicroscopic or minimal residual disease
- Maintenance - 2 years as an O/P
ALL Induction
What is the purpose
What is the regime
Aim
- Induce complete remission (no blasts with functional marrow)
- MRD at day 29 compared with day 8 checks this.
Either 3 or 4 drug regimen:
3 drug: Vincristine, steroid and asparaginase
- More is better with dosing but have to balance w toxicity
4 drug: Add anthracycline (doxorubicin, daunorubicin)
- Only used for B cell high risk disease and T-ALL
- Has higher risk of toxicity (cardio toxicity)
ALL CNS prophylaxis
What is the purpose
What is the regime
Without this, blasts will stay in CNS and induce CNS relapse
High dose methotrexate (intrathecal -> directly into CSF)
+/- radiation (but generally high dose MTX is adequate)
ALL Maintenance
Long-term oral-based treatment that contains the disease
- Oral 6MP
- Vincristine
- Steroid
‘Late effects’ of radiation tx
- Second tumour
- Endocrine dysfunction from cranial radiation and damage to HPA
- lung fibrosis
- Renal failure
- Bowel fibrosis
- Msk: osteonecrosis, fractures, spinal growth abnormalities, muscular hypoplasia
- Cardiomyopathy
Imatinib (Gleevac)
what is its use
MOA
Targeted therapy for use in philadelphia ALL (BCR ABL )
Works by blocking a protein called tyrosine kinase, which tells the leukaemia cells to grow and multiply. Without this signal, the cells die.
ALL: What to do when chemo does not work and there is no target for targeted tx?
Bone marrow (stem cell) transplant - use the immune system of a healthy donor to get rid of the leukaemic cells - Disease burden should be as low as possible before starting
Bispecific antibodies
- Recognise CD 19 and CD 3 on blasts -> engages T cells to fight the disease
Car T cells
- engineered to specifically recognise blasts
- can induce remission even in patients w neg MRD and high disease burden
Presenting sx/features of AML
*What features are different to ALL?*
*‘lumpy’ or ‘bleeding’* differentiates from ALL
>30% blasts on film (also ft Auer rods)
Bone marrow failure
- *DIC*
- Anaemia: pallor
- Thrombocytopaeani: purpura, bleeding
- Neutropaenia: recurrent fever or infections resistant to tx
Blastic infiltration
- *Prominent EXTRAMEDULLARY DISEASE (not a feature of ALL)
- > mass of leukaemia cells retro-orbital, skin or epidural location
- > gingival hypertrophy*
- Hepatosplenomegaly
- Bone pain
- CNS symptoms

What leukaemia is coagulopathy a complication of?
what is the typical IX findings for this?
APML (Acute promyelocytic leukaemia) which is a subclass of AML - t(15;17)
Results in DIC/fibrinolysis -> high risk of death from bleeding before 14 days
ix: Fibrinogen (low)
- D-dimer (elevated)
- Platelets (low)
- PT/APTT (high/prolongued)
Plt monitoring is critical, especially in first 15 days
- Plts need to be 30-50
- Fibrinogen > 1 (replace w FFP)
AML Risk assessment
Cytogenetics/molecular is critical risk factor
MRD early response
Down syndrome is favourable
Age and WCC are weak associations
AML treatment
- Chemotherapy, but risk of relapse associated
- -> induction, consolidation, further consolidation (no intensification or maintenance phases)
- Bone marrow transplant, if relapse of AMT
- > high risk of mortality (TRM) and late effects associated
Cytogenetic risk groups for AML (HR vs LR)
Low risk
- t(8;21)
- t(15;17) = APML
- inversion of chromosome 16 = inv(16)
Poor/high risk
- PR -7, -5 (monosomy 7 or 5)
- 5q- (deletion of long arm of chromosome 5)
- MRD >15%
Intermediate risk
- all others
Is T or B cell ALL higher risk?
T cell
What is the pathophys of renal impairment in TLS?
From precipitation of uric acid and phosphate in form of CaPh in the kidneys, causing tubular obstruction
What is spinal cord compression typically a complication of?
What are its classic presenting features?
Ix?
Mx?
*oncological emergency* caused by epidural mass compressing SC
Caused by:
Solid tumours
- Sarcomas
- Neuroblastoma
Hodgkin lymphoma
Mets
Sx
- back pain (incr on vertebral percussion)
- scoliosis, tenderness
- incontinence/urinary retention
- Change in sensation
- acute paraplegia
Ix - urgent imaging
Mx
- Dexamethasone
- Chemo
Lymphoma
- what is it?
- How are they different from leukaemias?
- types
Solid tumours of lymphoid origin - lymph nodes or extranodal lymphoid tissues (thymus, tonsils, spleen, GIT, liver or skin)
- Unlike leukaemias they do NOT originate from bone marrow and are not characterised first by their presence in the blood
- 2 types:
1. Hodgkin’s (40%)
2. Non-Hodgin’s lymphoma (60%)











