Oncology Flashcards

1
Q

What is cancer?

A
  • Abnormal cells dividing in an uncontrolled way
  • Gene changes
  • Stimulates own blood supply
  • Local invasion
  • Metastatic spread via blood or lymphatic systems
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2
Q

What is the epidemiology of childhood cancer?

A
  • Rare in <15
  • Scotland 130 per year
  • 1 in 500 <14 year olds
  • <1% of all cancer cases
  • M>F (slightly)
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3
Q

What types of malignancies are seen in paediatrics?

A
  • 33% Leukaemias
  • 25% brain tumours
  • 40% are extracranial solid tumours
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4
Q

What is the 5 year survival for childhood cancer?

A

80%

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5
Q

What is the basis of most childhood cancers?

A

Sporadic (some genetic basis)

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6
Q

How are childhood cancers classified?

A
  • International Classification of Childhood Cancer (ICCC)
  • Based on tumour morphology and (primary site)
  • Standard classification is essential for comparing incidence and survival across regions and over time periods
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7
Q

What are the most common types of cancer in children?

A
  • Leukaemia
  • CNS tumours
  • Lymphoma
  • Soft tissue tumours
  • Neuroblastoma
  • Renal tumours
  • Malignant bone tumours
  • Retinoblastoma
  • Germ cell tumours
  • Hepatic tumours
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8
Q

When are the peaks of childhood cancer?

A
  • Aged 0-4

- Adolescence

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9
Q

What are the causes of cancer in children?

A

Genetic: Down, Fanconi, BWS, Li-Fraumeni familial cancer syndrome
-Neurofibromatosis

Environment: radiation and infection

Iatrogenic: chemotherapy and radiotherapy induced

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10
Q

What are the steps in the diagnostic journey of childhood cancer?

A
  • Biological onset of disease
  • Symptom onset
  • Seek medical attention
  • Doctor recognises cancer as a possibility
  • Investigation, diagnosis and treatment
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11
Q

When should a child be immediately referred to oncology?

A
  • Unexplained petechiae

- Hepatosplenomegaly

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12
Q

When should a child have an urgent referral to oncology

A
  • Repeat attendance with the same problem and no clear diagnosis
  • New neuro symptoms or abdominal mass
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13
Q

When should a child be referred to oncology by phone call?

A
  • Rest pain, back pain and unexplained lump

- Lymphadenopathy

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14
Q

What are the 5 most common signs of cancer in young people?

A
  • Pain
  • A lump, bump or swelling
  • Extreme tiredness
  • Significant weight loss
  • Changes in a mole
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15
Q

What do oncologists need to find out?

A

What it is

  • Scans (MRI+US)
  • Biopsy and pathology
  • Tumour markers

Where it is
-Staging and scans, bone marrow

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16
Q

How is cancer treated in children?

A
  • Multimodal therapy based on specific disease and extent (plus patient factors)
  • MDT approach
  • Chemotherapy
  • Surgery
  • Radiotherapy
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17
Q

What are the acute risks of chemotherapy?

A
  • Hair loss
  • Nausea & vomiting
  • Mucositis
  • Diarrhoea / constipation
  • Bone marrow suppression – anaemia, bleeding, infection
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18
Q

What are the chronic risks of chemotherapy?

A
  • Organ impairment – kidneys, heart, nerves, ears
  • Reduced fertility
  • Second cancer
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19
Q

What are the acute risks of radiotherapy?

A
  • Lethargy
  • Skin irritation
  • Swelling
  • Organ inflammation – bowel, lungs
20
Q

What are the chronic risks of radiotherapy?

A
  • Fibrosis/scarring
  • Second cancer
  • Reduced fertility
21
Q

What oncological emergencies are there?

A
  • Sepsis / febrile neutropenia
  • Raised ICP
  • Spinal cord compression
  • Mediastinal mass (SVCS/SMS)
  • Tumour lysis syndrome
22
Q

What is a major cause of mortality/morbidity in childhood cancer?

A

Infection

23
Q

What are the risk factors for sepsis/ febrile neutropenia?

A
  • ANC < 0.5 x 10^9
  • Indwelling catheter
  • Mucosal inflammation
  • High dose chemo / SCT
24
Q

What organisms can be implicated in sepsis/febrile neutropenia?

A
  • Pseudomonas aeruginosa
  • Enterobacteriaciae eg E coli, Klebsiella
  • Streptococcus pneumoniae
  • Enterococci
  • Staphylococcus
  • Fungi eg. Candida, Aspergillus
25
Q

How does sepsis/febrile neutropenia present?

A
  • Fever (or low temperature)
  • Rigors
  • Drowsiness
  • Shock (tachycardia, tachypnoea, prolonged cap refill, reduced UO, metabolic acidosis)
26
Q

How is sepsis/febrile neutropenia investigated?

A
  • Blood culture, FBC, coag, UE, LFTs, CRP, lactact
  • CXR
  • Urine microscopy / culture
  • Throat swab
  • Sputum culture / BAL
  • LP
  • Viral PCRs
  • CT / USS
27
Q

How is sepsis/febrile neutropenia managed?

A
  • ABC approach
  • IV access
  • Oxygen
  • Fluids
  • Broad spectrum antibiotics
  • Inotropes
  • PICU
28
Q

What is the early presentation of raised ICP?

A
  • Early morning headache/vomiting
  • Tense fontanelle
  • Increasing HC
29
Q

What is the late presentation of raised ICP?

A
  • Constant headache
  • Papilloedema
  • Diplopia (VI palsy)
  • Loss of upgaze
  • Neck stiffness
  • Status epilepticus,
  • Reduced GCS
  • Cushings triad (low HR, high BP)
30
Q

How is raised ICP investigated?

A

Imaging mandatory (if safe)

  • CT good for screening
  • MRI best for more accurate diagnosis
31
Q

How is raised ICP managed?

A

Dexamethasone if due to tumour

  • Reduce oedema and increase CSF flow
  • 250 micro/kg IV STAT then 125 microg/kg BD

Neurosurgery - urgent CSF diversion

  • Ventriculostomy – hole in membrane at base of 3rd ventricle with endoscope
  • EVD (temporary)
  • VP shunt
32
Q

What cancers is spinal cord compression associated with?

A

Can complicate any paediatric malignancy

  • Affects 5 % of all children with cancer
  • 10-20 % Ewing’s or Medulloblastoma
  • 5-10 % Neuroblastoma & Germ cell tumour
33
Q

What is the pathological process of spinal cord compression?

A
  • Invasion from paravertebral disease via intervertebral foramina (40 % extradural)
  • Vertebral body compression (30 %)
  • CSF seeding (20 % intradural, extraspinal)
  • Direct invasion (10 % intraspinal)
34
Q

How can spinal cord compression present?

A

Symptoms vary with level

  • Weakness (90 %)
  • Pain (55-95 %)
  • Sensory (10-55%)
  • Sphincter disturbance (10-35%)
35
Q

How is spinal cord compression managed?

A
  • Urgent MRI
  • Start dexamethasone urgently to reduce peri-tumour oedema
  • Definitive treatment with chemotherapy is appropriate when rapid response is expected (Surgery or radiotherapy are other options)
36
Q

What does outcome of spinal cord compression depend on?

A

Outcome depends on severity of impairment rather than duration between symptoms and diagnosis

  • Mild impairment > 90 % recovery
  • Paraplegic 65 % recovery
37
Q

What paediatric malignancies is SVC/SMS syndrome associated with?

A
  • Rare <1 % of new paediatric malignancies

- Common causes include Lymphoma and other: neuroblastoma, germ cell tumour, thrombosis

38
Q

How does SVC syndrome present?

A
  • Facial, neck and upper thoracic plethora
  • Oedema
  • Cyanosis
  • Distended veins
  • Unwell
  • Anxious
  • Reduced GCS
39
Q

How does SMS present?

A
  • Dyspnoea
  • Tachypnoea
  • Cough
  • Wheeze
  • Stridor
  • Orthopnoea
40
Q

How should SVCS/SMS be investigated?

A
  • CXR
  • CT chest
  • Echo
41
Q

How should SVCS/SMS be managed?

A

-Keep upright & calm
-Urgent biopsy (ideally)
-Look to obtain important diagnostic information without GA
FBC, BM, pleural aspirate, GCT markers
-Definitive treatment is required urgently
-Chemotherapy is usually rapidly effective
-Presumptive treatment may be needed in the absence of a definitive histological diagnosis (steroids)
-Radiotherapy is effective
-May cause initial increased respiratory distress (surgery if insensitive)

42
Q

What is the pathogenesis of tumour lysis syndrome?

A
  • Metabolic derangement
  • Rapid death of Tumour Cells
  • Release of intracellular contents
  • At or shortly after presentation
  • Secondary to treatment
43
Q

What are the clinical features of tumour lysis syndrome?

A
  • Increased potassium
  • Increase urate, relatively insoluble
  • Increase phosphate
  • Decreased calcium
  • AKI (urate load and CaPO4 deposition in renal tubules)
44
Q

What is the treatment for tumour lysis syndrome?

A
  • Avoidance
  • ECG Monitoring
  • Hyperhydrate-2.5l/m2 -QDS electrolytes
  • Diuresis
  • Decrease uric acid
  • Treat hyperkalaemia
  • Renal replacement therapy
45
Q

How can uric acid be decreased in tumour lysis syndrome?

A
  • Urate oxidase uricozyme (rasburicase)

- Allopurinol

46
Q

How is hyperkaelamia treated in tumour lysis syndrome?

A
  • Ca resonium
  • Salbutamol
  • Insulin
47
Q

What should never be given in tumour lysis syndrome?

A

POTASSIUM