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Oncology Flashcards

1
Q

what is cancer?

A

group of abnormal cells that can divide in wring way

  • gene changes
  • stimulates own blood supply
  • local invasion
  • metastatic spread via blood or lymphatic system
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2
Q

how do we classify childhood cancer?

A
  • International Classification of - Childhood Cancer (ICCC)

Based on tumour morphology and (primary site)

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3
Q

most common childhood cancer?

2nd?

A

acute lymphoblastic leukaemia

  • CNS
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4
Q

age more likely to get caner?

A

0-4 years

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5
Q

most common cause of childhood cancer? give some examples?

A

genetic predisposition

  • Down - leukaemia
  • Fanconi
  • BWS -neuroblastoma or nephrpblastoma - US scan every 3 months
  • Li-Fraumeni Familial Cancer Syndrome - p53 mutation - family history of cancer
  • Neurofibromatosis - chromosome 17 mutation - soft tissue sarcomas, increased risk of brain tumours
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6
Q

child with petechiae or hepatosplenomegaly, new mass or neurological symtoms they should be?

A

Immediate referral

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7
Q

new mass or neurological symptoms a child should be?

repeat attendance, same problem, no clear diagnosis

A

urgent referral to paediatrician

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8
Q

when do you refer to a doctor for urgent investigation

A

rest pain, back pain and unexplained lump

lymphadenopathy - grater than >1cm diameter, growing and firm, not associated symptoms

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9
Q

under 5 years old - head start tumour symptoms

A 
- persistent vomiting
abnormal balace/ coordination tion, walking
- abnormal eye movement 
- fits and seizures
- abnormal head position
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10
Q

5-11 year old synths include

A

vision change and behaviour change

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11
Q

teenager head start symptoms

A

delayed or altered puberty

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12
Q

Oncological Emergencies?

A
  • Sepsis / febrile neutropenia
  • Raised ICP
  • Spinal cord compression
  • Mediastinal mass
  • Tumour lysis syndrome
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13
Q

risks of sepsis?

A
  • ANC < 0.5 x 109
  • Indwelling catheter
  • Mucosal inflammation
  • High dose chemo / SCT

(risk if had a catheter/ leukaemia)

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14
Q

organisms causing sepsis? 6)

A 
Pseudomonas aeruginosa
Enterobacteriaciae eg E coli, Klebsiella
Streptococcus pneumoniae
Enterococci
Staphylococcus 
Fungi eg. Candida, Aspergillus
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15
Q

presenting symptoms?

A
  • Fever (or low temp)
  • Rigors
  • Drowsiness
  • Shock
    Tachycardia, tachypnoea, hypotension, prolonged capillary refill time, reduced UO, metabolic acidosis
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16
Q

Management of sepsis

A

IV access
- Blood culture, FBC, coag, UE, LFTs, CRP, lactate
CXR

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17
Q

Management of sepsis - other investigations

A 
Urine microscopy / culture
Throat swab
Sputum culture / BAL
LP - meningitis
Viral PCRs - herpes
CT / USS - abscesses
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18
Q

management of shock in sepsis

A

ABC
Oxygen
Fluids
Broad spectrum antibiotics

Inotropes
PICU

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19
Q

presentation of raised ICP - early

A

early morning - headache/vomiting

  • tense fontanelle
  • increasing HC
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20
Q

presentation of raised ICP - later

A 
constant headache 
papilloedema 
diplopia (VI palsy) 
Loss of upgaze
neck stiffness
status epilepticus, 
reduced GCS 
Cushings triad (low HR, high BP, falling RR)
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21
Q

diplopia (VI palsy) - means you wouldn’t be able to ?

A

abduct the eye laterally

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22
Q

features of Cushing’s triad?

A

(low HR, high BP, falling RR)

23
Q

investigations for Raised ICP

- best imaging for diagnosis?

A

Imaging is mandatory (if safe)
CT is good for screening
MRI is best for more accurate diagnosis

24
Q

Management of raised ICP? - IMMEDIATE?
why?
how much?

A

Dexamethasone

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

25
Q

intervention for raised ICP

A

urgent CSF diversion

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

26
Q

Spinal Cord Compression - most commonly affects?

happens most commonly at?

A
  • 10-20 % Ewing’s or Medulloblastoma
  • 5-10 % Neuroblastoma & Germ cell tumour

diagnosis

27
Q

pathological processes of spinal cord compression - most common (4) types

A
  • Invasion from paravertebral disease via intervertebral foramina (40 % extradural)
  • Vertebral body compression (30 %)
  • CSF seeding (20 % intradural, extraspinal)
  • Direct invasion (10 % intraspinal)
28
Q

Presentation of spinal cord compression (4)

A
  • weakness (90 %)
  • pain (55-95 %)
  • sensory (10-55%)
  • sphincter disturbance (10-35%)
29
Q

Management of spinal cord compression?
first line?

definitive treatment?

A

MRI
- dexamethasone - reduce peri-tumour oedema

  • emergency chemotherapy or surgery/radiotherapy
30
Q

SVC (sup vena cava) syndrome or SMS - common causes?

A
  • Lymphoma!!! - Burkett’s

Other – neuroblastoma, germ cell tumour, thrombosis

31
Q

SVC (sup vena cava) syndrome blocks?

A

blocks flow of blood and airways from head and neck to the thorax

32
Q

presentation of SVC (sup vena cava) syndrome ?

A

facial, neck and upper thoracic plethora, oedema, cyanosis, distended veins, ill, anxious, reduced GCS

33
Q

presentation of SMS syndrome (5)

A

dyspnoea, tachypnoea, cough, wheeze, stridor, orthopnoea

34
Q

Investigations of SVC syndrome or SMS?

A
  • CXR / CT chest (if able to tolerate)

- Echo

35
Q

SVC syndrome or SMS - management

A

Keep upright & calm

  • urgent biopsy, drain pleural fluid
36
Q

SVC syndrome or SMS - management - how to get diagnostic information without a general anaesthetic

A

FBC, BM, pleural aspirate, GCT markers (alpha-fetoprotein + beta HCG)

37
Q

Definitive treatment is required urgently for SVC syndrome or SMS syndromes - what does this include?

A
  • chemo
  • steroids
  • radiotherapy
38
Q

CVAD-associated thrombosis should be treated by thrombolytic therapy such as?

39
Q

what is tumour lysis syndrome??

A

rapidly growing tumour dies
- releases intracellular contents to bloodstream

  • rise in potassium and rate acid levels,
40
Q

tumour lysis syndrome CLINICAL features - increase and decrease in what ?

A
  • rise in POTASSIUM , URATE, PHOSPHATE

- decrease in - PHOSPHATE

41
Q

what does tumour lysis syndrome cause?

A

acute renal failure

  • urate load
  • CaPO4 deposition in renal tubules
42
Q

Treatment of tumour lysis syndrome ?

A
  • avoidance , fluids
  • ECG Monitoring
  • Hyperhydrate-2.5l/m2
  • QDS electrolytes
  • Diuresis - furosemide
  • Never give potassium or phosphate
43
Q

what medications can reduce uric acid production in tumour lysis syndrome ?
- minor/ more advanced

A

Allopurinol

rasburicase

44
Q

How to treat hyperkalaemia

in tumour lysis syndrome ? (3)

A

Ca Resonium
Salbutamol
Insulin dextrose infusions

may need renal replacement therapy (dialysis)

45
Q

what do oncologists need to find out?

A

Scans (3D, MRI)
Biopsy / pathology - cell of origin
Cytogenetics- analysis
Tumour markers - blood levels - alpha feet protein - liver tumour

46
Q

amplification of what gene may show neuroblastoma?

47
Q

where do sarcomas often spread to?

48
Q

what is treatment of cancer dependent on?

A
  • Multimodal therapy based on specific disease and extent (plus patient factors)
  • MDT approach
  • National / international collaboration
  • Clinical research
49
Q

Treatment options can include what categories?

A 
Surgery - localised 
Chemotherapy - drug therapy 
Radiotherapy -
Immunotherapy
Bone marrow transplant
New targeted agents
50
Q

what are the acute risks of chemotherapy?

A

Hair loss
Nausea & vomiting
Mucositis - inflammation mouth and GI tract
Diarrhoea / constipation
Bone marrow suppression – anaemia, bleeding, infection

51
Q

what are the chronic risks of chemotherapy?

A

Organ impairment – kidneys, heart, nerves, ears
Reduced fertility
Second cancer

52
Q

what are the acute risks of radiotherapy

A

Lethargy
Skin irritation
Swelling
Organ inflammation – bowel, lungs

53
Q

what are the chronic risks of radiotherapy

A

Fibrosis / scarring
Second cancer
Reduced fertility

54
Q

late effects of childhood cancer?

A
  • growth
  • sexual development
  • organ
  • recurrent cancer
  • psychosocial effects

Paediatrics (49 decks)

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