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FRACP > Oncology > Flashcards

Oncology Flashcards

1
Q 
Leukaemia
When does ALL normally present 
How does it present 
Are there any signs 
What should be looked at on bone marrow aspirate 
(4 things) 
What indicates high risk
A

Preschool- peaks 4 yrs
Quick 2-3 weeks pallor, fatigue, weight loss, low grade fevers, irritable
Enlarged testis, chloromas

Morphology- myeloid or lymphoid
Immunoflorescence-CD markers
Cytogenetics- translocations
Enzyme studies

Under 1 or over 10, Philadelphia chromosome, more mature phenotypes, high leukocyte count (>50)

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2
Q

What translocation gives rise to the Philadelphia chromosome?
Which other translocation gives poor prognosis in ALL

A

9: 22
11: 23

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3
Q

What syndromes are associated with leukaemias

A

Downs
Wiscott Aldrich
Ataxia teliengeictasia
Fanconi anaemia

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4
Q

How long is the standard treatment of ALL?
Outline the phases
What is MRD?

A

2 yrs girls, 3 boys

Induction- weekly vincristine and IT Methotrexate, daily steroids, once PEG

Consolodstion- clearing cns disease

Intensification

Maintenance- daily mcp and daily mtx

Minimal residual disease- do a bone marrow after 28 days treatment to see if <5% blasts after induction

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5
Q

What translocation gives good prognosis in ALL

Which trisomy “?

A

12:21

Trisomy 4 and 10

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6
Q

What are the features of tumour lysis syndrome

What are risks for it

A

Hyperuricaemia phosphataemia and kalaemia
Hypo ca and mg

Leukaemia and lymphomas

Hyper hydrate
Allopurinol

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7
Q

What is the association of Down’s syndrome and leukaemias (3 things)

A

Increased risk 20 times normal
Do better in AML
Can get myelodysplastic syndrome from infancy so high risk of aml in the future

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8
Q

How does AML differ from ALL?

How does treatment differ?

A

Sicker, older, more likely to have signs (gum hypertrophy and blueberry muffin lesions)
Need to look for a bone marrow donor sooner

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9
Q

What translocations show good prognosis in AML

Which monosomy is bad

A

8:21, 15:17

7

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10
Q

Which subtype of AML has a specific treatment?

What is that treatment?

A

Juvenile APML

Retinoic acid

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11
Q

What is juvenile myelomonocytic leukaemia
What is it associated with?
What is the prognosis
Is it associated with Philadelphia chromosome?

A

Juvenile cml
Noonans syndrome and nf1
Poor if not noonans
No!

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12
Q

Lymphoma

Hodgkin and non Hodgkin- what are the features regarding:

  • number of nodes
  • how they spread
  • Extra nodal disease

Which subtype is more likely to involve mesenteric nodes

A

Hodgkin- single node, spread orderly, rare
NHL- multiple nodes, more sporadic spread, lots of extra nodal disease

NHL

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13
Q

Hodgkin lymphoma

How does it present?
What type of cells are seen on biopsy? Are they pathogonomic?
What staging system is used? What does it look for?
What gives a poor prognosis?
What is the most common histiological subtype ?

A

Slow onset, painless rubbery lymphadenopathy, B cell symptoms

Reed sternberg cells. No!

Ann arbour- LN involvement above or below diaphragm

B cell symptoms, Hugh tumour bulk, High stage
Nodular sclerosing

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14
Q

NHL

What is the most common subtype in children?
How do they present?
What abdominal pathology might make you think of it in an older child?
What is the classification staging?
What blood test monitors tumour burden?

A 
Burkitts 
Faster, lymphadenopathy SVC obstruction 
Intussussecption 
St Jude 
LDH
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15
Q

Brain tumours

What is the tentorium?
What are the most likely tumours 
-<1 
-1-10 yrs 
-over 10
A

Dura mater that separates the hemispheres and cerebellum

Supratentorial
Infratentorial
Supratentorial

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16
Q

Brain tumours

What are signs of supra and infratentorial tumours?

What is diencephalic syndrome?

What might Torticollis suggest?

What is parinaud syndrome?

A

Signs of raised ICP- headache seizures weakness behaviour changes
Signs of brainstem- vomiting, incoordination, visual change, gait change, papilloedema

Tumours in thalamus or hypothalamus- increased appetite and irritable, cahexia and emaciated

Cerebellum herniating

Pineal tumour- paralysis of upward gaze

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17
Q

Brain tumours
What is the most common histiological subtype?
What syndrome can it be associated with?
What is the prognosis?
Where is it found and what does it look like

A

Pilocytic astrocytoma (low grade glioma)
NF 1
Good- 80-90%
Cerebellar- cystic appearing

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18
Q

Brain tumours
What is an ependynoma

What is a medulloblastoma
Where are they normally found?
When does they present 
What is seen on imaging and histology 
What are good signalling pathways
A

Tumour from the lining of the ventricles

Primitive Neuroendocrine tumour 
Cerebellum 
Primary school age 
Non calcified, contrast enhancing mass
Homer Wright rosettes 
WNT sonic hedgehog
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19
Q

ATRT
What are they
How do they present
What is the prognosis
What is the youngest age you can have radiotherapy?
What genetic malformation are they associated with?

A 
Germ cell tumours 
Rapid onset usually <2 years 
Poor
3 years 
IN11- complete peerage partial deletion of ch 22
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20
Q

Neuroblastoma
What is it?
What 2 syndromes is it associated with
What gene shows bad prognosis

A

Tumour of the peripheral nervous system- neural crest cells
Beckwith wiedemann NF1
NNYC

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21
Q

Neuroblastoma
What subtype can have a very good prognosis
How do they present

A

M4 s
Spontaneously regresses
Widespread nodes, massive liver

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22
Q

Neuroblastoma

How do they typically present 
What is unique about the mass (2 things)
Where is the mass normally found 
What signs might be present 
How may a paraneoplastic syndrome present?
A

Large abdominal mass, weight loss, night sweats and fevers
Crosses the midline, hard craggy
Adrenal
Raccoon eyes and Horner syndrome, urinary or bowel obstruction
Opsomyoclonus, ataxia, diarrhoea and hypertension

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23
Q 
Neuroblastoma 
What is the best screening test 
What bloods monitor prognosis 
What is seen on ct 
What specialised imaging technique is used. What is needed to be given too
A

Vmas&HVAs
Ferritin and ldh
Calcification of the mass
MIBG scanning. Idodine

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24
Q

Neuroblastoma

What immune therapy is given

A

Anti GD 2 (glycoprotein)

25
Q

Neuroblastoma

Does it cause renal calyceal dilatation

A

No!

26
Q

Wilms
What genetic mutation will outline a bad prognosis
What is Denys Dash syndrome
What gene is associated with Denys drash

A

P53
Wilms plus abnormal male genitalia and nephropathy
WT1

27
Q 
Wilms 
How does it normally present 
Are they sick at diagnosis normally 
What is the best initial investigation. 
Where does it metastasise you 
Which renal tumours are more likely to met to the brain
A

Single smooth abdominal mass.
Hypertensive

No!

Abdominal ultrasound

Lungs and liver

Clear cell and rhabdoid

28
Q 
Retinoblastoma 
What gene is mostly involved?
which chromosome is it coded on?
What is the pattern of inheritance?
What is the difference between inherited and sporadic forms?
A 
RET 1
13
AD
Sporadic- usually unilateral
Hereditary- bilateral- one gene hit from birth, second sporadic mutation
29
Q

Retinoblastoma
How does it present in the developed world
How else can it present?
What type of tumour is it?

A

Squint
Leukocoria
Pain, unequal pupils, mass, fevers, visual loss
Small blue round cell

30
Q 
Rhabdomyosarcoma 
Where is the most common site?
What are three other common sites?
What type of tumour is it?
Which syndrome is it associated with?
How can it present
What two translocations are common
A 
Head and neck, trunk, limbs, GU tract 
Small round blue cell 
Li Frauneni syndrome 
Painful mass, longer than expected healing after an injury, bleeding or mass from vagina. Stridor and cough
1:13 2:13
31
Q 
Bone tumours 
When are they most likely to happen Ewing’s and osteo:
- location 
-X-ray findings 
- symptoms 
-genetics 
- Radiotherapy?
A

Adolescents
Ewing’s- diaphysis- pelvis chest wallBones and soft tissues. Lytic. Systemic upset. Ch 22 translocations. Yes of large or not fully ressected

Osteo- metaphysic, bone only- femur and tibia. Sunburst pattern. Pathological fractures or painful, slow to heal fractures. Retinoblastoma & li fraumeni. No

32
Q

Osteosarcoma
Where does it met to
What gives the biggest prognostic indicator?

A

Chest

Level of necrosis with pre op chemo

33
Q

Liver tumours
What is the most common type in children?
Which lobe do they commonly involve?
How do they present?
Which blood test will show it? How might that test also be useful?
Do they typically need chemo? Why?

A 
Hepatoblastomas 
R lobe
Large asymptomatic abdominal mass 
AFP. monitors response to chemo 
No >85% liver can be ressected with no complications
34
Q 
Germ cell tumours 
Are most gonadal or extra gonadal 
Where is the most common site
What is the most likely histiological type?
What will raised alpha FP show
What type of chemo is used
A 
Extra (gonadal in teens) 
Sacrococcygeal 
Teratomas 
If it’s malignant
Platinum based
35
Q

What are the three most common cancers to have secondary malignancies?

A

Hereditary retinoblastoma
Hodgkin lymphoma
Soft tissue sarcoma

36
Q

What are 5 small blue round cell to tumours?

A 
Ewing’s 
Rhabdomyosarcoma 
PNET 
Neuroblastoma
NHL
37
Q

What are the 5 points of the cell cycle?

Where does the p53 gene work

A

G0 G1 S G2 M

G1

38
Q

Which drugs work in M phase
Where in the cell cycle does asparginase work?
What works in the S phase
What acts in the G phase

A

Vincristine and vinblastane
G1
Methotrexate and 6MCP. Ara C
Bleomycin and etoposide

39
Q

Chemo side effects

Methotrexate

A

Bone marrow suppression

Nephro/hepato toxic

40
Q

Chemo side effects

Cytarabine

A

Cns side effects and fevers

41
Q

Chemo side effects

Vincristine

A

Peripheral neuropathy
Constipation
Fatal if given IT

42
Q

Chemo side effects

Asparginase

A

Anaphylaxis

43
Q

Chemo side effects
Cyclo/ifosfamide
What might help prevent it?

A

Renal tubulopathy ifos also encephalopathy

MENSA

44
Q

Chemo side effects

Carboplatin/ cisplatin

A

Hearing and neuro

Renal impairment

45
Q

Chemo side effects

Bleomycin

A

Pulmonary fibrosis

46
Q

What is a common side effect of etoposide

A

Allergy

47
Q

Chemo side effects

Cisplatin

A

Vomiting ++

48
Q

What stain on blood film may help identify blasts

A

MPO- myeloperoxidase

49
Q

Which chemo has high risk for secondary malignancies

What is the cancer type

A

Etoposide

AML

50
Q

How is Philadelphia chromosome positive leukaemia treated

A

Imatinib or dasatinib- tyrosine kinase inhibitors

51
Q

When will screening for beckwith wiedemann abdo tumours stop?
When is the highest risk period?

A

1st decade

1st year of life

52
Q

Phenotypically what is seen in Bloom syndrome

What tumours are likely

A

Short, photosensitive rash and T2dm

Leukaemia and lymphoma

53
Q

What tumours do inactivated p16 and 19 cause

A

T cell and pre B ALL

54
Q

How does rasburicase work

A

Enzyme oxidation to HPO and allantoin

55
Q

How does carT therapy work
What is the main side effect
What is it used for currently

A

Engineered T cells to kill cd19 cells
Cytokine storm
Relapsed ALL or primary refractory ALL

56
Q

Febrile neutropenia
How low do the neuts have to be
What is given for fungal cover
What is given for AML

A

<0.5
Ambisome
Taz and vanc

57
Q

Which 2 chemos cause mucositis

What is used to treat it

A

Doxyrubicin and methotrexate

Fluids and leukovorin rescue

58
Q

In tumour lysis syndrome, what precipitates in the tubules

“ if urine is alkaline

A

Uric acid

Calcium phosphate

59
Q

What is the most common cause of secondary HLH

A

Ebv

FRACP (23 decks)

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