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Skin Radiation therapy > pediatrics > Flashcards

pediatrics Flashcards

1
Q

most common paediatric cancer

A

ALL (acute lymphocytic leukaemia)

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2
Q

lymphoma is the ___most common paediatric cancer

A

3rd

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3
Q

age for lymphomas in children

A

common in 4-14 y.o.

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4
Q

what causes HD in kids

A

HD in kids is common in EBV in developing countries

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5
Q

what HD is common in what age group

A

nodular sclerosing is most common in adults and adolescents less common in children
mixed cellularity is more common in children

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6
Q

most children with lymphoma present with what kind of LN

A

cervical lymphadenopathy

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7
Q

is mediastinal involvement more common in children or adolescents with lymphoma

A

mediastinal involvement affects 75% of adolescents and is less common 33% in children 1-10y,o,

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8
Q

prognostic factors for lymphoma in chilren

A

stage is most important to determine treatment
b symptoms have a higher risk of relapse
T4 has worse prognosis
WBC count above 11500 hemoglobin less than 11 g/dl
lymphocyte depleted has a worse prognosis than other subtypes
children <10 have better prognosis

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9
Q

howccommon are the presentation of b symptoms in paediatric lymphoma pts

A

1/3 of patients present with b symptoms
fever >38c
night sweats
weight loss >10% of its body weight in 6 months

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10
Q

primary treatment for paediatric lymphoma patients

A

chemo

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11
Q

most common paediatric brain tumours

A 
low grade gliomas
medulloblastomas
gliomas
ependymomas
craniopharyngiomas
pineal region tumurs
embryonal rumours
choroid plexus tumours
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12
Q

treatment for low grade gliomas for patients <10 and >10

A

<10 SX+CX then XRT RESERVED FOR PROGRESSION

>10 XRT up front

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13
Q

planning for paediatric low grade gliomas CTV

A

CTV expansion of 5 mm for localized tumours and dose of 54/30

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14
Q

high grade glioma treatment

A

start with surgery adjuvant XRT5940/33

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15
Q

2nd most common types of paediatric tumours

A

brain tumours

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16
Q

XRT alone in lymphoma of paeds

A

Radiation alone is almost never done

Possible exception is the fully grown child with localized nodular lymphocyte predominant HD

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17
Q

dose for XRT for paeds

A

low dose 15-25.5Gy

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18
Q

is hodgkins or non hodgkins more common in paeds

A

Non hodgkins is more common

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19
Q

most common nodal areas involved in NHD

A

Abdomen is most common followed by mediastinum

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20
Q

use of XRT in paediatric brain tumours

A

reserved for unresectable or recurrent lesions 50-54Gy

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21
Q

CTV,PTV for low grade astrocytomas pediatric

A

CTV-1.5cm around GTV

PTV-.5cm around CTV

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22
Q

Treatment optic glioma

A

chemo for younger patients, 50-54Gy with IMRT, proton or 3DCRT

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23
Q

What can cause optic glioma in children

A

neurofibromatosis

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24
Q

where does ependymoma arise from

A

from the ependyma cells that line the ventricles

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25
Q

presenting symptoms of ependymoma paper like what other CNS tumour?

A

medulloblastoma

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26
Q

treatment of ependymoma in children

A

treated by a gross total resection XRT after surgery is generally given if CSF seeding is noted then CSI XRT is given 1cm CTV is treated to 5400-5940 cGy chemo is given neo or adjuvantly if the tumour is unresectable

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27
Q

medullablastoma is a _____fossa malignancy

A

posterior

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28
Q

medulloblastoma constitutes ___% of all childhood brain tumours

A

20

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29
Q

medulloblastoma arises from what type of cells

A

cerebellar stem cells

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30
Q

histologic appearance of medulloblastoma

A

small round blue cells

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31
Q

invasion of medulloblastoma

A

arises midline of cerebellum, invades 4th ventricles and brainstem and high propensity to invade CSF

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32
Q

Distant mets in medulloblastoma

A

can occur most likely to the bone

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33
Q

treatment for medulloblastoma

A

posterior occipital craniotomy is used followed by adjuvant XRT CSI 2340-5400 followed by chemotherapy

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34
Q

where do germ cell tumours arise from

A

develop from embryologic nests of tissue in midline brain usually in the suprasellar or pineal region

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35
Q

germinoma is radio ——–.

A

sensitive

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36
Q

what is the most common type of paediatric germ cell tumours

A

germinoma

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37
Q

treatment germ cell tumour

A

low dose csi followed by tumour boost to 50 Gyor cisplatinum based chemo followed by XRT boost
non germinomas are treated with all 3: cispltinum chemo, art and XRT boost

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38
Q

presentation of brainstem glioma

A

present with cranial nerve deficits that develop over weeks to months that affect vision, facial function and swallowing

39
Q

surgery for brainstem glioma

A

usually inresectable as brainstem gliomas usually involve the pons

40
Q

treatment of brainstem glioma

A

XRT is mainstay of treatment as brainstem gliomas are often unresectable there should be a 1-2cm margin dose is 54Gy

41
Q

where is the retinoblastoma gene located in children?

A

chromosome 13 a tumour supressor gene

42
Q

how is Rb diagnosed

A

discovered as a result of an abnormal light reflex, reflects white rather than red) can be discovered during a dr examination or from the flash of a camera

43
Q

retinoblastoma staging

A 
st dudes hospital staging 
intraocular disease
1a. retinal tumour single or multiple
1b.extension to lamina criborsa
Optical disease
2a.optical tumour
2b.optic nerve invasion 
intracranial mets
3a.+CSF fluid
3b.CNS mass lesion
44
Q

treatment of retinoblastoma

A

small focal tumours of the optic disc and the macula is treated with cryosurgery, photocoagulation, laser hyperthermia, local treatments are more commonly done with CX,
EBRT is used for inoperable unilateral disease or bilateral disease dose is 40-50Gy

45
Q

side effects of XRT in Rb

A

altered growth of the bony orbit, - vision, cataract formation, dry eye, and high risk of secondary cancer

46
Q

neuroblastoma is derived from what cells

A

cells of the neural crest

47
Q

what is different about neuroblastoma

A

it can spontaneously regress

48
Q

what oncogene is associated with neuroblastoma

A

n-myc

49
Q

where does neuroblastoma commonly occur in children

A

in the adrenal glands

50
Q

S&S neuroblastoma

A

include flushing and diahrrea abode mass, bowel disturbance,

51
Q

how common is mets in neuroblastoma in children

A

60% at presentation

52
Q

s&s of metastatic neuroblastoma cancer

A

fatigue, anemia, bleeding from bone marrow invasion, fever weight loss, bony mets, blue skin lesions, abode distension from liver involvement

53
Q

most important prognostic indicator in neuroblastoma

A

tumour stage is most important

54
Q

4s neuroblastoma category

A

occurs in infants less than 1 year many of these patients spontaneously regress

55
Q

staging system for neuroblastoma

A

stage1- confined to area of origin LN -, complete excision with or without microscopic disease
stage2a- unilateral tumour without complete excision ln-
Stage2b- unilateral tumour with or without completed excision,with +ipsilateral LN -contralateral LN
stahe3-tumour across midline with or without LN involvement , unilateral tumour with contralateral LN involvement or midline tumour with bilateral regional lN involvement
stage4-dissemination of tumour to distant LN, bone, bone marrow, liver or other organs
stage 4s- localized primary tumour as defined stage1,2 with dissemination to liver or skin

56
Q

what age group does neuroblastoma spontaneously regress in

A

in new borns

57
Q

treatment of neuroblastoma

A

localized disease without LN are cured by SX alone, for incomplete resections adjuvant XRT 500cGY (infants) 20Gy for children is added + multi agent cx (platinum, etopisode, cyclophosphamide, vincristine, doxorubicin

58
Q

side effects of art IN NEUROBLASTOMA

A

more common in children getting >20Gy than infants getting 500cGy, these side effects include: decreased or asymmetric growth of bone and soft tissues, lung fibrosis can occur if the lungs are in field, kidney and liver function can be impaired, `

59
Q

what type of cells does films tumour arise from

A

tumour of the kidney that arises from embryonal cells

60
Q

age for films tumours

A

median age is 3-4 y.o.

61
Q

what syndromes can cause films tumour

A

occurs more frequently in patients with WAGR syndrome (Wilms aniridia genitourinary malformations and mental retardation_) also common in patients with beck with Wireman syndrome and in patients with hemihypertrophy (one side of the body is larger than the other) and aniridia (absence o of the iris)

62
Q

Wilms tumours with unfavourable prognosis nd why?

A

anapaestic wilms tumours. clear cell sarcoma of the kidney Associated with bone mets, rhaboid tumour of the kidney –associated with spread to the CNS

63
Q

how do films tumours present

A

painless abdominal mass the enlarging mass can sometimes cause organs to rupture or bleed

64
Q

diagnostic methods for wilms tumour

A

CT scan of the chest and abdomen, the contralateral kidney should be examined as the contralateral kidney is involved in 4-8% of cases bone scant and brain cans can be done as rhaboid and clear ell tumours have a high tendency for mets

65
Q

Wilms staging system

A

national Wilms staging system
1. limited to the kidney but completely excised
2.beyond kidney but completely excised.
local tumour spillage or vessel invasion permitted but completely excised
3.residual nonhematogenous tumour confined to abdo
involved Ln, diffuse tumour spillage or grossly unresected tumour
IV. hematogenous mets usually liver blood bone or brain
V.bilateral kidney involvement at time of diagnosis

66
Q

treatment for Wilms

A

in europe neoadjuvant chemo or rads is given as there is a high propensity for wilms to have tumour spillage during surgery, surgery is performed ( nephrectomy)and then adjuvant XRT is given to the tumour bed, if there is tumour spillage then the whole abode is treated with XRT pdoses are 1080-2000cgy. XRT is not required for stage1,2 that are completely excised and received chemo 1080 is used for microscopic disease, LN mets, bilateral tumours, pulmonary mets( only get 1500) , gross residual disease is boosted to 20Gy

67
Q

XRT field size for wilms

A

for unilateral disease: width of 1 vertebral body +1cm contra laterally the growth plates of the long bones are shielded
sup- and inf = 1cm from the preoperative renal tumour

68
Q

chemo agents used for wilms

A

acitomycin-d + vincristine +doxorubicin for advanced stages

69
Q

side effects of treatment for wilms

A

for thoracic treatment of a prepubertal female breast development may be impaired, high doses of acitomycin-d can cause liver damage, because the child only has 1 kidney it is important that we are cautious if they get UTI which can lead to stones, infections or diseases from damaging the remaining kindye

70
Q

most common STS in kids

A

rhabdomyosarcoma

71
Q

what tis the tissue of origin in RMS

A

striated muscle

72
Q

age for STSD

A

MOST common in kids <10

73
Q

RMS is associated with translocations on what chromosome

A

13

74
Q

where is RMS most common

A

h&n 34%
abdo 25%
GU 23%
Extremities and trunk 17%

75
Q

where is embryonal subtype most commonly occur

A

orbit and GU

76
Q

STAGING OF rms

A 
intergroup RMS staging system 
tumour 
T1: confined to origin site
T2:extension to surrounding tissues
a.<5cm
b.>5cm 
histology
g1: favorable: embryonal, undifferentiated, mixed
G2:unfavourable alveoler
Nodes: N0: not clinically involved
N1: clinically involved by tumour
Mets
M0: no distant mets
M1:mets at time of diagnosis 
clinical system:
1:localized completely resected
2:grossly resected with microscopic residue or involved Ln
3:gross residual tumour
4:distant mets
77
Q

diagnosis of RMS

A

First an incisional biopsy is done to confirm histology ( alveolar, mixed, undifferentiated, embryonal )
physical exam, CT , US, MRI o BM biopsy and chest CT can determine mets

78
Q

what area of the body is mire prone and less prone to METS with RMS

A

not common with tumours of the orbit

more common with tumours of the extremities and trunk

79
Q

treatment of RMS

A

must determine f the patient is eligible for surgery, if so: removal of mass with margins is the first treatment, for tumours of the GU we want to preserve organ function therefore it is advisable to give cx +xrt rather than surgery for tumours that are unresectable or have +margins after sx cx+xrt is used with a 1cm margin around GTV

80
Q

dose RMS

A

36Gy in 180cGy fx are used for microscopic disease, 41.4gy for ln + disease and 50.4Gy for gross disease

81
Q

CHEMO AGENTS RMS

A

used adjuvantly after sx and is treated with vincristine, actinomycin D and cytoxan

82
Q

late effects RMS treatment

A

bone and soft tissue growth is affected in the XRT of the extremities, in the H&N dryness of the eyed or retinal damage can occur , fertility is affected after chemo for the pelvic region, secondary tumours can also occur most commonly (HD,ALL, STS)

83
Q

WHEN IS XRT used in ALL

A

When there is CNS or testicular involvement where there is less chemo penetration TBI is also used to prepare patient for BM transplant

84
Q

dose for petiatric all

A

1200-1800cGy

85
Q

typical treatment for ALL

A

Chemotherapy for 2 years is typical treatment

86
Q

treatment for langerhans cell histocytosis

A

abnormal proliferation of immune systems langerhans cells
focal bony lesions can be treated with surgical cutter age if fracture is a concern or if tumour is unresectable low dose XRT is given 400cgy-1200cGy steroids, vinblastine and cyclophosphamide can also be used

87
Q

HD treatment

A

chemo is initial treatment 15-25Gy is given following surgery

88
Q

XRT field for unilateral neck HD

A

Unilateral neck + ipsilateral supraclavicular; the SUP border should extend form the midpoint of the chin through the mid-tragus; this should provide a minimum of 2 cm margin at the tip of the mastoid; the INF border must be 1.5 cm below the clavicle; the lateral field border should be determined by the most lateral extent of disease on the CT study of the neck

89
Q

XRT field of the suoraclav and axilla for HD

A

Supraclavicular + mid/low neck + infraclavicular

Axilla +/- infraclavicular.supraclavicular

90
Q

XRT field the mediastinum / hill HD

A

Mediastinum + hila+ infraclavicular/supraclavicular; the SUP border should encompass the initial sup extent of disease + 2 cm; INF border should be placed 2 cm or at least one vert body below the lowest initial extent of disease; LAT borders will be treated based on the width of the disease and the mediastinum after chemo not the width of the original mass; 1.5 cm margin should be given on any residual mass and the normal mediastinal contour; lateral margins should cover the bilateral hila

91
Q

XRT FIELD of the paraAORTICS IF in HD

A

Paraaortics +/- spleen; SUP border placed at insertion of the diaphragm; INF border at the level of the aortic bifurcation; LAT border should cover the initial extent of disease with 1.5 cm margin

92
Q

XRT FIELDof the iliac HD

A

Iliacs + inguinal/femoral; if adequate superficial and deep coverage of these nodes can be obtained using only an anterior field with photons or an electron beam of appropriate, this is encouraged; SUP border 2-3 cm above and parallel to the inguinal fold; INF border should be parallel to the upper border; MED border should be the medial border of the obturator canal; LAT should be the lat border of the acetabuluM

93
Q

PROGNOSTIC INDICATORS OF NHD

A

Stage, serum lactate dehydrogenase and soluble interleukin-2-receptor levels

94
Q

role of XRT in NHD

A

Emergency treatment of mediastinal disease or spinal cord compression; treatment for pts who fail to obtain a complete remission after induction chemo; palliation of pain or mass effect; consolidation before bone marrow transplantation in patients with recurrent disease; over CNS lymphoma at diagnosis or relapse; leukemic transformation at diagnosis
30 Gy for small cell lymphocyte/blast to 45 Gy for large cell histiocytic
Palliation, total doses as low as 10 Gy

Skin Radiation therapy (40 decks)

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