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Tumor Ganas Mata: Alfa Sylvestris

Retinoblastoma is a rare eye cancer that affects young children, usually under 5 years old. It is caused by mutations in the retinoblastoma gene and presents as a white spot in the pupil or other eye abnormalities. Diagnosis is made through eye examination, imaging tests, and biopsy. Treatments include chemotherapy, radiation therapy, cryotherapy, and surgical removal of the eye. Early detection and treatment lead to survival rates over 90%.

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0% found this document useful (0 votes)
23 views53 pages

Tumor Ganas Mata: Alfa Sylvestris

Retinoblastoma is a rare eye cancer that affects young children, usually under 5 years old. It is caused by mutations in the retinoblastoma gene and presents as a white spot in the pupil or other eye abnormalities. Diagnosis is made through eye examination, imaging tests, and biopsy. Treatments include chemotherapy, radiation therapy, cryotherapy, and surgical removal of the eye. Early detection and treatment lead to survival rates over 90%.

Uploaded by

Azilu Fala
Copyright
© © All Rights Reserved
We take content rights seriously. If you suspect this is your content, claim it here.
Available Formats
Download as PPTX, PDF, TXT or read online on Scribd
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TUMOR GANAS MATA

Alfa Sylvestris
Jinak
A. Primer
Ganas
Jinak
TUMOR B.
Sekunder Ganas

C. Metastase

2
Retinoblastoma

Retinoblastoma is a disease that


causes the growth of malignant
tumors in the retinal cell layer of
the eye.
It is the most common eye tumor
in children (<5 yo)

3
The Prevalence of Retinoblastoma

Retinoblastoma is a childhood disease.


There is no known sex or racial
predilection.
Retinoblastoma affects 1 child for every
15,000 live births.
250-350 new cases are diagnosed each
year in the U.S., 90% of which occur
before the age of five.
Retinoblastoma can be either a hereditary
or non-hereditary disease
unilateral / bilateral

extraocular:

- through sclera
orbital cavity proptosis
-
through N.II intra
cranial
What Causes Retinoblastoma?

Retinoblastoma is caused by a
mutation on the 13th chromosome.
Possibly environmental factors
increase mutational events at the
retinoblastoma gene locus.
Symptoms of Retinoblastoma

Problems with eye A white spot on


movements the pupil of the
(crossed eyes). eye. cats eye
A persistent red Visual disturbance
irritation in the
eye.
Differences in pupil
size, iris color,
abnormal eye
movements,
bulging forward of
the eyes, tearing,
Sign :
- VA
- Leucocoria
- Strabismus
- Glaucoma
- Tumor mass in the vitreous with
calcification

8
Additional exam
- X Photo Ro
- USG B scan
- CT Scan
- PA durante op
- Lactic Dehidrogenase enzyme (LDH) in
humour aqeous paracintesa
(compared with level serum)
- Specific skin test for retinoblastoma
using crude
membrane extracts of retinoblastoma
cells
developed in tissue culture.
- Tapping paracintesa for tumour cells
in 9
HISTOPATHOLOGY

Flexner-Wintersteinerrosettes Homer-Wright rosette


HISTOPATHOLOGY

Fleurettes
Diagnosis

Untreated, Retinoblastoma is almost


always fatal.
Early examination is key to survival.
STAGING SYSTEMS REESE-ELLSWORTH
CLINICAL GROUPING

Stage I - Very Favorable Solitary tumor, less than 4


disk diameters (DD)* in size, at or beyond equator.
Multiple tumors, none over 4 DD in size, all at or
behind equator.
Stage II - Favorable Solitary tumor, 4 to 10 DD in
size, at or behind equator. Multiple tumors, 4 to
10 DD in size, at or behind equator.
Stage III - Doubtful Any lesion anterior to equator.
Solitary tumors larger than 10 DD behind equator.
Stage IV - Unfavorable Multiple tumors, some larger
than 10 DD. Any lesion extending anteriorly to ora
serrata. Stage V - Very Unfavorable Massive tumors
involving over half the retina. Vitreous seeding.
* 1 Disk Diameter (DD)= 1,6 mm.
Treatments

Chemotherapy
Cryotherapy (freezing treatment)
Enucleation ( removal of the eye)
External beam radiation therapy (radiation
treatment)
Localized plaque radiation therapy
(radiation therapy)
Photocoagulation (laser treatment)
Prognosis

The survival rate for Retinoblastoma


patients is more than 90%.
This is attributed to earlier diagnosis
and improved methods of treatment.
Determine the thing
that can and shall be
done, and then we
shall find the way.
- Abraham Lincoln
SQUAMOUS CELL
CARCINOMA
SCC keganasan ke-2 terbanyak pd
kelopak mata (9%)
US 105 kasus tiap 100.000 penduduk
Australia 166 kasus tiap 100.000
penduduk
SCC kelopak mata > conjungtiva
Invasi ke bola mata, struktur orbita,
lymphe node regional, metastese jauh
diagnosa awal sangat penting !
ETIOLOGI
Paparan sinar matahari kronis
Usia tua (60-70 th)
Orang muda dengan imunitas
(radioterapi, HIV)
Human papilloma virus pd pasien HIV
Zat kimia (minyak, tar, asap rokok,
arsenik, parafin)
Dermatosis prekanker
Pria (75%) > wanita (25%)
DIAGNOSIS KLINIS
Riwayat kelainan dan keganasan kulit
Status imun penderita
Riwayat paparan UV
Riwayat paparan zat kimia
Riwayat lesi jinak kelopak mata
Kelopak mata bawah > sering drpd
atas (1,4:1)
Tidak khas ! nodule, plak dg tepi
ireguler, luka kronis, fissura kulit, tepi
mengkilat, telengiektasis, ulserasi,
papiloma, cutaneous horn, lesi kistik
sering didaerah limbus,
pada fissura interpalpebra
sering mirip pterygium

Menjadi tumor ganas


kornea
bila menginvasi daerah
kornea
Pemeriksaan lain :
Hertel exophthalmometri
Palpasi lymphe node regional
Tes faal hepar
Analisa genetis untuk xeroderma
pigmentosum
Tes HIV
CTscan
POLA INVASI DAN METASTASIS
Dermis otot orbicularis superficial
Wajah, periosteum, pembuluh lymphe,
pembuluh darah, selubung syaraf
Klasifikasi BRODERS grade I,II,III,IV
Grade 1: 75% keratinocytes are well differentiated
Grade 2: >50% keratinocytes are well differentiated
Grade 3: >25% keratinocytes are well differentiated
Grade 4: <25% keratinocytes are well differentiated
Penyebaran lymphatic lnn. Preauriculer,
lnn. Submandibular,
Infiltrasi perineural n.trigeminus, syaraf
motoris ekstraokuli, n. fascialis
HISTOPATOLOGI
Sarang-sarang sel masuk ke dermis
disertai reaksi inflamasi kronis
Keratinisasi pada well differentiated
Undifferentiated sitoplasma eosinofilik,
mutiara keratin, jembatan interseluler
STADIUM KLINIS

T0 lesi in situ
T1 diameter < 2 cm
T2 diameter 2-4 cm
T3 diameter > 4 cm
T4 invasif pada tulang dan otot
TERAPI

PEMBEDAHAN
Bedah eksisi dengan :
Tehnik Mohs
Vriescope
Diikuti dengan bedah rekonstruksi

Kadang diperlukan eksenterasi orbita dan


eksisi en bloc bila telah melibatkan tulang
RADIOTERAPI
Bila ada KI bedah atau menolak operasi
SCC lebih resisten dosis lebih
Kelemahan :
Tepi tidak terkontrol
Komplikasi post radiasi
Kunjungan berulang kali
Tidak dapat :area yang pernah
diradiasi, tumor di tengah kelopak,
usia < 40 th, xeroderma
pigmentosum
CRYOTERAPI
Kelebihan : biaya, nyaman, potensiasi
kataraktogenik , dapat diulang
Tidak dapat : tumor terfiksasi di
periosteum, pada canthus medialis,
diameter >10 mm, lesi tidak jelas
tepinya, lesi melebihi conjungtiva fornix
Nitrogen cair semprot dengan
melindungi bola mata
ES depigmentasi, bulu mata hilang,
hipertrofi scar, ektropion, epifora,
hiperplasia pseudoepitelomatous
KEMOTERAPI
Sebagai terapi tambahan untuk SCC
kelopak mata lanjut
Cisplatin, atau kombinasi dengan
doxorubicin, bleomycin, isotretinoin, -
interferon
FOLLOW UP

Curiga SCC kelopak mata evaluasi 6-12


bulan
Telah mengenai lymph node 2-3 bulan
selama 2 th pertama
PENCEGAHAN

Sunscreen SPF 15 wajah dan kelopak mata


bawah, dan dioleskan tipis-tipis pada
kelopak mata atas dan dahi
Pakaian dan topi pelindung
Menghindari paparan sinar matahari pk.
10.00-15.00 WIB sore
Menurunkan 78%
It isn't the things that happen
to us in our lives that cause us
to suffer, it's how we relate to
the things that happen to us
that causes us to suffer.
- Pema
Chodron
BASAL CELL CARCINOMA
Most common human malignancy
Elderly patients
Chronic exposure to sunlight
Slow growing, locally invasive, non
metastating
Nodulo-ulcerative BCC
shinny, firm, pearly nodule,
small dillated blood vessel on
its surface
growth slow central
ulceration, raised rolled edges
(rodent ulcer)

Sclerosing BCC
difficult to dx infiltrates
laterally beneath the epidermis
plaque
palpation better than
inspection to determine the
tumor.
Treatment
Surgical excision remove the entire tumour but
preserve as much normal tissue as possible
together with 4 mm margin tissue which looks
clinically normal
large tumour frozen section or Moh
micrographic surgery
Reconstruction the defects
Radiotheraphy for nodulo-ulcerative BCC with
no involvement of medial canthal area and
unsuitable for/refuse surgery
Treatment
Cryotheraphy small superficial
BCC
Laser microsurgery well-
circumscribed BCC of the lid margin
without conjunctival extention
A education isnt how much you have
committed to memory, or even how much
you know,
its being able to differentiate between what
you know and what you dont.

-Anatole France
MELANOMA MALIGNA
ORIGIN :
- arising from PAM (primary acquired
melanosis) with atypia 75 %
- arising from a pre existing naevus 20 %
- primary melanomais the least common
6th decade
Signs MM conjunctiva :
A solitary, black or grey nodule containing
dilated feeder vessels which may become
fixed to the sclera
Amelanotic tumours are pink, smooth, fish-
flesh app.
A common site is the limbus (may arise
everywhere)
Therapy :
Circumscribe melanoma
wide excision with clearence and cryotherapy to
prevent reccurence
incomlete clearence + re excision and
cryotherapy
follow up every 6-12 monthly suspicious
area biopsy and impression citology
Diffuse melanoma excision and cryotherapy or
mitomicin C
Orbital recurences local resection and
raadiotherapy
Lymph node involve excision and radiotherapy
Palliation chemotherapy for metastatic disease
Prognosis
5 ysr 12 %
10 ysr 25 %
Metastase : regional lymph nodes,
lung, brain, liver
Signs MM eyelid :
Rare, but lethal
Superficial spreading melanoma plaque
with an irregular outline and variable
pigmentation
Nodular melanoma blue-black nodule
surrounded by normal skin
Melanoma arisin gfrom lentigo maligna
(slowly expanding pigmented macule in
elderly Hutchinson freckle)
Signs MM ciliary body :
In the sixth decade with visual symptoms
Discovered incidentally
Pupillary dilatation and gonioscopy
Dilated episcleral blood vessels in the
same quadrant of tumour

Extraocular extension through sclera


Pressure to the lens astigmatism,
subluxation

Erosion iris root


Retinal detachment caused by post
extension

Anterior uveitis
Annular/ circumferential growth
360- worst prognosis e.c difficulty
to diagnose
Diagnostic
Triple mirror contact lens
Transillumination for amelanotic
melanoma
USG
Biopsy
Therapy
Enucleation large tumour and
affecting the anterior choroid,
secondary glaucoma
Iridocyclectomy small medium
tumours involving less than one third
of the angle
Radiotherapy
Signs MM choroid :
Sixth decade of life
Decrease VA or VF defect
Third patients very brief balls of light
traveling across the visual field two-three
times a day in the subdued lighting
Elevated subretina, dome shaped, brown
or grey mass, mottled with dark brown/
black pigment/ amelanotic.
Mushroom shape app if breaks through
Brunch membrane
Secondary exudative RD
Choroidal folds, haemmorrhage,
secondary glaucoma, cataract, and
uveitis
Diagnosis
Binocular indirect ophthalmoscopy
Indirect slit lamp biomicroscopy
USG
FFA
ICG
MRI
FNAB

METASTASIS lung, mammae, GIT


TREATMENTS
Brachytherapy tumours < 10 mm in
elevation and < 20 mm in basal dia.
External radiotherapy more posterior (>
4 mm of the disc)
Transpupillary thermotherapy (w/ diode
laser) small tumours, location near the
fovea or optic disc
Trans scleral local resection = excision
tumours with the rim of healthy choroid
under a partial thickness scleral flap too
thick for radiotherapy, < 16 mm in dia.
Stereotatic radiosurgery large tumours
with preservation of visual function in
selected case
Enucleation very large tunours, visual
loss
Exenteration extensive extraocular
extension or orbital recurrences
Palliation chemo therapy /
immunotherapy metastatic disease

PROGNOSIS
Lung metastatic < 1 year, Liver metastatic <
6 mo
All our dreams can come
true, if we have the courage
to pursue them.
Walt Disney

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