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Molluscum contagiosum
Molluscum contagiosum
Definition / general
• Infectious disorder caused by molluscum contagiosum
poxvirus
• Multiple nodules on skin, trunk or anogenital region, due
to skin to skin contact or sexual transmission
• Exuberant lesions appear in adults with AIDS
Gross description
• Observation
• Oral cimetidine
• Excision if on eyelid margin to prevent
infection of ocular surface
• Controlled cryotherapy
• Curretage
Basal Cell Carcinoma of eyelid
• Most common eyelid malignancy
• 90-95% of malignant eyelid tumours
• Risk factors
– Fair skinned, blue eyed, red-haired/ blond
– Middle aged/older persons
– Irish, Scottish, Scandinavian ancestry
– Cigarette smoking
– Prolonged sun exposure within first 2 decades
• Systemic associations
– Basal cell nevus syndrome (Gorlin syndrome): AD
• Multiple nevoid basal cell CA
• Skeletal anomally (mandible, maxilla, vertebrae)
– Xeroderma pigmentosum :AR
• Extreme sun sensitivity
• Defective repair mechanism for UV light induced DNA damage
Clinical features
• Location
– Lower eyelid (50-60%)
– Medial canthus (25-30%)- deeply invasive
– Upperlid
– Lateral canthus
• Origin
– Stratum basale or stratum germinativum of the epidermis
and the outer root sheath of the hair follicle
– Occur only in hair bearing tissue
Nodular basal cell CA
– Firm, raised, pearly nodule
– Telangiectatic vessels
– Central ulceration
– Histology-
• nests of basal cells originate from basal layer
• Peripheral palisading
• Nest of atypical cells break through to the surface
epithelium
Morpheaform type
– less common
– Aggressive
– Firm and slightly elevated
– Margins may be indeterminate
– Chronic inflammation of lid margin with madarosis
– May be mistaken for blepharitis
– Histology :
• no peripheral palisading
• Thin chords and strands of tumour cells in fibrotic stroma
Histology
• Excisional biopsy
– When lesions are small
– Do not involve eyelid margin
– Eyelid margin lesions are centrally located away from lateral canthus
and puncum
– In incomplete removal, borders should be marked
– Should be oriented vertically to minimize vertical traction
Surgical resection – Intraoperative histologic
confirmation
– Treatment of choice • Frozen section
– Surgeon excise tumour with
– Recurrent rate is lower 1-2 mm margins, oriented on
– BCC involving medial canthal a drawing
region • Mohs micrographic surgery
• Need removal of lacrimal – for recurrent,
drainage system – deeply infiltrated
• Reconstruction should not – Morpheaform type/ SCC
be done until it is confirmed – Tumour in medial canthal
to be tumour free region
– Ensures complete cancer
– Orbital invasion removal with preserving
• Orbital exentertion maximal healthy tissues
• Mortality rate is 3% – Difficult to identify the
tumour margins when the
tumour has invaded the
orbital fat
Reconstruction of the eyelid
• High power
– Cohesive collection of epitheliod cells -Ovoid
– Cytoplasm- Brown pigmented-melanocytic lesion (normal cells pink in
colour)
– Bleeched sample to see features of nucei/mitoses
– Nuclei
• Pleomorphism/ hyperchromatism/ mitoses
– Some show apoptotic bodies
• Shrunken cells
• Pyknotic nuclei ( round ball like)
Low power- raw sample
Conjunctival melanoma- high power (from web source)
Differential diagnosis
• Conjunctival nevus
• Conjunctival melanoma or secondary
melanocytic deposit
– Well differentiated:
• Contain ovoid to sauamous cells with foamy, finely vacuolated
cytoplasm and distinct cell borders
• Better differentiated cells are usually in center of nests, often near
tarsus and meibomian glands
• Lobules lack peripheral palisading
• More pleomorphic, hyperchromatic and atypical than BCC
• Abundant mitoses ( Differentiate from sebeceous hyperplasia)
• Lympho-plasmocytic infiltration
– Anaplastic:
• Often scant cytoplasm with indistinct vacuoles
• Central necrosis, pagetoid involvement of overlying skin
Vacuolation
Fat- dissolves in Xylene
Glycogen- dissolves in alcohol
Normal sebeceous glands
High power
• Treatment options
• Signs
– Immunohistochemistry
• Keratin (in ductal areas)
• Actin, myosin, fibronectin and S-100 ( in myoepithelial areas)
• High power
– Myxoid appearance of cell cytoplasm
– Ground glass apprearance ( GAGs)
– Basaloid cells arrenged in regular chords
– Ductal structures ( can show metaplasia)
• Epithelial components form nests or tubules lined by 2 layers of
cells
– Outermost layer (myoepithelial cells)
» Blending with stroma
» Myxoid stroma- Contain heterogenous elements( Cartilage and
bone)
– Inner layer
» Epithelial and myoepithelial components derived from
epithelium
Management
• En bloc excision
Complete removal of tumour (with pseudo
capsule,margin of orbital tissue)
• Low power
– Areas of irregular basaloid growth with cribriform change
– Peripheral areas with normal glandular architecture with
acni
– Multiple pools of mucin impart a swiss-cheese appearance
to the basophilic lobules
– (Perineural invasion, focal tumor necrosis may be seen)
Under high power
• Normal acini
– Lined by regularly arranged basaloid epithelial cells
– Lumens are filled with mucin
– Cellular polarity is present.
• Abnormal acini
– Basaloid ovoid cell clusters
– Mitotic figures
– Abundant Nuclear:cytoplasm ratio
– Loss of aciniform structure/polarity
– Comedonecrosis
– Fibrous desmoplastic stroma
• Alternative
– Globe sparing intra-arterial chemotherapy
Retinoblastoma
• Most common malignant ocular tumour in childhood
• Neuroblastic tumour
• Occurs due to somatic and germline mutation of RB-
tumour suppressor gene located at Q14-Ch13
• M=F
• 60% unilateral (somatic)
• 40% bilateral (germline)
How do they present?
• Most common –leucocoria
– Strabismus
– Hyphema
– Periocular inflammation
– Proptosis
– Pseudohypopyon
– Nystagmus…..
Diagnosis
A. It’s mainly a clinical diagnosis
• By identifying the ocular features
• Characteristic calcification
• 03 patterns of growth
• Endophytic (towards vitreous)
• Exophytic
– Grows subretinally
– Exudative RD
– Overlying vessels are large and tortuous
• Diffuse infiltrative
– Mimics pan-uveitis
– Diffuse retinal infiltration without a distinct mass
– pseudohypopyon
B.) Imaging
• MRI orbits and brain (CT is not recommended)
– Confirm diagnosis
– Evaluate extension
• USS- intraocular calcification
C.) FNAB ( in situations where clinical diagnosis
is difficult
• Vitreous sampling ( risk of seeding)
How do RBs spread?
Vitreous seeding-CB/Iris/AC
Through TM-
Conj. Lymphatics-> preauricular and cervical lymphnodes
Through sclera
To orbit
Genetic basis
• Somatic (60%)
– Non hereditory
– Mutations occur in a retinal cell
– Unilateral/unifocal
• Germline (40%)
– Mutation in one of the 02 allels
• Inherited by parents (10%)
• Occurs spontaneously (90%)
– Requires a 2nd hit ( Knudson theory)
IHC
– LCA ( leucocyte common antigen; CD45)
• + in lymphocytes/ - in RB
– Synaptophysin ( neuro-endocrine marker)
• + in RB/ - in lymphocytes
Flexner Wintersteiner rosettes
High risk histologic features associated with
metastasis
polymorphism monomorphic
Pleomorphism of nuclei
Oncologist involvement
Investigations – depending on the histological type
– CBC
– Liver spleen USS
– CXR
– Serum immunoprotein electrophoresis
– CT thorax and abdomen – mediastinal and retroperitoneal nodal involvement
– Bone marrow biopsy
• Treatment
• Radiotherapy – for localized disease – mainstay
• 2000 – 3000 cGY
• Surgical cure – can not achieve due to infiltrative nature
• Chemotherapy
Choroidal melanoma
HISTOLOGY
Low power
– General appearance
• Darkly stained discoid lesion of choroid
• Visible scleral rim
• Overlying thin sheet like retina with underlying SRF
High power
– fascicular arrangement of spindle shaped cells
– Nuclei are elongated/ cigar shaped
– Features of dysplasia
• Condensed hyperchromatic appearance
• Mitotic figures
– Mitotic count is very low comparatively
– Detection of even a single mitotic figure is significant
Modified Callendar Classification
• Spindle cell nevus- spindle cell A ( cigar shaped,
no nucleolus)
• Spindle cell melanoma- spindle cell B (larger, oval
shaped, prominent nucleolus)
• Epitheliod melanoma ( large, oval or round,
prominent nucleolus,polymorphsm)
– worst prognosis
• Mixed- epitheliod/spindle cell B
Clinical risk factors of melanoma related
mortality
• Large tumour size
• CB extension
• Extra scleral extension
• Older age
• Faster tumour growth
• Tumour regrowth after globe conservative
therapy
Histologic and molecular features affecting survival
Histological
• Tumour cell type
– Epithelioid- worse prognosis
– Mixed- intermediate
– Spindle B- best prognosis
• The mean of the 10 largest melanoma cell nucleoli
• Intrinsic tumour extravascular matrix pattern ( closed loops and
networks- increase risk of mets)
• High mitotic or cell proliferative indexMicrovascular density
• Large number of tumour infiltrating lymphocytes and macrophages
Molecular
– Monosomy 03
– BAP-1 mutation
Clinical evaluation
• History
• Slit lamp+ gonioscopy
• Post. segment with indirect oph.
• Fundal photograph
• B- scan
• OCT
• FAF
• Evaluation for metastasis
– Liver imaging
– LFT
– Chest X –Ray
– If any of above are abnormal
• Triphasic liver CT/ MRI abdomen
• If a metastatic lesion is found- biopsy
Treatment
Options
– Enucleation
– Conservative
• Ionizing radiation
• Adioactive plaque brachytherapy
• External beam radiation
• Charged particle therapy
• Steriotactic radiation therapy
• PDT
• TTT
• Local excision of tumour
Choice of treatment depend on 04 factors
– Size, location and extent of tumour
– Vision status of affected eye and fellow eye
– Age and general health
– Patient and physician preference
• Enucleation (COMS large tumour trial; Iry enucleation Vs pre-
enucleation EBR))
– Large tumour size
– Optic disc invasion
– Extensive involvement of the CB or angle
– Irreversible loss of useful vision
– Poor motivation to keep the eye
• Brachytherapy (COMS medium size tumour trial; enucleation Vs I125
Brachytherapy)
– Small to medium size tumours (< 20mm base diameter and up to
10mm thickness)
– Presence of useful vision.
• Charge particle radiation
– When brachytherapy is unsuitable ( large tumour size, posterior
location)
Metastatic disease