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Neoplasia Flashcards

1
Q

most common primary intra-ocular tumour in adults

A

uveal melanoma

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2
Q

most common primary intra-ocular tumour in children

A

retinoblastoma

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3
Q

Most common malignant lacrimal gland tumour

A

Adenocystic carcinoma

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4
Q

Most common benign orbital tumour in adults

A

Cavernous haemangioma

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5
Q

Most common benign orbital tumour in children:

A

Capillary haemangioma

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6
Q

Most common malignant orbital tumour in children:

A

Rhabdomyosarcoma

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7
Q

enviromental carcinogenesis

A

chemicals, radiate, virusees

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8
Q

conjuncitval papilloma

A

caused by HPV 6 and 11
16 and 18 are high risk carcinoma

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9
Q

EBV

A

burkitt’s lymphoma

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10
Q

carcinogenesis of HPV

A

HPV produces the E6 protein which binds to and inactivates p53 leading to
uncontrolled DNA replication

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11
Q

carcinogensis of EBV

A

EBV produces a protein that makes the cell resistant to apoptosis

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12
Q

xeroderma pigmentosum

A

Autosomal recessive
o Deficiency in DNA nucleotide excision repair (NER) mechanisms leading to
multiple skin tumours
o Photosensitivity, multiple solar keratoses, skin cancers

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13
Q

neurofirbomatosis

A

o Autosomal dominant (1:4000)
o Neurofibroma: derived from endoneurium. Spindle cells on histology
o Schwannoma: derived from Schwann cells. Palisaded spindle cells and
myxoid areas

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14
Q

NF1

A

o Defect in NF1 gene on chromosome 17q
 Multiple neurofibromas, cafe-au-lait spots, axillary freckling and risk
of sarcoma
 Associated with optic nerve glioma, Lisch nodules, lid neurofibroma,
choroidal naevi, phaeochromocytomas and retinal astrocytoma

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15
Q

NF2

A

o NF-2 (1:40,000) does not actually cause neurofibromas but causes acoustic
neuroma/schwannoma, meningioma, glioma, combined hamartoma of the
RPE and early cataract. Mutation is at 22q

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16
Q

li-fraumeni syndrome

A

germ-line mutation of p53
high risk of childhood sarcoma and breast cancer

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17
Q

von hippel lindau syndrome

A

o Autosomal dominant cancer syndrome
o Mutation on chromosome 3
o Capillary haemangiomata of the retina (aka retinal angiomata), renal cell
carcinoma, phaeochromocytoma, haemangioblastoma of the cerebellum

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18
Q

proto-oncogenes

A

normal genes that stimulate cell division

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19
Q

tumour suppressor genes

A

normal genes that inhibit cell division

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20
Q

oncogenes

A

abnormal/cancerous genes that cause uncontrolled proliferation

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21
Q

benign tumours

A

can undergo malignant change possibly after acquiring genetic
mutations eg. pleomorphic lacrimal gland adenomas can transform to
adenocarcinoma

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22
Q

chronic inflammation

A

chronic lymphocytic infiltrates in the lacrimal gland
associated with Sjogren’s syndrome can develop into lymphoma

23
Q

intraepithelial neoplasia

A

actinic keratosis showed
pleomorphism and dysplasia and can become squamous cell carcinoma if they
breach the basement membrane

24
Q

hamartoma

A

 Non-neoplastic tumour of normal tissues for the site
 Typically involve blood vessels and melanocytes

25
haemangiomas
proliferation of blood vessels  Capillary (small vessel) and cavernous (large vessels with septations) can affect the eyelids, orbit and choroid
26
sturge-webder syndrome
encephalo-trigeminal angiomatosis) causes extensive haemangiomas (phakomatoses). It is a sporadic (not hereditary) mutation in the GNAQ gene o Choroidal haemangiomas o Vascular proliferation in the angle: glaucoma
27
naevi
abnormal proliferation of melanocytes (neural crest derived cells)  Found in the conjunctiva, iris, choroid and retina  Can occasionally progress to melanoma  Benign features: clear margins, no overlying subretinal fluid, no orange pigment/lipofuscin
28
beign astrocytic haematroms
astrocytes forming a matrix of calcification  Associated with tuberous sclerosis (fundal astrocytomas)  Stable round nodule projecting into vitreous
29
choriostoma
Non-neoplastic tumour of normal (ectodermal) tissues in an abnormal location include: dermoid, dermolipomas, phakomatous choristoma
30
dermoid
may be composed of fat, fibrous tissue, hair follicles, sweat glands (ectodermal elements).  Seen as nodules on the bulbar conjunctiva  Well-defined, white-pale yellow lesions  No malignant potential  May be associated with Goldenhar’s syndrome
31
phakomatous choristoma
eyelid nodule composed of lens capsular material!
32
squamous papilloma
includes molluscum contagiosum (poxvirus) and viral warts (HPV)
33
basal cell papilloma
appearnce: sessile, pedunculated, papipillary shepd aka seborrhoeic keratosis histo: acanthonic proliferation of basal cells, keratin filled cysts
34
adenoma
benign tumour of glandular tissue  Can arise from eyelid sweat glands, sebaceous glands, meibomian glands  Sebaceous adenomas are commonly seen as a yellow mass at the caruncle
35
keratocathoma
Rapidly growing but spontaneously resolving tumour of the epidermis  Can mimic an SCC  Nodule that grows over only a few weeks  Elevated, “heaped” shoulder  Central ulcer/crater  Typically resolves within 2-3 months but can leave a scarh
36
histology of keratocathoma
Central mass of keratin (pink with H&E stain)  Hyperplastic epidermis with clear demarcation between this raised edge and normal skin surface  Demonstrate hyperkeratosis (of the epidermis) and sometimes also dyskeratosis (keratinisation within the dermis)
37
epidermoid cyst
Demonstrate dyskeratosis (purely)  Histologically: keratin-filled cavity within the dermis lined by keratinised xtratified squamous epithelium
38
meningiomas
Slow-growing tumours of the meninges  Most commonly detected primary intracranial neoplasms  Most sporadic but may be familial  Associated with NF2 (22q) and MN1 (also on 22q)
39
intracranial meiningiomas
Intracranial meningiomas cause raised ICP which can cause papilloedema  Meningiomas arising from the olfactory groove or sphenoid can cause  Optic atrophy  CN VI nerve palsies: false localising sign
40
histopathology of meininingioma
psammoma bodies
41
basal cell carcinoma
>90% of malignant eye tumours  Caucasians over 50 years old
42
assoicaitons with basal cell carcinoma
 Sunlight exposure  Gorlin-Goltz syndrome (aka basal cell naevus syndrome). Autosomal dominant mutation of PTCH gene on 9q  Xeroderma pigmentosa: autosomal recessive, extreme sensitivity to UV light  Albinism: usually autosomal recessive (lack of melanin)  Bazex syndrome: X-linked dominant disorder of hair follicles  Male gender  Arsenic exposure  Immunosuppression  Fair skin/caucasian
43
appearance of BCCs
 Nodular (or solid)  Central ulcer  Rolled edge  Morphoeiform type: scirrhous (hard/fibrous) plaque  Occasionally pigmented
44
histological types of BCCs
nodular superfical infiltrative / scelorising micronodular
45
histology of nodular BCCs
well-defined islands of proliferating basal cells with peripheral palisades. Cystic degeneration can occur (nodulocystic)
46
histology of superficial BCCs
scaly plaque showing lobules of cells budding into superficial dermis from the epidermis or localised to the dermal-epidermal junction. There may be big gaps between the collections of cell
47
histology of infiltraitive / scelorising
morphoeic clinically. More aggressive. Strands of tumour cells in a fibrous stroma and ill-defined border with reduced peripheral palisading
48
histology of micronodular
more aggressive. Multiple small nodular collections of cells.
49
squamous papilloma histology
Epithelial acanthosis Hyperkeratosis Central fibrovascular core
50
seborrheic keratosis histology
Lesion above skin surface Acanthotic proliferation of basaloid cells Varying degrees of hyperkeratosis Keratin filled cystic inclusion
51
inverted follicular keratosis histology
Endophytic proliferation of basaloid, squamous elements Squamoid eddies Acantholysis
52
keratoacanthoma histology
Cup-shaped nodular elevation Thickened epidermis with islands of well differentiated squamous epithelium Neutrophil infiltration Central mass of keratin
53

Pathology (6 decks)

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