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Repeating KHIO 1 > 4 Ocular lesions > Flashcards

4 Ocular lesions Flashcards

1
Q

Conjunctiva anatomy:

A

Membrane from limbus > globe (bulbar) > fornix > palpebrae
Squamous cells near limbus, columnar near fornix.
Stroma, fibrovascular connective tissue

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2
Q

Dermoid:

A

Benign Congenital conjunctival yellow mass, fine hairs present. Appears near limbus.
Leads to astigmatism.
Surgery might help vision, will leave scar.
Isolated lesion or with Goldenhar’s syndrome (hearing loss)

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3
Q

Squamous Papilloma:

A

Usually benign tumor from HPV infection of conj.
Pink vascular bumps from fornix, or outer lid.
Severe fornix > irritation, chronic mucous, blood tears.
Treated with cryo, cimetidine prevents regression

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4
Q

Conjunctival cysts:

A

Epithelial swelling following inflammation, surgery, trauma.
Clear epithelial cavity filled with serous fluid.
Benign, Easily excised

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5
Q

Actinic keratosis

A

Scaly dry skin (like exzema)

From UV, unlikely squamous carcinoma

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6
Q

Conjunctival intraepithelial neoplasia:

A

CIN
Premalignant cellular proliferation through epithelium.
Vascular fleshy growth of abnormal epithelial cells

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7
Q

Conjunctival squamous cell carcinoma/neoplasia:

A

OSSN
Malignant Extensive vascular fleshy growth.
Usually extending from limbus to fornix or cornea
Alcohol epitheliectomy (cornea), lamella scleroconjunctivecotomy (conj.), cryo (remaining bulbar components)
Usually wont spread globally unless immunocompromised
Mitomycin C / interferon prevent regression

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8
Q

Melanocytic tumors of conjunctiva:

A

Nevus (most common)
Racial melanosis
Primary acquired melanosis (PAM)
Malignant melanoma

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9
Q

Conjuntival Nevus:

A

Benign melanocytes in stroma. (10yo-30yo when notices)
Small elevated lesion, variable pigmentation, interpalpebral limbus.
<1% chance of formation to malignant melanoma
Colour change can initiate growth and malignancy

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10
Q

Primary aquired melanosis:

A

Melanocytes near basal epitheilum.
Brown pigment, scattered through conj. (usually Caucasian)
Atypia melanocytes =50% risk malignant melanoma
Biopsy with cryo, mitomysic C prevents recurrence

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11
Q

Malignant conjuntival melanoma:

A

Commonly ~60yo from PAM, otherwise nevus/de novo.
Melanocytes penetrate conj. Stroma
Pigmented vascular elevation, anywhere on conj./cornea
Metastases to facial lymph, brain, lung, liver commonly
Recurrence occurs 25% in 5 years, 65% by 15 years
treated with alcohol epithiliectomy, lamellar sclerconjunctivectomy, cryo

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12
Q

Conditions resembling melanocytic tumours:

A 
Pingueculum
Pterygium
Conjunctival cysts
Adrenochrome pigment from epinephrine drops
Mascara/gunpowder deposit
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13
Q

Pyogenic granuloma:

A

Elevated vascular red mass on conj, can bleed.
Proliferative chronic inflammation from trauma/surgery
Excised or cryo, unlikely to metastasize

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14
Q

Non-malignant choroid/retina lesions:

A

Congentical hypertrophy of the retinal pigment epithelium (CHRPE)
Choroidal naevi

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15
Q

Uveal melanoma:

A

Usually from separate tumour metastasis (Female breast cancer, or male lung cancer)
Otherwise malignant melanoma (from nevi 5%)
50% further metastasis (1/2 die in 8 months)
60% metastasise to liver (then lung 25%/bone/brain)

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16
Q

Uveal melanoma risk factors:

A

Light iris/skin colour
Choroidal nevi
(Asia) 45 - (europe/males) 60 yo
Cooks (cooking oil), welders (carcinogenic gas)
Iris nevi (5% malignancy), choroidal nevi (0.0005%)

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17
Q

Choroidal naevi likelihood to from malignancy

A

> 2mm
Orange lipofuscin/drusen
Irregular boarders
Serous RD

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18
Q

Uveal melanoma symptoms:

A 
Loss VA, Myodesopsia (floaters), photopsia, VF defects, high IOP (glaucoma), iris color change
Or asymptomatic (most common, after myosesopsia)
Macula, painless VA loss
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19
Q

Uveal melanoma treatments:

A

Enucleation, or Radiotherapy:
Brachytherapy, iodine-125 plaque near lesion
Proton beam/steriotactic radiotherapy: (large/close to ON tumor)
Transpupilliary thermotherapy (heating via contact lens)

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20
Q

Uveal melanoma prevalence and location of tumour:

A

5-10 cases per million
90% choroid, 6% ciliary, 4% iris
Asia/Africa has least (0.5/million)
Australia has most (11/million)

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21
Q

How uvea is protected from UV:

A

Vitreous humour blocks light in pos.

Lens/cornea resist UV

22
Q

Uveal melanoma good/bad prognosis

A

Fusiform A/B (HLA-A immune cells), good
Epithelioid cell (HLA-B immune cells), bad
Mixed, mild
Increased vasculation, bad

23
Q

Cutaneous melanoma vs uveal melanoma:

A

Both come from melanocytes with alternate MAP kinase signalling
Cutaneous, spread via lymph
Uveal, spread via blood

24
Q

Uveal melanoma genetics:

A

Chromosome 3 monosomy (bad)/ disomy (better)
Mutation of BRCA-associated protein 1 gene (BAP1) worse prognosis (mono 3)
Mutation of G protein subunit alpha gene (GNA11/GNAQ), better prognosis

25
Q

Clinical prognosis of uveal melanoma:

A

50% metastasise in 15 years, resulting in 6-12month life expectancy
Repeat imaging 6months
Liver/lung MRI

26
Q

OSSN prevalence, and cause

A

Mostly from UV, HIV, HPV
Highest rates in africa
Lesions mainly occur in the nasal sector, usually unilateral

27
Q

Limbal OSSN initiation physiology:

A

Basal cells in Limbal epithelial crypts proliferate, to surface then below basement membrane.
UV Damages DNA for prymidine dimers for p53 tumor-suppressor gene allows passage of GI checkpoint and immunosuppresion.
HPV (activated by UV/de novo) promotes proliferation and inhibits p53.
Vit A def. Impairs tumor surveillence
Telomerase reactivation > increased division
VEGF > angiogenisis
Matrix metalloproteinases (MMPS) > intracellular matrix destruction

28
Q

Cells that form limbal OSSN:

A

Limbal stem cells in basal epithelial crypts (extensions of palisades of vogt)
10% of basal cells, most nasally.
Slow life cycle, used for cornea repair.

29
Q

OSSN treatment

A

Excision
Topical chemotherapy
Mitomycin C / 5-fluoruracil / interferon alpha-2b following surgery

30
Q

HPV in OSSN:

A

Invades basement membrane via abrasions.
V-DNA incorporates with DNA
Cells elevate, normally would deactivate, but HPV’s E7 protein allows them to remain proliferative
It’s E6 protein inhibits cell cycle arrest of cancerous cells by inhibiting p53
HPV is activated by immunosuppression or UV

31
Q

Cell division cycle:

A

Interphase (S) DNA synthesized > Gap 2 (G2) > mitosis (M) > Gap 1 (G1)

32
Q

Function of p53 tumour suppressor system:

A

Phosphoprotein in nucleus to apoptosis from stress at G1-S

Also prevents DNA damage, help repair and mediate communication

33
Q

Photo immunosuppression:

A

UV suppresses immunity
UVB 290-320nm is more potent than UVA 320-400nm
UVB (5%) / UVA (90%)

34
Q

HIV in OSSN

A

Infects Helper T-cells (CD4+) initiating apoptosis.
Increases action of HPV (and other viruses)
Induces inflammation via C-reactive protein / interleukin-6 level increase

35
Q

Vitamin A in ocular surface

A

Maintains integrity (loss > abrasions > HPV entry), assists immune (CD4+/Treg) in tumour surveillance, promote stem differentiation (loss results in cancer cells)

36
Q

OSSN following activation:

A

Uncontrolled replication (telomerase reactivation via cancer cells)
Angiogenesis (VEGF > feeder vessels)
Metastasis (MMPs degrade matrix allowing invasion to other tissue)

37
Q

Uveal melanoma genetics (proteins):

A

Cyclogenase (COX-2), poor prognosis marker
CD200/HVEM levels reduced
T cells express LAG3 instead of CTLA-4 or PD-1
PD1 levels increased at tumour site

38
Q

signalling pathway of uveal melanoma

A

Mutation in GPCR receptor genes (GNA11/GNAQ)
Modifies many signal cascades in melanocytes
GPCR is activated by serotonin receptor 2A/B, mutation in this receptor also lead to melanosis

39
Q

genetic mechanisms in uveal melanoma metastasis

A

BAP1 tumor suppressor gene forms enzyme that binds to suppressor proteins (BARD1/BRCA1) forming tumor suppressors.
Mutation of BAP1 leads to poor DNA repair and metastasis
SF2B1 mutation ruins splisosome function

40
Q

mechanisms in uveal melanoma development

A

Hypoxia, leads to angiogenesis and cell motility (increased HIF > CD31/VEGF presence)
Oxidative stress, ROS/NRS accumulation, and antioxidant imbalance

41
Q

Congenital hypertrophy of the retinal pigment epithelium presentation

A

Flat, round lesions (usually several and unilateral)
May depigment over time
Overlaying retina may degenerate

42
Q

Cysts of moll:

A 
Blocked apocrine (sweat) gland
Dome shaped, translucent, near lashes usually nasal/temporal
43
Q

Cysts of zeiss:

A 
Blocked zeiss (sebaceous) gland
Dome shaped, white/yellow under lashes usually nasal/temporal
44
Q

Chalazion:

A

Inflammation due to meibomian blockage, most common.
Painless/irritable bump in tarsal plate, associated with blepharitis.
Treated via compress before incision

45
Q

Hordeolums (stys)

A

Infection and blockage of meibomian (large) or zeiss/moll (small)
Treated with oral antibiotic + compress
Can present with orbital cellulitis

46
Q

Molluscum contagiosum:

A

Molluscum contagiosum viral infection of meibomian gland

White/pink bump, usually self resolving

47
Q

Xanthelasma:

A

Soft white tissue
Aggregate of macrophages
Completely benign

48
Q

Eyelid naevus:

A

Flat (young) or Elevated (>20yo) bump before lash
Can be pink or pigmented
Transormation to melanoma is rare

49
Q

Seborrheic keratosis

A

is papilloma
Most common elderly benign lesion
Waxy pigmented on lid (like bumpy birthmark)

50
Q

lid Basal cell carcinoma

A

Most common OSSN
Slow non-pigmented growth
Late stage will necrosis leaving black scab
Unlikely metastasis

51
Q

lid Squamous cell carcinoma

A

Non-pigmented growth, tend to crust / ulcer (has blood flow)
Unlikely tumor
aggressive

Repeating KHIO 1 (15 decks)

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