Conjunctiva Flashcards

1
Q

What is the blood supply of the conjunctiva?

A

supplied by the anterior ciliary and palpebral arteries.

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2
Q

What is the conjunctiva?

A

a transparent mucous membrane that lines the inner surface of the eyelids and the anterior surface of the globe, terminating at the corneoscleral limbus.

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3
Q

What are the divisions of the conjunctiva?

A
  • The palpebral conjunctiva starts at the mucocutaneous junction of the lid margins and is firmly attached to the posterior tarsal plates. The tarsal blood vessels are vertically orientated.
  • The forniceal conjunctiva is loose and redundant.
  • The bulbar conjunctiva covers the anterior sclera and is continuous with the corneal epithelium at the limbus.
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4
Q

What is the epithelium of the conjunctiva?

A

non-keratinizing and around five cell
layers deep. Basal cuboidal cells evolve into flattened polyhedral cells, subsequently being shed from the surface. Mucus-secreting goblet cells are located within the epithelium,
being most dense inferonasally and in the fornices.

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5
Q

What is the stroma of the conjunctiva?

A

richly vascularized loose connective tissue. The accessory lacrimal glands
of Krause and Wolfring are located deep within the stroma. Secretions from the accessory lacrimal glands are essential components of the tear film.

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6
Q

What is Conjunctiva associated lymphoid tissue (CALT)?

A

critical in the initiation and regulation of ocular surface immune responses. It consists of lymphocytes within the epithelial layers, lymphatics and associated blood vessels, with a stromal component of lymphocytes and plasma cells, including follicular aggregates.

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7
Q

What are some clinical features of conjunctival inflammation?

A

Discharge- watery (viral/allergic conjunctivitis), mucoid (chronic allergic conjunctivitis and dry eye), mucopurulent (chlamydia/bacterial conjunctivitis), moderately purulent (acute bacterial conjunctivitis), severe purulent (gonococcal infection)

Conjunctival reaction- hyperaemia (diffuse and beefy red seen in bacterial infection and away from limbus). Haemorrhages in viral conjunctivitis, Chemosis (local from TED, Allergic conditions, SVC syndrome and nephrotic syndrome). Membranes (pseudomembranes, true membranes of which removal causes tearing caused by severe adenoviral conjunctivitis, gonococal and bacterial infections, diptheria. Infiltration- papillary response and chronic inflammation. Subconjunctival cicatrization- scarring from trachoma. Due to loss of goblet cells and can lead to entropion. Follicles- viral and chlamydial conjunctivitis. Parinaud oculoglandular syndrome. Papillae- bacterial/allergic conjunctivitis/chronic blepharitis/CL wear, SLK, FES.

Lymphadenopathy- viral infections. Can occur in Chlamydial/severe bacterial infection (gonococcal) and parinaud oculoglandular syndrome. Preauricular lymph node affected.

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8
Q

How to macroscopially differentiate between a follicle and papillae?

A

Papillae- a vascular core is present.
Micropapillae form a mosaic-like pattern of elevated red dots as a result of the central vascular channel,

Follicles are multiple, discrete, slightly elevated lesions resembling translucent grains of rice, most prominent in the fornices. Blood vessels run around or across
rather than within the lesions.

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9
Q

Histological difference between follicle and papillae?

A

Follicle- Histology shows a subepithelial lymphoid germinal centre with central immature lymphocytes and mature cells
peripherally

Papillae- folds of hyperplastic conjunctival epithelium with a fibrovascular core and subepithelial stromal infiltration with inflammatory cells

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10
Q

What are the causes of acute bacterial conjunctivitis?

A

The most common isolates are Streptococcus pneumoniae,
Staphylococcus aureus, Haemophilus influenzae and Moraxella catarrhalis. A minority of severe cases are caused by the sexually transmitted organism Neisseria gonorrhoeae, which can readily invade the intact corneal epithelium. Meningococcal (Neisseria meningitidis) conjunctivitis is rare and usually affects
children.

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11
Q

Symptoms and signs of bacterial conjunctivitis?

A

Redness, grittiness, burning and discharge.
Usually bilateral and 1 eye infected 1-2 days before the other.
Eyelids stuck together on waking.

Vision usually normal.
Eyelid oedema/erythema (gonococcal)
Conjunctival injection
Hyperacute purulent discharge
Superficial corneal PEE’s
PUK in gonococcal and meningococcal infection progressing to perforation

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12
Q

What investigations can be performed for bacterial conjunctivitis?

A

Ix not routinely performed but indicated in:
1) Severe cases (binocular swabs and scrapings to excude Gonococcal and Meningococcal conjunctivitis
2) Culture on chocolate agar/Thayer martin for N. gonorrhoea
3) PCR for less severe cases such as chlamydial/viral infections

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13
Q

What is the treatment for bacterial conjunctivitis?

A

Topical antibiotics QDS for upto 1 week such as CPL, Quinolones, Macrolides, fusidic acid.

Gonococcal and meningococcal conjunctivitis treated with quinolone, gentamicin, CPL or bacitracin 1-2 hourly

Systemic abx in gonococcal infection. Refer to GUM. H influenza in children treated with Co-amoxiclav orally.

Topical steroids can reduce scarring in (pseudo) membranous conjunctivitis

CL wear discontinued for at least 48 hours after complete resolution

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14
Q

What percentage of bacterial conjunctivitis resolve in 5 days without treatment?

A

60%

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15
Q

What is Giant fornix syndrome and how is it treated?

A

uncommon entity causing chronic pseudomembranous purulent conjunctivitis due to retained debris in a big upper fornix leading to colonization with S. aureus. in an elderly patient with levator disinsertion.

Treatment involves repeated fornix sweeps with cotton bud and topica/systemic abx. Intense topical steroid may be appropriate.

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16
Q

What are the 2 forms that Chlamydia Trachomitis exist in?

A

They exist in two principal forms: a robust infective extracellular ‘elementary body’ and a fragile intracellular replicating ‘reticular body’.

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17
Q

Which chlamydial serotypes is Adult chlamydial inclusion conjunctivitis caused by?

A

serovars (serological variants) D–K of C

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18
Q

What % of Chlamydial conjunctivitis transmission is ‘eye to eye’

A

10%

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19
Q

Which chlamydial serovars cause Trachoma

A

A,B,Ba,C

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20
Q

What are the symptoms and signs of chlamydial conjunctivitis?

A

Symptoms
Subacute unilateral/bilateral redness/watery eyes and discharge

Signs
Watery or mucopurulent discharge
Tender preauricular lymphadenopathy
Large follices inferior fornix
SPK
Perilimbal subepithelial corneal infiltrates after 2-3 weeks

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21
Q

How to investigate suspected Chlamydial conjunctivitis?

A

Tarsal conjunctiva scrapings for NAAT PCR
Giemsa staining for basophilic intracytoplasmic bodies
Enzyme immunoassay
McCoy cell culture- highly specific
Swabs for bacterial culture and serology

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22
Q

How to treat chlamydial conjunctivitis?

A

Refer to GUM specialist.
Systemic Azithromycin/Doxycycline/Erythromycin/ Amoxicillin/Ciprofloxacin
Topical abx Erythromycin/tetracycline ointment
Reduce transmission risk until 1 week after azithromycin
Retest in 6-12 weeks

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23
Q

What is the pathogenesis of Trachoma?

A

recurrent infection with Chlamydia serotypes A-C elicits a chronic immune response consisting of a cell-mediated delayed hypersensitivity (Type IV) reaction to the intermittent presence of chlamydial antigen and
can lead to loss of sight.

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24
Q

2 stages of Trachoma?

A

Active inflammatory stage
Cicatricial chronic stage

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25
Q

WHO grading of Trachoma?

A

TF = trachomatous inflammation (follicular): five or more follicles (>0.5 mm) on the superior tarsal plate

TI = trachomatous inflammation (intense): diffuse involvement of the tarsal conjunctiva, obscuring 50% or
more of the normal deep tarsal vessels; papillae are present

TS = trachomatous conjunctival scarring: easily visible fibrous white tarsal bands

TT = trachomatous trichiasis: at least one lash touching the globe

CO = corneal opacity sufficient to blur details of at least part of the pupillary margin

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26
Q

What happens in active trachoma?

A

○Mixed follicular/papillary conjunctivitis associated with a mucopurulent discharge. In children under the age of 2 years the papillary component may predominate.

○Superior epithelial keratitis and pannus formation

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27
Q

What happens in Cicatricial trachoma?

A

○Linear or stellateconjunctival scars in mild cases, or broad confluent scars (Arlt line) in severe disease.

○Although the entire conjunctiva is involved, the effects are most prominent on the upper tarsal plate.

○Superior limbal follicles may resolve to leave a row of shallow depressions (Herbert pits)

○Trichiasis, distichiasis, corneal vascularization and cicatricial entropion

○Severe corneal opacification.

○Dry eye caused by destruction of goblet cells and the ductules of the lacrimal gland.

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28
Q

What is the SAFE strategy for managing Trachoma?

A

Surgery for trichiasis,
Antibiotics for active disease,
Facial hygiene
Environmental improvement.

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29
Q

Whys are systemic tetracyclines not used in children under 12 years of age?

A

Tooth staining

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30
Q

What is ophthalmia neonatorum?

A

as conjunctival inflammation developing within the first month
of life. It is the most common infection of any kind in neonates, occurring in up to 10%.

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31
Q

What are the causes of Ophthalmia Neonatorum?

A

*Organisms acquired during vaginal delivery: C. trachomatis, N. gonorrhoeae
*Staphylococci are usually responsible for mild conjunctivitis.
*Topical preparations used as prophylaxis
*Congenital nasolacrimal obstruction. Despite poor neonatal tear production

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32
Q

What are the timing of onset for different organisms causing Ophthalmia Neonatorum?

A

○Chemical irritation: first few days.
○Gonococcal: first week.
○Staphylococci and other bacteria: end of the first week.
○Herpes simplex virus (HSV): 1–2 weeks.
○Chlamydia: 1–3 weeks.

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33
Q

What are the characteristics of discharge in the organisms causing Ophthalmia Neonatorum?

A

○A mildly sticky eye may occur in staphylococcal infection, or with delayed nasolacrimal duct canalization (mucopurulent reflux on pressure over the lacrimal sac).

○Discharge is characteristically watery in chemical and HSV infection, mucopurulent in chlamydial infection, purulent in bacterial infection and hyperpurulent in gonococcal conjunctivitis.

○Pseudomembranes are not uncommon in chlamydial conjunctivitis.

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34
Q

Treatment for Ophthalmia Neonatorum?

A

Prophylaxis with 2.5% poviodine
Chemical conjunctivitis with artificial tears
Mild conjunctivitis broad spectrum topical abx like CPL.
Moderate-severe cases Ix with microscopy and treatment with broad spectrum abx liek CPL/Erythromycin
Severe conjunctivitis with systemic illness take samples and treat with broad spectrum abx like erythromycin. Cover for chlamydia
Chlamydial infection treated with PO erythromycin for 2/52
Gonococcal conjunctivitis treated systemically with 3rd gen Cephalosporin
HSV with high dose intravenous aciclovir under paediatrics

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35
Q

What are the common causes of viral conjunctivitis?

A

Viral conjunctivitis is a common external ocular infection, adenovirus (a non-enveloped double-stranded DNA virus) being the most frequent (90%) causative agent.

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36
Q

How can viral conjunctivitis present?

A

Non specific acute follicular conjunctivitis
Pharyngoconjunctival fever (PCF)
Epidemic Keratoconjunctivitis (EKC)
Acute haemorrhagic conjunctivitis
Chronic/relapsing adenoviral conjunctivitis
HSV
Systemic viral infections
Molluscum contagiosum

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37
Q

What is Non specific acute follicular conjunctivitis?

A

most common clinical form of viral conjunctivitis and is typically due to adenoviral infection by a range of serological variants. Unilateral watering, redness, irritation and/or itching and mild photophobia occur, the contralateral eye generally being affected 1–2 days later, often less severely.

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38
Q

What is Pharyngoconjunctival fever (PCF)?

A

caused mainly by adenovirus serovars 3, 4 and 7. It is spread by droplets within families with upper respiratory tract infection. Keratitis develops in about 30% of cases but is seldom severe. Symptoms are essentially as above, though sore throat is typically
prominent.

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39
Q

What is Epidemic Keratoconjunctivitis (EKC)?

A

caused mainly by adenovirus serovars 8, 19 and 37 and is the most severe
ocular adenoviral infection. Keratitis, which may be marked, develops in about 80%. Photophobia may be correspondingly prominent.

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40
Q

What is Acute haemorrhagic conjunctivitis?

A

occurs in tropical areas. It is typically caused by enterovirus and coxsackievirus, though other microorganisms may present similarly. It has a rapid onset and resolves within 1–2 weeks. Conjunctival haemorrhage is generally marked

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41
Q

What are the signs of viral conjunctivitis?

A

*Eyelid oedema
*Lymphadenopathy: tender preauricular
*Conjunctival hyperaemia and follicles
Keratitis (adenoviral). Epithelial microcysts, PEE’s, focal white subepithelial/anterior stromal infiltrates, small pseudodendritic epithelial formations
*Anterior uveitis- mild
*Molluscum contagiosum- pale waxy umbilicated nodule on lid margin

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42
Q

How to investigate viral conjunctivitis?

A

*Giemsa stain- mononuclear cells in adenoviral conjunctivitis and multinucleated giant cells in
herpetic infection.
* NAAT eg. PCR are sensitive and specific for viral DNA.
*Viral culture with isolation is the reference standard but is expensive and fairly slow. Sensitivity is variable but specificity is around 100%.
*A immunochromatography test takes 10 minutes to detect adenoviral antigen in tears; sensitivity and
specificity are excellent.
* Serology for IgM or rising IgG antibody titres to adenovirus
has limitations and is rarely used.
*Investigation for other causes such as chlamydial infection may be indicated in non-resolving cases.

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43
Q

How to treat viral conjunctivitis?

A

*Spontaneous resolution of adenoviral infection 2-3 weeks
*Reduction of transmission risk with hand hygiene
*Molluscum- lesions self limiting but remove in immunocompromised
*Topical steroids- Pred 0.5% QDS for severe membranous conjunctivitis. Use with caution suppress inflammation and corneal infiltrates recur after stopping.
*Discontinue lens wear
*Cold or warm compress
*Artificial tears

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44
Q

What is seasonal allergic conjunctivitis?

A

‘hay fever eyes’), worse during the spring and summer, is the more common. The most frequent allergens are tree and grass pollens, although
the specific allergen varies with geographic location.

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45
Q

What is Perennial allergic conjunctivitis?

A

Causes symptoms throughout the year, generally worse in the autumn when exposure to house dust mites, animal dander and fungal allergens is greatest. It is less common and tends to be milder than the seasonal form.

46
Q

What are the symptoms and signs of seasonal/perennial allergic conjunctivitis?

A

*Symptoms. Transient acute or subacute attacks of redness, watering and itching, associated with sneezing and nasal discharge.
*Signs. Normal vision. Conjunctival hyperaemia with a relatively mild papillary reaction, variable chemosis and lid oedema.

47
Q

Treatment for seasonal/perennial allergic conjunctivitis?

A

Artificial tears
Mast cell stabilisers (sodium cromoglicate)
PO antihistamines
Dual action antihistamines and mast cell stabilizers eg olopatidine, ketotifen act rapidly
NSAID- rarely used
Topical steroids effective

48
Q

What is Vernal keratoconjunctivitis?

A

(VKC) is a recurrent bilateral disorder
in which both IgE- and cell-mediated immune mechanisms play
important roles. It primarily affects boys and onset is generally
from about the age of 5 years onwards. There is remission by the
late teens in 95% of cases, although many of the remainder develop
atopic keratoconjunctivitis.

49
Q

Types of VKC

A

Palpebral VKC- involves upper tarsal conjunctiva associated with significant corneal disease
Limbal disease affects black and Asian patients
Mixed VKC- featrures of both palpebral and limbal disease

50
Q

Symptoms of VKC?

A

intense itching, which may be associated with lacrimation, photophobia, a foreign body sensation, burning and thick mucoid discharge. Increased blinking is
common.

51
Q

What do you see in palpebral VKC?

A

Early disease- papillary hypertrophy on superior tarsal plate
Macropapilla (<1mm). Progression to giant papillae (>1mm) can occur.
Mucous deposition between giant papillae
Keratopathy SPEE’s with mucous on the cornea.

52
Q

What do you see in Limbal disease VKC?

A

Gelatinous limbal conjunctival papillae associated with white cellular collections (Horner Trantas Dots)

53
Q

What is the pathogenesis of Atopic Keratoconjunctivitis (AKC)?

A

a rare bilateral disease that
typically develops in adulthood (peak incidence 30–50 years)
following a long history of atopic dermatitis (eczema). Asthma is
also extremely common in these patients. About 5% have suffered
from childhood VKC

54
Q

What are the differences in presentation of VKC and AKC?

A

*Fewer eosinophils on conjucntival scrapings in AKC
*Symptoms unremitting in AKC
*Skin changes more in AKC (Eczematoid changes/ dryness/scaling)
*Madarosis common
*Hertoghe sign- absence of lateral eyebrows
*Dennie Morgan folds -lid skin folds caused by persistent rubbing
*Conjunctival involvement usually inferior in AKC with cicatricial changes seen in AKC over VKC.
*Horner trantas dots seen in both.
*PEE’s over inferior 1/3 of cornea
*Peripheral vascularization and scarring more in AKC
*Presenile shield like subcapsular cataracts common in AKC
*RD commoner in AKC after cataract surgery

55
Q

How to manage AKC and VKC?

A

*Allergen avoidance
*Cool compress
*Lid hygiene
*BCL
*Mast cell stabilizers
*Topical antihistamines
*Combined antihistamine/vasconstrictor
*Combined antihistamine/mast cell stabilizer
*NSAID
*Topical steroids
*Steroid ointment
*Antibiotics
*NAC
*Ciclosporin if steroids ineffective
*Calcineurin inhibitors eg Tacrolimus
*Systemic oral antihistamine/abx/immunosuppresive *agents
*Surgery with superficial keratectomy. *Surface maintenance/restoration surgery

56
Q

What is non-allergic eosinophilic conjunctivitis?

A

NAEC seen in middle aged women with concurrent dry eyes. Similar pathogenesis to allergic eosinophilic rhinitis. Conjunctival eosinophilia present without significant IgE levels in serum/tear film. Treatment with 1-2 week course of topical steroid for exacerbations and maintenance with topical mast cell stabilizers/NSAIDS/antihistamines

57
Q

What is the pathogenesis of Giant (mechanically induced papillary conjunctivitis)?

A

Occurs secondary to mechanical stimuli of tarsal conjunctiva eg contact lens wear CLPC. Risk increased by build up of proteinaceous debris on CL surface. Ocular prosthesis, exposed sutures and scleral buckles.

58
Q

What is mucus fishing syndrome?

A

in a variety of underlying anterior segment disorders, patients develop
or exacerbate a chronic papillary reaction due to repetitive manual
removal of mucus. Giant papillae can also be seen in other conditions such as VKC and AKC.

59
Q

Symptoms and signs of Giant (mechanically induced papillary conjunctivitis)?

A

*FB sensation, redness, itching, increased mucus production, blurring and loss of CL tolerance. Symptoms may be worse after lens removal. Patients should be questioned about CL cleaning and maintenance.

Signs
*Variable mucous discharge
*CL protein deposits
*Excessive CL mobility
*Ptosis due to irritative spasm and tissue laxity secondary to chronic inflammation

60
Q

How to treat Giant (mechanically induced papillary conjunctivitis)?

A

*Removal of stimulus eg CL wear/exposed sutures/scleral buckle
*Assessment of fit/status of ocular prosthesis
*Filtering bleb excision/revision
*Change CL solution if preservatives
*Switch to monthly then daily lenses
*Cessation of CL wear
*Prosthesis polishing/cleaning/coating
*Topical mast cell stabilizers PF.
*Antihistamines/NSAIDS
*Topical steroids

61
Q

What is Mucous Membrane Pemphingoid (MMP)?

A

also known as ocular cicatricial pemphigoid (OCP), comprises a group of chronic autoimmune mucocutaneous blistering diseases.
An unknown trigger leads to a Type II (cytotoxic) hypersensitivity response
resulting in antibodies binding at the basement membrane zone (BMZ), the activation of complement and the recruitment of inflammatory cells, with localized separation of the epidermis from the dermis at the BMZ and subsequent progression to scarring. Studies of HLA typing have found an increased susceptibility
to the disease in patients with HLA-DR4. The HLA-DQB1 allele in particular shows a strong association with OCP and other forms of pemphigoid disease.

62
Q

Who is the target population for OMMP (Ocular mucous membrane pemphingoid)

A

The disease typically presents in old age and affects females more commonly than males by a 2: 1 ratio.

63
Q

What is Foster’s classification system for OMMP?

A

Diagnosis is principally clinical, but biopsy of involved mucous
membrane often shows supportive changes (linear antibody and
complement BMZ deposition).

○Stage I: early stage associated with chronic conjunctivitis, tear dysfunction and subepithelial fibrosis.
○Stage II: forniceal shortening, particularly inferiorly.
○Stage III: symblepharon formation.
○Stage IV: surface keratinization and cicatricial ankyloblepharon.

64
Q

Symptoms of MMP?

A

Conjunctiva- Papillary conjunctivitis/diffuse hyperaemia.
Fine lines of subconjunctival fibrosis and shortening of inferior fornix.
Symblepharon
Flattening of plica/keratinization of caruncle
Dry eye

Eyelids- trichiasis/chronic blepharitis/keratinization of lid margin
Ankyloblepharon

Cornea- epithelial defects with drying and exposure
Infiltration and peripheral vascularization
Keratinization and conjunctivalization of corneal surface
End stage disease characterized by symblepharon/corneal opacification

65
Q

What is a symblepharon?

A

Symblepharon (plural: symblephara)
formation refers to adhesion between the bulbar and palpebral conjunctiva

66
Q

What is an ankyloblepharon?

A

An adhesion at the outer canthus
between the upper and lower lids

67
Q

Systemic treatment for MMP?

A

Dapsone- 1st line treatment mild-mod disease. Contraindicated in G6PD deficiency. Sulfasalazine better tolerated sometimes.
Antimetabolites (azathioprine/methotrexate/mycophenolate) mild-mod disease if dapsone contraindicated/poor tolerated.
Steroids rapid disease control side effects limit long term use. IOP monitoring needed
Rituximab/immunoglobulins

68
Q

Local treatment for MMP?

A

Artificial tears
Topical steroids/ciclosporin/tacrolimus
Retinoic acid reduce keratinization
Antibiotics when indicated
Lid hygiene low dose tetracycline for blepharitis
Subconjunctival mitomycin C can be used temporarily.
CL with caution to prevent corneal damage from trichiasis/dehydration

69
Q

When is reconstructive surgery done for MMP?

A

*Aberrant eyelashes
*Punctal occlusion to aid tear retention.
*Lateral tarsorrhaphy or botulinum toxin-induced ptosis may be used to promote healing of corneal epithelial defects.
*Entropion repair: conjunctival incision is avoided if possible.
*Cataract surgery is commonly required.
*Mucous membrane autograft/amniotic membrane transplant
*Limbal stem cell transfer for corneal re-epithelialization
*Keratoprosthesis in end stage disease

70
Q

What is Steven Johnson Syndrome?

A

a cell-mediated delayed hypersensitivity reaction, usually
related to drug exposure. A wide range of medications have been
incriminated, including antibiotics (especially sulfonamides and
trimethoprim), analgesics including paracetamol (acetaminophen),
nevirapine (widely prescribed as a part of combination therapy for
HIV infection), cold remedies and anticonvulsants.

Infections due to microorganisms such as Mycoplasma pneumoniae and HSV and some cancers have also been implicated. Because symptoms often take weeks to develop, in many cases the precipitant cannot be identified.
Mortality overall is around 5% in SJS (death is commonly due to infection), but is considerably higher in TEN.

71
Q

What are the symptoms and signs of SJS?

A

Symptoms- redness/mild-severe grittiness, photophobia, watering and blurry vision.

Acute signs-haemorrhagic crusting of lid margins, papillary conjunctivitis, conjunctival (pseudo)membranes, keratopathy with PEE’s.

Late signs- conjunctival cicatrization with forniceal shortening and symblepharon formation, cicatricial entropion, keratopathy eg scarring/vascularization, watery eyes due to fibrosis

72
Q

What are the systemic features of SJS

A

Skin biopsy to make the diagnosis

Symptoms- Flu like symptoms can be severe may last upto 2 weeks before lesions occur.

Signs- blistering mucosal lesions, haemorrhagic lid crusting, purpuric vesicular skin lesions on extremities, face and trunk.

73
Q

What are the systemic treatment options for SJS?

A

*Removal of the precipitant eg discontinuation of drugs and treatment of suspected infection.
*General supportive measures such as maintenance of adequate hydration, electrolyte balance and nutrition (especially protein replacement) are critical.
*Systemic steroids remain controversial.
*Other immunosuppressants including ciclosporin, azathioprine, cyclophosphamide and intravenous immunoglobulin may be considered in selected cases, but are controversial
*Systemic antibiotics may be given as prophylaxis against skin or other systemic infection, avoiding those known to be at higher risk of precipitating SJS/TEN.

74
Q

Ocular treatment for acute disease in SJS?

A

*Daily review cornea and check symblepharon formation
*Topical lubricants
*Prevent corneal exposure
*Topical steroids for irits/conjunctival inflammation
*Topical cycloplegia for comfort
*Lysis of developing symblephara with sterile glass rod/cotton bud
*Scleral ring may prevent symblephara formation
*Treat bacterial keratitis if developing
*IOP monitoring

75
Q

Ocular treatment for chronic disease in SJS?

A

Lubrication
Topical transretinoic acid may reverse keratinization
Treatment of aberrant lashes
BCL (gas permeable scleral lenses)
Mucous membrane grafting for forniceal reconstruction
Corneal rehab with superficial keratectomy for keratinization, lamella corneal grafting for superficial scarring. LSCT, keratoprosthesis

76
Q

What is graft-versus-host disease?

A

Ocular graft-versus-host disease (GVHD) occurs in patients who
have undergone allogenic haematological stem cell transplantation, an operation that is undertaken on an estimated 25,000 individuals annually worldwide

Clinically it manifests in a similar fashion to SJS

77
Q

What % of people develop ocular manifestations after stem cell transplantation?

A

40-60%

78
Q

Ocular features of GvHD?

A

Keratoconjunctivitis sicca
Conj hyperaemia with (pseudo)membrane formation
Chronic inflammation leading to cicatricial changes
Corneal SPEE’s, marginal keratitis, filamentary keratitis, corneal erosion, thinning, ulceration, perforation

79
Q

What is the treatment for ocular GvHD?

A

Artificial tears
Topical cyclosporine
Systemic treatment (oral steroids)

80
Q

What is superior limbic keratoconjunctivitis (SLK)?

A

a relatively uncommon chronic disease of the superior limbus and the superior bulbar and tarsal conjunctiva. It affects one or both eyes of middle-aged women, approximately 50% of whom have abnormal thyroid function (usually hyperthyroidism).

81
Q

What % of people with abnormal thyroid function have SLK?

A

3%

82
Q

What is the pathogenesis of SLK?

A

the result of blink-related trauma between the upper lid and
the superior bulbar conjunctiva, precipitated in many cases by tear
film insufficiency and an excess of lax conjunctival tissue.

83
Q

What are the symptoms of SLK?

A

FB sensation, burning, mild photophobia, mucoid discharge, frequent blinking.
Conjunctiva- hyperaemia, limbal papillary hypertrophy, petechial haemorrhages, keratinization on biopsy or impression cytology

Cornea- SPEE’s separated from the limbus by normal epithelium. Filamentary keratitis in 1/3 cases. Mild superior pannus. Keratoconjunctivitis sicca in 50%

84
Q

How to investigate suspected SLK?

A

Thyroid function testing
Biopsy or impression cytology may show keratinization of superior bulbar conjunctiva.

85
Q

How is SLK treated?

A

*Topical- lubricants, NAC, mast cell stabilizers and steroids, topical rebamipide, ciclosporin, retinoic acid for keratinization, autologous serum drops
*Soft CL
*Supratarsal steroid injections
*Temporary superior+/- inferior punctal occlusion
*Resection of superior limbic conjunctiva
*Conjunctival ablation to affected area
*Treatment of thyroid dysfunction

86
Q

What is ligneous conjunctivitis?

A

rare potentially sight- and even
life-threatening disorder characterized by recurrent, often bilateral fibrin-rich pseudomembranous lesions of wood-like consistency that develop mainly on the tarsal conjunctiva.

87
Q

What does histopathology of ligneous conjunctivitis show?

A

amorphous subepithelial deposits
of eosinophilic material consisting predominantly of fibrin

88
Q

How does Ligneous conjunctivitis present and what are the signs?

A

*conjunctivitis, usually in childhood (median age 5 years), although onset may be at any age. A conjunctival lesion is commonly noted by parents.

*Enlarging red-white lobular conjunctival masses which may be covered by thick yellow-white mucoid discharge
*Corneal scarring, vascularization, infection or melting.

89
Q

How is ligneous conjunctivitis treated?

A

*Discontinue antifibrinolytic drugs
Surgical removal with diathermy from the base of the lesion. Preop topical plasminogen to soften pseudomembranes
*After membrane removal, hourly heparin and steroids commenced until wound re-epithelialized
*Recurrence retarded with long term use of ciclosporin and steroids
*IV or topical plasminogen
*Amniotic membrane transplant
*Prophylactic heparin

90
Q

What is Parinaud Oculoglandular syndrome?

A

a rare condition consisting of chronic low-grade fever, unilateral granulomatous conjunctivitis with surrounding follicles and ipsilateral
regional (preauricular) lymphadenopathy.

91
Q

What are the causes of Parinaud oculoglandular syndrome?

A

synonymous with cat scratch disease (caused by Bartonella henselae), although several other causes have been implicated, including tularaemia, insect hairs (ophthalmia nodosum), Treponema pallidum, sporotrichosis, tuberculosis and acute C. trachomatis
infection.

92
Q

What is factitious conjunctivitis?

A

Self-injury (factitious keratoconjunctivitis) is most often intentional, but can also occur inadvertently, as in mucus fishing
syndrome and removal of contact lenses. Damage may be the result of either mechanical trauma or of the instillation of irritant but readily accessible household substances, such as soap. Occasionally over-instillation of prescribed ocular medication is responsible.

93
Q

Symptoms and signs of factitious conjunctivitis?

A

Symptoms disproportionate to signs.
Inferior conj injection and staining with Rose Bengal with quiet superior bulbar conjunctiva
Linear corneal abrasions/persistent ED/focal corneal perforations
Secondary infection with Candida
Sterile ring infiltrate and hypopyon
Corneal scarring

94
Q

How to manage factitious conjunctivitis?

A

*Exclude other diagnoses.
*Close observation may be required.
*Confrontation often leads to failure to return for review.
*A psychiatric opinion may be appropriate.

95
Q

What is a pinguecula?

A

an innocuous but extremely
common asymptomatic elastotic degeneration of the conjunctival
stroma. A yellow–white mound or aggregation of smaller mounds
is seen on the bulbar conjunctiva adjacent to the limbus

Calcification sometimes present

96
Q

Where is a pinguecula normally sited?

A

Nasally>temporal limbus.

97
Q

Difference between pterygium and pinguecula?

A

pinguecula resembles pterygium histologically. The distinction is that the limbal barrier to extension has remained intact with a pinguecula,
though transformation can occur.

In contrast to pingueculae, pterygia
encroach onto the cornea, invading the Bowman layer

98
Q

What is the treatment for pinguecula?

A

*Usually unneccessary to treate
*Irritation with lubrication
*Pingueculitis with lubrication/short course topical steroid
*Excision for cosmetic reasons. Low recurrence compared to pterygium.
*Thermal laser ablation can be effective

99
Q

What is a pterygium?

A

a triangular fibrovascular subepithelial ingrowth of degenerative bulbar conjunctival tissue over the limbus onto the cornea.

Develops in patients who
have been living in sunny countries and, as with pinguecula, may
represent a response to ultraviolet exposure and to other factors
such as chronic surface dryness.

100
Q

What do pinguecula and pterygium show histologically?

A

shows elastotic degenerative changes in vascularized subepithelial
stromal collagen

101
Q

Symptoms and signs of pterygium?

A

○Most small lesions are asymptomatic.
○Irritation and grittiness are caused by a dellen – localized drying – effect at the advancing edge due to interference with the precorneal tear film
○Intermittent inflammation/ pingueculitis
○Linear epithelial iron deposition (Stocker line) may be seen in the corneal epithelium anterior to the head of the pterygium
○Fuchs islets are small discrete whitish flecks consisting of clusters of pterygial epithelial cells often present at the advancing edge.

102
Q

What are the 3 parts of a pterygium?

A

a ‘cap’ (an avascular halo-like zone at the advancing edge),
a head
a body

103
Q

What is the treatment for pterygium?

A

Medical- sunglasses reduce UV exposure
Surgery- Simple excision with bare sclera technique

104
Q

What is the bare sclera technique for pterygium excision?

A

○pterygium is excised from the cornea and conjunctiva leaving bare sclera
○Conjunctival autografting. The donor conjunctival patch is usually harvested from the superior or upper-temporal
para-limbal region. The graft is sutured into position using 10-0 nylon sutures. The site heals rapidly. Conjunctival grafts can be secured with tissue glue (for example: TISSEEL fibrin glue) rather than sutures, thus shortening operating time and reducing postoperative irritation.
○Adjunctive treatment with mitomycin C or beta-irradiation can be used in place of patching techniques.
○ Peripheral lamellar keratoplasty may be required for deep lesions.

105
Q

What are concretions?

A

extremely common and are usually associated with ageing, although they can also form in patients with chronic
conjunctival inflammation such as trachoma.

appear as multiple tiny cysts containing yellowish–white deposits of epithelial debris including keratin, commonly located subepithelially in the inferior tarsal and forniceal conjunctiva. Become calcified and erode through overlying epithelium causing irritation

106
Q

What is conjunctivochalasis?

A

appears as a fold of redundant conjunctiva interposed between the globe and lower eyelid, protruding over the lid margin.

It is probably a normal ageing
change that may be exacerbated by inflammation and mechanical
stress related to dry eye and lid margin disease.

107
Q

How to treat conjunctivochalasis?

A

topical lubricants and treatment of any blepharitis. A short course of topical steroids or another anti-inflammatory agent may be helpful. Conjunctival resection can be performed in severe cases

108
Q

What is a retention cyst?

A

thin-walled lesions on the bulbar
conjunctiva containing clear or occasionally turbid fluid.

109
Q

What do retention cysts show histologically?

A

a fluid-filled internal cavity
lined by a double epithelial layer.

110
Q

How can retention cysts be treated?

A

by simple puncture with a needle under topical anaesthesia, but
recurrence is common. Bleeding should be encouraged within
the ruptured cyst as it may promote adhesion of the walls and reduce the chance of recurrence. Cyst wall excision under topical anaesthesia can be carried out for recurrent cyst formation.

111
Q

What is a subconjunctival haemorrhage?

A

common phenomenon that is often idiopathic and apparently spontaneous, occurring particularly in older individuals. It may result from
surgery, conjunctivitis and trauma. The haemorrhage is usually
asymptomatic but a momentary sharp pain or a snapping or popping sensation is sometimes felt.