OPTOM 353B Flashcards
Corneal layers and its characteristics
Epithelium –> 50um thick and Statified squamous epithelium
Bowmans layer –> Acellular + 10um thick + Dense collagen fibrils
Stroma –> 90% corneal thickness + Layers of Parallel collagen fibrils w keratocytes
Descemets membrane –> Basement membrane of endothelium + 10um thick + Hexagonal fibrils
Endothelium –> Single layer of very thin flat cells + Covers posterior Descements membrane + Major role in corneal hydration
Importance of the endothelium and what does it require
Major role in corneal hydration for transparency, it needs high energy in the single layer of cells for the pump-leak model to function
Function of eye lids
Decrease FB contact and light. 15000 blinks per day to remove FB and pathogens. Has pumps and renews tear fluid maintaining the optical surface
Lipid layer function
Stops aqueous evaporation
Aqeuous and Mucus layer function
Removes free floating microbes, FB and debris. Also has anti-inflam and anti-microbrial proteins like lysozymes
Characteristic of epithelium and function
Tight junctions reducing microbe penetration
Has nerve endings and anti-oxidant production
Minor role in corneal hydration
How often is the epithelium replaced
every 5-7 days due to rapid healing and cell migration
Keratitis
Cornea inflammation giving the cardinal signs and loss of function.
Inflammation signs like epithelial cell loss, immune cell infiltration, corneal swelling and neo-vas.
What does fluorescein staining indicate
Depth of local tear film, it stains disruputed cell-cell junctions. Also absorbs blue light and emits higher wavelength yellow-green light.
Staining is painless
What is SPK
Superficial punctate keratitis
Small pinpoint defects in superficial corneal epithelium and stains w fluorescein. Also assoc. w other ocular disorders
What do stromal infiltrates in the anterior stroma represent
Inflammatory cell migration form limbal vasculature and tear film, can be infectious/non-infectious, epithelium either intact/not-intact
Epithelial oedemas
Means endothelial dysfunction. Leads to epithelial bullae formation causing light scatter. More effect on vision compared to corneal stromal oedemas due to endothelial pump dysfunction. Results in decreased corneal transparency.
Corneal neo-vas.
Corneal pannus is the infiltration of sub-epithelium with fine blood vessels
What is mirobial keratitis
Bacteria/Virus infection from compromised epithelium. Corneal excavations w tissue necrosis. Sight threatening ; Only few bacteria can penetrate epithelium.
What can cause microbrial keratitis
Contact lenses, trauma and herpetic diseases
Microbial keratitis characteristics
Have FB sensation, photophobia and increased pain.
Epithelial defect gives mucopurulent discharge, secondary sterile anterior chamber reaction in the central or periphery
How does microbial keratitis occur
Bacteria colonises stromaa and becomes antigenic releasing enzymes and toxins resulting in immune reaction and inflammation
Then polymorphonuclear leukocytes aggregate and phagocytoses bacteria.
Stroma damage by bacterial enzymes seen
Factors that increase corneal infection risk
CL lens w pathogens on it. Mechanical microtraumas from CL —> Pathogens enter stroma —> Immune reaction and inflammation
Signs of Corneal Infection
Red eyes, epithelial defects, corneal opacification and hypopyon
What is PEDAL
Pain, Epithelial defect, Discharge, Anterior chamber reaction and Location ( usually central )
Acronym to identify lesions that are related to infections
Viral keratitis
Majourity population seroposutuve for HSV antibodies
HSV 1 for the face, lips and eyes
HSV 2 is genital herpes
Primary HSV 1 infection in childhood via droplet with mild fevers and remians dormant in the trigeminal ganglion and the virus activates later in life
What is HSK and its classification
Herpes simplex keratitis
Classification either epithelial, stromal and endothelial.
Epithelial –> Dendritic or geographic ulcer
Stroma –> Stromal necrotic and interstitial keratitis
Endothelial –> Disciform endothelitis
Epithelial HSK
Unilateral w reduced vision.
Signs –> Conjunctival injections, reduced corneal sensation, branching of dendritic ulcer where dendrites can coalesce giving geographic ulcers
Stromal necrotic HSK
Rare w tissue necrosis and viral invasion.
Signs –> Conjunctival injections, cheesy necrotic stroma, anterior uveitis w keratic precipitates ( KPs ) and a vascularised scar
Keratic precipitates
Seen in anterior segment inflammation. Punctate KPs are inflammatory cellular deposits on the corneal endothelium
New vs Old KPs
New –> White and round
Old –> Irregular, faded and pigmented
Endothelitis
HS reaction to viral antigen. Has gradual onset, painless w blurred vision
Signs –> Reduced corneal sensation + Epithelial/stromal oedemas + KPs local to underlying lesion + Anterior chamber inflammation + elevated IOP
What is HZO
Herpes zoster ophthalmicus, from VZV which is dormant in dorsal root ganglion and reactivates as herpes zoster
Gives painful skin rash in trigeminal nerve path. Nasocilliary nerve affected affecting the eye.
Prevalence increases w age
HZO signs and symptoms
Prodromal fever + headaches and Malaise giving vessicular rash over cutaneous branches of the opthalmic nerve where 50% people get epithelial keratitis within 2 days
Epithelial HZO giving a pseudo-dendritic appearance
Complications of long term HZO
Nerve damage giving palsie + Scarring giving ectropion and increased IOP from trabecular meshwork scarring + Chronic inflammation + Dry eye due to tear duct damage
Acanthamoeba Keratitis
Either active as Trophozoites or dormant as cysts
Infection associateed w risk factors like epithelial defects and soft contact lens wear –> hard to diagnose and often treated as smthn else
Acanthamoeba keratitis signs and symptoms
Excruciating pain from attacks on corneal nerves, photophobia and blurred vision
Conjunctival infections, epithelial and sub-epithelial infiltrates w enlarged abscesses seen
Fungal Keratitis
Leads to severe sight loss where corneal infections from yeast like candida
Fungal keratitis risk factors
Ocular trauma, topical steroid therapy and pre-existing ocular/systemic immuosuppressive diseases
Fungal keratitis signs and symptoms
Marked pain and photophobia as presentation where px presents wihtin weeks ratehr than days of red eye
Signs –> Corneal infiltrates and oedemas + Anterior chamber reactions and hypopyopn
What are degenerations
Assoc. w systemtic diseases + inflammation + Age + Thinning corneal tissue + Unilateral
What are dystrophies
Inherited corneal disease, Autosomal dominant + Bilateral/Symmetry/Early onset and progressive
What is Arcus Senilis
In elderly, has white perilimbal band w clear zone + Phospholipid/cholesterol deposition in stroma + Px asymptomatic w no treatment needed
What is Arcus Juvenilis
Rare + Small part of peripheral cornea and Assoc. w genetic high blood cholesterol
Vogt’s limbal girdle
Common and age related + Sub-epithelial degeneration + w/wo calcium deposits in nasal and temporal perilimbal cornea w no visual significance
What is Dellen and how does it occur
Localised thinning of peripheral cornea w the dehydration and compaction of cornea
From Tear film instability assoc. w scarring and vascularisation. Pooling of fluorescein seen but epithelium is intact
Band keratopathy
Uncommon calcium deposits in sub-epithelial, bowmans and anterior stroma due to age related, chronic ocular inflammation, metabolic disruption and hereditary
Vision affected is central and cuase ocular irritation and begins nasally or temporally, expands centrally
Terrien’s Marginal degeneration
Non-inflamm progressive thinning or peripheral corneal stroma superiorly + Lipid deposits between collagen layers + intact epithelium + Bilateral + Slow progression + Assoc. w Vascularisation + Decreased vision caused by irregular astigmatism.
What is Mooren’s Ulcer
Peripheral ulcerative keratitis that is uni/bilateral, has autoimmune response to stromal antigens
Mooren’s ulcer signs and symptoms
Redness, pain, photophobia and decreased vision. Epithelial defects and healing assoc. w thinning and corneal vascularisation
Rosacea Keratitis
Skin disease w itching and flushing of facial skin.
Has prominent blood vessels w butterfly rash patterns aggravated sun exposure w dry eye and blepharitis.
Assoc. w margincal keratitis and Neo-vas.
What is RCE
Recurrent Corneal erosion. syndrome.
From unstable epithelial to basement membrane, uni/bilateral.
Dystropic RCE assoc. w corneal dystrophies. Post traumatic RCE follows superficial corneal trauma.
RCE signs and symptoms
Has recurrent ocular surface pain, blurred vision and photophobia.
Localised epithelial injuries w microcysts after healing seen
Corneal dystrophies
Genetic abnormalities in corneal structure and funcrion. This is autosomal dominant and treatment involves corneal graft
Where can corneal dystrophies occur
Epithelial –> Epithelial basement membrane dystrophy + Messman’s
Stromal –> Reis-Bucklers + Granular + Lattice + Macular
Endothelial –> Fuchs endothelial dystrophy + Posterior polymorphous dystrophy
What is epithelial basement membrane dystrophy ( EMBD )
Autosomal dominant assoc. w recurrent corneal erosion syndrome affecting central cornea if involved
EMBD signs and symptoms
Epithelial cells poorly attached to basement membrane
Maps –> Multilaminar basement membrane extending into epithelium
Dots –> Deep epithelial cells migrating to surface and trapped under abnormal basement membrane
Fingerprints –> Folds of reduplicated basemenr membrane within epithelium
Meesman’s Dystrophy
Autosomal dominant w tiny cysts in epithelium, has minimal effect on VA but has recurrent erosions
Reis-Bucklers Dystrophy
Bilateral and starts from young age. Damage to bowmans layer and anterior stroma.
Sub-epithelial opacities central but most dense in mid-periphery. Has loss of hemi-desmosomes causing recurrent lesions
Granular dystrophy
Autosomal dominant w granular deposits of hyaline in central anterior stroma w clear zones in between.
Decreased vision when opacities are confluent and has recurrent corneal erosions
Lattice dystrophy
Has stromal amyloid deposits w poor epithelial adhesion. There is Type 1 and 2 autosomal dominant and Type 3 autosomal recessive
Explain the lattice dystrophy types
Type 1 AD –> Most common w fine branched lines in anterior or mid stroma w periphery spared
Type 2 AD –> Thicker lines and begins peripherally
Type 3 AR –> Coarser lines limbus to limbus
Macular dystrophy
Autosomal recessice w Mucopolysaccharide deposits in stromal keratocytes.
Corneal thinning and progressive visiion loss where px needs corneal transplant. Does not lead to RCES
Fuchs endothelial dystrophy
Progressive and more in women. Autosomal dominant but can be recessive.
Starts asa endothelial dystrophy and progresses to Fuch’s endothelial dystrophy where vision loss and has pain is epithelial bullae is present
Corneal Guttata
Collagen deposits on Descemet’s membrane, the Guttata is visible on slit lamp exam, w endothelial cell loss
Pleomorphism and Polymegathism seen
Stages of Fuchs endothelial dystrophy
- Guttata and thickening of descemets membrane from collagen deposits
- Progressive loss of endothelial cells causing breakdown in barrier function and active transport givng corneal oedema
- Denegerative pannus and scarring w permanent vision loss ( May need corneal graft )
Posterior polymorphus dystrophy
Autosomal dominant affecting descemets membrane and endothelium. Has bubble like lesions on endothelium and has band like lesions across the endothelium
What can posterior polymorphus dystrophy cause
Compromises endothelium, where there is abnormal endothelial cells growing into the angle giving glaucoma.
What is the cause of blindness in developed countries
Trauma from chemical burns, thermal, abrasion and UV
Corneal wound healing process
Endothelium heals fast, epithelial cells migrate to site in 4 hours.
Stromal injuries heal slowly. Descements ,embrane also heals slowly and scars easily.
Endothelium has limited miotic or regenerative capacity where cells change shape and spread to cover defect
Consequences of Alkali burns on eyes
More severe than acid burns as it penetrates cornea and anterior chamber. Alkali combines w lipids causing cell disruption
Sloughing of corneal epithelium seen, stromal cell necrosis leads to oedema or corneal stroma.
Keratoconus
Non-inflammatory cental or paracentral thinning of stroma giving progressive corneal potrusion and steepening resulting in myopia and astigmatism. Has reduced vision and corneal scarring
Keratoconus treatment
KC begins w progression between age 10-40.
Treat w rigid gas permeable CLs. Some px need corneal graft due to poor VA. Aim is to prevent progression and the need for graft
Why is there variation in keratoconus studies
Due to different study inclusion criteria and factors like genetic predisposition and environmental cofactors
Keratoconus associations and symptoms
Assoc. w –> Asthma, hay fever and eczema, presents as sporadic disorder
Symptoms such as decreased vision, has glare sensitivity, monocular double vision, itchy eyes and sometimes pain.
Irregular astigmatism
Non-uniform steepening of cornea w blurred vision or monocular diplopia.
From corneal denegerations, corneal surgery and trauma
Keratoconus signs
Corneal thinning, central/paracentral ectasia, steep keratometry readings, changing in refraction w increasing astigmatim and myopia. Also abnormal retinoscope reflex
Will see prominent corneal nerves, Vogt’s striae and fleischer’s ring
If KC is advanced then Munson’s signs seen and corneal hydrops
Types of cones in KC
Nipple, Oval anf Keratoglobus
What will we see in retinoscopy w px of KC
Scissoring or swirling reflex that is hard to neutralise.
Oil droplet sign seen in dilated pupils in Opthalmoscopy
What is Vogt’s striae
Vertical white ligns in corneal stroma or Descemets membrane, will see this under high magnification w white light. Could be from mechanical stress
What is Fleischer’s ring
Iron pigment ring deposits at base of cone in deep layers or corneal epithelium, seenw blue cobalt filter
Munsons’ sign
Advanced KC where superfical corneal swelling seen due to breaks in the bowmans layer.
Looks like a V shaped protrusion of the lower eyelid during a down gaze
Corneal hydrops
Ruptured descemet’s membrane allowing AH to flow into cornea giving swelling of stroma and epithelium.
Symptoms of Corneal hydrops
Px has sudden and painful vision loss. Gives corneal opacification w vascularisation
Leads to flattened cornea on respution so px may need corneal graft to improve vision
What is KC severity based on
The best spectacle corrected VA, Keratometry readings, inferior and superior differences in corneal pachymetry
There is forme Fruste keratoconus where ther eis non-inflammatory thinning of cornea w no clinical signs
What happens in KC ( Keratoconus )
Stroma becomes compact and fibrils are lost in anterior stroma. The thinning due to re-orientation of stromal collagen and reduced keratocytes in anterior stroma
KC etiology
Apoptosis from enzyme release follwing chronic epithelial injury
Function of Keratocytes
Maintain, repair of stroma and collagen/GP/GAGs synthesis. All maintains transparency
What do rigid gas permable contact wear do
Endothelial pleomorphism, polymegathism and thinning
Is KC and endothelial cell abnormality associated
Maybe as KC has ndothelial cell abnormalities, but most KC px also wear RGP CLs so the endothelium is not directly due to the disease
KC management
Spectacles, soft CLs, Rigid CLs, Intacs corneal implants, Corneal collagen cross linking and corneal transplant
Glx and CLs use in KC
Glx used in early stages, but does not correct irregular astigmatism.
Soft CLs drape over the cornea contour so not good for correction
RGPs treats moderate KC but w increasing cone height the RGPs become unstable or cause corneal scarring
Intacs and Corneal implants use in KC
Thin and semi-circular plastic ring segments inserted into corneal stroma under anaesthesia.
This flattens cornea and reduces distortion improving vision –> Gives reduced central K readings, Px selection also important
Corneal collagen cross-linking use in KC
Newer treatment slowing KC progression and strengthens corneal tissue. Involves corneal epithelium removal/Vitamin B/UVA light exposure and potential for endothelial damage
Corneal transplants
Done when cornea becomes very thin and no other treatments give good vision. in NZ, 50% of corneal grafts is for KC and close monitoring for graft rejection
What is PKP
Penetrating keratoplasty, for full thickness corneal transplant if significant stromal scarring or unknown endothelial status –> Has long post-op recovery time
What is DALK
Deep anterior lamellar keratoplasty, for partial thickness transplant. There is a selective transplant of corneal stroma where the stroma is involved but the endothelium is healthy which decreases risk of endothelial rejection
What is pellucid marginal degeneration
Rare, bilateral corneal ectasia. It is non-inflammatory w a peripheral band of severe thinning of the inferior cornea.
Thinner area is flatter but superior cornea is steepest w Severe VA reduction. The clear band of normal cornea separates thinned cornea from limbus.
What is the conjunctiva
Thin transparent vascularised mucous membrane
What does the conjunctiva consist of?
- Palpebral/Tarsal Conjunctiva –> Lines posterior aspect of eyelid and adherent to tarsal plate
- Forniceal Conjunctiva –> Loop between eyelid and globe
- Bulbar conjunctiva –> Covers globe surface, loosely attached to underlying Tenon’s capsule and inserts centrally ay corneoscleral limbus
Where are Lymphatic vessels
In the superficial and deep plexus in the substantia propia
Describe the medial and lateral lymphatics
Laterial is pre-auricular/parotid lymph nodes
Medial is submandocular lymph nodes
Term for external ocular infection
Lymphadenopathy
What is conjunctivitis, and its signs and symptoms
Inflammation of conjunctiva
Signs –> Discharge, chemosis, follicles, papillar and membranes seen
Symptoms –> Ocular discomfort, redness, discharge and lacrimation
VA unaffected
What is the redness seen in conjunctivitis
Diffuse, involving entire conjunctival surface. Hyperemia seen due to increased redness of conjunctival blood vessels.
Injection seen due to vasodilation of conjunctival blood vessels where intensity increases going away from the limbus. Different to ciliary injection
What is the discharge seen in conjunctivitis
Exudate from conjunctival epithelium from dilated vessels
Discharge quality depends on the causative agent such as if it is watery, mucoid, mucous-purulent and severe purulent
What is the Chemosis in conjunctivitis
Macroscopic severe conjunctival swelling where protein rich exudtaes through the walls of inflamed blood vessels. This results in translucent blisters that protrude through the clsoed eyelid.
What are the follicles in conjunctivitis
Supepithelial foci of hyperplastic lymphoid tissue within conjunctival stroma. Multiple slightly elevated yellow-white nodukes seen. It is avascular but assoc. w vascularisation and viral/chlamydial conjunctivitis
What is the papillae in conjunctivitis
Conjunctival epithelial hyperplasia, has vascular core w various inflammatory cells that develop in the palpebral and limbal bulber conjunctiva
Has a non-specific inflammatory response where it is assoc. w CL wear and floppy eyelid syndrome
What are the membranes in conjunctivitis
True membrane infiltrate superficial layers of conjunctival epithelium.
If removed then tearing anf bleeding will occur.
The cause of this is Steven-Jognson syndrome where pseudomembranes are coagulated exudates that is adherent to inflamed conuunctival epithelium which can be peeled away keaving epithelium intact. Due to bacterial conjunctivitis from S.Pyogenes
Bacterial Conjunctivitis
Bacteria infection from contact w infected secretions such as S.epigermis/auerus/pneumoniae/influenzae.
Common and has muco-purulent discharge w eyelids often glued tgt upon waking. It is unilateral but becomes bilateral in couple days
Viral conjunctivitis
AKA Adenoviral keratoconjunctivitis AKA Pink eye.
Due to adenocirus fiving pharyngoconjunctival fever ( PCF ) and Epidemic Keratoconjunctivitis ( EKC ). Very contagious w water discharge, follicles and lymphadenopathy.
Development to keratitis is common
Viral Conjunctivitis process
Unilateral redness becoming bilateral very quickly, followed by corneal epitheliopathy. Finally subepithelial infiltrates after a week
How is viral conjunctivitis spread
By respiratory or ocular secretions, so STAY at home until symptoms settled.
Frequent hand washing, avoiding touching eyes, and cover while sneezing recommended. Do not share towels and utensils.
This why sterilising equipment is important
Allergic Conjunctivitis
Non-infectious conjunctivitis due to allergen reaction w contact to the conjunctiva
Pinguecula
Denegeration of elastic tissue and collgen in the conjunctival stroma from response to chronic UV exposure and surface dryness
What is seen in Pinguecula
Yellow-white elevated lesion on bulbar conjunctiva adjacent to limbus, it is more nasal than temporal but usually bilateral
Becomes larger if inflamed
Pterygium
Fibromuscular subepithelial ingrowth of degenrative conjunctival stroma and can be transformed from a pinguecula
Enroaches the limbus onto the cornea invading the bowmans layer
Pterygium characteristics
High vascular conunctival overgrowth extending onto the cornea. Deposits of iron seen in corneal epithelium at apex known as Stocker’s line. There is chronic irritation and vision impairment
Conjunctivochalasis
Excess conunctival tissue between the globe and lower lid. It is benign and age related.
Bilateral, redundant bulbar conjunctiva that protrudes over lid margin in inferior bulbar conjunctiva.
Symptoms –> Dry eye and Epiphora
Conjunctival Naevus
Melanocyte proliferation in junction of conjunctival epithelium and the supepithelial tissue
Conunctival Naevus Characteristics
Benign, unilateral, solitary, flat or slightly elevated
Common in juxtalimbal location, less then 1% risk of malignancy
Ethnic melanosis
Common in darker skin pigmentation. Similar to Narvi but its hypermelanosis w normal number of melanocytees. This is bilateral and develops in early years and stable in adulthood
Conjunctival melanoma
Unregulated proliferation of atypical melanocytes w stromal invasion with serious malignancy
Black/grey solitary nodule located at limbus with high metastasis and reccurence rates
Can arise from pre-existing nevus but mostly from PAM ( Primary acquried melanosis )
What is Primary Acquired Melanosis
Acquired unilateral condition of middle aged white individuals involving the limbus and bulbar conjunctiva.
What are the types of PAM
- PAM w/o atypia –> Benign proliferation of normal melanocytes in basal conjunctival epithelium
- PAM w atypia –> Pre-malignant proliferation of atypical melanocytes in all epithelial layers, up to 50% chance of malignancy wihtin 5 years
PAM management
Small lesions without nodules and vascularisation is monitored yearly.
Larger lesions of suspicion require excision. We want to get all the acquired melanotic lesions of the conjunctiva and reviewed by ophthalmologists
Conjunctival papilloma
Proliferation of squamous epithelial cells in conjunctiva. The acquired benign tumours assoc. w HPV type 6 and 11 occuring in various locations.
Conjunctival papilloma Characteristics
It is Sessile ( Rounder ) or pedunculated ( More bumpy ) morphology which is either uni/bilateral and found in juxtalimbal areas.
Symptoms depends on size and location and rarely undergoes malignancy
Conjunctival Intraepithelial Neoplasia ( CIN )
Unregulated proliferation of atypical squamous epithelial cells in conjunctiva, most common ocular surface tumours
CIN process
CIN –> Carcinoma in situ –> Squamous cell carcinoma
CIN characteristics
Unilateral and slightly elevated within the interpalpebral fissure at the limbus. It is slow growing, where redness, FB sensation and mild irritation is seen in older white men.
Subconjunctival Haemorrhage
The rupture of conjunctival blood vessels where blood accumulates between conjunctiva and episclera.
How does subconjunctival haemorrhage occur
Mostly idiopathic, can be from surgery or trauma but liely from older ageS
Subconjunctival haemorrhage symptoms
No pain but there is discharge and inflammation and it looks worse than it feels, there is spontaneous resolution in 1-2 weeks
What is the outer tunic
Opaque, fibrous and protective outer layer of the eye that forms 5/6th of the connective tissue of the globe surface
Anterior vs Posterior sclera
Anterior sclera becomes cornea at limbus
Posterior sclera fuses w optic nerve dural sheath
Thickness ranges form 0.3-1mm, thickest at posterior pole covered by fascial sheath
What makes up the conjunctiva
- Episclera –> Loose and vascularised, connected to the tenons capsule
- Scleral Stroma –> Dense and fibrous collagen tissue that intermingles w networks of fine elastic fibres
- Lamina Fusca –> Innermost thin layer containing melanocytes that blends w the suprechoroid and supraciliary lamellae of the uveal tract
Scleral Stroma Vascular Supply
It is Avascular so the blood comes from the episcleral vascular bed
- Superficial episcleral plexus that runs under the tenons capsule. The vessels are straight w radial configuration
- Deep episcleral plexus resting on superficial surface of sclera
What overlies the anterior sclera also
Layers of conjunctival vessels
What is episcleritis
Inflammation within Tenons blood vessels and episcleral
Episcleritis classifications
- Simple episcleritis which is most common, can be sectoral or diffuse, and spontaneous resolution within weeks
- Nodular episcleritis that is tender with congested red nodules w localised injection. It lasts longer than simple episcleritis
Episcleritis signs and symptoms
Idiopathic, unilateral affecting young to middle age adults. Ocular redness, discomfort, lacrimation also seen
What is scleritis
Oedema and cellular infiltration of the entire thickness of the sclera.
Either infectious or non-infectious ( Most common )
Who does scleritis affect more
Middle aged adults between 4-6th decade in life. More females affected non-infectioudly
Males affected infectiously
Scleritis signs and symptoms
Acute or gradual onset of ocular redness and lacrimation, the ocular pain radiates to the forehead and interferes w sleep
VA reduced w photophobia
Scleritis classification
based on anatomical sites of inflammation and its associated vascular changes
Anterior scleritis
Either mostly non-necrotising or Necrotising w or w/o inflammation
Anterior non-necrotising scleritis types
- Diffuse which is widespread vascular congestion and dilation assoc. w oedema. It resembles simple episcleritis, more in females in 5th life decade. Can recur
- Nodular which are local granulomatous inflammation that resemble nodular episcleritis. Nodules have deeper blue-red colour and tender to palpitation. Same age and concidence as diffuse. BUT 1/4 people get visual impairment
Anterior necrotising scleritis types
With or Without inflammation
Anterior necrotising scleritis with inflammation
Most severe and aggressive form of scleritis.
Goes from Distortion and occlusion of deep vascular plexus –> Scleral necrosis giving spread and coalesce w other necrotic areas –> Scleral thinning giving bluish tinge from increased visibility of underlying area
Onset is 60 Y/O, bilateral presentation and can result in loss of one eye. 25% mortality rate within 5 year onset.
Anterior necrotising scleritis without inflammation
Goes from Necrotic yellow scleral plaques in uninflamed sclera –> Enlargement, spread, coalescence giving slow and progressive scleral thinning exposing underlying uvea –> Staphyloma formation occuring but perforation of globe rare
In women w longstanding rheumatoid arthritis, it is bilateral and painless w no effective treatment
Posterior Scleritis
Scleritis primarily arising posterior to equator affecting women 2x more especially w those already w systemic disease. 85% get visual impairment
Posterior scleritis presentation
Eyelid oedema, ptosis and diplopia. The fundus seen to have ONH swelling, mecular oedema, ERD and choroidal folds
It is bilateral in 35% cases
Scleritis clinical examination
Record time, mode of onset, description of any associated ocular pain and discomfort and any underlying systemic issues
Slit lamp exam in daylight, diffuse lighting w ND filter and red free filter. Blanch w 1gtt phenylephrine 2.5%. Dilation performed to exclude posterior involvement
What are the 3 lines of defence
- Barriers preventing infection
- General response to infection
- Immunity against specific pathogens
What is the eyes 1st line of defence
The orbit, eyelid and blinking which stops microbe-cornea attachment
What is the eyes 2nd and 3rd line of defence
- The vascularised conjunctiva ( B-cells and macrophages )
- Tears that contain plethora of antimicrobial molecules ( Lysozymes, Lactoferrin and transports WBCs )
How does the eye being immune privileged affect its regeneration and immune response
Eye is evolved to limit inflammation, as it cant regenerate it preserves vision.
The privilege is due to lack of blood or lymph vessels in the eye, having the Blood retinal/aqueous barrier and immunosuppressive molecules
What is Sympathetic ophthalmia and how does it occur
It is known as spared eye injury which is bilateral granulomatous uveitis
From injury to one eye causing intraocular inflammation meaning that the eye is no longer privileged as the eye is exposed to sequestered antigens to the adaptive immune response
What happens in sympathetic ophthalmia
BE attacked by immune system via T4 HS which is T cell mediated. It manifests 5 days to several years form injury.
Untreated = Bilateral Blindness
What does re-exposure to allergen do to the body
Each re-exposure to the allergen gives HS response that becomes faster and more severe each time
T1 HS is immediate or known as anaphylactic
T4 HS is delayed or cell-mediated via T cells
What is the process of T1 HS and its time of onset
Onset within 30 mins of exposure, known as allergic reaction
- Sensitisation by allergen binding to IgE and then binding to mast cells and basophils
- Allergen re-exposure causes mast cell degranulation releasing inflammatory mediators
Plasma cells produce IgE
What is Acute allergic conjunctivitis
Common T1 HS conjunctival reaction like pollen.
Either seasonal or perennial allergic conjunctivitis. And anaphylactic drug allergy
Hallmark is bilateral itchy eyes
Acute allergic conjunctivitis Signs
Conjunctival injections, erythematous and oedematous lids, chemises and watery discharge
What is the process and onset of T4 HS
Onset is 24-72 hours after allergen exposure such as poison ivy, Mantoux test and seen in transplant rejection
- Sensitisation by allergen that causes T-cell maturation
- Activation of mature T cells on re-exposure causing 2 responses either TH cells or cytotoxic T cells
What is allergic contact dermatitis
Known as contact allergic blepharoconunctivitis which is non-infectious inflammation.
It is a T4 HS to eyedrops or cosmetics. Involvges skin like Eczematous dermatitis, periorbital oedema, erythema, skin lichenfication and peri-ocular itching w mucoid discharge
What is Phylctenular Keratoconjunctivitis
T4 HS due to S.Aureus which is small pink-grey gelatinous nodules on the bulbar conjunctiva. It is composed of B cells and plasma cells.
Self resolves in 2-3 weeks and can extend into cornea
What is Type 4b HS
A combination of T1 and T2 HS.
IgE and T cell mechanisms play a role where there is feedback cycle of chronic inflammation w elevated humoral response
What is Vernal Keratoconjunctivitis ( VKC )
Severe ocular allergy that affects children and young adults where male is dominated
VKC symptoms
Itchiness, lacrimation, photophobia and mucoid discharge
Worse in spring and summer so this is more seasonal than perennial
Has concomitant atopy like asthma
What is Atopic Keratoconjunctivitis ( AKC )
Persistent and severe form on ocular allergies that develops in adult hood
AKC symptoms
Like VKC but worse, this is more perennial than seasonal so this condition is worse in winte
How is AKC presented
Atopic dermatitis and asthma. Also assoc. w sinal visual morbidity. AKC in tarsal conjunctiva seen as diffuse infiltration and scarring
What is Giant papillary conjunctivitis
AKA mechanically induced papillary conjunctivitis. It is a Non-HS that has inflammation of the tarsal conjunctiva
How is giant papillary conjunctivitis contracted
It is secondary to second CL wear, exposed sutures mucous fishing syndrome due to concurrent allergy that adheres w CLs and the surface of antigen foreign bodies
Giant papillary conjunctivitis symptoms
Same symptoms such as VKC and AKC.
T2 vs T3 vs T5 HS
- T2 is antibody mediated cytotoxicity
- T3 is immune complex mediated
- T5 is stimulatory
What is associated with T2 HS
Auto-immune disorders and allergic reactions to blood transfusions and drugs via IgG/IgM which induces cell destruction
T2 HS process
- Initial allergen contact w IgG/IgM produced by plasma cells that circulate around the body
- IgG/IgM - cell interactions such as phagocytosis, complement activation and ADCC
What is Cicatricial pemphigoid
Known as Mucous membrane pemphigoid, it is chronic and sub-epithelial blistering autoimmune disease.
A T2 HS giving complement activation causing epidermic-dermis separation resulting in scars.
Occurs w older age w more females than males affected
What is Ocular Cicatricial pemphigoid
Has non-specific symptoms of chronic bilateral conjunctivitis, also ask px about lesions on other body parts
How is diagnosis of ocular cicatricial pemphigoid confirmed
With immunofluorescence of biopsy where IgG/A/M and C3 along basement membrane of conjunctival epithelium
Stages of ocular cicatricial pemphigoid
- Early stage where conjunctivitis causes dry eye and papillary conjunctivitis
- Intermediate stages has forniceal shortening and the keratinisation of the caruncle
- End stage has severe conjunctival fibrosis and ankyloblepharon
What is associated with T3 HS
Rheumatoid arthritis, serum sickness mediated by immune complexes which are antigen-antibody aggregations
T3 HS process
- Antibody production from allergen contact causing immune complexes that circulate around the body
- Has Immune complexes that deposit in tissues which initiates immune cascade such as phagocytosis and complement activation
Larger immune complexes give higher risk of tissue damage
What is Sjogren’s Syndrome
A T3 HS, systemic autoimmune disease affecting exocrine glands, can affect kidneys and the liver.
Affects women 9:1 in their 50s. This can be primary or secondary and assoc. w higher risk of malignant non-Hodgkin lymphoma
Sjogren’s syndrome signs
Dry eye giving burning and FB sensation, crusting of eyelids and transient blurry vision. Can perform TBUT and phenol red threat test
Dry mouth with dry fissured tongue
Dry slim which is reduced sweating
Enlarged parotid gland seen
What is T5 HS and its process
Mediated by antibodys.
- Antibody production on contact w allergen
- Antibody binding to cell surface activating cell function so it acts as agonist
What does T5 HS ultimately do
Overstimulates cell function leading to cell destruction
What is Grave’s disease
T5 HS, autoimmune disorder giving thyroid hormone overproduction resulting in hyperthyroidism. Triggered by AB production that reacts w TSH receptors
Who does Grave’s disease affect and its signs
Women in their 50s
symptoms like unexplained weight loss, sweating palpitations and fatigue
30-50% of people w Grave’s disease have ophthalmopathy
What is the TSH feedback loop
Pituitary gland produces TSH –> TSH binds to TSH receptor –> Stimulates hormone synthesis in thyroid cell –> Hormones produced bind to pituitary gland –> Regulates production of thyroid hormones in the pituitary gland
What is Grave’s Ophthalmopathy
Thyroid eye disease ( TED ) is a common extra-thyroidal manifestation of Grave’s.
The TRAb reacts against TSH receptors on orbital fat and connective tissues
What are the stages of Grave’s Ophthalmopathy and its signs
- Active inflammatory stage
- Fibrotic quiescent stage
Soft tissue will be inflamed where peri-orbital and lid swelling is seen w conjunctival hyperemia. Optic neuropathy also seen
What are cataracts and its signs
Opacification to the lens where too much opacification leads to visual impairment
Cloudy and diminished lens is seen.
What is used to evaluate cataracts
VA w std high contrast test
Px w cataracts also sensitive to glare
How to assess cataracts
Via pupil dilation then performing direct opth, retinoscopy, slit lamp and photography for grading
Treatments for cataracts
- IOL replacing cataract lens for treatment or couching which is an ancient technique.
- ICCE ( Intra-capsular cataract extraction ) removes lens and surrounding capsule. IOL put in the anterior chamber
- ECCE ( Extracapsular cataract extraction ) replaces ICCE where now the lens substance is removed w the posterior capsule left intact, the IOL here is placed in the posterior chamber - Phacoemulsification which emulsifies by vibration and removed by suction, this is less invasive and has faster wound healing
How is the lens transparent
Its avascular, no intracellular organelles, compact cortical fibre structure, RI matching in the nucleus and has microcirculation system transport
How does the microcirculation system work
Active ion transport driving fluid fluxes, regulating cell volume, nutrient delivery, waste removal and maintaining RI gradient
What are the cataract morphologies
- Anterior subcapsular ( ASC )
- Cortical
- Nuclear
- Posterior subcapsular ( PSC )
Anterior sub-capsular ( ASC ) morphology
Opacity beneath anterior lens capsule, assoc. w fibrous metaplasia of lens epithelium due to injury to lens epithelium. This leads to formation of ASC fibrous plaques that wrinkles lens capsule and disrupts tissue order.
Least common location and due to ocular trauma
Cortical opacity morphology
Involves anterior, posterior or equitorial cortex in inferonasal quadrant initially. Assoc. w biochemical changes to lens fibres giving fibre cell swelling from ionic imbalances
What is the consequence of cortical opacities
Forms typical cuneiform or radial opacities which can progress to cortical liquefaction due to morgagnian globule formation from age and Diabetes.
Most common location but least visually significant
What affect do cortical opacities have on the lens
Impairs regulation of fibre cell volume due to failed osmotic regulatory systems
Gives imbalance of in/outward water diffusion giving water accumulation, results in fibre cell swelling, water clefts and vacuoles showing a cuneiform and wedge shaped opacities.
Seen w retro illumination
Nuclear opacity morphology
Seen in central lens from biochemical changes to lens fibres where modified crystallin proteins accumulate
Nuclear opacity signs and symptoms
Yellow hue due to urochrome pigment deposition and gets brown when advanced. Age, UV and smoking are risk factors, it is also assoc. w myopic shift
What is a major factor in getting nuclear opacities and how does it work
Oxidative stress due to light absorption by lens substance
Failed ROS scavenger system allows ROS to damage lens where GSH is main antioxidant so in nuclear cataracts the GSH is reduced
More ROS the more cross linking of lens crystallin proteins ( Protein aggregation ) giving refractive index mismatching and opacities
Posterior Subcapsular ( PSC ) opacity morphology
In front of posterior lens capsule due to lens epithelial cell migration along the posterior capsule at the lens equator
What does posterior subcapsular opacity do to the lens
Forms grainy PSC depositions. Diabetes and corticosteroid use increases the chance of this.
Even a little opacity will affect vision due to its density and location
What is the WHO grading criteria for cataracts
NUC-1/2/3
- Cortical part more transparent than central part
- Even opacity throughout the lens
- Central worse than peripheral for opacity
How is the grading for cataracts done
With retro illumination, we want to see if opacity has reached the central lens
Example : NUC-2 + Cen for grade 2 w central opacity
What is LOCS III
Cataract grading system for research and is very detailed. Grading done w dilation to see the full cataracts
Cataract etiology classification and its examples
- Acquired –> Senile, Traumatic, Toxic, Assoc. w systemic disease or Secondary
- Congenital –> Hereditary, Assoc. w syndromes and Intrauterine infection
How does traumatic cataract affect people
Gives unilateral cataract in young people, 65% of ocular trauma gives cataract
Types of traumatic cataracts
Penetrating, Blunt, Electric shock, Infrared radiation and Ionising radiation
Penetrating Trauma
Sharp objects penetrates lens and lens capsule = Focal non-progressive opacities
Blunt Trauma
Extreme force against the eye or face. The cataract takes days-years to develop. The Cataract is transient, static and progressive.
Rosette ASC/PSC opacity most common known as sunflower cataracts.
Concurrent Vossius ring may be present
Electric Shock Trauma
Diffuse/milky-white opacity, Sometimes is snowflake-like opacities in stellate subcapsular distributionI
Infrared radiation Trauma
IR exposure from heating glass or molten metal from an occupation aka glassblowers cataracts.
Opacities seen at any location and causes true exfoliation of anterior lens capsule
Ionising radiation
High exposure to ionising radiation, generally PSC opacities seen so it takes months to years to manifest
What is Toxic Cataracts
Associated w abuse of drugs or toxic substances
Drugs that cause Toxic Cataracts
- Corticosteroids such as anti-inflammatory drugs like Prednisone. Only steroids w gluco-corticoid activity does this which gives PSC opacities. The duration and dose affects this
- Phenothiazines which are anti-psychotic medications. ASC deposits in stellate configuration. The opacities are Dose and duration dependent
- Amiodarone which is an anti-arrhythimic drug treating atrial fibrillation. Seen as punctate/yellow-white ASC opacities
Causes of Systemic disease cataracts
- Diabetes mellitus
- Myotonic Dystrophy
- Atopic Dermatitis
How does diabetes increase risk of cataracts
Cataracts that is 2-5x more common in DM px (Duration of DM and metabolic control). Adults have cortical/PSC opacities, children have snowflake like cortical opacities. This makes it difficult to assess the retina.
Osmotic stress from high glucose increases ROS which gives loss of lens fibres giving swelling and loss of cell volume regulation giving cataracts
How does Myotonic dystrophy increase risk of cataracts
Multi-system disease of not being able to relax and muscle wasting. There is autosomal dominant inheritance where 1–% of the px get bilateral cataracts
Myotonic dystrophy process
At 3rd decade the px will have fine iridescent cortical opacities known as christmas tree cataracts.
At 5th decade we will see cortical and PSC opacities and later on it will be hard to distinguish from typical cortical cataracts
How does Atopic dermatitis increase risk of cataracts
Common form of chronic eczematous dermatitis ( T1 HS ). This is often bilateral and has shield like ASC plaque that wrinkles the anterior capsule
PSC opacities also common
What is secondary cataracts
Cataract from other primary ocular diseases
Causes of secondary cataracts
- Chronic anterior uveitis which is a common cause of secondary cataracts. Correlated to duration and severity inflammation and the corticoid steroid treatment. Gives ASC and PSC opacities
- Acute congestive angle closure
- Hereditary fundus dystrophies resulting in RP
What are congenital cataracts
Present at birth but diagnosed later. Autosomal dominance inheritance giving chromosomal abnormalities, metabolic disorders and intrauterine infections. 2/3 cases are bilateral
How to manage congenital cataracts
Find out the cause and determine visual significance. Should be surgically removed early if it is sight threatening otherwise is can lead to strabismus or amblyopia.
What happens if congenital cataracts are not managed
Long term visual rehabilitation from aggressive ambylopia treatment, high powered glx or CLs or IOL implant when older.
What is PXO ( Posterior capsular opacification )
A late complication of uncomplicated cataract surgery ( 25% cases ). The lens epithelial cells proliferate to re-colonise denuded regions of the anterior capsule and colonises previously cell-free posterior capsule.
What is seen in PXO
Patterns of PCO such as vacuolated, fibrosis type, soemmering ring.
How to treat PXO
Nd:YAG laser capsulotomy
