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64 Cards in this Set
- Front
- Back
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Describe microcornea |
• Bilateral, familial, AD inheritance • <10mm horizontal • Associated with shallow anterior chamber and narrow angle |
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Describe megalocornea |
• Bilateral; Non-progressive • >13mm (12mm in neonates) horizontal Ø • No associated glaucoma BUT is associated with PSC cataract |
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Describe corneal dystrophies |
• They are usually inherited anomalies affecting both eyes • They develop slowly from early life • There are lots of them, but most are very rare |
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Describe corneal disorder degenerations |
• A degeneration is an acquired abnormality in response to inflammation, trauma or ageing • They are not inherited and may be unilateral or bilateral • They develop in later life • They often affect the peripheral cornea • They are common compared to dystrophies |
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Give the inflammation related degenerations of the cornea? |
• Band keratopathy • Saltzmann’s nodular degeneration • Lipid keratopathy |
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Give the trauma related corneal disorder degenerations |
• Climatic droplet keratopathy |
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Give the age related corneal disorder degenerations |
• Arcus senilis • Cornea guttata |
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Describe band keratopathy |
• Bilateral, asymmetrical • Uncommon (prevalence <1/1000) • More common in much older patients (>80yo) • Follows-on from chronic uveitis in conditions such as juvenile idiopathic arthritis • May occur in patients with raised blood calcium levels, e.g. in renal failure |
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What are the symptoms of band keratopathy? |
• Chronic uveitis • HLA B27 associated systemic disease • Blurred vision • Glare • Discomfort |
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What are the signs of band keratopathy? |
• Diffuse horizontally oriented grey opacity, starting in the peripheral cornea at the level of the anterior stroma • Develops towards central cornea through time • Discrete calcium crystals may be visible in band • Overlying epithelial defects • Reduced VA, dependent upon central corneal involvement |
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What is the pathophysiology of band keratopathy? |
• Calcium salts are present in tear film • Inflammation allows penetration of tear fluid into cornea through epithelium and anterior stroma, more in periphery where corneal permeability is highest • Salt deposition gradually accumulates leading to diffuse opacities and eventually crystalline deposits • Opacity, corneal irregularity lead to discomfort and visual acuity loss |
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What is the management of band keratopathy? |
• Ocular lubricants for pain relief • Bandage contact lenses • Chelation or PTK to remove deposits • Recurrence is common |
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What are the associated conditions of band keratopathy? |
• Chronic uveitis • HLA B27 associated systemic disease • Hyperparathyroidism • Renal failure |
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Describe climatic droplet keratopathy (CDK) |
• Bilateral, symmetrical • Rare – requires chronic UV light exposure • Mechanical trauma from dust and sand • Familial • Develops in Bowman’s layer • AKA Labrador keratopathy, spheroidal degeneration |
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What are the symptoms of CDK? |
• Appropriate ocular exposure • FH+ • Burning sensation • Sensitivity to wind • Blurred vision if advanced |
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What are the signs of CDK? |
• Small, golden globules in anterior cornea • Similar distribution and progress to band keratopathy, but less likely to affect central cornea • Epithelial irregularity and opacity in later stages • Reduced VA in later stages |
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What is the pathophysiology of CDK? |
Deposition of degenerate collagen due to an elastotic degeneration (as in pingueculae) |
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What is the management of CDK? |
• Protection from UV and dust, i.e. wrap around sunglasses or avoidance of environment • Ocular lubricants • Superficial keratectomy • If serious, a penetrating keratoplasty |
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What are the associated conditions of CDK? |
• Pterygium • Pingueculae |
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Describe arcus senilis |
• Peripheral corneal disease • Bilateral, symmetrical • Extremely common (practically everyone >80yo) • Increases with age • Typically not seen before age 50 • Affects Descemet’s layer first, then anterior stroma |
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What are the symptoms of arcus senilis? |
None |
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What are the signs of arcus senilis? |
• Narrow white band, initial deep in cornea, but later both deep and superficial, appears as an arc • Initially near lower limbus, then upper, then grows round to form a ring • Clear corneal zone nearly always visible between ring and limbus |
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What is the pathophysiology of arcus senilis? |
Cumulative lipid deposition from limbal vasculature |
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What is the management of arcus senilis? |
• Explanation and reassurance only if in elderly • Blood tests for lipid metabolic disorders if in young or middle aged individuals (Corneal Arcus) |
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What are the associated conditions of arcus senilis? |
• Hypercholesterolaemia younger Px’s < 40 yrs • Coronary heart disease; Atherosclerosis; Stroke |
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What types of infection are associated with the cornea? |
• Bacterial • Viral • Fungal • Amoebic |
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What types of inflammation are associated with the cornea? |
• Irradiation • Chemical • Exposure • Allergic |
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Describe bacterial keratitis |
• Unilateral • Much more serious than bacterial conjunctivitis. Sight threatening • May cause loss of stromal tissue or corneal perforation • 65% associated with contact lens use. Relative risk 10x-40x. Contact lenses give bacteria food, warmth, and something easy to stick to. • Rare: annual incidence 4/100,000 over 1800 CL related cases/year |
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What are the symptoms of bacterial keratitis? |
• Contact lens wear • Dry eye • Recent ocular trauma • RCEE • Photophobia • Pain • Watery discharge (mucopurulent if conjunctiva gets infected too) |
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What are the signs of bacterial keratitis? |
• Red eye • Blepharitis • Greyish white infiltrate in cornea with overlying epithelial staining • Corneal stromal oedema • Anterior uveitis |
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What is the pathophysiology of bacterial keratitis? |
• A breach in the corneal surface allows penetration of bacteria • Bacteria colonize, release enzymes and toxins and induce an immune response • Immune response promotes inflammation and discharge from conjunctiva and iris • Immune cells create infiltrate and oedema in cornea • Stromal cells cannot tolerate the chemical burden and die, causing thinning, eventual scarring, and possible perforation |
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What is the management of bacterial keratitis? |
• Culture of corneal swabs and CL/CL case swabs if appropriate • Broad spectrum topical antibiotic therapy started immediately • Topical steroids should be used after the infection is resolving to minimise the resultant corneal scarring and thinning |
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What are the associated conditions of bacterial keratitis? |
• Bacterial conjunctivitis • Dry eye • Herpes Zoster/Simplex • Corneal trauma • Recurrent corneal epithelia erosion (RCEE) |
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What are the three types of viral keratitis? |
Adenoviral Bilateral Herpes Simplex (HSK) Herpes Zoster (HZO) |
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Describe adenoviral bilateral viral keratitis? |
• Common, annual incidence 1% • Incubation 4-10 days, resolves 10-14 days |
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Describe herpes simplex (HSK) viral keratitis |
• HSV-1 • Unilateral • Common, 90% have HSV1, annual incidence 8/100,000, more common in children • Secondary to primary infection and dormant period in V |
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Describe herpes zoster (HZO) viral keratitis |
• VZV • Unilateral • Common virus, 90% have VZV, annual incidence 20-40/100,000, incidence doubles each decade from 50 • Secondary to primary infection |
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What are the symptoms of adenovirus bilateral viral keratitis? |
• Mild burning • Watery discharge • Photophobia • Blurred vision • URTI |
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What are the symptoms of HSK/ HZO? |
• Viral prodrome • Variable pain • Watery discharge • Photophobia • Variable vision • Ipsilateral skin lesions • Post herpetic neuralgia (HZO) |
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What are the signs of adenovirus viral keratitis? |
• Watery discharge • Follicular conjunctivitis • Scattered subepithelial areolar (snow balls) • corneal opacities • Palpable pre-auricular lymph nodes |
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What are the signs of HSK? |
• Cold-sore skin lesions on both lids • Watery discharge • Conjunctivitis • Corneal oedema • AC inflammation • Dendritic corneal epithelial ulcer, staining with fl and RB • Later amoeboid ulcer |
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What are the signs of HZO? |
• Characteristic skin lesions following course of V1 (Ophthalmic division/nasociliary branch) • Hutchinson’s sign • Conjunctivitis • Palpable pre-auricular lymph nodes • Multiple corneal microdendites peripheral and central • Disciform keratitis (as in HSK) • Scleritis/episcleritis |
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What is the pathophysiology of HZO? |
• Trigeminal root dormancy as in HSK • Virus is more disseminated through V1 than in HSK, hence more of the eye is inflamed • Later dermal scarring can cause entropion and trichiasis |
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What is the management of HKC/ HZO? |
• Avoid trigger factors such as trauma and UV exposure • Avoid contagion (HZO) • Topical antivirals • Topical steroids to control inflammation and prevent scarring • Oral acyclovir • Cycloplegics if uveitis |
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What are the associated conditions of HSK? |
• Cold sores • Uveitis |
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What are the associated conditions of HZO? |
• Chickenpox • Every ocular, intraocular and adnexal inflammation |
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Describe fungal keratitis? |
• Dense, round sub-epithelial corneal infiltrate with surrounding satellite lesions • Concomitant intraocular inflammation • Steroids promote fungal growth, anti-fungals are toxic to the cornea and several are needed to be effective against all fungi • PK is often needed before fungus spreads |
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Describe amoebic keratitis? |
• Bilateral, rare (incidence 1/1,000,000) • Principle infective organism is acanthamoeba • Principle means of infection is through soft contact lenses • Protozoa with hard to kill cystic form (trophozite) • Organism feeds on bacteria and fungi in lens cases • Early infection resembles HSK and slow developing until stroma is invaded • Appears to respond to anti-viral or anti-bacterial treatment, but survives in cystic form |
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What are the symptoms of amoebic keratitis? |
• Contact lens usage (esp with tap water) • Lake or pool swimming • Hot tub usage • 50% discomfort, 50% more pain than signs indicate • Photophobia • Blurred vision |
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What are the signs of ameobic keratitis? |
• Central punctate epitheliitis and limbitis • Pseudo-dendrites • Stromal infiltration along course of corneal nerves • Stromal ring infiltrate |
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What is the pathophysiology of amoebic keratitis? |
• Water borne organism feeds on bacteria in lens case or stagnant water • Corneal infection leads to slow initial growth, then more rapid growth as the epithelium is penetrated and the corneal nerves are used as conduits for invasion • Central replication leads to ring infiltrate • Corneal stromal necrosis, thins and may perforate |
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What is the management of amoebic keratitis? |
• Stop CL wear • Emergency referral to eye casualty • Topical anti-amoebic and trophozoicidal drugs • Concomitant treatment with antibiotics and steroids (remove food supply and reduce inflammation) • PK may be necessary if stromal invasion occurred |
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Describe radiation (UV Keratitis)? |
• Bilateral, acute, common • ~25% of workplace ocular injuries in industrial cities • ~10% of all ocular injuries • Most damage from l=260-290nm (man made light sources) |
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What are the symptoms of UV keratitis? |
• Welding/Electrical flash • Sunbed use • Exposure to high altitude/highly reflective sunny environments • Exposure 8-12 hrs prior to onset of Sx • Intense FB sensation with lacrymation, photophobia and blurred vision |
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What are the signs of UV keratitis? |
• Epiphora • Blepharitis • Sunburn • Corneal and conjunctival superficial punctate staining with fluorescein • Normal tarsal conj and superior cornea |
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What is the pathophysiology of UV keratitis? |
• Superficial epithelial damage to exposed ocular surface • Photochemical cellular damage where absorbed energy is enough to disrupt cellular membranes • Resultant oedema and cellular debris causes blur and pain, hence reflex tearing, osmotic changes and further pain |
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What is the management for uv keratitis? |
• Reassurance: self limiting condition, usually better within 48hrs • Advice for hazard avoidance • Tear lubricants, cold compresses and sunglasses for symptomatic relief |
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What is the clinical information for dystrophies? |
Dystrophies, which usually start early in life, affect both eyes symmetrically, are inherited, are quite rare, but many will affect central vision and cause pain due to RCEE associated with the growth abnormality |
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What is the clinical information for EMB? |
The most common dystrophy, EMB dystrophy, is the least damaging and requires the mildest forms of management. |
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What is the clinical information for keratoconus? |
Keratoconus, despite being a dystrophy is usually asymmetric and only 10-20% go on to require surgical management. |
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What is the clinical information for degenerations? |
Degenerations, which usually start late in life, may be symmetrical or asymmetric, do not have easily identified inheritance patterns and are common. They typically affect the peripheral cornea and do not affect vision. The most commonly observed degenerations are age-related, but degenerations can also arise from external factors such as inflammation and exposure. The latter are more likely to affect vision and cause pain. |
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What is visible in dystrophies and degenerations? |
In dystrophies and degenerations, corneal opacities are visible, but they do not directly stain with fluorescein. Infective corneal opacities will stain with fluorescein. |
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Which dystrophies warrant emergency referral to eye casualty? |
Bacterial keratitis, fungal keratitis, and amoebic keratitis are all sight-threatening conditions and require emergency referral to eye casualty. |
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What is the clinical information for viral keratitis? |
Viral keratitis is by far the most common form of infective keratitis and is treated only with palliative measures, unless there are skin lesions involved indicating the presence of one of the herpetic viruses. |
