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126 Cards in this Set
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Chemical burns
1. Acidic 2. Alkali 3. Radiation |
1. Acid: denatures and precipitates tissue protein. Sulfuric acid is most common. Pathology:causes suppurative necrosis of the conjunctiva and corneal epithelium
2. Alkali: denatures but does not precipitate proteins, causes saponification of fat leading to deeper penetration of chemicals. Lime is most common, Lye causes the most serious injury. Pathology conjunctival and corneal epithelial loss, conjunctival and corneal necrosis, ischemia from thrombosis of conj and episcleral vessels. 3. Radiation: UV light cause Punctate epithelial keratitis and Ionizing radiation cause superficial keratitis, stromal damage, corneal drying from keratinization of conjunctiva |
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How to treat chemical burns?
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1. Copious irrigation, debride any necrotic tissue, remove any particulate matter, check pH.
2. topical and oral sodium ascorbate 3. collagenase inhibitor (acetyl cysteine, EDTA 4. topical steroids first 5-10days ONLY 5. topical antibiotics 6. anti-glaucoma meds 7. cycloplegia 8. Citrate |
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Corneal striae
1. Horizontal 2. Vertical |
Horizontal: Haab striae--> horizontal striae seen in congenital glaucoma
Vertical: Birth forcep trauma, rupture of descemet and endothelium |
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Iron lines
What level of deposition? |
Hudson Stahli - interpalpebral
Ferry - Filtering bleb Stocker - Pterygium head Fleisher - keratoconus Deposition of iron at the epithelium |
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Guidelines for surgical intervention in hyphema
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1. Optic atrophy: IOP >50 for 5 days. IOP > 35 for 7 days
2. Corneal blood staining: First signs of corneal blood staining. IOP > 25 for 6 days 3. PAS: Total hyphema for 5 days, diffuse total hyphema for 9 days 4. Sickle cell: IOP >25 in 24hrs, IOP >30 transiently |
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1. Treatment of hyphema
2. Treatment of hyphema in sickle cell 3. What is rebleed risk? |
1. Bed rest, head of bed elevated, avoid any anticoagulation (ASA), Shield eye, control IOP (avoid miotics), cycloplegia, topical steroids, control Bp, antiemetics, surgery if meets criteria
2. Beta blockers are safe, AVOID: carbonic anhydrase inh (increase ascorbic acid, metabolic acidosis), epinephrine and alpha agonist (vasoconstriction, deoxygenation), hyperosmotics (hemoconcentration) all lead to increase sickling 3. Risk of rebleed at 2-5 days, use of aminocaprioc acid can help decrease rebleed |
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Papillae
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Small to large elevations with central vascular tufts. Are non specific reactions to conjunctival inflammation.
Usually seen in Bacterial and allergic conjunctivis |
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Follicles
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small avascular mounds of lymphocytes and plasma cells. Mostly in inferior fornix except in trachoma.
Seen in: viral infections, chlamydia |
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Ichthyosis
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hereditary skin disorder results in excessive dry skin and scaling. most common is ichthyosis vulgaris: AD, ocular involvement causes eyelid scaling, cicatritial ectropion, conjunctival thickening. X-linked ichthyosis causes corneal opacities.
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contact dermatoblepharitis
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inflammation of eyelid due to type 4 allergic reaction. Begins 24-72 hrs post exposure. causes eczema, leathery skin, scaling eyelids, hyperpigmentation, scarring, lower lid ectropion.
Meds assoc: 1. cycloplegics- atropine 2. aminoglycosides: neomycin, gentamycin, tobramycin 3. antivirals: idoxuridine, trifluridine 4. preservatives: Thimerosal, EDTA treatment: stop trigger, topical steroids |
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Floppy eyelid syndrome
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Easily everted eyelids, cause chronic papillary conjunctivitis from lid autoeversion during sleep resulting in mechanical irritation. Assoc: obesity, keratoconus, eye rubbing, sleep apnea
treatment: lubrication, tape/patch/shield eyes during sleep, consider horizontal eyelid tightning procedure. |
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Giant Papillary conjunctivitis
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Allergic reaction to some material whether a contact lens, exposed suture, ocular prosthesis. Will see in vernal and atopic keratoconjunctivitis.
Giant papilla >1.0mm on upper palpebral conjunctiva. Remove the trigger, topical allergy medication, avoid thimerosal. symptoms resolve months before papillae resolve |
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Atopic keratoconjunctivitis
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A type 1,4 hypersensitivity adult onset, hx of atopy, eczema, hay fever, asthma. Present with itching, burning, photophobia, tearing, blurry va. Have papillary conjunctivitis, symblepharon formation, corneal neo, corneal scarring.
Assoc: keratoconus, subcapsular cataracts(maltese cross pattern), HSV keratitis. Pathology: mast cell infiltration on conjunctival epithelium. Treat with topical allergy meds, systemic antihistamine, cyclosporine. |
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Vernal conjunctivitis
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A seasonal allergic conjunctivitis. occurs in young boys and resolves by puberty. have Fhx atopy and stopic dematitis. Will have itching, photophobia, pain. present with cobblestone papillae, limble follicles, horner trantas dot (accum eosinophils), ropy mucus, pseudomembrane, keratitis, shield ulcer
Have high IgE in tears. Pathology of conj have mast cells, eosinophils, basophils. treat with topical allergy meds, cyclosporine. |
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Ligneous conjunctivitis
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occurs in children girls, a bilateral pseudomembranous conjunctivits, acute onset with a chronic course. present with a vascular, raised, friable, woody lesion of palpebral conjunctiva. Removing it bleeds. Can affect all mucous membranes (mouth, vagina) Pathology shows acellular, eosinophilic hyaline material, granulation tissue.
Treat with excision and will bleed, topical and oral steroids, topical antiiotics, acetylcysteine, hyaluronidase, alpha chymotrypsin, daily debridement. Consult ENT to make sure respiratory tract not invovled. |
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Superior limbic keratoconjunctivits
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Occurs in females, bilateral recurrent inflammation of superior bulbar and palpebral conjunctiva. Assoc with contact lens wear and thyroid dysfunction Have foreign body sensation, burning, photophobia, blurred vision. Present with redundant superior bulbar conjunctiva, thickening, hyperemia. stains with rose bengal, papillary conjunctivitis, filamentary keratitis. schrimer's decreased. Must check for thyroid dysfunction. Treatment: scarring of superior conjunctiva, pressure patch, bandage contact lens, mechanical scraping, topical silver nitrate (avoid silvernitrate stick), thermo cautery, resession or resection of conjunctiva
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Filamentary Keratitis
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Strands composed of epithelium and mucus. due to increase turnover epithelium and mucus production. Assoc conditions: KCS, SLK, recurrent erosions, bullous keratopathy, prolong patching, HSV keratitis, neurotrophic keratitis, trauma, atopic keratitis, adenoviral conjunctivitis, medicamentosa, ptosis. NOT seen in OCP. Treat with mucomyst, lubrication, remove filaments, bandage contact lens, treat underlying disorder
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Neurotrophic keratitis
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Occurs when there is corneal anesthesia from CN 5 lesion. Cause epithelial abnormality. Can have non-healing epithelial defect, infection, perforation. Etiology: HSV, HZV, stroke, surgery, irradiation, tumor. Always test corneal sensation. treat with lubrication, antibiotic ointment, tarsorrhaphy, rule out an infection by culturing.
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Pemphigus Vulgaris
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No extensive scarring like OCP. skin condition that rarely affect eyes. Antigen antibodies are within the epithelium. Does not involve the substantia propia or dermis.
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Ocular cicatricial pemphigoid
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Occurs in old women, a bullous disease of mucous membrane leading to scarring. Due to autoimmune complexes (IgA) in the basement membrane. assoc with HLA B12, Meds(pilo, phopholine iodide, timolol, epinephrine, idoxuridine). presents with symblepharon, ankyloblepharon, trichiasis, entropion, subconj fibrosis, dry eyes, corneal ulcer, corneal neo and scarring. Can have bullous lesion in face, scalp, inguinal area, and mucous membrane causing strictures and dysphagia.
pathology: antigen antibody complexes at BMZ. treatment: lubrication, immunosuppresive, dapsone (rule G6PD first can cause hemolysis), cyclophosphamide, surgery. |
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Stevens Johnson Syndrome
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Occurs in young, triggered by drugs (sulfa, antibiotics, barbiturates, phenytoin, infection (herpes, mycoplasma), idiopathic. Cause pseudomembrane conjunctivitis, symblepharon, epithelial defect, trichiasis, corneal scarring, vascularizaton, erosions, ulcers.
systemically: have erythema multiforme, targetoid bullous lesions. Minor form: no mucosal invovlement, Major form has mucous membrane ulceration. Pathology: occurs at mucocutanous junction. early on has epithelial thinning, stromal lymphocytic infiltration. Late: has epidermalization, keratinization, subepithelial fibrosis. treat: topical antibiotics, steroids, lubrication, symblepharon lysis. |
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Conjunctival cicatrization
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Stevens Johnson Syndrome
Ocular cicatricial pemphigoid atopic keratoconjunctivits chemical burns trachoma SCC infectious conjunctivitis scleroderma |
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Limbal stem cell deficiency
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limbal stem cells at basal layer of limbus, 25-33% of limbal stem cell need to be intact to ensure normal ocular resurfacing. normal limbus act as barrier to corneal vascularization and conjunctival invasion.
can occur from destruction of stem cells (chemical burn, SJS, infection, contact lens wear) or dysfinction of stem cells (aniridia, MEN, neurotrophic) Have decrease vision (irregular surface), reccurent corneal ulceraton, pain, tearing. Conjunctivization, corneal vascularization, poor epithelium, chronic inflammation. Pathology: bowman's membrane destruction. fibrous ingrowth. Diagnosis: via impression cytology, goblet cells in cornea, cornea epithelium stains with flourecein shows wave of irregularity. Treatment: limbal stem cell transplant, autograft, allograft, a poor candidate for PK. |
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Phlyctenulosis
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Local corneal or conjunctival inflammation due to cell mediated or delayed response to a microbial antigen. Assoc with TB and staph blephroconjunctivits. Present in limbus, bulbar conj, cornea as a small round elevated grey hyperremic nodule. They can necrose and ulcerate leading to involuton and wedge shaped scar --> corneal thinning.
For cases due to staph blepharoconjunctivits must perform lid hygiene, antibiotics, topical steroid with caution. rule out TB |
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Hemorrhagic conjunctivitis
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coxsackie A24
picorna (enteroviris 70) EKC (adenovirus 8,19) have preauricular adenopathy, follicular conjunctivitis, subconj heme, punctate epithelial keratitis, incubation 24hrs, resolve in 1 week. |
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Herpes simplex and its ocular presentations
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Congenital
vesicular blepharitis acute follicular conjunctitivitis primary HSV epithelial keratitis recurrent HSV - epithelial keratitis - necrotizing keratitis - trophic ulcer - disciform keratitis - keratouveitis |
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HSV vesicular blepharitis
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Can be primary or secondary HSV. Have eyelid skin vesicular lesions
treat with antiobiotic ointment to skin lesions. warm or cool soaks to lesion. If involves the lid margin use viroptic 1% 5x/day 1 week |
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HSV acute follicular conjunctivitis
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can be primary or recurrent. present with preauricular lymphadenopathy, conjunctival injection with acute unilateral follicular conjunctivitis. treat with viroptic 1% 5x/day, discontinue when resolved
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Primary HSV epithelial keratitis
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Presents as unilateral blepharoconjunctivitis. follicular with preauricular lymphnode. can develop lid vesicles, epithelial keratitis
Can diagnose culture vesicular fliuid, scraping for vesicle base for cytology and presence of virus, antigen detection, PCR. look for intranuclear viral inclusions and multinucleated giant cells. treatment: usually self limited, use antivirals. triggers for recurrence are: fever, stress, trauma, UV light. |
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HSV epithelial keratitis
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Have dendritic ulcer, live virus at the base of epithelium, dendrite base stains fluorecein while the sides stain rose bengal.
Treat with viroptic 1% 9x/day for 1-2 weeks then taper. Antiviral toxicity: idoxuridine>vidrabine>trifluridine> acyclovir. Use of topical steroids can help reduce scarring, taper slowly. Idoxuridine can cause follicular conjunctivitis, corneal epitheliopathhy, punctal stensis Bilateral herpes simplex more common in ocular atopy |
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HSV disciform keratitis (non-necrotizing keratitis)
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Have a disc shaped stromal edema with intact epithelium. A type 4 hypersensitivity reaction. can have granulomatous Kp, iritis, and increase IOP. culture negative. Pathology shows a granulomatous reaction.
Treatment: mild conditions: cycloplegia only. severe or central: cycloplegia, predforte QID, viroptic 1%QID, can add antibiotic ointment |
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HSV necrotizing keratitis
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(uncommon) a type 3 hypersensitivity. has multiple diffuse, whitish corneal stromal infiltrates with or without epithelial defects, can have stromal inflammation, thinning, and neoveascularization. Iritis, hypopyon, glaucoma can be present. Rule out bacterial superinfection.
Treatment: Treat as a severe disciform keratitis (cycloplegia, topical steroids, topical antiviral, antibiotic ointment) First priority is to treat any epithelial defect and bacterial superinfection with antibiotic drops and ointment. |
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HSV trophic ulcer
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A chornic sterile ulceration with smooth margins that persists or worsens with antiviral therapy, can have stromal melting and perforation. does not stain with rose bengal. treat with aggresive lubrication, tarsorraphy, bandage contact lens
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HSV keratouveitis
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Mark corneal edema, ac reaction, and KPs
will ahve significant bulbar injection possile hypopyon, rubiosis, hyphema, elevated IOP, live virus present. Treatment: topical steroids, oral or topical antivirals, control IOP |
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Study: Herpetic eye disease Study (HEDS)
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1. Is oral acyclovir effective in treating stromal keratitis in addition to topical steroids and antivirals? NO
2. Is topical steroids effective in treating stromal keratitis with viroptic? YES, decreases persistence and progression of stromal keratitis by 68% and shortens duration. 3. does oral acyclovir help HSV keratouveitis? NOT CONCLUSIVE 4. Does oral acyclovir in epithelial keratitis help progression of stromal keratitis or iritis? NO 5. Does oral acyclovir help prevent recurrent ocular HSV? YES, especially those with previous stromal keratitis 6. What are the determinants for recurrent HSV keratitis: Hx stromal keratitis increases risk of subsequent stromal keratitis. NOT epithelial keratitis. |
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What is Wessely's ring?
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Occur in HSV keratitis a type 3 hypersensitivity
Ring of HSV antigen precipiate and neutrophils around stromal edema. |
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Herpes Zoster Ophthalmicus
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vesicular skin rash involving V1 dermatome will not cross midline. Frontal nerve distribution affected most. Hutchingson sign is involvement of tip of noce in distribution of nasociliary branch, can predict ocular involvement. Can present with lid vesicles, lid cicatricial changes, follicular conjunctitis. Cornea can have P.E.E, dentrites (no bulbs, no ulcer, no staining), mucous plaques, disciform keratitis, bullous keratopathy, neurotrophic keratopathy. Iris, segmental atrophy, argyll roberson pupil. uvietis with glaucoma. Retina assoc with CRAO, ARN, PORN, optic neuritis, ishemic optic neuropathy. CN palsy 3,4,6. Diagnosis with skin lesions, tzank prep, serology, culture, ELISA.
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Complication of HZO
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1. Post herpetic neuralgia
2 .meningoencephalitis and myelitis (occur in cranial zoster, dissemination, immnuocompromised) 3. granulomatous arteritis 4. orbitla apex syndrome |
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Treatment of HZO
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Skin rash <72hours: oral acyclovir 800 5x/day, famciclovir 500 TID or valacyclovir 1000 TID for 7 days.
skin rash > 72hours: warm compresses, bacitrain ointment Conjunctival lesion:erythro ointment. warm compress Corneal pseudodendrites: lubrication, topical steroids Stromal keratits: topical steroids Uveitis: topical steroids, cycloplegia, erythromycin ointment Neurotrophic keratitis: rule out bacterial infection, lubrication, erythromycin ointment. If sterile, consider tarsorraphy Scleritis: treat as in scleritis Retinitis, chorioditis, optic neuritis, CN palsy: acyclovir IV, and oral steroids. Increase IOP: control IOP can be from steroids, adjust Post-herpetic neuralgia: amitrptyline, capsaicin cream or doxepin. |
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Epstein Barr virus
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Cause Stromal keratitis
diagnose with antibodies causes lymphocytosis and elevated LFTs |
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Crytalline keratopathy
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caused by strep viridans, candica
associated with chronic steroid use. Present with cracked glass without epithelial defect |
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Corneal deposit due to antibiotic use
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Topical ciprofloxaxin can cause chalky white precipitate withing a epithelial defect
These are precipitates of cipro crystals. Discontinue cipro to allow crystal to resolve |
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Epidemic keratoconjunctivitis
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Caused by adenovirus (DNA) 8,19,37. Bilateral mostly
Present with a preauricular lymphadenopathy, follicular conjunctivitis, watery, lid swelling, pseudomembrane, subconj heme, sympblepharon, subepi infiltrates, corneal erosions. Assoc with pharyngitis, rhinitis. Treat: lubrication, cool compress, peel pseudomembrane, steroids for 1 week then taper. hand washing. |
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Thygeson's
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90% BIL, spontaneous remssion and exacerbations. Have photophobia, FB sensation, burning, tearing, much more symptomatic than seen clinically. Find: punctate, gray opacities in K epithelium, stains in acute attacks. No conjunctivitis, k edema, or iritis. Treat with lubrication, topical steroids to help symptoms and improve lesions but will prolong the course.
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Trachoma
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Caused by chalmydia trachomatis A-C
WHO classification TF: follicles in sup tarsus >5 .5mm TI: inflammed and thick tarsus TS: Scarring and fibrosis of tarsus TT: trichiasis, misdirected lashes CO: corneal opacification, VA <20/60 present: follicles, conjunctivcal scarring, tarsal shortning (entropion), trichiasis, corneal abrasion, corneal scarring, cicatrized limbal follicles (herberts pits) Pathology: epithelial cells with interstitial bodies, leber's cells treat with systemic and topical tetracycline for active disease. lubrication for dry eye and trichiasis. surgical correction of entropion. |
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Adult inclusion conjunctitivits
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caused by chlamydia trachomatis D-K. Chronic follicular conjunctivitis, assoc with vaginitis, urethritis, cervicits
Present with bulbar follicles, subepi infiltrates, corneal pannus, peripheral SEI, stringy mucous discharge. diagnosis: direct immunofluorescence test, chlamydial culture (topical fluorescein can interfere), conjunctival scraping for giemsa: look for basophilic intracytoplasmic inclusion bodies. Treat with azithromycin 1g single dose. For sexual partners doxy 100mg BID or erythro 500mg for 7 days. Topical erythro, tetracycline. |
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Classification of corneal ulcers
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non-immune: trauma, eyelid abnormality, neurotrophic K, acne rosacea, keratomalacia, gold toxicity
systemic immune: KCS, sjogren's, OCP, SJS, RA, SLE, Wegeners, Polyarteritis Nodosa. Locally immune: Mooren's, staph marginal keratitis, vernal keratoconjunctivits infectious: bacterial, fungal, viral, protozoan |
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List organisms that penetrate intact epithelium
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Neisseria
Listeria Shigella H. Aegytus Corynbacterium Haemophillus influenzae |
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List organisms that penetrate a epithelial defect
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Mostly any organism
Staph Strep Pseudomonas |
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Bacterial keratitis
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Increase risk: corneal trauma, surgery, contact lens, epithelial ulceration, dry eye, lid abnormality. Signs of improvement: decrease in infiltrate size, stromal edema, endothelial plaque, ac rxn, hypopyon, reepothelialization.
Treatment: culture first. Small and medium size infiltrate can ise moxifloxacin. Vision threatning: tobramycin or gentamicin 15mg/ml with fortified cafazon 50mg/ml or vancomycin 25mg/ml Q1 hours staggered. Treat with loading dose: 1 drop Q5min x 5. 1 drop Q15min x3, then Q30min. Cycloplegia for comfort, can also add oral fluoroquinolone |
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Staph marginal keratitis
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Is due to hypersensitivity reaction to staph antibodies.
Starts off subepithelial infiltrate with peripheral clear zone. progress to shallow ulcer adjacent to conjunctiva. Injected. Pt can have pain, photophobia. Assoc with blepharitis. Treat: warm compress, lid hygiene, bacitracin ointment. topical steroids or steroid/ABX combo. doxycycline |
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Bacteria commonly found in eyelash
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most do not cause ocular disease.
Staph epidermitis Strep viridans moraxella corynebacterium ** gram negatives never found pathologic organism H influenzae pseudomonas strep pneumo staph aureus bacillus neisseria |
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Phthiriasis palpebrum
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infection of lice of lashes
spread via direct contact, sexually transmitted. causes blepharoconjunctivitis Find: follicules, injection, eggs and lice Treatment: remove the eggs and lice, topical ointment to suffocate the lice, delousing creams, shampoo |
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Hyperacute purulent conjunctivits
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A copius purulent discharge, conjunctival injection, chemosis. caused by neisseria gonorrheae. Present preauricular lymphadenopathy, K infiltrate, corneal perforation in 48hours.
GRam stain show: gram - diplococci treatment: systemic ceftriaxone, IM if no K invovled, IV if corneal involvement. Treat for chlamydia also with erythromycin or doxy. |
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Acanthamoeba keratitis
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Risk: cleaning contacts with homemade solution, swimming or hot tube with contacts. prevent by dissinfecting with heat 75C and hydrogen peroxide systems. Presents with pain out of proportion to clinical findings. Early findings: epithelial cyst, enlarge corneal nerves. late findings: ring shaped infiltrate, corneal edema, iritis, hypopyon, scleritis, can perforate. Diagnosis with giemsa, calcoflour white, culture with non-nutreint agar with e-coli overlay. Pathology show a double walled cyst in stroma.
Treatment: debridement is curative if limited to epithelium. 1. Stop Contacts. 2. polyhexamethyl biguinide .02% Q1H 3. Propamidine .1% 4. neosporin drops 5. itraconazole 400mg load then 100-200QD 6. cycloplegia 7. oral NSAIDS. Can PK if medical failure but recurs. |
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Newcastle disease
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A RNA virus, cause unilateral follicular conjunctivitis with pneumonitis and preauricular lymphadenopathy. Occur in poultry handlers, self-limited, lasts 1 week.
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Salzmann's nodular degeneration
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common in older females, post inflammatory changes due to chronic inflammation, blue white elevated nodules. Seen in phlyctenulosis, trachoma, IK, staph hypersensitivity.
Pathology: replacement of bowman's by hyaline and fibrillar material. treatment superficial keratectomy, PTK. |
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spheroidal degeneration
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Bilateral, males > females, asymptomatic. Due to actinic exposure and old age.
Type 1- most common, involves peripheral corneal Type 2-Assoc with other corneal conditions, can involve the central cornea Type 3-involves the conjunctiva Presents as a tranlucent, golden brown spherical protein deposit (superficial, stroma, conjunctiva) pathology-extracellular basophilic material |
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Band keratopathy
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interpalpebral band of white opacity, begins at the limbus. involves the bowman's mainly
Causes: uveitis, intersitial keratitis, superfical keratitis, phthisis, sarcoid, trauma, silicone oil, hypercalcemia, Vit D intoxication, fanconi, hyperphosphatemia, gout, milk-alkali, myotonic dystrophy, mercury exposure pathology- calcification of epithelial BM, bowmans, anterior stroma. There is destruction of bowmans. Treat with Disodium EDTA chelation. |
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DDx kayser fleisher ring
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Wilson's disease
Intraocular Copper FB Chronic hepatitis primary biliary cirrhosis chronic cholestatic jaundice multiple myeloma |
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Wilson's disease
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AR, increase in copper due to deficiency in ceruloplasmin, copper deposits in the basal ganglia(tremor, ataxia, dysarthria), liver (cirrhosis), eye(kayser-fleischer ring, copper in descemets, starts superior, inferior, medial, temporal) lens (sunflower cataract).
Treat with Oral penicillamine, followed by oral zinc. Kayser fleischer ring resolves with adequate treatment |
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corneal verticillata
what causes? |
Whorl-like opacity in basal epithelium
amiodarone, chloroquine, hydroxychloroqine, indomethacin, phenothiazine. fabry's |
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Keratoconus
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Bilateral, cornea ectasia with inferior corneal protrusion, thinning is at the maximal cone apex. onset at puberty.
Present with corneal protrusion, apical scarring, fleischer ring, vogts striae, prominent K nerves, scissoring reflex, munson sign, rizzutti sign, hydrops (acute edema, clouding due to break of descemets. Pathology: breaks in bowman's, stromal folds, superior scarring, stromal thinning, breaks at descemet will lead to curled edges if hydrops. diagnosis: corneal topography, irregular astigmatism, central or inferior steepening. treat: rigid contact lens, PK, supportive treatnment if hydrops(cycloplegia, pressure patch, sodium chloride ointment) |
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Systemic conditions associated with keratoconus
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Down syndrome
atopy (eye rubbing) marfan's Ehlers Danlos Osteogenesis imperfecta |
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Ocular conditions associated with Keratoconus
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Anridia
RP VKC Leber's congenital amaurosis ectopia lentis CHED PPMD |
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Posterior keratoconus
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Discrete post corneal indentation with stromal haze and thinning. unilateral, nonprogressive.
Anterior corneal is normal. Vision is good. Can have irregular astigmatism Pathology: loss of stromal substance, thin descemets, descemet and endothelium intact |
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Pellucid marginal degeneration
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Typical in 20-40s, BIL corneal thinning below the protrusion. Pathology looks like keratoconus. Diagnose with corneal topography, irregular against the rule astigmatism. inf annular pattern of steepening. Treat with PK, contact lenses.
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Keratoglobus
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sporatic, globular corneal ectasia. assoc with connective tissue disease and lebers congenital amaurosis.
Present with BL corneal thinning in the mid periphery, at base of protrusion. treat with regid contact lens and PK. |
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Name corneal dystrophy
anterior stromal endothelial |
Anterior:
Map dot fingerprint Meeseman gelatinous Droplike Reis Bucker Thiel Benke Stromal: granular lattice Avellino macular central crystalline fleck central cloudy post amorphous CHSD Endothelial: Fuchs Post Polymorphous dystrophy CHED |
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What are the inheritance pattern of the dystrophies?
Name the BIGH-3 dystrophies |
All autosomal dominant except: Macular, gelatinous droplike, Lattice type 3, CHED are all AR.
BIGH-3 (5q31): granular, lattice type 1,3, avellino, Reis Bucklers |
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Corneal dystrophies with systemic disease
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Corneal dystrophies are usually not associated with systemic disease.
except: central crystalline dystrophy assoc with hypercholesterolemia Type 2 lattice, assoc with systmic amyloidosis |
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Map dot fingerprint
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AD, most common anterior corneal dystrophy. BIL in middle age women. present with pain, redness, tearing, decrease vision from reccurent erosions and corneal scarring.
have irregular loose epithelium with map,dot, finger print lines. develop recurrent erosions commonly. Pathology: epithelial reduplication with excess subepithelial and intraepithelial production of BM. Treatment: none unless symptomatic. Erosion treat with lubrication, muro 128, bandage contact lens, epithelial debridement, ant. stromal puncture, laser PTK, debride scar |
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Meeseman's
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AD, has minimal symptoms and good vision. have tiny epithelial vesicles, most interpalpebral. Pathology: epithelial cells contain PAS + material called peculiar substance. thick epithelial BM. No treatment needed.
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Gelatinous drop-like
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AR, rare, occurs in young children. cause decrease vision, photophobia, tearing. Present with a central mulberry subepithelial opacity.
Pathology: shows absent bowman's, +amyloid |
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Reis Bucklers
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AD, BIGH-3, occurs in early life, dystrophy at anterior bowmans. present with subepithelial, irregular rings, scalloped edges, geographic gray white reticular opacification. Most central.
Cause painful erosions and corneal scarring. pathology: absent bowman's and replacement with connective tissue. has irregular saw tooth epithelium. stains masson's trichrome. Treat with PK but recurrence is common. |
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Thiel Benke's dystrophy
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Clinically exactly same as reis bucklers. Only way to differentiate is via electron microscopy. reis bucklers has rod shape bodies. Thiel behkes has curly fibers.
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Granular dystrophy
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AD, BIGH-3, most common stromal dystrophy, deposits occur early in childhood, hyaline deposit. presents as a white granular deposition in the central anterior stroma with interveing clear spaces. Involves central cornea most. Recurrent erosions are rare. Pathology shows hyaline deposit, stain masson's trichrome. Treat with PK, PTK
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Lattice dystrophy
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BIGH-3, amyloid deposit in the stroma early childhood, have branching refractile lines in the ant stroma. best seen with retroillumination, peripheral cornea clear. recurrent erosions with scarring common. 3 typpes
Type 1: AD, classic lattice, central, no systmic amyloidosis Type 2: (meratoja) AD, has systemic amylodsosi, central then spread to periphery Type 3: AR, adult onset, limbus to limbus, no recurrent erision. Pathology shows amyloid staining with congo red, thioflavin T, crystal violet, birefirngence with dichroism. Treatment:PK, recurrence common |
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Macular dystrophy
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AR, error in sysnthesis of keratan sulfate, most severe but least common of the classis stromal dystrophy. Cause decrease vision, have gray white stromal dystrophy at al levels, extend to periphery with diffuse clouding, no intervening clear spaces. pathology show mucopolysaccharide deposit, stains with alcian blue and colloidal iron.
Treatment with PK, erosions are rare.PTK not useful because the lesions run deep into stroma |
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Fleck dystrophy
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AD, a congenital non-progressive, unilateral condition stromal dystrophy. Think as a mix of macular with snyders. vision not affected so patients asymptomatic. Have dandruff-like specks and ring shape opacities. extend to periphery in the stroma. Corneal has decrease sensation. Assoc with limbal dermoids, keratoconus, central cloudy dystrophy of francois, pseusoxanthoma elasticum, atopy. Pathology: mucopolysacharrides and lipid deposits, stain with alcian blue and colloidal iron, sudan black, and oil o red for lipids.
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Schnyder crytalline corneal dystrophy
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AD, slowly progressive, present with yellow-white crystal beneath bowmans in a central pattern (in 50% patients). Have dense arcus, decrease corneal sensitivity. no recurrent erosions. Assoc with hypercholesterolemia, short forearm and genu valgum. Pathology: stains with old-o-red. show cholesteral and fat deposits. can recur in graft check lipid panel.
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Fuch's dystrophy
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AD, commonly in post menopausal women, have blurry vision typical in the morning, pain when bullae ruptured. Has guttata, stromal edema, descemet folds, epithelial bullae, subepithelial fibrosis (beaten bronze) pathology shows guttata, thick BM, atrophic endothelium, cell dropout, endothelial cell polymegathism and pleomorphism, stromal edema. Patients with cell count <1000, CCT > 640, and corneal edema will have great chance of corneal decompensation post cataract sx. Treatment: hypertonic ointment, bandage contact lens, control IOP, conjunctival flap, PK, DSEAK. Can use hairdrier in am.
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Posterior polymorphous Dystrophy
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AD, occur early in life. slowly progressive. vision usually normal. The endothelium behaves like the epithelium. Cells migrate to angle causing angle closure glaucoma 14%. Present with group vesicles, gray lesions, bands, scalloped edges, stromal edema, corectopia, iridocorneal adhesions. Pathology: thick descemets, abnomal multi layer epithelial like endothelial cells. endothelial cells resemble epithelium (+keratin, microvilli, desmosomes, easy culture growth), have intracellular desmosomes. treat with PK but can recur
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Recurrence of corneal dystrophy after PK
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Recur: Ries bucklers, lattice, granular, macular.
RB>lattice>granular>macular |
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Peripheral ulcerative keratitis
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unilateral periphral ulceration due to elevated collaginase, melting stops when epithelium heals.
Assoc with dry eyes (sjogrens), RA, Wegeners, polyarteritis nodosa, SLE, scleroderma. Diagnosis: by blood test CBC, ESR, ANA, RF, ANCA. Treatment: lubrication, punctal occlusion, tarsorrhaphy, consider immunosuppresion, conjunctival resection. Treat underlying disease. |
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Mooren's Ulcer
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A chronic painful, progressive ulceration. Begins nasal or temporal proceeds circumferential. Type 2 hypersensitivity. Assoc Hep C, Crohn's, hydradenitis. Causes pain, blurry vision from significant astigmatism. Has undermined leading edge with overhanging margin.
USA type: unilateral in elderly Africa type:severe BL disease in young that leads to perforation. Pathology: plasma cells, immunoglobulin, complement. Treatment:steroids, immunosuppresion, NSAIDS, bandage contact lens, conj recession or resection. may need corneal gluing, PK for perforation. |
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Terrien's marginal degeneration
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BL, painless, progressive, stromal thinning, starts superior. occur in young. Has a leading lipid edge, steep central and sloping peripheral edge. Epithelium is intact. Circumferential progression. Causes against the rule astigmatism. Can perforate with trauma, rarely spontaneous
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Multiple endocrine neoplasia
(MEN) |
Type 1- Chromosome 11, pituitary, parathyroid, pancreas tumors. Ocular finding is visual field loss from pituitary tumor.
Type 2A- Chomosome 10, medullary thyroid carcinoma, pheochromocytoma, parathyroid. have enlarged corneal nerves. elevated calcitonin, vanillymandelic acid Type 2B- AD, chromosome 10, medullary thyroid carcinoma, pheochromocytoma, GI neuroma, marfinoid. Has enlarged corneal nerves, conjunctival neuroma, eyelid neuroma, dry eye, prominent perilimbal vessels. |
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DDx enlarged corneal nerves
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MEN 2B
refsum syndrome Hansen disease (leprosy) Riley day syndrome neurofibromatosis acanthamoeba |
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DDx for more visible corneal nerves
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keratoconus
ichthyosis fuch's corneal edema congenital glaucoma |
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List of contact lens related problens
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1. SPK- mechanical or CL soln
2. 3-9 oclock staining - poor wetting, refit lens 3. abrasion - start antibiotics, DO NOT PATCH 4. infiltrates- start antibiotics 5. Edema- altered metabolism, decrease wear time 6. Giant papillary conjunctivitis-sensitive to lens material, mechanical irrtation, stop CL, topical allergic medications 7. SLK- sensitivity to CL , Stop CL 8. neovascularization of cornea- chornic hypoxia, refit lens, increase oxygen transmission, stop CL wear 9. Corneal warpage- hard>RGP>soft. irregular astigmatism. Stop CL wear repeat refraction until stable. |
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Graft vs. Host disease
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A bone marrow transplant complication. Ocular findings: KCS (main finding), corneal sloughing, cicatricial conjunctivitis, lagophthalmos, entropion, microvascular retinopathy, optic neruropathy (can be from cyclosporin use)
Stages of conjunctivits: 1. hyperemia, 2. hyperemia with chemosis 3. pseudomembrane 4. pseudomembrane with corneal sloughing Other findings in acute GVHD, maculopapular rash in palm and sole, pruritus, GI diarrhea, elevated liver enzymes. In chornic GVHD, lichenoid skin ,sjogrens like syndrome. treatment: cyclosporine, high dose steroids. In stage 2 or higher patients 12% acute GVHD, 90% mortality. |
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Primary acquired melanosis
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A unilateral, flat, diffuse, patchy, brown pigmentation. waxes and wanes. proliferation of intraepithelial melanocytes. No cysts seen. analogous to lentigo maligna of the skin.
Occurs in middle age white. 30% have malignant transformation. If becomes nodular must have excisional biopsy. PAM without atypia low risk of melanoma. PAM with atypia 46% risk of melanoma. treat with close observation with photos, biopsy, and excise if malignant. |
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Secondary acquired conjunctival melanosis causes
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Pregnancy
topical epinephrine addison's disease radiation |
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conjunctival intraepithelial neoplasia
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premalignant lesion, replacement of conjunctival epithelium by dysplastic squamous cells. Has a translucent gelatinous appearance.
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Carcinoma in situ
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Total replacement of epitheliumby malignant cells to invasion through BM. assoc with HPV 16, 18, actinic exposure. pathology: dysplastic epithelium spreading anterior to bowman's
Treatment: wide local excision with cryo. remove invovled corneal epithelium |
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Conjunctival squamous cell carcinoma
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Most common malignant epithelial tumor of the conjunctiva. rarely metastasize. common in africa and middle east. Pathology shows: invasive malignant squamous cells with penetration through the BM.
Treat: wide excision 4mm beyond margin with removal of surrounding conjunctiva and scleral lamella, cryotherapy (cryo decrease, recurrence from 40- less than <10%). Enucleation if intraocular spread. Exenteration if intraorbital spread. |
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Conjunctival squamous papilloma
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A Benign proliferation of the conjunctival epithelium. can be sessile or pedunculated fleshy mass.
Sessile has broad base, occurs in older at limbus often. Pedunculated cause by HPV, occurs in children located near the caruncle, recurs after excison, but can regress spontaneously. Pathology-vascular, cores covered by acanthotic nonkeratinized, stratified squamous epithelium. Treatment: excisional biopsy with cryo. rare risk for malignant transformation |
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pterygium
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Interpalpebral, wing shape, fibrovascular tissue invading the cornea. assoc with actinic exposure. have stocker line. astigmatism with the flattening meridian of the pterygium. decrease VA if crosses axis. Pathology: elastoid degeneration with destruction to bowman's. treatment: observe or excise. 50% recurrence rate in primary excision.
15% amniotic membrane 5% conjunctival graft mitomycin during surgery |
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sclerocornea
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scleralized cornea, can be peripheral or entire cornea. non-progressive. 50% sporatic 50% hereditary. 90% bilateral. Limbuss indistinct. Assoc with cornea plana 80% persistent pupillary membrane, congenital glaucoma. Corneal transplant has poor prognosis
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DDx blue sclera
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sclera is blue due thinning and visualization of underlying uvea
ehlers danlos, hurlers, turners, marfans, osteogenesis imperfecta, scleromalicia perforans, congenital glaucoma |
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Conjunctival lymphoma
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Smooth fleshy, salmon patch color mass. common in the fornic. can be bilateral. 20% assoc with systemic disease.
Spectrum of disease: 1. Benign reactive lymphoid hyperplasia 2. Atypical lymphoid 3. lymphoma needs immunohisto chemical studies to differentiate between them they all look the same clinically. Require systemic work up:CT, bone scan, SPEP. Treatment: RT, local chemo, surgery |
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Mucoepidermoid carcinoma
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rare SCC variant that contains malignant goblet cells. occurs in the old >60yo. very aggressive, invades the globe via the sclera. suspect in recurrent SCC. Pathology: epidermoid and mucinous components, stains mucicarmine, alcian blue, colloidal iron. Treatment: wide local excision with cryo, high recurrence.
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Donor screening
contraindications for donor corneas |
septicemia
HIV Hep B,C Creutzfeldt Jakob rabies subacute sclerosing panencephalitis PML Lymphoma leukemia systemic malignancy with ocular mets anterior segment tumors Prior intracular surgery **choroidal melanoma no a contraindication! |
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Storage of grafts, What are the techniques for preservation?
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1. cryopreservation
2. preservation in 4C moister chamber (48hrs) 3. McCarey-Kaufman - TC-199, Dextran, gentamicin stored in 4C (48hrs) 4. K-sol- chondritin sulfate in TC199 at 4C 5. Corneal storage media- mercaptoethanol and chondroitin sulfate. 6.Dexol- minimal essential mediam with dextran and chondritin sulfate 7. Optisol- K-sol, dexsol, CSM, vitamins, amino acids, antioxidants --> keeps cornea thinner. |
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Study: Collaborative Corneal Transplant treatment study
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ABO blood typing to check for incompatability, possible risk of rejection
HLA matching not cost effective or advantageous high risk rejection: vascularization of 2 quadrants of cornea preveous graft rejection glaucoma extensive PAS trauma a hereditary surface disorder |
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Radial keratotomy
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Deep radial corneal incisions to correct low to mod myopia
The effect depends on 1. number of incision: more incision more effect 8max 2. depth, deeper more effect 3. size of optical zone, smaller more effect 4. patient age: older more effect 5. sex: men more effect Techniques: downhill or uphill. complication: under or over correction, perforation, infection, scarring, irregular astigmatism, progressive hyperopia glare, fluctuating VA. remember that inferotemporal cornea the thinnest. |
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Photorefractive keratectomy
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Laser ablation of the cornea to correct myopia, hyperopia, and astigmatism
Adv:precise, minimal adj tissue damage Disadv: involve visual axis, risk haze, scarring, regression, needs removal of epithelium contraindications: collagen vascular diseases, autoimmune dz, pregnancy, corneal ectasia, keloid, isotretinoin, amiodarone, sumatriptan. Caution: unstable refraction >.5D/yr, disease affecting wound healing, herpes keratitis, ocular inflammation Complications: under and over correction, haze, scarring, delay re-epitheilization, sterile infiltrate, infection, decentered ablation, central island, irregular astigmatism, regression, glare, halo, dry eye, (glaucoma, cataracts) from steroid use |
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PRK corneal haze and treatment complications
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corneal haze- risk and severy increase with deeper ablations and UV exposure. Results in decrease VA with regression. Treat with oral Vit C 1000mg/day for 1 week presurgery and 2 weeks post surgery
avoid sunlight Treatment complications: 1. enhance under or over corrections, wait 3mo when refraction and corneal topography stable. 2. Haze: topical steroids, mitomycin for 2 min, diamond burr, PTK will change refractive error. 3. Irregular astigmatism- rigid gas permeable contact lens, wave front guided retreatment |
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Superficial keratectomy
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Indications: excision of superficial layers of cornea (epithelium, bowmans, ant stroma), no replacement tissue
Use to: 1. remove hyplastic or necrotic tissue 2. excision retained FB 3. tissue biopsy 4. excision scar, corneal dystrophy technique: 1. mechanical 2. Phototherapeutic keratectomy This laser ablates scar tissue and normal tissue at different rate, cause uneven surface. hyperopic shift, Mitomycin can help decrease post op scarring, oral vit C to decrease haze |
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Descemet's stripping and automated endothelial keratectomy
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endothelium stripped and replaced by a donor lenticle composed of endothelium, descemets, and thin stroma.
- indicated in fuch's dystrophy, pseudophakic bullous keratopathy. complicated by endothelial rejection, separation or displacement of lenticle |
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Endothelial corneal graft faliure
Endothelial corneal graft rejection |
failure: Graft becomes edematous without inflammatory signs:
1. tissue contained marginal endothelial cells 2. loss of endothelial cells later in the post op period, poor surgery 20-25% have endothelial graft rejection |
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Penetrating keratoplasty
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Most common indictation in
Adults: aphakic or pseudophakic bullous keratopathy, fuchs, keratoconus, graft failure, corneal scar Children: peters anomaly Success: 90% clear 1 year, 65% HSV clear 1 year. complications:rejection, failure, glaucoma, recurrent pathology, suprachoroidal or expulsive heme, endophthalmitis |
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Corneal graft rejection
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rarely occurs in 2 weeks, usually 6 months. If treated early can be reversible.
3 forms: epithelial rejection: immune response to donor epithelium, lymphocytes cause a linear epithelial ridge seen early post op 1-13mo. Subepithelial rejection: looks like adenovirus keratitis endothelial rejection: most common form, most serious since endothelium only replaced by graft. Khodadoust line, inflammatory precipitate as endothelium damaged --> stroma thickening, epithelium edematous. treatment frequent steroids. |
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Laser in situ keratomileusis (Lasik)
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Combination of keratomileusis and PRK to correct myopia, hyperopia, astigmatism.
Corneal falp created, laser ablaton on the stromal bed. Adv: rapid healing, less pain, less haze, less post op meds disadv:complications with microkeratome |
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Cogan's syndrome
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autoimmune disorder causing stromal keratitis, vertigo, hearing loss. occurs in young can have URI prodrome. early findings are subepi infiltrates. Rule out syphillis and other infections first this is a diagnosis of exclusion. treat with topical steroids and oral streoids to prevent heairng loss
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Collagen types in cornea
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Type 1 - Stroma
Type 3 - healing stroma Type 4 - basement membrane **bowman's is not a real BM, is consists of compact stromal fibers contain type 1, 5, 6 |
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Central cloudy dystrophy of francois
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non-progressive, vision not affected. have polygonal gray areas in atn stroma looks like crocodile shagreen
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tetracycline
side effects |
inhibits 30S ribosome, take on empty stomach. binds calcium, antaacids, iron. used for chlamydia, rosacea, meibomianitis, sclera melting.
Side effects:GI upset, increase photosensitivity, tooth discoloration in children, decrease OCP effectiveness, teratogenic, nephrotoxic, hepatoxic, can potentiate coumadin |
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topical fluorecein properties
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nontoxic, water soluble
detects disruption of intracellular junctions no antiviral properties ** rose bengal has antiviral and toxic properties |
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properties of aqueous tear deficiency
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1. decrease tear lysozyme and lactoferrin levels
2. decrease tear meniscus (.3mm or less) 3. increase in tear osmolarity |
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What is recommended to prevent transmission of adenovirus for tonometer tips?
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Cleaning of tonometer tips with 1% bleach for 10 minutes
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Oculodermal melanocytosis
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combined pigmentation of skin and ocular surface (uvea, sclera, episclera). 5% bilateral, increase risk glaucoma and malignant transformation. malignant melanoma can occur in skin, conj, uvea, orbit. uveal melanoma risk 1 in 400.
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Keratomileusis
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Technique to correct myopia or hyperopia, a lamellar section removed, frozen and then shaped. It is then replaced.
Contraindicated in glaucoma |
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Keratophakia
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Technique used to correct aphakia, donor lenticle is placed between the cornea and microkeratome created lamellar section.
Contraindicated in thin cornea, infants, glaucoma |
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Epikeratophakia
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Used to correct myopia, hyperopia. The epithelium is removed, donor lenticle is then placed. It is preferred method for children since it is reversible.
Pathology shows 2 bowman's membrane (patient's and donor's) |
