7 - Cornea1 Flashcards
Dellen
= DEHYDRATED STROMA
Area of cornea that wets poorly -> stromal dehydration + corneal thinning -> positive staining/pooling of fluoro
Seen adjacent to areas of elevation (e.g. pterygia)
Asymptomatic or complaints of FBS, other dry eye symp
Exposure keratopathy
- pathophys
- signs/symp
= EYELID ISSUE
Abnormal or incomplete lid closure:
- CN7 issue: Bell’s (idiopathic), cerebrovascular accident, aneurysm, MS, HS/ZV, sarcoid
- orb.oculi issue: surgery causing ectropion, TED, floppy eyelid, #1 NOCTURNAL LAGOPHTHALMOS
Signs: vary from mild SPK (esp INFERIOR 1/3rd) to corneal ulceration, decr corneal sensitivity is common
Symp: redness/FBS/burning that’s WORSE IN THE MORNING
Filamentary keratopathy
- who
- pathophys
Hx of multiple episodes, chornic symptoms of irritation and dryness
CHRONIC INFLAMMATION of cornea -> oc surf dz
#1 = keratoconj-itis sicca
-others: floppy eyelid, slk, corneal erosion, cls overwear, neurotrophic k
Filamentary keratopathy
-signs/symp
Signs: filaments = mucus + degenerated epithelial cells
- remain attached to corneal surface
- range from 0.5 to 10mm
- early = comma-shaped, late = stringy
- will stain with fluoro
Symp: mild-severe FBS, photophobia, epiphora, blur, blepharospasm
Superficial punctate keratitis
- pathophys
- signs/symp
Non-specific inflammation of corneal epithelium
-cls wear, corneal infxn, dry eye, blepharitis, etc.
Pinpoint defects in corneal epi - stains with fluoro
-localized, scattered, confluent (severe)
Asymptomatic; blur, irritation, fbs, photophobia, redness, tearing
Thygeson’s superficial punctate keratopathy
- who
- pathophys
Rare, 2nd-3rd decade, hx of recurrent episodes, no sex predilection
UNKNOWN ETIOLOGY
- may be viral, autoimmune
- no known associated condns
Thygeson’s superficial punctate keratopathy
-signs/symp
Signs: BILATERAL (90%), small, multiple, asymmetric GRAY-WHITE clusters of superficial INTRAEPITHELIAL raised CENTRAL corneal lesions (“crumb-like” opacities)
- acute attacks: last 1-2mo, light fluoro staining, exacerbations within 6-8wks
- remissions: no staining
Symp: FBS, photophobia, tearing, OCCASIONAL BLURRED VISION
-overall, eye is relatively quiet (no ac rxn, conj injection)
3 condns to think of when see intraepithelial corneal defects
Thygeson’s
Herpes
Meesman’s
Neurotropic keratopathy
- who
- pathophys
Past surgical procedures, cls wear, systemic dz, meds
Damage to sensory supply anywhere from trigeminal nucleus to corneal nerve endings -> CN V1 neuropathy -> decr corneal sensitivity + decline in corneal regeneration/wound healing
Neurotropic keratopathy
-common causes
Directly affecting V1: HSV, HZV, DM, LASIK
-also RCEs/dystrophies, medications (timolol, betaxolol, diclofenac sodium)
Damage to CN 7 -> impaired reflex tearing -> chronic damage to ocular surf + disruption to V1
Neurotropic keratopathy
-signs/symp
Signs: decr corneal sensitivity
- early: SPK, perilimbal injection
- late: sterile inferior oval ulcer (-) signs of inflammation
Symp: redness, tearing, decr vision, fbs, swollen eyelids
-CORNEAL FINDINGS»_space;> SYMPTOMS INDICATE
Recurrent corneal erosion
-pathophys
POOR HEMIDESMOSOME ATTACHMENTS to underlying basement membrane
2 scenarios: past abrasian (trauma), dystrophy (EBMD)
-incr risk if abrasion results from organic etiology (fingernail, stick)
Recurrent corneal erosion
-signs/symp
Signs: abrasion of varied size that stains with fluoro
Symp: recurrent, ACUTE PAIN WORSE IN MORNING UPON WAKENING, lacrimation, photophobia, blur
Thermal/UV keratopathy
- who
- pathophys
Prolonged skin exposure, welding, skiing/mountaineer, sunlamps
Epithelium + Bowmans absorb <300nm (UVC)
Excessive UVC absorption -> hyperactivation of K+ channels -> loss of intracellular K+ -> cell death
Thermal/UV keratopathy
-signs/symp
Signs: confluent SPK - stains with fluoro
Symp: pain, photophobia, blur
-WORSE 6-12hrs AFTER INCIDENT
Dry eye disease
- definition
- who is most likely to have it
Multifactorial dz of the tears and ocular surface that results in symptoms of discomfort, visual disturbance, and tear film instability with potential damage to ocular surface
Older, menopausal women
Dry eye disease causes
-medications
Anticholinergic (anti-PNS) effects:
- STop ACH
- anti-histamines/psychotics/depressants/anxiety
- muscle relaxant (cyclobenzaprine)
- ipratropium (via muscarinic blockade)
Other: isotretinoin, BBs, contraceptives, HRT, ADHD, diuretics
Dry eye disease causes
- sytemic diseases
- environmental factors
Big 4: TED, RA, Sjogren’s, Lupus
Fans, dusty environ, low humidity
Dry eye disease
-signs/symp
Signs:
- general: decr TBUT, incr tear osmolarity
- aqueous deficient: THIN TEAR MENISCUS/LAC LAKE/PRISM (<0.2mm), decr Schirmer + phenol red thread (<10mm in 15sec)
- evaporative: decr TBUT, poor expression/atrophy of meibomian gland
- other: conj hyperemia, tear film debris, staining with lissamine green (classically 3/9 o’clock)
Symp: burning, dryness, tearing, itching, blinking, photophobia, cls intolerance, fbs
-WORSE AT THE END OF THE DAY
Dry eye disease
-interpretations of:
—Schirmer 1 + 2
—phenol red thread
S1 = WITHOUT ANESTHETIC = basal, reflex, emotional secr
- normal >10mm in 5 min
- abnorm <5mm in 5 min
S2 = WITH ANESTHETIC = ONLY BASAL (krause, wolfring) secr
-normal >5mm in 5 min
Phenol
-normal >10mm in 15sec
Dry eye disease
-primary mechanisms (2)
Tear HYPEROSMOLARITY -> inflammatory cascade -> damages ocular surf + releases inflamm mediators into tears
- normal/avg: 308 mOSm/L
- dry eye is >308 OR >8 difference between eyes
TF INSTABILITY
-can be secondary to hyperosmolarity or disease process
2 divisions of aqueous deficient dry eye
Sjogren’s
Non-sjogren’s
Primary vs secondary sjogren’s
P: dry eye, dry mouth
S: TRIAD - dry eye, dry mouth, autoimmune CT dz
- RA, SLE, polyarteritis nodosa, wegener’s
- ACCOUNTS FOR 50% OF DRY EYE CASES!
Non-sjogren’s aqueous deficient dry eye
Secondary to LACRIMAL GLAND DYSFUNCTION
Primary lac gland deficiency: #1 AGE-RELATED
Secondary lac gland deficiency: ABC
- attacked gland (sarcoid, lymphoma, aids, graft vs host)
- blocked gland duct (trachoma, pemphigoid, erythema multiforme, burns)
- cut nerves (cls wear*, diabetes, bells, drugs, neuro k, surgery)
- ~50% of cls wearers have dry eye symptoms
Evaporative dry eye
-3 main causes
MGD
Vit A deficiency
Contact lens wear
Evaporative dry eye
-intrinsic causes
Pathology in lid structure/dynamics #1 MGD Lid position disorders: ptosis, nocturnal lagophthalmos Low blink rate: intense concentration, computers, Parkinson’s -results in poor expression of meibum -> hyperkeratinize -> obstruction -> intraductal htn due to build-up -> duct dilation -> mg atrophy
Evaporative dry eye
-extrinsic causes
Independent of lid pathology
Oc surf dz: vit A deficiency (xerophthalmia), topical anesthetics/preservatives
Contact lens wear
All corneal ectasias can cause
Hydrops = splitting of Descemet’s
List 3 corneal ectasias
Keratoconus
Pellucid marginal degeneration
Keratoglobus
Keratoconus
-who
Usually sporadic
6-13% of cases are AD
Commonly presents around puberty
53% have hx of atopy
Keratoconus
-pathophys
Non-inflammatory, progressive, degenerative dz of unknown etiology
Stromal collagen FIBRIL DISPLACEMENT due to loss of adhesion between fibrils -> corneal thinning + protrusion due to degeneration of fibrils by MMPs
Assoc with eye rubbing, atopy, cls wear, ocular condns, systemic condns
- ocular: allergic (vkc, akc, fes), connective tissue abnorm (fuchs, ppmd, granular, lattice), hereditary (aniridia, rp, lebers, rop, cone dystrophy)
- systemic: TDOME (turners, downs, oi, marfans, ehlers)
Keratoconus
-signs/symp
Signs:
- early: fleischer’s ring (iron), scissors reflex, irregular mires, inferior topography steepening
- late: vogt’s striae (vert lines in desc, disappear with pressure), muson’s sign, rizzuti’s sign (conical reflection on nasal cornea with temporal lighting), hydrops
- 53% with mod-severe develop scarring
Symp: progressive decr vision, photophobia, glare, monocular diplopia, ghost images
-acute vision loss + pain if hydrops develops
Keratoconus
-mild vs mod vs severe
Mild: <48D
Mod: 48-54D
Severe: >54D
Pellucid marginal degeneration
- who
- pathophys
Early adulthood (20-40), no sex predilection
Unknown etiology
Thought that COLLAGEN ABNORMALITIES -> thin, weakened area with crescent-shaped inferior distribution
IOP causes corneal protrusion right above area of thinning (NOT WITHIN area of thinning, as with keratoconus)
Pellucid marginal degeneration
-signs/symp
No pain
Bilateral, inferior corneal thinning: 4 to 8 o’clock, 1-2mm from limbus
High ATR astig
Topography: “kissing doves” or “crab claws”
Keratoglobus
- who
- pathophys
- signs
Congenital, AR (tho may be acquired from advanced k-con, trauma, exophthalmos)
Assoc with Ehlers-Danlos, blue sclera, Leber’s congenital amaurosis
Diffuse corneal thinning - concentrated in periphery
Can result in acute corneal edema due to rupture in descemet’s
