• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/130

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

130 Cards in this Set

  • Front
  • Back
Dellen
-Depression; reversible
-Dehydration/thinning of cornea adjacent to raised corneal/limbal lesions (ptyrigium/bleb)
Exposure Keratopathy
-Eyelid issue that leads to K problem
-Incomplete lid closure
-Bell's palsy (CN7)
-Thyroid
-Lagophthalmos
-Floppy eyelid syndrome
Filamentary Keratopathy
Chronic inflammation (ie dry) of cornea leads to strands of epithelial cells in mucous form (like rubbing hands together)
-Filaments will stain
Superficial Punctate Keratitis
-Epithelial defects
-Most common causes: DES, BAK preservative (Travatan Z has no BAK), aminoglycosides (mean to K)
Preservative: Thimerosal
-Mercury
-Toxic
-Don't use more than 3 weeks
-In Viroptic
Thygeson's superficial punctate keratopathy
-U R a HERO if you dx this
-Recurrent episodes of foreign body sensation (6-12 yrs) with no inflam/redness
-Intraepith crumb-like opacities in central K
Neurotropic Keratopathy
-CN5v1 damage leads to desensitization and delayed corneal healing
-Corneal FINDINGS are worse than symtoms
-Hx: stroke, herpes, diabetes
Recurrent Corneal Erosion
-Past K abrasion (especially wood,fingernail) or ABMD (Cogan's) leads to poor adhesion
Thermal/UV keratopathy
-Welding, Skiing, Sunlamp
-Worse 6-12 hours after incident
Dry eye dx (how much wetting?)
PRT (phenol red thread) and Schirmer's: 10mm in 5 minutes
If unanesthetized, Schirmers = 15 mm
Keratoconus
-See it at puberty (eye now full-grown)
-Frequent eyeglass changes
-50% had topical allergies as kid
-Fleischer's ring
-Vogt's striae (stromal vertical lines)
-Munson's sign=downgaze, lower lid
-Hydrops=ruptured Descemet's
Systemic causes of Keratoconus
"TDOME"
Turner
Down's
Ostiogenesis imperfecta
Marfan's
Ehlers Danlos
Iron deposits in cornea:
Fleischer's ring
Hudson Stahli lines
Stocker's line
Ferry's line
Kayser-fleischer ring
Fleischer's -base of cone
Rust ring-foreign body
Hudson Stahli- benign line, lower K of elderly
Stocker's-ptergium
Ferry-Bleb
Kayser-fleischer- copper from **Wilson's disease (liver); causes cataracts at young age (hepatolenticular degen)
Pellucid Marginal Degeneration
-*Kissing doves,Crab claws
-Inferior corneal thinning
-Early adult-hood (not puberty like keratoconus)
-High ATR
Which of the following can happen in pellucid and keratoconus:
Fleischer ring
Hydrops
Scarring
Vogts striae
Pellucid: only hydrops
Keratoconus: everything
Which K dystrophies are Autosomal Dominant and Autosomal Recessive?
All are AD except Macular Dystrophy
Anterior Basement Membrane Dystrophies (names)
-Most common K dystrophy
-Weak/abnormal adhesion between epithelium and basement menbrane
-ABMD, Map-dot, EBMD, Cogan's
-50% of patients with K erosions have ABMD
Meesman's Dystrophy
-Ant K dystrophy (epithelium)
-1st year of life
-100's of cysts
Reis-Buckler
Anterior K dystrophy
Bowman's replaced with collagen
Four types of Stromal dystrophies and respective substance
Marilyn Monroe got high in Los Angeles Sniffing Fat
Macular-mucopolysaccaride
Granular-hyline
Lattice-Amyloid
Schnyder-Hyperlipedemia
Macular dystrophy
-Stromal K dystrophy
*Only autosomal recessive
(Mac Daddy=different from others)
-Most severe stromal dystrophy
-Mucopolysaccharide deposits within stroma (cloudy cornea)
Granular Dystrophy
-Most common stromal dystrophy (Gr = Greatest)
-Hyline deposits in central stroma
Lattice Dystrophy
-Stromal K dystrophy
-Lattice-like lines of amyloid deposits in stroma
Schnyder's dystrophy
-Stromal K dystrophy
-Ring of crystals in central stroma
-Associated with hyperlipidemia
Fuchs Endothelial Dystrophy
Older women
Endothelial guttata, edema
(Guttata in periph=Hassal-Henle)
Pleomorphism(shape), Polymegathism (size)
Increased Pachs
At birth: 3,000 endoth cells
Age 70: 2,000
Edema: 500
Posterior Polymorphous Dystrophy
-*Early in life
-Patches of vesicles
-Typically benign
-Can get secondary angle closure (15%) from metaplasia of endoth cells growing into angle
Megalocornea
-X-linked (males)
-Horizontal diameter of 13mm
(11.7 is normal)
-High myope
-Lens/glaucoma problems
-Connective tissue dz: Marfans, Ehlers-Danlos syndrome, osteogenesis imp
Microcornea
-Diameter less than 10mm
-Hyperope, glaucoma (shallow angle)
Haab's Striae
Horizontal cracks in Descemet's from increase IOP
-Congenital glaucoma
Posterior Embryotoxin
Anteror displaced Schwalbe's line
(glaucoma risk)
Axenfeld's Anomaly/Syndrome
Anomaly=posterior embryotoxin+prominent iris strands
50% develop glaucoma (syndrome)
Rieger's anomaly
Posterior embryotoxin + Axenfeld's + displaced pupil/iris atrophy
-50% develop glaucoma
Reiger's Syndrome
-Anomaly + Mental retardation and skeletal abnormalities
-50% develop glaucoma (Axenfeld syndrome)
Progression of diseases for line/strands/glaucoma/iris/pupil?
PARR
Post Embr = line
Axen anom = strand (syndr=glaucoma)
Rieger's anomaly = pupil/iris
Rieger's syndrome = body
Peter's anomaly
-Central corneal opacity with iris adhesions
-50% glaucoma
Aniridia
75% glaucoma
Foveal hypoplasia
Chorodial coloboma
Limbal dermoid
Dense connective tissue that is commonly located at inferotemporal limbus
Bacterial Keratitis
-Most common etiology of infectious keratitis (*aka ulcer)
-*Infiltrate w/ overlying epi defect (ulcer)
Gram(+) bacteria
Staph, Strep, Clostridium, Corny, antrax
Bacteria that can penetrate intact epithelium
"Canadian Professional National Hockey League" CPNHL
Corneybacterium diphtheriae
Pseudomonas aeruginosa
Neisseria gonorrhea
Haemopilis
Listeria
Fungal Keratitis
-Feathery edges
-Plate on Sabouraud's agar

Three main risk factors:
1-Trauma involving vegetable matter
2-Long-term steroids use
3-Chronic ocular surface dz (dry eye, neurotrophic keratopathy)
What fungus is part of normal flora?
aspergillus
fusarium
candida
pneumocystis pneumonia
Candida
Acanthamoeba Keratitis
-"I can't believe ya" (acanthamoeba) would do that w/your CLs
*-Pain is greater than signs suggest (looks like SPK but more pain)*
-CL hygiene (tap water, swiming)
-Ring ulcer (late finding, transplant time)
-Culture in heat killed e.coli plate
HSV
-Edges of ulcer stain well with rose
-Center stains w/fluorescein
-*Disciform keratitis (disc shaped stromal keratitis due to endothelitis and edema)
-Interstitial Keratitis
-Giemsa stain culture>giant cells
-If epithelium is intact>steroids
-Stromal scarring = decr acuity
-#2 cause of corneal blindness (#1=trauma)
HZV
-Reactivation of chicken-pox virus
-If young, think imunocomp.
-*Prodrome (fever, malaise, tingling)
-Post herpetic neuralgia BAD pain
-Hutchingson's sign=higher risk of ocular involvment (nasociliary nerve of CNV)
-*No terminal bulbs (stuck-on appearance)
-*The entire lesion stains with rose and poorly with NaFl (HSV stains edges with Rose, all with NaFl)
Interstitial Keratitis
Stromal swelling without primary involvment of epi or endo.
**Syphilis 90%**
-*Triad:Saddle nose, hutchinson's teeth, Frontal bossing (signs of congenital syphilis)
3 disease that cause Peripheral Ulcerative Keratitis (PUK)
Mooren's ulcer
Staphylococcal Marginal Keratitis
Collagen vascular disorders (RA, lupus, Wegener)
Mooren's Ulcer
-Vasculitis of Limbal vessels>necrosis>ulcers
-Independant of systemic disorder
-Mid-stage ulcer with overhanging edge
(think, Jared Moore cliff hanging)
-Unilateral, benign, older
Staph marginal keratitis**
-Immune-mediated result of under-treated chronic bleph (staph)
-Multiple stromal infiltrates with no epi staining
(Infiltrate is sign of immune system, NOT infection)
Corneal signs of Collagen vascular disorders
-RA, Lupus, polyarteritis nodosa, wegener granulomatosis)
-Peripheral corneal thinning (that's where the antibodies can access)
-Associated scleritis/episceritis
-K sicca
Terrien's Marginal Degeneration
-Men over 40
-Progressive thinning in periphery
-ATR astigmatism
-Only one that starts superiorly
Salzmann's nodular Degeneration
-Female predilection
-Blue-grey stromal opacities (nodule)
-Seen with K sicca
Band K
-Gout, hypercalcemia, JRA, iritis
-Calcium deposits like "swiss cheese" on anterior surface of bowmans
Corneal Arcus
-Lipid deposition on bowmans and decemet's
-Unilateral arcus *Carotid Disease*
-If under 40 lipid profile is warranted
Corneal graft rejection
Khodadoust line-endo (WBC; dd=endo)
Krachmer's spots-stroma
Type 4 hypersensitivity
Absolute counterindications for refractive sx
<21yo, refractive instability, keratoconus, contact lens warpage, immunosuppression (systemic steroids), active HSVeK, Connective tissue disease, unrealistic expectations
Potential complications of LASIK (laser in situ keratomileusis)
Ectasia (keratoconus), DLK (diffuse lamellar keratitis), higher incidence of dry eye
Potential complications of PRK (photorefractive keratectomy)
Regression, glaucoma (steroids), corneal haze
Potential complications of RK (radial keratotomy )
(radial incisions) Hyperopic shift, diurnal fluctuations
NS
-Refractive error shift
-Etiology
-Myopic shift, "second sight"
-Diffusion of glutathione from aqueous to nucleus of lens diminishes w/age
Cortical
-Refractive error shift
Hyperopic shift
PSC
Affect near vision more than distance
-systemic steroids
-X-rays
Presenile Cataracts
DM, myotonic dystrophy (PSC christmas tree), wilson's, hypocalcemia, *atopic dermatitis*

Get MAD about cataracts early in life
Tramatic cataracts - clinical manifestation
Vossius ring
Toxic cataracts
Chlorpromazine: stellate cataracts
Amiodarone: deposits
Miotics: vacuoles
Gold salts: gold deposits
Disease that can cause lens subluxation
Marfan's (up and out), Ehlers-danlos, homocystinuria
Most serious complication of Marfan's
RD
(also superotemporal lens sublux)
When measuring axial length to determine IOL power for cataract surgery, 1mm represents how many diopters?
3 D
Drug C/I before sx
Anticoagulents, Tamsulin (flowmax), prostaglandins
Acute postoperative bacterial endophalmitis
-Prognosis
-Infecting agent
1/1000, 50% go blind in that eye
-Staph epidermis
-Hypopyon
-Occurs within days
PCO (after-cataract)
-2-6 months after sx
-Elschnig pearls (type of PCO in children)
Post Sx Cystoid Macular Edema
-Called Irvine-Gass syndrome
-Happens in 6-10 weeks
-Can be prostaglandin-induced
Asteroid hyalosis
-Unilateral 75%
-Usually asymptomatic
-Calcium-phosphate soaps
Synchysis Scintillans
-Golden brown cholesterol crystals that often settle in inferior vitreous
-Occurs after chronic uveitis, vitreous heme, trauma
PVD
-Prevalence approximates age (50yo=50%, 75yo=75%)
-Acute onset of floaters, flashes of light, decreased VA
-Weiss ring
-Tobacco dust (Shafer's sign) w/retinal break
-10% have RD
Vitreous Heme
-Diabetes**
-Trauma, HTN, BRVO, PVD, ARMD, Sickle,
-Pre-retinal is boat-shaped
What systemic conditions can cause tractional detachments?
Diabetes, sickle cell ret, ROP, Ocular ischemic syndrome, vascular occlusion
Does a CRVA or a CRVO release VEGF?
Ischemia vs hypoxia?
CRVO: sick retina can release VEGF
CRAO: dead retina can't release VEGF

Ischemia is reduced blood flow, which results in hypoxia.
However, hypoxia can occur if blood has insufficient O2
CRVO
-All 4 quadrants
-Collateral veins can form over weeks-months and drain retina to choroid
-Usu involves artery compressing vein (due to HTN, DM)
-90-day glaucoma from NVI
-Ischemic=10DD of non-purfusion, 20/200 or worse
-Non-ischemic 20/40 or better
-Concern: Macular disease (isch, edema, ret heme), Neo (heme, glaucoma, RD, vitr heme)
BRVO most common quadrant
-Superior temporal
-Most common vasc occlusive dz
-Concern: same as CRVO
(macular ischemia/edema, neo)
CRAO
-White in all 4 quadrants
-HTN 67%
-Emboli are usually (1)*calcific from heart (2) Hollenhorst cholesterol from carotid
-CRAO more common than BRAO
-20/400 or worse unless cilioretinal artery is present (15-20% of population; from choroid)
-APD, cherry red spot
*Narrowed arteries may be only sign patient had CRAO
-Giant cell arteritis, collagen vascular disease, sickle
BRAO
90% involve temporal
-Mostly Hollenhorst
-Leave permanent VF defect when resolve
Diabetic Ret
-Leading cause of new cases of blindness in US in ages 20-74
**-NEO in DM is always pre-retinal
-Damage to pericytes
-Snowflake cataracts
-Worry about:
1-Macular edema/ischemia
2-Neo:pre ret hemes, tractional ret detatchmnt, NVI/glaucoma
Rule of 4-2-1
Patient is labeld severe NPDR (10-50% develop PDR in 1 year) if they have one or more:
4)severe hemes in 4 quadrants
2)venous beading in 2 quadrants
1)Irma in 1 quadrant
Proliferative diabetic ret
5% of diabetics have PDR (95% NPDR)
Vitreous or preret hemes, tractional RD, neo, glaucoma
Treatment for PDR is delayed untill High Risk Characteristis (HRC)are shown, what are they?
1)NVD greater than 1/4 DD
2)Any NVD/NVE with vitreous or pre-ret heme
CSME criteria
-Most common reason for legal blindnes in Diabetic Ret
-To be diagnosed with CSME, one of the following must be present:
1)Thickening within 1/3DD of foveal center
2)Exudate within 1/3DD
3)Thickening of at least 1DD within 1DD
Hypertensive Ret
-Vessels constrict (autoregulate) to decr flow
-Vision is usually unaffected unless macular edema (macular star - exudates) serous RD, vein occlusion, papilledema
HTN Ret grading
1) Increased light reflex, narrowing
2) Nicking
3) Hemes, CWS, exudates
4) Papilledema, macular star

Color shows at 3
Retinal macroaneurysm
-Circinate exudates
-60+ yo women
-HTN/atherosclerosis
Ocular Ischemic Syndrome
-65 yo man
-Gradual vision loss, pain, amaurosis fugax
-Unilat midperiph dot/blot
-NVD, NVI
-Atherosclerosis, Arteritis
Amaurosis Fugax
1) Monoc vision loss (seconds to minutes)
2) Carotid artery embolus
Coats
-8yo boy with unilateral leukocoria (ddx retinoblastoma, ROP), strab
-Tons of exudates (can lead to exudative RD)
ROP
-Born less than 36 weeks
**Temporal retina subject to neo and tractional RD
-Temporal retinal vessels develop around 9mo
ARMD
-Chief cause of vision loss in 50+ Caucasians
-Dry:asymptomatic or gradual VA loss, *drusen, mottling,
-Worst form of dry ARMD:
Geographic atrophy
-Wet:Sudden, distortion (amsler)

PED can happen w/dry or wet
Pathophysiology of Dry and Wet AMD
Dry: disease of RPE, Bruch's, and choriocapillaris
Wet: abnormal RPE and choriodal neovascular membrane (CNV) w/subret fluid
4 types of leakage associated with wet ARMD
1)Sub-RPE heme:grey-green
2)Sub-RPE detachment: plasma under RPE (also called **PED); can happen in dry or wet
3)Sub retinal heme
4)Sub retinal detachment (plasma-serous retinal detatchemt)

(2 fluids, 2 potential spaces)
4 big risk factors for dry going wet?
*multiple soft drusen
*focal hyperpigmentation
HTN
smoking
Central Serous Choroidopathy
-Type A middle aged men
-Sudden unilater vision loss/metamorphopsia
-Bruch's breakdown
-40% recurrence
-Macular serous detatchment
-Fluorescein angiography: gradual pooling or smokestack
-Self-resolve 1-3 months
Histoplasmosis
-Whites, Ohio/MS valley
-Fungus
-30% recurrence
-Chorioretinitis (no vitritis like toxo)
*Triad:
1) Peripapillary atrophy
2) Punched out lesions
3) Maculopathy (CNV)
High myopia
>6D
-Axial length> 26mm
-Oblique insertion of disc
1) Fuchs' spots (hyper pigmentation)
2) *Lacquer cracks (yellow streaks)
3) *Macular holes
4) Posterior staphyloma
Lacquer cracks
Fine yellow lines that represent large breaks in bruch's
-Neo can occur
Epiretinal membrane
-Glial cells from retina grow out a hole in ILM
-Contraction of membrane can wrinkle retina
-Mild=cellophane
-Severe=pucker
-Cause: PVD, RD, sx, trauma idiopathic
Macular Hole
-Women (...)
-Round red spot, vision 20/200
-Stages:1)yellow, 2)hole/pseudo operculum, 3)hole with operculum, 4)hole+detatchment
-PVD, if other eye already has PVD no risk
Cystoid macular edema
-Post cataract sx (Irvine-Gass)
-Prosaglandin induced
Macular Photostress Test
-Look at light for 10 sec
-Time to read 1 line less than BVA
-Should be <1min
Retinitis Pigmentosa
(triad)
-Dominates (*Autosom Dom) periph & central
-Usually heritable but also associated with Usher's syndrome (hearing loss) 5%
-*Most common retinal dystrophy
-Night blindness/tunnel vision
-By 30yo 75% are symptomatic
-Triad: bone-spicule pigment, arteriolar attenuation, waxy optic disc pallor
Cause of RP?
Testing?
Retinal signs centrally?
Cause: progressive loss of RPE
Test: ERG (scotopic reduced)
Signs: CME, ERM, mac holes, PSC
Stargardt's
-Typically diagnosed between age 6-20
*Vision loss out of proportion to fundus appearance.
-Most common hereditary macular dystrophy
-Fundus flavimaculatus (stargardt's without macula involvment)

Signs:
-Yellow flecks shape: pisciform (fish tail)
-*Beaten-bronze macular pattern
-Salt and pepper pigment changes (syphilis)
-Dark choroid
Differentials for bull's eye maculopathy
Stargardt's, cone dystrophy, chloroquine/hydroxychloroquine, thioridazine toxicity
Best's Disease
(Vitelliform dystrophy)
-"Best macular dystrophy to have until 50 yo"
-"Who has the best egg (eog)"
-Young 5-10yo
-Bilateral, Yellow round egg yolk lesion (lipofuscin in RPE) under fovea; scrambled egg = bad
-CNV
-Abnormal EOG. Normal ratio (light peak:dark trough ratio) is 1.8; Best is about 1
Gyrate Atrophy
-Young, by 10
-Night blindness (nyctalopia)
-Scalloped areas of periph chorioret atrophy
-Deficient in mitochondrial enzyme ornithine aminotransferase
Rhegmatogenous Retinal Detatchments
-RD caused by hole/tear
-Floater, flashes, curtain
-Demarcation line>chronic RD
Signs and causes of Rhegmatogenous RD
Signs: undulating retina, Shafer's sign (pigment cells; aka tobacco dust), low IOP

Causes: atrophic holes, vitreo-retinal traction tears (PVD), weaker connection between RPE and photoreceptors
*LATTICE DEGEN*
-*Found in 6-10% people
-Only 1% of people w/lattice will develop RD
-Bilateral, temporal, superior
Non-Rhegmatogenous
-Tractional from Proliferative DB ret
-Serous from ARMD
Retinoschisis
-Splitting of outer plexiform layer
-4-7% general population >40yo
-Dome shaped bullous elevation located inferior/temporal that doesn't move (not RD)
-Absolute VF defect
-May have retinal breaks (outer or inner)
Angiod Streaks
"PEPSI"
-Pseudoxanthoma elasticum is most common cause
-Streaks from the disc like spokes
-Elastic layer of Bruch's membrane
Risk factors for POAG:
-IOP: only one we can control
-Race: Afr Am 4-5x more likely
-Family history: 16%
-Age
-Thin corneas
POAG
-IOP >21 mm Hg
-If damage at lower IOP=normal tension gl
-Signs: focal vertical thinning, notching, NFL defect, C/D ratio, drance heme
Port-Wine Stains
Vascular birthmarks highly associated w/ipsilateral glaucoma (45%).

Rarely associated w/systemic disorders (Sturge-Weber Syndrome)
Pseudoexfoliation Syndrome
-Caucasians, Scandinavian decent, 60 yo
-White, flaky amyloid deposits on pupil margin, lens capsule, TM
-Sampaolesi's line: pigmentation on Schwalbe's line (also seen in pigment dispersion syndrome)
-Happens in older people (epithelial cells and BM get old and release stuff)
Pigmentary Dispersion Glaucoma
-Caucasians, 30 yo
-High ant chamber pressure causes iris to bow posteriorly, zonules scrape off pigment (50% develop glaucoma)
-Signs: transillumination defects, Krukenberg's spindle (vertical pigment line), TM pigment, Scheies line (pigment on lens)
Normal Tension Glaucoma
-NFL/VF damage at lower pressures (&lt;21)
-Before dx, take diurnal IOP readings
-Signs similar to POAG but drance heme (splinter heme) is more common
-Ddx: myocardial infarction, anemia, syphilis, vasculitis
Primary Angle-Closure Glaucoma
-Acute or subacute (intermitten)
-Periph iris pushes anteriorly, blocking TM
-Cause: lens growth w/age
-Cause: mid-dilated pupil, highest risk after dilation and pupil constricts to mid position
-2 causes: pupillary block (more common; hyperopes) and plateau iris syndrome
-Vomit, intense oc pain, HA, halos, nausea
-Lower IOP (50-100) and do PI
-Greatest threat: CRAO
Glaucomflecken
Type of cataract (anterior subcapsular opacities from lens epith ischemia) associated with previous primary angle-closure glaucoma
Neovascular Glaucoma
(Secondary Angle-Closure Glaucoma)
-Cause: CRVO, Diab, CRAO (ret ischemia)
-Sign of neovasc glaucoma: rubeosis of iris
-Examine pupil margin for neovasc tufts
-Neo in angle makes fibrovasc membrn, impedes aqueous outflow
Uveitic Glaucoma
(Secondary Angle-Closure Glaucoma)
-Cause: periph ant synechiae, post syn
-Iris inflammed & sticky (adheres to TM/lens)
Glaucomatocyclitic Crisis
A type of Inflammatory Glaucoma
(Secondary Angle-Closure Glaucoma)
-aka Posner-Schlossman syndrome
-Cause: acute trabeculitis
-40-60 IOP, angles open
-Recurrent unilat attacks
Fuch's Heterochromic Iridocyclitis
A type of Inflammatory Glaucoma
(Secondary Angle-Closure Glaucoma)
-Chronic non-granulomatous anterior uveitis
-Glaucoma & cataracts
-Unilat, iris different color