Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Anterior Segment Disease > 2: Cornea > Flashcards

2: Cornea Flashcards

1
Q

Bowman’s layer damage

A
  • does not regenerate
  • will be replaced by epithelial cells or stroma-like fibrous tissue
  • however, very resistant to damage by shearing, penetration, or infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

stromal damage

A
  • leads to scarring/opacification
  • newly formed connective tissue components differ slightly from original tissue; alignment and organization of collagen fibrils are not as precise
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Descemet’s membrane damage

A
  • can be secreted and re-formed by stromal keratocytes and endothelium
  • however, very resistant to damage by shearing, penetration, or infection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

epithelial damage

A
  • heals within hours to days (turnover time for entire corneal epithelium is 7-10 days)
  • if the basement or hemidesmosomes are damaged, takes months to heal completely; if hemidesmosomes are malformed, can lead to recurrent corneal erosion
  • increases risk of infection due to break in epithelial barrier
  • generally scar-free
  • can result in mild stromal edema; loss of tight junctions between surface cells allows fluid from tear film to enter K
  • if trigeminal nerve damage or limbal stem cell damage, wound healing will be impaired
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

endothelial damage

A
  • endothelial cells do not regenerate
  • with cell loss, neighboring cells generally enlarge and flatten to cover the area of loss: results in enlarged endothelial cells (polymegathism), irregularly shaped cells (pleomorphism), and a decrease in cell density
  • can result in stromal edema: loss of cells = loss of metabolic pumps; moderate to severe edema in the stroma will cause folds in Descemet’s membrane; corneal edema is directed towards posterior stroma (anterior stroma has more tightly packed lamellae of collagen making it more resistant to edema); cause Descemet’s membrane to buckle giving the appearance of vertical folds (striae)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

bacterial keratitis (microbial keratitis, corneal ulcer, bacterial ulcer)

A

bacterial infection of the cornea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

bacterial keratitis (microbial keratitis, corneal ulcer, bacterial ulcer) etiology/associations

A

corneal epithelial defect with subsequent bacterial infection:

  • epithelial defect is most commonly the result of contact lens wear, particularly if extended
  • epithelial defects can also occur from trauma, surgery, ocular surface disease (e.g., herpetic keratitis, dry eye, trichiasis, severe allergic eye disease, corneal anesthesia)
  • most common bacteria include Staph and Strep species, Pseudomonas aeruginosa, and Moraxella catarrhalis

some bacteria can penetrate an intact cornea (no epithelial defect)

  • keratitis usually occurs as a result of a severe conjunctivitis
  • includes Neisseria gonorrhoeae, Neisseria meningitidis, Haemophilus influenzae, Corynebacterium diphtheriae)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

bacterial keratitis (microbial keratitis, corneal ulcer, bacterial ulcer) demographics

A

most commonly occurs in CL wearers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

bacterial keratitis (microbial keratitis, corneal ulcer, bacterial ulcer) laterality

A

unilateral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

bacterial keratitis (microbial keratitis, corneal ulcer, bacterial ulcer) symptoms

A
  • red eye
  • ocular pain with tearing and photophobia
  • mucous discharge
  • blurred vision
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

bacterial keratitis (microbial keratitis, corneal ulcer, bacterial ulcer) signs

A
  • conjunctival injection
  • infectious corneal ulcer (stromal thinning with overlying epithelial defect and an associated stromal infiltrate): size of epithelial defect is approx. = to size of stromal infiltrate; typically located centrally or paracentrally
  • stromal edema
  • AC rxn (WBCs in the AC); if severe, hypopyon can form
  • mucopurulent/purulent discharge
  • eyelid edema in severe cases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

bacterial keratitis (microbial keratitis, corneal ulcer, bacterial ulcer) complications

A
  • corneal scarring

- corneal perforation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

bacterial keratitis (microbial keratitis, corneal ulcer, bacterial ulcer) management

A
  • d/c CL wear
  • topical broad spectrum antibiotic(s)
  • H. influenzae and N. gonorrhoeae require systemic treatment in addition to a topical antibiotic
  • oral analgesic as needed
  • cycloplegic for pain
  • evaluate daily to monitor for improvement in s/s; improvement should occur in 24-48 hours of initiating tx with resolution in 1-2 weeks
  • if not resolving with tx, ulcer larger than 2 mm or in the visual axis, consider culturing
  • if not resolving with tx, consider an amniotic membrane in addition to a topical antibiotic
  • if severe inflammation persists after bacterial infection is under control, consider a topical steroid
  • if significant stromal thinning occurs, limit the risk of corneal perforation by treating with ascorbic acid (promotes collagen synthesis) and citric acid or a tetracycline (inhibits collagenolysis); also discuss eye protection
  • if medical therapy fails, corneal perforation occurs, or there is visually significant corneal scarring, refer out for penetrating keratoplasty (PKP, full thickness corneal transplant); another option for corneal perforation is an amniotic membrane transplantation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

bacterial keratitis (microbial keratitis, corneal ulcer, bacterial ulcer) pearls:

  • infectious keratitis is commonly _____; in general, corneal infections are treated as _____
  • when infectious keratitis is present, check IOP ____
  • with patients in significant pain from a corneal issue, consider _____, but never ___
A

bacterial;
bacterial unless high suspicion for another organism;
using non-contact method or iCare;
instilling a topical anesthetic during exam to aid in evaluation the eye;
prescribe an anesthetic for ocular pain!!!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

fungal keratitis

A

fungal infection of the cornea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

fungal keratitis etiology/associations

A
  • corneal epithelial defect with subsequent fungal infection
  • if filamentous fungi (e.g., Aspergillus and Fusarium species), epithelial defect is most commonly the result of trauma with vegetative matter or contact lens wear, particularly if extended
  • if non-filamentous fungi (e.g., Candida species), epithelial defect is most commonly the result of ocular surface disease (e.g., herpetic keratitis, dry eye, trichiasis, severe allergic eye disease, corneal anesthesia)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

fungal keratitis demographics

A

no predilection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

fungal keratitis laterality

A

unilateral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

fungal keratitis symptoms

A
  • red eye
  • ocular pain with tearing and photophobia
  • mucous discharge
  • blurred vision
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

fungal keratitis signs

A
  • conjunctival injection
  • infectious corneal ulcer (stromal thinning with overlying epithelial defect and an associated stromal infiltrate): size of epithelial defect < size of stromal infiltrate; infiltrate has feathery edges if filamentous fungi; typically located centrally or paracentrally
  • satellite lesions surrounding the primary infiltrate
  • stromal edema
  • AC rxn (WBCs in AC); if severe, hypopyon can form
  • mucopurulent/purulent discharge
  • eyelid edema in severe cases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

fungal keratitis complications

A
  • corneal scarring

- corneal perforation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

fungal keratitis management

A
  • d/c CL wear
  • culture to confirm diagnosis; may have bacterial co-infection
  • topical anti-fungal; consider epithelial debridement to facilitate antifungal penetration
  • oral antifungal in addition to topical antifungal for deep ulcers
  • oral analgesic as needed
  • cycloplegic for pain
  • evaluate daily to monitor for improvement in s/s; stability of infection after initiation of tx is often a favorable sign; resolution may take weeks to month
  • if not resolving with tx, consider an amniotic membrane in addition to a topical antifungal
  • if significant stromal thinning occurs, limit the risk of corneal perforation by treating with ascorbic acid (promotes collagen synthesis) and citric acid or a tetracycline (inhibits collagenolysis); also discuss eye protection
  • if medical therapy fails, corneal perforation occurs, or there is visually significant corneal scarring, refer out for penetrating keratoplasty (PKP, full thickness corneal transplant); another option for corneal perforation is an amniotic membrane transplantation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

fungal keratitis pearls:

-do not use ____ for fungal keratitis

A

topical steroids (can promote replication of microorganism)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

acanthamoeba keratitis

A

protozoal infection of the cornea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

acanthamoeba keratitis etiology/associations

A
  • corneal epithelial defect with subsequent acanthamoeba infection
  • epithelial defect is most commonly the result of contact lens wear, particularly if extended
  • infection typically occurs when a contact lens wearer uses nonsterile water to clean lenses or exposure to water while wearing contact lenses
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

acanthamoeba keratitis demographics

A

most commonly occurs in CL wearers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

acanthamoeba keratitis laterality

A

unilateral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

acanthamoeba keratitis symptoms

A
  • red eye
  • ocular pain with tearing and photophobia; pain is usually out of proportion to early clinical findings
  • mucous discharge
  • blurred vision
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

acanthamoeba keratitis signs

A
  • conjunctival injection
  • early findings: epitheliitis with pseudodendrites, whorls, epithelial ridges, and/or diffuse subepithelial microcysts; subepithelial infiltrates (SEIs)- sometimes along the corneal nerves, producing a radial keratoneuritis
  • late (3-8 weeks): ring-shaped corneal stromal infiltrate
  • stromal edema
  • AC rxn; if severe, hypopyon can form
  • minimal mucous discharge
  • eyelid edema in severe cases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

acanthamoeba keratitis complications

A
  • corneal scarring

- corneal perforation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

acanthamoeba keratitis management

A
  • d/c CL wear
  • culture to confirm diagnosis; may have bacterial and/or fungal co-infection
  • topical antiprotozoal; consider epithelial debridement to facilitate antiprotozoal penetration
  • topical propamidine isethionate (disinfectant and antiseptic) in addition to topical antiprotozoal
  • oral antifungals in addition to the above treatment have shown success
  • oral analgesic as needed
  • cycloplegic for pain
  • evaluate daily to monitor for improvement in s/s; stability of infection after initiation of tx is often a favorable sign; resolution may take 1-12 months; tx is usually continued for 3 months after resolution of inflammation due to concern for recurrence
  • if not resolving with tx, consider an amniotic membrane in addition to a topical antiprotozoal
  • if sever inflammation persists after acanthamoeba infection is under control, consider a topical steroid
  • if significant stromal thinning occurs, limit the risk of corneal perforation by treating with ascorbic acid (promotes collagen synthesis) and citric acid or a tetracycline (inhibits collagenolysis); also discuss eye protection
  • if medical therapy fails, corneal perforation occurs, or there is visually significant corneal scarring, refer out for penetrating keratoplasty (PKP, full thickness corneal transplant); another option for corneal perforation is an amniotic membrane transplantation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

acanthamoeba keratitis pearls:
-early misdiagnosis as _____ is relatively common; presentation of 2 disease can be quite similar in the early stages; ____ typically responds well to appropriate tx

A

HSV keratitis;

HSK

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

marginal keratitis

A
  • also called Staphylococcal Hypersensitivity, Marginal Sterile Infiltrate, and/or Marginal Sterile Ulcer
  • inflammation of the peripheral cornea
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

marginal keratitis etiology/associations

A
  • type IV hypersensitivity reaction to staphylococcal antigens
  • commonly associated with chronic staphylococcal blepharitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

marginal keratitis demographics

A

typically occurs between the ages of 45-65 years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

marginal keratitis laterality

A

bilateral > unilateral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

marginal keratitis symptoms

A
  • mild red eye
  • mild ocular pain with tearing and photophobia
  • chronic eyelid crusting and dryness from blepharitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

marginal keratitis signs

A
  • sectoral conjunctival injection (in area of infiltrate)
  • stromal inifiltrate(s) (WBCs) near the limbus; infiltrates are small, round, and well defined; can coalesce and become circumferential; separated from the limbus by a clear zone
  • sterile ulcer (stromal thinning with overlying epithelial defect in the area of the stromal infiltrate); size of epithelial defect < size of infiltrate
  • minimal to no AC rxn
  • mild pannus
  • blepharitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

marginal keratitis complications

A

corneal scarring

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

marginal keratitis management

A
  • eyelid hygiene and warm compress for blepharitis
  • topical antibiotic (low dose antibiotics on the eyelids may have to be maintained indefinitely)
  • if moderate to severe, topical steroid in addition to topical antibiotic
  • oral doxycycline if blepharitis is refractory to eyelid hygiene and warm compress
  • if patient is a CL wearer, d/c CL wear
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

marginal keratitis pearls:

  • condition is generally _____
  • CL wearers can develop _____
A

chronic and recurrent;
similar sterile infiltrates (also due to hypersensitivity rxn to staphylococcal antigens; often seen in pts who sleep in CLs; may not be a clear zone between infiltrate and limbus; most pts present with mild to no symptoms and do not come in for an exam; if active inflammation, tx includes d/c CL wear until resolution, topical lubrication, and discuss CL hygiene)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

phlyctenular keratoconjunctivitis (phlyctenulosis)

A

inflammation of the cornea and conjunctiva

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

phlyctenular keratoconjunctivitis (phlyctenulosis) etiology/associations

A
  • type IV hypersensitivity reaction to staphylococcal antigens; may also be a hypersensitivity reaction to tuberculosis
  • commonly associated with chronic staphylococcal blepharitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

phlyctenular keratoconjunctivitis (phlyctenulosis) laterality

A

unilateral or bilateral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

phlyctenular keratoconjunctivitis (phlyctenulosis) symptoms

A
  • mild red eye
  • ocular pain with tearing and photophobia
  • chronic eyelid crusting and dryness from blepharitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

phlyctenular keratoconjunctivitis (phlyctenulosis) signs

A
  • sectoral conjunctival injection (in area of phlyctenule)
  • conjunctival phlyctneule (small, white subepithelial inflammatory nodule); at or near the limbus
  • corneal phlyctenule (small, white subepithelial inflammatory nodule); juxtablimbal; migrates toward center of cornea with trail of neovascularization; may have an overlying epithelial defect
  • blepharitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

phlyctenular keratoconjunctivitis (phlyctenulosis) complications

A

corneal scarring (typically in the shape of a triangle)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

phlyctenular keratoconjunctivitis (phlyctenulosis) management

A
  • eyelid hygiene and warm compress for blepharitis
  • topical antibiotic (low dose antibiotics on the eyelids may have to be maintained indefinitely)
  • if moderate to severe, topical steroid in addition to topical antibiotic
  • oral doxycycline if blepharitis is refractory to eyelid hygiene and warm compress
  • if patient is a CL wearer, d/c CL wear
  • if suspicion for TB, order lab work
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q 
phlyctenular keratoconjunctivitis (phlyctenulosis)  pearls:
-condition is generally \_\_\_\_\_
A

chronic and recurrent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

peripheral ulcerative keratitis (PUK)

A

inflammation and subsequent thinning of the peripheral cornea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

peripheral ulcerative keratitis (PUK) etiology/associations

A
  • white blood cells release collagenase and protease that destroy corneal stroma
  • collagen vascular disease and vasculitis; most common diseases include RA, SLE, GPA, PAN
  • local or systemic infection; most common infections include staph, strep, gonococcal, herpes simplex, herpes zoster, lyme, syhpilis, TB
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

peripheral ulcerative keratitis (PUK) laterality

A

unilateral > bilateral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

peripheral ulcerative keratitis (PUK) symptoms

A
  • red eye
  • ocular pain with tearing and photophobia
  • blurred vision
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

peripheral ulcerative keratitis (PUK) signs

A
  • sectoral conjunctival injection (in area of corneal thinning)
  • crescent-shaped corneal ulceration (stromal thinning with overlying epithelial defect); juxtalimbal; may have surrounding infiltrate
  • may have accompanied scleritis and/or anterior uveitis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

peripheral ulcerative keratitis (PUK) complications

A
  • corneal scarring

- corneal perforation; can rapidly occur, within days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

peripheral ulcerative keratitis (PUK) management

A

infectious:

  • aggressive topical lubrication
  • treat w/ appropriate anti-infective
  • amniotic membrane to relieve symptoms and facilitate healing

non-infectious:

  • aggressive topical lubrication
  • topical antibiotic
  • oral steroids
  • oral immunosuppressants for long-term therapy
  • bandage contact lens or amniotic membrane to relieve symptoms and facilitate healing
  • recommend eye protection
  • if etiology is unknown, order lab work based on most likely etiologies
  • if systemic etiology, refer out for systemic treatment
  • cyanoacrylate adhesive can arrest corneal melting
  • if significant stromal thinning occurs, limit the risk of corneal perforation by treating with ascorbic acid (promotes collagen synthesis) and citric acid or a tetracycline (inhibits collagenolysis); also discuss eye protection
  • if corneal perforation occurs, refer out for amniotic membrane transplantation or penetrating keratoplasty; PKP has a high failure rate due to graft melt from PUK recurrence
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
57
Q

peripheral ulcerative keratitis (PUK) pearls:

  • very rare
  • chronic and recurrent
  • _____ is most common systemic association of PUK
  • ~35% of patients also have ____
  • topical corticosteroids suppress corneal inflammation, but _____
  • ____ is a similar condition
A

RA;
scleritis with necrotizing scleritis being most common;
they are usually best avoided in cases of PUK as they can contribute to corneal melt by suppressing collagen production;
Mooren’s ulcer (symptoms, signs, tx are similar; idiopathic; diagnosis of exclusion)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
58
Q

Terrien’s marginal degeneration

A

progressive circumferential thinning of peripheral cornea

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
59
Q

Terrien’s marginal degeneration etiology/associations

A

idiopathic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
60
Q

Terrien’s marginal degeneration demographics

A

typically occurs over the age of 30

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
61
Q

Terrien’s marginal degeneration laterality

A

bilateral > unilateral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
62
Q

Terrien’s marginal degeneration symptoms

A
  • asymptomatic

- blurred vision

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
63
Q

Terrien’s marginal degeneration signs

A
  • peripheral stromal thinning; starts superiorly, spreads circumferentially
  • mild pannus over the area of thinning
  • irregular astigmatism
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
64
Q

Terrien’s marginal degeneration management

A
  • monitor q6-12 months: slit lamp exam, photos
  • recommend glasses or eye shield for protection
  • correct refractive error with glasses/CLs
  • watch for: corneal scarring, corneal perforation (rare; epithelium usually remains intact)
  • corneal consultation when perforation seems likely or when astigmatism becomes uncorrectable
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
65
Q

Terrien’s marginal degeneration pearls:

-_____ is a similar finding that occurs in the elderly

A

Furrow degeneration:

  • non-progressive
  • stromal thinning is peripheral to arcus senilis
  • no tx necessary
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
66
Q

keratoconus (KCN)

A

progressive central or paracentral (inferior to visual axis) stromal thinning accompanied by protrusion of the cornea in the area of thinning

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
67
Q

keratoconus (KCN) etiology/associations

A
  • unknown etiology
  • systemic associations: Down, Ehlers-Danlos, and Marfan syndromes
  • ocular associations: atopic disease (i.e., AKC), Leber congenital amaurosis, retinitis pigmentosa, chronic eye rubbing
  • family hx of keratoconus in 10% of patients
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
68
Q

keratoconus (KCN) demographics

A

typically presents during teenage years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
69
Q

keratoconus (KCN) laterality

A

bilateral > unilateral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
70
Q

keratoconus (KCN) symptoms

A

blurred vision- progressive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
71
Q

keratoconus (KCN) signs

A
  • central or paracentral (inferior to visual axis) stromal thinning accompanied by protrusion of the cornea in a cone shape; maximal thinning at the apex of the protrusion; central or paracentral steepening on corneal topography
  • progressive myopia and irregular astigmatism; scissoring reflex on retinoscopy; “egg-shaped” mires on keratometry; abnormal corneal topography
  • oil-droplet reflex on retroillumination (cone-shape of the cornea produces a dark, round shadow)
  • Rizutti’s sign
  • Munson sign
  • Fleischer ring
  • Vogt striae; temporarily disappear with pressure on the globe
  • superficial apical scarring in advanced disease, due to breaks in Bowman’s layer
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
72
Q

Rizutti’s sign

A

triangle of light on iris when penlight shined from opposite side

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
73
Q

Munson sign

A

bulging of the lower eyelid when looking downward

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
74
Q

Fleischer ring

A

epithelial iron deposits at the base of the cone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
75
Q

Vogt striae

A

fine, vertical, deep stromal stress lines

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
76
Q

keratoconus (KCN) complications

A

corneal hydrops (influx of aqueous into the cornea due to a rupture in Descemet’s membrane); symptoms include a red eye, sudden decrease in vision, pain with tearing and photophobia and signs include conjunctival injection, corneal edema, AC rxn

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
77
Q

keratoconus (KCN) management

A
  • monitor q3-12 months: corneal topography, slit lamp exam, photos
  • discuss avoidance of rubbing eyes
  • correct refractive error with glasses/CLs (soft, RGP, scleral)
  • if CLs cannot be tolerated or produce unsatisfactory results, refer out for intracorneal ring segment transplantation or keratoplasty
  • consider referral for corneal collagen cross-linking (CXL)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
78
Q

intracorneal ring segment transplantation

A
  • must have minimum corneal thickness of 400 um, clear central cornea, and CL intolerance
  • ring segments made of PMMA are implanted in deep corneal stroma
  • goal is to reduce corneal irregularity and facilitate CL tolerance
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
79
Q

keratoplasty

A
  • penetrating keratoplasty (PKP)- full thickness corneal transplant
  • deep anterior lamellar (DALK)- partial thickness corneal transplant (epithelium to deep anterior stroma)
  • may have residual astigmatism, necessitating CL correction for optimal acuity
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
80
Q

corneal collagen cross-linking

A
  • minimum of 400 um thickness required
  • large area of corneal epithelium removed, riboflavin drops instilled, exposed to UVA light x30 minutes
  • goal is to “cross-link” molecular bonds in the cornea to strengthen it and slow down (ideally eliminate) progression
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
81
Q

hydrops management

A
  • treat with hypertonic saline, cycloplegic, optional large diameter BCL for comfort, and educate the patient on eye protection
  • Descemet’s break usually heals in 6-10 weeks, edema clears, and a variable amount of stromal scarring occurs
  • to speed recovery, refer for pneumatic descemetopexy (placement of air or gas in the anterior chamber)
  • if scarring occurs or becomes chronic, refer out for penetrating keratoplasty (PKP, full thickness corneal transplant)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
82
Q

keratoconus (KCN) pearls:

  • most common _____
  • KCN severity based on keratometry values: mild= ____, moderate= ____, severe= _____;
  • ____% of patients develop hydrops
A 
corneal ectasia (1 in 2000 people);
<48D;
48-54D;
>54D;
2-3
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
83
Q

pellucid marginal degeneration (PMD)

A

progressive inferior peripheral stromal thinning accompanied by protrusion of the cornea above the thinned area

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
84
Q

pellucid marginal degeneration (PMD) etiology/association

A

unknown etiology

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
85
Q

pellucid marginal degeneration (PMD) demographics

A

typically presents during the ages of 20-40

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
86
Q

pellucid marginal degeneration (PMD) laterality

A

bilateral > unilateral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
87
Q

pellucid marginal degeneration (PMD) symptoms

A

blurred vision- progressive

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
88
Q

pellucid marginal degeneration (PMD) signs

A
  • crescent-shaped band of inferior stromal thinning accompanied by protrusion above the band; band ~1-2 mm in height and ~1-2 mm from the limbus; inferior “crab claw” or “kissing doves” pattern of steepening on corneal topography
  • irregular astigmatism; abnormal corneal topography
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
89
Q

pellucid marginal degeneration (PMD) complications

A

corneal hydrops (influx of aqueous into the cornea due to a rupture in Descemet’s membrane); symptoms include a red eye, sudden decrease in vision, pain with tearing and photophobia and signs include conjunctival injection, corneal edema, AC rxn

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
90
Q

pellucid marginal degeneration (PMD) management

A
  • similar to keratoconus

- keratoplasty has a higher failure rate in PMD because it requires larger grafts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
91
Q

pellucid marginal degeneration (PMD) pearls:

-in contrast to keratoconus, ______ do not occur

A

scarring, Vogt striae, and Fleischer ring

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
92
Q

arcus senilis (circumsenilis, arcus)

A

lipid deposition in the corneal stroma

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
93
Q

arcus senilis (circumsenilis, arcus) etiology

A
  • age-related

- in patients < 40 years, MAY be due to hyperlipidemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
94
Q

arcus senilis (circumsenilis, arcus) demographics

A

typically occurs over the age of 40

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
95
Q

arcus senilis (circumsenilis, arcus) laterality

A

bilateral

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
96
Q

arcus senilis (circumsenilis, arcus) symptoms

A
  • asymptomatic

- may notice a gray or white ring around eye

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
97
Q

arcus senilis (circumsenilis, arcus) signs

A
  • gray to white band around the cornea
  • starts as an arc superior and inferior and extends circumferentially
  • separated from the limbus by a clear zone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
98
Q

arcus senilis (circumsenilis, arcus) management

A
  • none if age-related

- in patients < 40, order a lipid panel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
99
Q 
arcus senilis (circumsenilis, arcus) pearls:
-most common \_\_\_\_\_
A

peripheral corneal opacity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
100
Q

crocodile shagreen

A

opacities in the corneal stroma; opacities are most likely vacuoles within the cytoplasm of keratocytes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
101
Q

crocodile shagreen etiology

A

age-related

102
Q

crocodile shagreen demographics

A

typically occurs over the age of 40

103
Q

crocodile shagreen laterality

A

bilateral

104
Q

crocodile shagreen symptoms

A

asymptomatic

105
Q

crocodile shagreen signs

A

gray or white polygonal stromal opacities separated by relatively clear spaces; starts in the peripheral cornea

106
Q

crocodile shagreen management

A

none

107
Q

limbal girdle of Vogt

A

elastotic degeneration at the limbus; may also have deposition of calcium

108
Q

limbal girdle of Vogt etiology

A

age-related

109
Q

limbal girdle of Vogt demographics

A

typically occurs over the age of 40

110
Q

limbal girdle of Vogt laterality

A

bilateral

111
Q

limbal girdle of Vogt symptoms

A

asymptomatic

112
Q

limbal girdle of Vogt signs

A

whitish superficial band at the limbus; typically at 3 and 9 o’clock; may have chalk-like flecks (calcium)

113
Q

limbal girdle of Vogt management

A

none

114
Q

corneal dystrophies

A

group of genetic, inherited disorders in which there is a bilateral, progressive accumulation of deposits within corneal layers

115
Q

epithelial basement membrane dystrophy (EBMD)

A
  • also called Anterior Basement Membrane Dystrophy (ABMD), Map-Dot Fingerprint Dystrophy, and/or Cogan’s Dystrophy
  • thickening of the corneal epithelial basement membrane with absence of hemidesmosomes and deposition of fibrillary protein between the BM and Bowman’s layer
116
Q

epithelial basement membrane dystrophy (EBMD) etiology

A

genetic abnormality

117
Q

epithelial basement membrane dystrophy (EBMD) demographics

A

typically becomes apparent during teenage years

118
Q

epithelial basement membrane dystrophy (EBMD) laterality

A

bilateral

119
Q

epithelial basement membrane dystrophy (EBMD) symptoms

A
  • asymptomatic
  • ocular irritation (e.g., burning, FBS)
  • blurred vision
120
Q

epithelial basement membrane dystrophy (EBMD) signs

A
  • intraepithelial diffuse gray patches (maps), creamy white cysts (dots), or fine refractile lines (fingerprints) in the corneal epithelium
  • negative staining with Fl due to raised areas of epithelium
121
Q

epithelial basement membrane dystrophy (EBMD) complications

A

recurrent corneal erosion (RCE)

122
Q

epithelial basement membrane dystrophy (EBMD) management

A
  • monitor: slit lamp exam, photos
  • topical lubrication (for prophylaxis of RCE)
  • if significant discomfort or reduced vision, refer for superficial keratectomy or keratoplasty (superficial keratectomy= smoothing of the corneal surface by removal of epithelium down to Bowman’s layer)
  • treat RCE
123
Q

epithelial basement membrane dystrophy (EBMD) pearls:

  • most common _____
  • ____% of patients develop RCE; accounts for ____% of RCE cases
A

corneal dystrophy;
~10;
~30

124
Q

Fuch’s dystrophy

A

accelerated endothelial cell loss with subsequent polymegathism (change in cell size) and pleomporphism (change in cell shape)

125
Q

Fuch’s dystrophy etiology

A

genetic abnormality

126
Q

Fuch’s dystrophy demographics

A
  • typically becomes apparent during the ages of 45-65

- women > men

127
Q

Fuch’s dystrophy laterality

A

bilateral

128
Q

Fuch’s dystrophy symptoms

A
  • asymptomatic

- decreased vision, worse in the morning

129
Q

Fuch’s dystrophy signs

A
  • Guttata centrally (accumulation of collagen in Descemet’s membrane; secreted by damaged endothelial cells); seen as tiny dark spots int he endothelium that progress to beaten-metal appearance
  • endothelial pigment
  • central stromal edema
  • central epithelial edema in advanced cases
  • stromal opacification in advanced cases
130
Q

Fuch’s dystrophy complications

A

bullous keratopathy:

  • bullae (water blisters) form in the cornea as a result of severe stromal edema
  • bullae may rupture (lead to an epithelial defect) and cause significant pain
131
Q

Fuch’s dystrophy management

A
  • monitor: slit lamp exam, photos, specular microscopy, pachymetry
  • to treat corneal edema: hypertonic saline (sodium chloride, Muro 128), use of hairdryer in the morning
  • if ruptured bullae, treat with a topical antibiotic (for prophylaxis of bacterial infection) and BCL (for comfort) in addition to hypertonic saline
  • if decreased vision, refer for keratoplasty
132
Q

Fuch’s dystrophy pearls:

  • _____ can cause endothelial cell loss and worsen the condition
  • _____ can be non-progressive and not cause K edema
  • _____ can be a normal aging change; termed ____ and typically occur _____
A 
cataract surgery;
guttata;
guttata;
Hassell-Henle bodies;
in the peripheral cornea
133
Q

posterior polymorphous dystrophy (PPMD)

A

metaplasia (transformation of one differentiated cell type to another differentiated cell type) of endothelial cells; endothelial cells become epithelial-like (raised vs. flat and can divide)

134
Q

posterior polymorphous dystrophy (PPMD) etiology

A

genetic abnormality

135
Q

posterior polymorphous dystrophy (PPMD) demographics

A

typically becomes apparent during teenage years

136
Q

posterior polymorphous dystrophy (PPMD) laterality

A

bilateral > unilateral

137
Q

posterior polymorphous dystrophy (PPMD) symptoms

A
  • asymptomatic

- decreased vision

138
Q

posterior polymorphous dystrophy (PPMD) signs

A
  • classic vesicle-like lesions in posterior cornea (circular or oval transparent cysts with a gray halo)
  • band lesions (AKA snail tracks) in posterior cornea (horizontal lesions with parallel, scalloped edges)
  • stromal edema is rare
139
Q

posterior polymorphous dystrophy (PPMD) complications

A

secondary open angle glaucoma; corneal endothelial cells may migrate over the TM and impair aqueous outflow

140
Q

posterior polymorphous dystrophy (PPMD) management

A
  • monitor q6-12 months (slit lamp exam, photos, IOP, gonio, ON photos, ON OCT, GCC, VF)
  • if glaucoma develops, tx is similar to POAG
  • if decreased vision, refer for keratoplasty
141
Q

Meesman epithelial dystrophy

A

thickening of the corneal epithelial basement membrane with epithelial cysts filled with cellular debris

142
Q

Meesman epithelial dystrophy etiology

A

genetic abnormality

143
Q

Meesman epithelial dystrophy demographics

A

typically becomes apparent in 1st decade

144
Q

Meesman epithelial dystrophy laterality

A

bilateral

145
Q

Meesman epithelial dystrophy symptoms

A
  • asymptomatic

- blurred vision

146
Q

Meesman epithelial dystrophy signs

A

tiny intraepithelial vesicles in the interpalpebral zone extending limbus to limbus

147
Q

Meesman epithelial dystrophy complications

A

RCE

148
Q

Meesman epithelial dystrophy management

A
  • monitor (slit lamp exam, photos)
  • topical lubrication (for prophylaxis of RCE)
  • if significant decrease in vision, refer for superficial keratectomy or keratoplasty
  • treat RCE
149
Q

Reis-Bucklers corneal dystrophy

A

hyaline-like deposits accumulate in Bowman’s layer and anterior stroma; stain red with Masson’s trichrome stain

150
Q

Reis-Bucklers corneal dystrophy etiology

A

genetic abnormality

151
Q

Reis-Bucklers corneal dystrophy demographics

A

typically becomes apparent in 1st decade

152
Q

Reis-Bucklers corneal dystrophy laterality

A

bilateral

153
Q

Reis-Bucklers corneal dystrophy symptoms

A
  • asymptomatic

- blurred vision

154
Q

Reis-Bucklers corneal dystrophy signs

A

irregular, gray-white, reticular opacities; initially in Bowman’s layer and anterior stroma centrally; progress to deeper stroma sparing the periphery

155
Q

Reis-Bucklers corneal dystrophy complications

A

RCE

156
Q

Reis-Bucklers corneal dystrophy management

A
  • monitor (slit lamp exam, photos)
  • topical lubrication (for prophylaxis of RCE)
  • if significant decrease in vision, refer for keratoplasty
  • treat RCE
157
Q

Thiel-Behnke corneal dystrophy

A

curly collagen fibrils accumulate in Bowman’s layer and anterior stroma

158
Q

Thiel-Behnke corneal dystrophy etiology

A

genetic abnormality

159
Q

Thiel-Behnke corneal dystrophy demographics

A

typically becomes apparent in 1st decade

160
Q

Thiel-Behnke corneal dystrophy laterality

A

bilateral

161
Q

Thiel-Behnke corneal dystrophy symptoms

A
  • asymptomatic

- blurred vision

162
Q

Thiel-Behnke corneal dystrophy signs

A

irregular, gray-white, honeycomb-like opacities; initially in Bowman’s layer and anterior stroma centrally; progress to deeper stroma sparing the periphery

163
Q

Thiel-Behnke corneal dystrophy complications

A

RCE

164
Q

Thiel-Behnke corneal dystrophy management

A
  • monitor (slit lamp exam, photos)
  • topical lubrication (for prophylaxis of RCE)
  • if significant decrease in vision, refer for keratoplasty
  • treat RCE
165
Q

lattice dystrophy

A

amyloid deposits accumulate between the epithelial basement membrane and Bowman’s layer as well as in stroma; stain with Congo red stain

166
Q

lattice dystrophy etiology

A

genetic abnormality

167
Q

lattice dystrophy demographics

A

typically becomes apparent in 1st decade

168
Q

lattice dystrophy laterality

A

bilateral

169
Q

lattice dystrophy symptoms

A
  • asymptomatic

- blurred vision

170
Q

lattice dystrophy signs

A
  • refractile white dots that coalesce into linear opacities; described as “glass like” (broken glass appearance); initially in anterior stroma centrally; progress to deeper stroma sparing the periphery
  • intervening stroma becomes cloudy
171
Q

lattice dystrophy complications

A

RCE

172
Q

lattice dystrophy management

A
  • monitor (slit lamp exam, photos)
  • topical lubrication (for prophylaxis of RCE)
  • if significant decrease in vision, refer for keratoplasty
  • treat RCE
173
Q

granular corneal dystrophy, type 1

A

hyaline-like deposits accumulate between the epithelial basement membrane and Bowman’s layer as well as in stroma; stain red with Masson’s trichrome stain

174
Q

granular corneal dystrophy, type 1 etiology

A

genetic abnormality

175
Q

granular corneal dystrophy, type 1 demographics

A

typically becomes apparent in 1st decade

176
Q

granular corneal dystrophy, type 1 laterality

A

bilateral

177
Q

granular corneal dystrophy, type 1 symptoms

A
  • asymptomatic

- blurred vision

178
Q

granular corneal dystrophy, type 1 signs

A

discrete gray-white crumb-like opacities separated by clear stroma; resemble sugar granules or bread crumbs; initially in anterior to mid stroma centrally; progress to deeper stroma sparing the periphery

179
Q

granular corneal dystrophy, type 1 complications

A

RCE

180
Q

granular corneal dystrophy, type 1 management

A
  • monitor (slit lamp exam, photos)
  • topical lubrication (for prophylaxis of RCE)
  • if significant decrease in vision, refer for keratoplasty
  • treat RCE
181
Q

granular corneal dystrophy, type 2 (Avellino dystrophy, combined granular-lattice dystrophy)

A

hyaline-like and amyloid deposits accumulate between the epithelial basement membrane and Bowman’s layer as well as in stroma; stain red with Masson’s trichrome and Congo red stains

182
Q

granular corneal dystrophy, type 2 (Avellino dystrophy, combined granular-lattice dystrophy) etiology

A

genetic abnormality

183
Q

granular corneal dystrophy, type 2 (Avellino dystrophy, combined granular-lattice dystrophy) demographics

A

typically becomes apparent during teenage years

184
Q

granular corneal dystrophy, type 2 (Avellino dystrophy, combined granular-lattice dystrophy) laterality

A

bilateral

185
Q

granular corneal dystrophy, type 2 (Avellino dystrophy, combined granular-lattice dystrophy) symptoms

A
  • asymptomatic

- blurred vision

186
Q

granular corneal dystrophy, type 2 (Avellino dystrophy, combined granular-lattice dystrophy) signs

A

discrete gray-white crumb-like opacities separated by clear stroma combined with deeper linear opacities (sugar granules and broken glass)

187
Q

granular corneal dystrophy, type 2 (Avellino dystrophy, combined granular-lattice dystrophy) complications

A

RCE

188
Q

granular corneal dystrophy, type 2 (Avellino dystrophy, combined granular-lattice dystrophy) management

A
  • monitor (slit lamp exam, photos)
  • topical lubrication (for prophylaxis of RCE)
  • if significant decrease in vision, refer for keratoplasty
  • treat RCE
189
Q

macular corneal dystrophy

A

GAGs accumulate within epithelium, Bowman’s layer, stroma, Descemet’s, endothelium; stain blue with Alcian blue

190
Q

macular corneal dystrophy etiology

A

genetic abnormality

191
Q

macular corneal dystrophy demographics

A

typically becomes apparent during 1st decade

192
Q

macular corneal dystrophy laterality

A

bilateral

193
Q

macular corneal dystrophy symptoms

A

blurred vision

194
Q

macular corneal dystrophy signs

A

gray-white crumb-like opacities with stromal haze between deposits; initially in anterior stroma centrally; progress to deeper stroma extending limbus to limbus

195
Q

macular corneal dystrophy complications

A

RCE

196
Q

macular corneal dystrophy management

A
  • monitor (slit lamp exam, photos)
  • topical lubrication (for prophylaxis of RCE)
  • if significant decrease in vision, refer for keratoplasty
  • treat RCE
197
Q

Schnyder corneal dystrophy

A

phospholipids and cholesterol accumulate within basal epithelial cells, Bowman’s layer, and stroma; stain with Oil-Red-O and Sudan Black stains

198
Q

Schnyder corneal dystrophy etiology

A

genetic abnormality

199
Q

Schnyder corneal dystrophy demographics

A

typically becomes apparent during teenage years to 20s

200
Q

Schnyder corneal dystrophy laterality

A

bilateral

201
Q

Schnyder corneal dystrophy symptsom

A

blurred vision

202
Q

Schnyder corneal dystrophy signs

A
  • ring or disc-like central opacities with or without crystalline opacities; initially in anterior stroma centrally; progress to deeper stroma sparing the periphery
  • prominent arcus senilis; progresses centrally leading to a diffuse haze
203
Q

Schnyder corneal dystrophy management

A
  • monitor (slit lamp exam, photos)
  • topical lubrication (for prophylaxis of RCE)
  • if significant decrease in vision, refer for keratoplasty or superficial keratectomy
  • order lipid profile (has been linked with hypercholesterolemia and hyperlipidemia in some patients)
204
Q

congenital hereditary endothelial dystrophy

A

congenital focal or diffuse thickening of Descemet’s membrane endothelial degeneration

205
Q

congenital hereditary endothelial dystrophy etiology

A

genetic abnormality

206
Q

congenital hereditary endothelial dystrophy demographics

A

present at birth

207
Q

congenital hereditary endothelial dystrophy laterality

A

bilateral

208
Q

congenital hereditary endothelial dystrophy symptoms

A

blurred vision

209
Q

congenital hereditary endothelial dystrophy signs

A

stromal edema

210
Q

congenital hereditary endothelial dystrophy management

A
  • monitor (slit lamp exam, photos)

- if decreased vision, refer for keratoplasty

211
Q

Thygeson’s superficial punctate keratitis

A

opacities within the corneal epithelium (unknown composition)

212
Q

Thygeson’s superficial punctate keratitis etiology

A

idiopathic

213
Q

Thygeson’s superficial punctate keratitis demographics

A

typically presents between the ages of 20-30

214
Q

Thygeson’s superficial punctate keratitis laterality

A

bilateral

215
Q

Thygeson’s superficial punctate keratitis symptoms

A
  • ocular irritation
  • photophobia with tearing
  • mild decreased vision
216
Q

Thygeson’s superficial punctate keratitis signs

A
  • multiple small, gray-white corneal epithelial opacities; often central; slightly elevated; stain lightly with fluorescein
  • minimal to no conjunctival injection, corneal edema, or AC rxn
217
Q

Thygeson’s superficial punctate keratitis management

A
  • self-limiting within 1-2 months (typically resolves completely with no scarring)
  • aggressive topical lubrication for mild symptoms
  • topical steroid for moderate to severe symptoms
  • Restasis, Xiidra, or tacrolimus may be an alternative or adjunctive treatment to a steroid
  • BCL for comfort
218
Q

Thygeson’s superficial punctate keratitis pearls:

-chronic course of exacerbations and remissions over the course of _____

A

10-20 years

219
Q

band keratopathy

A

linear band of calcium that deposits at the level of Bowman’s layer and anterior stroma

220
Q

band keratopathy etiology/associations

A
  • unknown etiology
  • most commonly develops following chronic ocular disease (e.g., uveitis, corneal edema, dry eye, exposure keratopathy, glaucoma, phtisis bulbi), trauma, and ocular surgery (esp. retinal detachment repair with silicone oil)
  • less commonly associated with hypercalcemia, hyperphosphatemia, gout, corneal dystrophy, myotonic dystrophy, long-term exposure to irritants (e.g., mercury fumes)
  • may be congenital
221
Q

band keratopathy demographics

A

depends on etiology

222
Q

band keratopathy laterality

A

unilateral or bilateral

223
Q

band keratopathy symptoms

A
  • asymptomatic
  • grittiness/FBS
  • decreased vision
  • corneal whitening
224
Q

band keratopathy signs

A

white linear plaque of calcium at the level of Bowman’s layer and anterior stroma; commonly has a swiss cheese appearance; typically within the interpalpebral fissure; separated from the limbus by a clear zone

225
Q

band keratopathy management

A
  • treat the underlying condition
  • mild symptoms (i.e., FBS): aggressive topical lubrication, BCL for comfort
  • moderate to severe (i.e., irritation not relieved by lubricants, obstructing vision): refer for chelation using disodium ethylenediamine tetraacetic acid (EDTA)
226
Q

Salzmann’s nodular degeneration

A

superficial corneal nodules composed of hyaline deposition between corneal epithelium and Bowman’s layer or beyond into stroma

227
Q

Salzmann’s nodular degeneration etiology/associations

A
  • unknown etiology
  • most commonly develops following chronic ocular surface disease (e.g., MGD, pterygium, dry eye, exposure keratopathy, prior corneal surgery)
  • may also be idiopathic
228
Q

Salzmann’s nodular degeneration demographics

A
  • typically occurs between ages of 45-65

- women > men

229
Q

Salzmann’s nodular degeneration symptoms

A
  • asymptomatic
  • FBS
  • blurred vision
230
Q

Salzmann’s nodular degeneration signs

A
  • elevated, smooth gray or blue-gray nodules anterior to Bowman’s layer; may extend into stroma; usually midperipheral; single or multiple; base may be surrounded by epithelial iron deposits
  • irregular astigmatism
231
Q

Salzmann’s nodular degeneration complications

A

RCE

232
Q

Salzmann’s nodular degeneration management

A
  • treat the underlying condition
  • correct the refractive error; topography can show associated astigmatism within the visual axis
  • if significant discomfort or reduced vision due to progressive increase in astigmatic error, refer for superficial keratectomy or keratoplasty
233
Q

exposure keratopathy

A

corneal drying due to prolonged exposure

234
Q

exposure keratopathy etiology

A
  • lagophthalmos (incomplete eyelid closure)

- incomplete blink

235
Q

exposure keratopathy demographics

A

no predilection

236
Q

exposure keratopathy laterality

A

unilateral or bilateral

237
Q

exposure keratopathy symptoms

A
  • ocular redness
  • ocular irritation (e.g., burning, FBS, pain)
  • tearing
  • blurred vision
238
Q

exposure keratopathy signs

A
  • inadequate blinking or closure of the eyelids
  • conjunctival injection
  • conjunctival staining with Lissamine green and Rose bengal; inferior 1/3 or in the interpalpebral region
  • superficial punctate keratitis (SPK); inferior 1/3 or as a horizontal band in the interpalpebral region
  • corneal epithelial breakdown; typically inferior
  • corneal stromal melt; typically inferior
239
Q

exposure keratopathy management

A
  • treat the underlying condition
  • aggressive topical lubrication
  • eyelid taping or patching qhs in addition to topical lubrication
  • punctal plugs in addition to topical lubrication
  • BCL or scleral contact lens
  • topical antibiotic for epithelial defects
  • amniotic membrane in addition to topical antibiotic for non-healing corneal epithelial defects
  • if significant stromal thinning occurs, limit the risk of corneal perforation by treating with ascorbic acid (promotes collagen synthesis) and citric acid or a tetracycline (inhibits collagenolysis); also discuss eye protection
  • if medical therapy fails, refer for surgery
240
Q

exposure keratopathy complications

A
  • microbial keratitis

- corneal perforation

241
Q

exposure keratopathy pearls:

  • damage to CN V can _____
  • CN V plays an important role in _____
  • causes of CN V damage include _____
A

exacerbate any corneal issue (neurotrophic keratopathy);
wound healing, the blink reflex, and tear production and secretion;
HSV and HZO keratitis, CL wear, refractive surgery, keratoplasty, diabetic neuropathy, chemical injury stroke

242
Q

iridocorneal endothelial syndrome (ICE syndrome)

A

represents a spectrum of 3 diseases linked by a fundamental defect of corneal endothelium and variable iris abnormalities:

  • progressive iris atrophy (essential iris atrophy)
  • Chandler’s syndrome
  • Cogan-Reese syndrome (iris nevus syndrome)
243
Q

iridocorneal endothelial syndrome (ICE syndrome) etiology

A

unknown etiology

244
Q

iridocorneal endothelial syndrome (ICE syndrome) demographics

A
  • typically occurs between the ages of 20-50

- women > men

245
Q

iridocorneal endothelial syndrome (ICE syndrome) laterality

A

unilateral

246
Q

iridocorneal endothelial syndrome (ICE syndrome) symptoms

A
  • asymptomatic
  • blurred vision, worse in the morning
  • may note an irregular pupil or iris appearance
  • monocular diplopia
247
Q

iridocorneal endothelial syndrome (ICE syndrome) signs

A
  • corneal endothelial changes (loss of endothelial mosaic similar to Fuch’s dystrophy); fine, beaten metal appearance
  • variable corneal edema; more severe in Chandler syndrome
  • iris abnormalities; progressive iris atrophy: marked iris thinning leading to iris atrophy, holes and corectopia (displacement of the pupil); Chandler’s syndrome: mild iris thinning and corectopia; Cogan-Reese syndrome: fine, pigmented nodules on the iris surface, ectropio uveae, and variable iris atrophy
248
Q

iridocorneal endothelial syndrome (ICE syndrome) management

A
  • to treat corneal edema: hypertonic saline, use of hairdryer in morning
  • if severe endothelial dysfunction and cornea edema does not clear, refer for keratoplasty
  • if glaucoma develops, treatment is similar to POAG; IOP lowering drops may improve corneal edema
249
Q

iridocorneal endothelial syndrome (ICE syndrome) complications

A
  • secondary open angle glaucoma; corneal endothelial cells may migrate over the TM and impair aqueous outflow
  • secondary closed angle glaucoma; corneal endothelial cells may migrate over the anterior iris and form peripheral anterior synechiae (which then contract and close the angle)
250
Q

iridocorneal endothelial syndrome (ICE syndrome) pearls:

  • _____ is the most common variant (50% of ICE syndrome cases)
  • a _____ disease, but in some cases, subclinical abnormalities of the corneal endothelium may be seen _____
A

Chandler syndrome;
unilateral;
in the asymptomatic fellow eye

Anterior Segment Disease (22 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions