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Ophthalmology Boards Review > Cornea > Flashcards

Cornea Flashcards

1
Q

What are the causes and associations of acute hemorrhagic conjunctivitis?

A

Causes
• Enterovirus type 70
• Coxsackie A24
• Adenovirus type 11
Associations
• Follicular conjunctivitis
• Subconjunctival hemorrhage

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2
Q

What is the percentage of patients with conjunctival lymphoid tumor that have extraocular lymphoma?

A

• 20%
• Non-Hodgkin’s B cell
• Most common in > 50 years old or
immunocompromised

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3
Q

What is the inheritance pattern and extraocular malignancies associated with ataxia telangiectasia?

A

• Autosomal recessive
• Increased risk of breast cancer and T cell leukemia

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4
Q

What biomolecules make up the corneal stroma?

A

• Type 1, 5, and 6 collagen
• Proteoglycans (dermatan and keratan sulfate) in a
higher ratio posterior than anterior stroma

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5
Q

What is the most common branch of cranial nerve V1 involved in herpes zoster infection?

A

• V1 frontal branch

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6
Q

What are the causes of enlarged and prominent corneal nerves?

A

○ Enlarged corneal nerves
• Multiple endocrine neoplasia (MEN) type 2B
• Medullary carcinoma of thyroid gland, pehochromocytoma, mucosal neuromas, marfanoid habitus
• Phytanic acid storage disorder (Refsum disease)
• Leprosy (Hansen disease)
• Familial dysautonomia (Riley-Day syndrome)
• Neurofibromatosis
• Acanthamoeba perineuritis
○ Prominent corneal nerve
• Keratoconus
• Ichthyosis
• Fuch’s corneal dystrophy
• Corneal edema
• Congenital glaucoma

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7
Q

Where do lateral eyelid lymphatics drain?

A

• Preauricular lymph nodes

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8
Q

Where do medial eyelid and conjunctiva lymphatics drain?

A

• Submandibular and submental lymph nodes

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9
Q

What is congenital hereditary stromal dystrophy?

A

• Rare
• Present at birth
• Bilateral opacification of central stroma with white
flakes
• Clear peripherally
• Moderate to severe visual loss
• Non progressive or slowly progressive
• Mutation in decorin gene on chromosome 12”• Rare
• Present at birth
• Bilateral opacification of central stroma with white
flakes
• Clear peripherally
• Moderate to severe visual loss
• Non progressive or slowly progressive
• Mutation in decorin gene on chromosome 12

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10
Q

What is the mutation in macular corneal dystrophy?

A

• Carbohydrate sulfotransferase 6

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11
Q

What is gelatinous corneal dystrophy?

A

• Autosomal recessive
• Mutation in tumor associated calcium signal
transducer 2
• Initially resembles band keratopathy
• Eventually lesions resemble “mulberries”
• 100% recurrence rate after PKP

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12
Q

What dystrophies do mutations in TGF beta-1 (5q31) cause?

A

• Lattice type 1
• Avellino/granular corneal dystrophy 2
• Reis-Bucklers/Thiel Benke
• Granular corneal dystrophy 1
“LARGe” 5 letters, chromosome 5

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13
Q

What is the water content of the cornea?

A

• 78%
• Maintained by intact epithelium and endothelium
(water pump of endothelial cells)

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14
Q

What is hereditary hemorrhagic telangiectasia (Rendu-Osler-Weber disease)?

A

• Autosomal dominant
• Telangiectasias of conjunctiva, nasopharynx, GI, brain,
etc
• Abnormal blood vessels in adulthood results in
bleeding → iron deficiency anemia
• Fragile vessels in conjunctiva can bleed with minimal
eye rubbing

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15
Q

What are the surgical risk factors in posterior polar cataract and Mittendorf dot cataract?

A

• Risk of posterior capsule breaks
• Avoid hydrodissection, instead perform
hydrodelineation

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16
Q

What does tear osmolarity measure and how is it affected in dry eye?

A

• Measures aqueous tear deficiency
• Elevated in aqueous tear deficiency (>300 mOsm/L)
• This test is not necessarily diagnostic of dry eye in
isolation
• There can be variable results at the same appointment
• Results should be considered in context of clinical signs

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17
Q

What is tear lactoferrin?

A

• Made by acinar cells of lacrimal gland
• Binds iron, prevents bacterial growth
• indirect measure of lacrimal gland function
• helps differentiate aqueous tear deficiency from
evaporative dry eye
• This test is not necessarily diagnostic of dry eye in
isolation
• There can be variable results at the same appointment
• Results should be considered in context of clinical signs

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18
Q

How is tear IgE affected in allergic conjunctivitis?

A

• Elevated in allergic conjunctivitis

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19
Q

What is tear MMP-9 and how is it affected in dry eye?

A

• Inflammatory cytokine
• Released by epithelial cells in response to stress
(blepharitis)
• Elevated MMP-9 suggest evaporative dry eye

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20
Q

What is the treatment for a gonococcal infection?

A

• One time intramuscular ceftriaxone 1 g
Or
• One time spectinomycin intramuscular
Or
• Oral fluoroquinolone 5-7 days
Plus
• Eye lavage every hour
Plus
• Treatment for chlamydia (high rate of concurrence) –
azithromycin or doxycycline

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21
Q

What is the treatment for chlamydia?

A

• Azithromycin 1g (single dose)
Or
• Doxycycline 100 mg BID 7 days
Or
• Erythromycin 500 mg QID x 7 days

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22
Q

What is the basic secretion test?

A

Measures basal secretion:
• Topical anesthetic
• Blot off excess fluid
• Check at 5 minutes
• <3 mm = abnormal
• 3-10 mm = equivocal

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23
Q

What is the Schirmer I test?

A

• Do NOT use topical anesthetic
• Measures basic and reflex tears
• Check at 5 minutes
• <5.5mm at 5 mins = abnormal
• >15 mm at 5 mins = epiphora

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24
Q

What is the Schirmer II test?

A

• Uses topical anesthetic
• Measures reflex secretion
• Nasal mucosa stimulated
• Check at 2 minutes
• <15 mm at 2 mins = abnormal

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25
Q

What are the complications of using Valtrex in immunocompromised patients?

A

• Thrombotic thrombocytopenic purpura
• Hemolytic uremia syndrome

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26
Q

What are the signs of cornealc edema?

A

• Waite-Beetham lines = faint deep stromal wrinkles,
early sign
• D-folds = stroma increased thickness 10% or more

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27
Q

What is Thiel Benke?

A

• Autosomal dominant
• TGFB1 gene mutation
• Affects Bowman layer
• Distinguish from Reis Bucklers via electron microscopy,
shows “curly fibers” in Thiel-Behnke only
• Bowman’s layer is replaced by fibrocellular material,
forms “saw-tooth” pattern
• Clinically = honeycomb opacities at Bowman level,
spare peripheral cornea
• Recurrent erosions are common - less frequent and
less severe than Reis-Buckler

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28
Q

Which protein does TGFB1 gene code for and which chromosome is it located on?

A

• Keratoepithelin
• Chromosome 5q31

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29
Q

What is Mikulicz syndrome?

A

• Lacrimal gland enlargement + Salivary gland
enlargement + Keratoconjunctivitis sicca

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30
Q

What is Wilson’s disease?

A

• Autosomal recessive
• Kayser-Fleischer ring – brown discoloration of
peripheral descemet’s membrane
• Sunflower cataract - copper in anterior capsule in
petaloid configuration
• Decreased serum ceruloplasmin
• Treatment with systemic D-penicillamine (binds
copper) can lead to disappearance of K-F ring

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31
Q

What causes a sunflower cataract?

A

• Copper in anterior capsule in petaloid configuration
• Seen in Wilson’s disease

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32
Q

What is Cogan’s syndrome?

A

• Autoimmune disease
• Hearing loss + vertigo + stromal keratitis
• Young adults w/recent UR
• Associated with polyarteritis nodosa
• Treatment - topical steroids for keratitis and oral
steroids for hearing loss
• If not treated, causes deafness
• Rule out syphilis before any steroids

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33
Q

What is megalocornea?

A

• Non-progressive
• Bilateral
• X-linked recessive
• Normal histo
• Horizontal corneal diameters 13 mm or more
• Can have glaucoma (not congenital glaucoma)
• IOP normal
• Normal axial length, corneal thickness and contour
• Deep AC
• Associated with Marfan syndrome

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34
Q

What are the causes of neurotrophic ulcers?

A

• Topical medications: beta blockers, CAIs, NSAIDs,
trifluridine
• Topical anesthetic abuse
• Corneal HSV/VZV – zoster with patchy hypoesthesia
• BAK preservative
• CN V palsy (surgery for trigeminal neuralgia) - diffuse
hypoesthesia
• Diabetes
• Chronic contact lens wear
• LASIK
• Familial dysautonomia (“Riley-Day syndrome”)
• Leprosy

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35
Q

What is the triad for congenital glaucoma?

A

• Triad: photophobia, tearing, blepharospasm
• Increased horizontal diameters (normal for newborns
9.5-10.5 mm)

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36
Q

What are ideal methods to obtain corneal bacterial cultures?

A

• Best by platinum Kimura spatula (heats and cools
rapidly)
• Also, metal blade, calcium alginate, Dacron swab

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37
Q

What are the least ideal methods to obtain corneal bacterial cultures?

A

• Cotton swabs, can inhibit growth

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38
Q

What is the best way to obtain corneal viral cultures?

A

• Dacron swab
• Calcium in calcium alginate and wood from cotton
swab can inhibit viral recovery

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39
Q

What is the best way to obtain anaerobic bacteria culture?

A

• Thioglycolate broth

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40
Q

What is the best way to obtain aerobic bacteria culture?

A

• Blood agar
• Chocolate agar
• Thioglycollate broth (also for anaerobic bacteria)

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41
Q

What is the best way to culture Neisseria species?

A

• Thayer-Martin agar

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42
Q

What is the best way to culture fungi?

A

• Sabouraud’s agar

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43
Q

What is the best way to culture mycobacteria and Nocardia species?

A

• Lowenstein Jensen

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44
Q

What is the best way to culture non-tuberculous mycobacteria?

A

• Middlebrook agar

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45
Q

Subepithelial infiltrates are associated with which viral conjunctivitis?

A

• Adenovirus EKC
• 1-3 weeks after acute infection
• WBCs + immune complex deposits
• Treat with topical steroids.

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46
Q

What causes toxic ulcerative keratopathy?

A

• Caused by topically applied medications. Due to
impaired epithelial wound healing

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47
Q

What is vernal keratoconjunctivitis?

A

• Giant papillary conjunctivitis
• Horner-Trantas dots = degenerated eosinophils
• Shield ulcer

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48
Q

What is scleromalacia perforans?

A

• Painless
• Minimal inflammation
• Necrotizing scleritis
• Requires systemic workup for underlying autoimmune
disease
• Associated with rheumatoid arthritis
• Positive for rheumatoid factor (autoantibody against
IgG)
• Underlying autoimmune conditions are associated
with significant mortality if not treated appropriately
• Rarely spontaneous perforation
• Associated with globe rupture after minimal trauma

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49
Q

What bacteria does cefazolin cover?

A

• More gram positive coverage

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50
Q

How do acidic chemicals cause ocular damage?

A

• Denature and precipitate proteins in the tissues they
contact
• Precipitated proteins then serve as type of barrier to
further damage by acidic chemical
• Ocular tissues have higher buffering capacity for acidic
compounds

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51
Q

How do alkali chemicals cause ocular damage?

A

• Saponification of fatty acids in cell membranes
(corneal epithelium) leads to cellular disruption
• After corneal epithelium is destroyed, alkali chemical
easily penetrates and destroys collagen fibrils and
proteoglycans in the stroma
• Very strong alkali chemicals can eat through cornea
and enter anterior chamber
• High incidence of severe glaucoma

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52
Q

What is Lattice Corneal Dystrophy 1 (LCD1)?

A

• Autosomal dominant
• Mutation in TGFBI, 5q31
• Gene defect causes abnormal protein folding causing
amyloid accumulation
• Localized corneal amyloidosis
• Stains with Congo red
• Metachromasia if stained with crystal violet
• Amyloid deposits, apple-green in color under polarized
light, “birefringence”
• “Dichroism” = deposits alternate in color from red to
green when viewed through rotating polarizing filter
• Glasslike branching lines in the stroma
• Deposits start in anterior cornea (subepithelial and
anterior stroma) then progresses posteriorly
• Starts centrally and progresses centrifugally

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53
Q

Which corneal dystrophies have the highest rates of recurrence in corneal transplant patients?

A

• Most common – Reis-Bucklers
• 2nd most common – Lattice
• 3rd most common – Granular
• Least common - Macular

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54
Q

What is the age of presentation of the corneal stromal dystrophies?

A

• Youngest – macular
• 2nd youngest – lattice
• Oldest - granular dystrophy

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55
Q

What is Meretoja syndrome/LCD2?

A

• Familial amyloidosis
• Finnish type/gelsolin type
• Mutation in 9q32-34/gelsolin gene
• Corneal-lattice like changes with systemic amyloidosis
• Characteristic features = masked facies,
dermatochalasis, lagophthalmos, pendulous ears,
dry/lax skin, cranial and peripheral nerve palsies,
orthostatic hypotension, cardiac conduction
abnormalities, problems with perspiration
• Increased incidence of glaucoma (NOT a feature of
LCD1)
• NOT a dystrophy

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56
Q

What is a Gundersen flap?

A

• Incising and then rotating piece of conjunctiva so it
covers cornea
• Indicated if persistent epi defect in a poor visual
potential eye

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57
Q

What are posterior polar cataracts/Mittendorf dots?

A

• Autosomal dominant
• Usually bilateral
• Develop early in life
• Remnant of fetal hyaloid artery
• Location usually center of lens - vision worse under
photopic conditions (bright light); better under
scotopic conditions (dim light)
• Fused with posterior capsule
• Surgery is associated with increased risk of posterior
capsule breaks, vitreous loss, and other associated
complications
• Avoid hydrodissection, instead do hydrodelineation to
avoid disruption of cataract and posterior capsule
adhesions
• Strategies “inside-out” and “reverse flower bloom”
techniques are used

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58
Q

What are conjunctival nevi?

A

• Present in 1st or 2nd decade of life
• Color from light brown to amelanotic
• 50% have epithelial inclusion cysts
• Limbal nevi tend to be flat, while nevi of bulbar
conjunctiva, plica semilunaris, and caruncle tend to be
raised
• Observation generally recommended
• Excision is recommended is growth occurs
• ALWAYS biopsy if lesions are on palpebral conjunctiva,
tarsal conjunctiva, caruncle, plica semilunaris, or fornix

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59
Q

What is complexion-associated melanosis (racial melanosis or benign acquired melanosis)?

A

• Darker complexions
• More noticeable near limbus
• Bilateral and symmetric
• Occur in adulthood
• Does not typically lead to malignant transformation

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60
Q

What is primary acquired melanosis (PAM)?

A

• Unilateral & asymmetric
• Non cystic
• Most common in light-pigmented and middle aged
patients
• Premalignant; progress to melanoma 30-50%
• Risk factors for progression: 3 clock hours of
conjunctival pigmentation, involve caruncle, plica,
fornix, or palpebral conjunctiva
• Indication for removal >2 clock hours involvement
• Cellular atypia is most important factor for predicting
progression
• Without atypia, rarely turns malignant → follow q6-12
months
• PAM with mild atypia → follow closely
• PAM with moderate to severe atypia → high risk of
progression → remove entire pigmented conjunctival
lesion; if too large to remove, then topical MMC

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61
Q

What is conjunctival melanoma?

A

• Occurs in middle to late adulthood
• Nodular and vascular
• Mortality 25%
• Common in bulbar conjunctiva or limbus
• 25% are amelanotic
• >50% rate of recurrence
• Origin from PAM (70%), nevus (5%), de novo (25%)
• Excision of lesion include 2 mm uninvolved margin,
avoid touching pigmented area of lesion to prevent
seeding

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62
Q

What factors suggest poor prognosis for conjunctival melanoma?

A

• Palpebral/caruncle/lid margin/fornix
• Invasion to deeper tissues
• >1.8 mm thickness
• Pagetoid or full thickness intraepithelial spread
• Lymphatic invasion
• Mixed cell type
• De novo origin (not starting out as PAM or nevus)
• Tumors NOT involving limbus
• Residual tumor at surgical margin after excision

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63
Q

How to excise pigmented conjunctival lesions?

A

• Include 2 mm uninvolved margin
• Avoid touching pigmented area of lesion to prevent
seeding
• Avoid incisional biopsies because may spread the
tumor

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64
Q

What is the frequency of eyelashes/cilia replacement?

A

• Naturally: q3-5 months
• Cut: 2 weeks
• Pulled out: 2 months
• Twice as many cilia along upper lid compared to lower
lid

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65
Q

What are sessile papillomas of conjunctiva?

A

• Most common at the limbus
• Flat with corkscrew vessels
• Appearance of strawberry
• When associated w/HPV 16, 18 or 33, likely to be
dysplastic or carcinomatous
• Signs of dysplasia = leukoplakia and symblepharon

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66
Q

What are pedunculated conjunctival papilloma?

A

• Associated with HPV 6, 11 (children); HPV 16 (adults)
• Fibrovascular core and grow out from surface
• Most common from inferior fornix
• Proliferate in immunocompromised
• Generally observe
• Remove with complete excision and cryotherapy
• Incomplete excision leads to proliferation

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67
Q

What is congenital Hereditary Endothelial Dystrophy (CHED)?

A

• Autosomal recessive
• Corneal edema
• Present at birth and does not get worse - “stationary”
• Nystagmus due to reduced visual sensory input from
birth

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68
Q

What is keratoconus?

A

• Most common corneal ectasias
• Thinning of cornea at the apex of the cone
• Topographic abnormalities at a young age
• Develops initially in puberty to early adulthood
• Progressive thinning
• Munson’s sign; Rizzutti sign; Vogt lines; Fleischer ring
• Associated with painful episodes of corneal hydrops,
apical scarring
• Due to fragmentation of Bowman’s layer → cornea
bows forward
• Steep corneas, >50 D
• High astigmatism
• Bilateral disease
• Risk factors: atopy, eye rubbing, Marfans, floppy eyelid
syndrome, mitral valve prolapse

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69
Q

What is hydrops in keratoconus?

A

• Sudden rupture of Descemet’s membrane leading to
acute corneal edema
• Treatment: cycloplegic, hypertonic agent, BCL,
aqueous suppressants
• Can cause scarring that eventually leads to corneal
transplant

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70
Q

What is keratoglobus?

A

• Rare corneal ectasia
• Globular overall corneal curvature
• Thinnest in the periphery
• Generalized protrusion of cornea
• Present at birth
• Commonly associated with corneal perforation and
rupture
• Strong associated with Ehlers-Danlos syndrome type 4
and blue sclera
• Associated with flexible joints, bone fractures,
deafness, teeth abnormalities

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71
Q

What is pellucid marginal degeneration?

A

• Bilateral ectatic disorder
• Inferior thinning approximately 1-2 mm in width
• Protrusion of cornea above thinning (corneal apex
above area of thinning)
• Corneal scarring, episodes of hydrops, iron lines - less
common compared to keratoconus
• “Crab claw” configuration = against the rule
astigmatism superiorly, with the rule astigmatism
inferiorly
• Pachymetry and correlating to topography to
differentiate from other entities

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72
Q

Which systemic infection is Mooren-like PUK ulcer associated with?

A

• Hepatitis C

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73
Q

Which systemic condition is superior limbic keratoconjunctivitis associated with?

A

• Autoimmune thyroid disease

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74
Q

What is Schnyder crystalline corneal dystrophy?

A

• Mutation in UBIAD1 gene
• Rare, progressive stromal dystrophy
• Starts with central corneal opacification at all levels,
next develops in the periphery, then mid-periphery,
then loss of corneal sensation
• Loss of photopic vision when pupil is constricted
• Vision improves under scotopic vision when pupil is
dilated, light passes around central cholesterol
• Check cholesterol levels → associated with
hyperlipidemia/hypercholesterolemia

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75
Q

What are the corneal findings in congenital glaucoma?

A

• Corneal edema
• Haab’s striae – horizontal lines

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76
Q

What is the prevalence of the 3 main corneal stromal dystrophies?

A

• Most common – Granular
• 2nd most common – Lattice
• 3rd most common - Macular

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77
Q

What corneal findings are associated with birth trauma?

A

• When forceps are used, compression of globe
vertically which stretches the cornea horizontally
• Vertical pattern of Descemet’s tears
• Left eyes are more commonly affected than right eye
• Usually unilateral
• Differential diagnosis includes PPMD, the edges are
scalloped with wide endings, in Haabs striae the
borders are smooth with tapered ends

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78
Q

What are systemic associations with corneal crystals?

A

• Multiple myeloma
• Waldenstrom macroglobulinemia
• Benign monoclonal gammopathy
• Crystals are in all layers of cornea

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79
Q

What is Fabry disease?

A

• X linked recessive
• Defect in alpha galactosidase A
• Sphingolipidoses
• Corneal verticillata (opacities in epithelium in whorl
like pattern)
• Secondary deposition in the basal epithelial layer
• Posterior spokelike cataracts
• Comma-shaped conjunctival aneurysms
• Macular edema
• Retinal vessel dilation
• Systemic findings: renal failure, peripheral neuropathy

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80
Q

What is Hunter’s syndrome inheritance pattern and ocular findings?

A

• X linked recessive
• Pigmentary retinopathy

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81
Q

What are the causes of corneal verticillata?

A

• Fabry disease
• Multiple sulfatase deficiency
• Generalized gangliosidosis
• Amiodarone

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82
Q

What is positive versus negative fluorescein staining of cornea?

A

● Positive staining: areas of epi disruption
○ Examples – epi defects
● Negative staining: area of interest projects above the
surrounding tear film
○ Examples - zoster pseudodendrites and SPK

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83
Q

What is the most common risk factor for fungal keratitis?

A

• Trauma with vegetable matter

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84
Q

What are normal age-related endothelial cell counts?

A

• At birth: approx. 4,000
• Young adults: approx. 3,000
• 60 years: approx. 2,500
• Cell count decreases linearly until age 60 years, then
slower rate

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85
Q

What is acanthamoeba keratitis?

A

• Severe eye pain out of proportion to clinical
appearance of cornea
• Epitheliopathy with or without pseudodendrites
• Perineural infiltrates (pathognomonic)
• Ring infiltrate - late stage
• Cyst form is highly resistant
• PHMB 0.02% and chlorhexidine 0.02% are biguanides
and cysticidal
• Propamidine isethionate 0.1% and hexamidine 0.1%
are diamidines and cysticidal
• Steroids used with caution if used too early they can
induce cyst formation

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86
Q

What is Descemet’s membrane?

A

• True basement membrane
• Basement membrane of corneal endothelium
• Type 4 collagen
• At birth, Descemet’s membrane 3-4 microns thick and
increases to 10-12 microns in adults
• Two zones, anterior banded developed in utero.
posterior non-banded zone, deposited by endothelial
cells throughout life

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87
Q

What are conjunctival papillae?

A

• Central vascular tuft represented by “red dot” in the
middle of the bump, surrounded by edema and
inflammation

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88
Q

What are corneal stem cells?

A

• Located at limbus, in palisades of Vogt region
• Radially oriented fibrovascular ridges, perpendicular to
corneal margin
• More concentrated in the inferior and superior limbus
• Limbal stem cells from palisades migrate centripetally
to create basal epithelial level

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89
Q

What is stromal keratitis secondary to herpes simplex?

A

• Mainly an autoimmune phenomenon
• Main treatment - topical steroids
• Topical antiviral used to prevent outbreak of epithelial
keratitis
• HEDS study - topical PF q2h and topical trifluridine QID.
Showed no benefit to adding oral acyclovir to topical
prednisolone and trifluridine

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90
Q

What is Granular corneal dystrophy 1?

A

• Early age onset
• TGFBI gene mutation
• Deposition of hyaline material that stains red with
Masson trichrome stain
• Clear spaces between opacities that look like bread
crumbs, becomes more confluent with age, does not
extend to limbus
• Maintain good vision
• Photophobia, glare, recurrent erosions

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91
Q

What is granular corneal dystrophy 2 (Avellino corneal dystrophy)?

A

• Appearance of both granular and lattice dystrophies
• Corneal opacities described as stellate (star-like),
snowflake, icicle
• TGFBI gene mutation, keratoepithelin protein,
chromosome 5q31
• Deposition of hyaline material that stains red with
Masson trichrome stain or Congo red

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92
Q

What is associated with unilateral arcus senilis in elderly patient?

A

• Contralateral carotid artery disease and ocular
hypotony

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93
Q

What is associated with unilateral arcus senilis in an young patient (<40 years old)?

A

• Hyperlipoproteinemia (check lipid panel)

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94
Q

What is Mooren’s ulcer?

A

• Involves only cornea
• Very painful
• Associated with helminthic infection

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95
Q

What is peripheral ulcerative keratitis?

A

• Main association with rheumatoid arthritis
• Also associated with HSV, VZV, TB, gonorrhea, syphilis,
AIDs
• Involves cornea and sclera
• Unilateral
• Peripheral corneal infiltration with epithelial loss
• Very painful

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96
Q

What type of iris atrophy is associated with HSV?

A

• Patchy

97
Q

What type of iris atrophy is associated with VZV?

A

• Sectoral

98
Q

What is a clinical finding ophthalmologists may use in primary HSV diagnosis?

A

• Enlarged preauricular lymph node

99
Q

What are clinical findings in secondary HSV (previously sensitized immune system)?

A

• Stromal keratitis
• Endotheliitis
• Uveitis

100
Q

What is cryptophthalmos?

A

• Partial or complete failure of eye to form

101
Q

What is pseudo cryptophthalmos?

A

• Eyelids fail to separate and gives appearance of eye
not forming

102
Q

What is ankyloblepharon?

A

• Part or all of the eyelid margin fails to separate

103
Q

What is Heerfordt syndrome?

A

• Type of systemic sarcoidosis
• Granulomatous uveitis
• Constitutional symptoms
• Parotid swelling
• Facial nerve paralysis

104
Q

What is Lofgren syndrome?

A

• Systemic sarcoidosis
• Bilateral hilar adenopathy
• Arthropathy
• Fever
• Erythema nodosum

105
Q

What are causes of giant papillae?

A

• Vernal associated conjunctivitis
• Contact lens associated conjunctivitis

106
Q

What is atopic keratoconjunctivitis?

A

• Small/medium papillae
• Extensive corneal vascularization with opacification
• Year round disease
• Posterior subcapsular or multifaceted or shield-shaped
anterior subcapsular cataracts
• Cell-mediated immunity decreased - more susceptible
to herpes simplex keratitis and colonization of eyelids
with staph aureus

107
Q

What is a chalazion?

A

• Sterile inflammation
• Antibiotics do not help the process
• Tetracycline (doxycycline) and macrolide
(erythromycin) work due to anti-inflammatory
properties

108
Q

What is meibomian gland dysfunction?

A

• Hyperemia of eyelid margin
• Faster tear breakup time
• Posterior telangiectatic vessels
• Keratin plugging

109
Q

What is keratocyte distribution and density in corneal stroma?

A

• Parallel and between corneal lamellae
• More numerous in the anterior stroma
• Responsible for digesting and producing stromal
molecules
• Least numerous posteriorly
• Population declines with age

110
Q

What is the most detrimental type of corneal graft rejection?

A

• Endothelial graft rejection, leads to inflammation and
death of grafts endothelial cells. Because they cannot
replace themselves, this types of rejection is most
detrimental
• Also most common type of corneal graft rejection

111
Q

What is the least detrimental type of corneal graft rejection?

A

• Epithelial and stromal rejection
• Treated with topical steroids
• Once inflammation resolved, corneal epithelium and
stroma generally return to normal

112
Q

What is a Fleischer ring?

A

• Iron line deposited at the base of the cone
• Landmark for peripheral edge of cone
• Use cobalt blue light to detect early signs
• Seen in keratoconus

113
Q

What is Munson’s sign?

A

• Lower eyelid is displaced secondary to bulging cornea
• Seen in advanced keratoconus

114
Q

What is Rizzuti sign in keratoconus?

A

• Conical reflection on nasal cornea is seen when
penlight is shone from temporal side

115
Q

What are Vogt lines?

A

• Vertical/fine parallel lines in posterior
stroma/Descemet’s membrane
• Digital pressure on the eye makes the lines disappear
• Distinguish from superficial linear scars that occur
from previous hydrops episodes
• Seen with keratoconus

116
Q

What is macular corneal dystrophy?

A

• Autosomal recessive (unlike other corneal stromal
dystrophies)
• Gene CHST6, carbohydrate sulfotransferase, chrom. 16
• Least common corneal stromal dystrophies in North
America
• Most severe vision loss of the 3 classic stromal corneal
dystrophies
• Age of presentation is the youngest in macular dystrophy,
then lattice then granular
• Usually noticed in adolescent years
• Associated with severe photophobia and recurrent
erosions
• Diffuse, fine, superficial clouding in central cornea which
extends peripheral (limbus to limbus) and full thickness by
2nd decade
• Accumulates GAGs within keratocytes and endothelial
cells, and under epithelium
• Stain with Alcian blue, colloidal iron, PAS, metachromatic
dyes

117
Q

What is Bietti crystalline corneoretinal dystrophy?

A

• Retinal dystrophy
• Peripheral corneal crystals
• Nyctalopia due to retinal degeneration
• Defect in lipid metabolism

118
Q

What is the differential diagnosis for corneal crystals?

A

• Macular dystrophy (mucopolysaccharide)
• Granular dystrophy (hyaline)
• Lattice dystrophy (amyloid)
• Bietti’s and Schnyder’s
• Ciprofloxacin deposits
• Strep Viridans - infectious crystalline keratopathy
• Cystinosis
• Multiple myeloma
• Monoclonal gammopathy

119
Q

What is conjunctival intraepithelial neoplasia?

A

• Consists of dysplastic cells involving varying amount of
epithelial layer
• Do not penetrate basement membrane
• Standard treatment: excision of lesion with 3-4 mm
margins, cryotherapy to bordering conjunctiva
• Topical treatment: interferon alpha-2b (low side effect
profile and tolerability); MMC, 5-FU

120
Q

What are corneal keloids?

A

• Rare
• Chalky white lesions
• After corneal trauma or perforation
• Due to vigorous fibrotic response after trauma
• Glistening and jelly like
• Congenital keloids - associated with Lowe syndrome,
ALC syndrome (acromegaly, cutis gyrata, corneal
leukoma), Rubinstein-Taybi syndrome

121
Q

What is ocular cicatricial pemphigoid?

A

• Autoantibodies directed against bullous pemphigoid
antigen II in the basement membrane zone
• Bilateral
• Inferior forniceal depth less than 8mm
• Severe disease treated with cyclophosphamide

122
Q

How is PUK treated?

A

• Most important is to address the underlying systemic
autoimmune disease
• Recessing the conjunctiva distances blood vessels
carrying cell mediators to the peripheral cornea

123
Q

What is Parinaud’s oculoglandular syndrome?

A

• Granulomatous conjunctivitis + regional
lymphadenopathy + constitutional symptoms
• Unilateral
• Presents 1 week after exposure to causative
microorganism
• Most common cause: cat scratch disease due to
Bartonella henselae
• Other causes, tularemia (rabbits), sporotrichosis,
tuberculosis, syphilis
• Treatment: azithromycin or doxycycline

124
Q

What is the ocular effect of the Dieffenbachia plant?

A

• House plants that contain needle shaped calcium
oxalate crystals – raphides
• Cause acute keratoconjunctivitis associated needle-like
crystals in the cornea when sap of this plant gets into
eyes

125
Q

What is the thinnest location of the cornea?

A

• Typically inferotemporal quadrant (thinnest zone of
cornea 1.5 mm temporal to geographic center)

126
Q

What are the risk factors for graft rejection?

A

• Deep stromal neovascularization
• Peripheral corneal thinning
• Ocular surface disease

127
Q

What is microsporidia?

A

• Classified as fungi
• Rare cause of conjunctivitis or epithelial keratitis in
immunocompromised (AIDS)
• Scraping of conjunctiva show gram positive spores
• Treat with topical fumagillin

128
Q

What is ocular melanocytosis?

A

• Focal proliferation of subepithelial melanocytes
• Pigmentation of episclera
• Not mobile
• 50% - ipsilateral dermal melanocytosis (Nevus of Ota),
proliferation of dermal melanocytes in periocular skin
V1 and V2
• 10% develop glaucoma
• Risk of uveal melanoma is 1:400 (much greater than
sporadic risk in general population)
• Only 5% are bilateral

129
Q

What is reactive arthritis?

A

• Caused by gram negative bacterial dysentery
(Salmonella, Shigella, Yersinia)
• Nongonococcal urethritis
• >75% are HLA B27 positive
• Papillary conjunctivitis (most common ocular finding)
“Can’t see, can’t pee, can’t climb a tree”

130
Q

What are the causes of chronic follicular conjunctivitis?

A

• Chlamydia - inclusion conjunctivitis or trachoma
• Toxic follicular conjunctivitis (i.e. glaucoma drops,
antiviral drops)
• Molluscum

131
Q

What is the differential diagnosis for cloudy cornea in an infant?

A

• Sclerocornea
• Trauma
• Ulcer
• Mucopolysaccharidoses/metabolic storage disease
• Peters anomaly
• Congenital hereditary endothelial dystrophy (CHED)
• Congenital hereditary stromal dystrophy
• Dermoid
• Congenital glaucoma

132
Q

What is Peters anomaly?

A

• Most common indication for corneal transplant in
children
• Localized absence of corneal endothelium and
Descemet’s membrane underneath a central corneal
opacity
• Inherited sporadically
• Bilateral in 80%
• Glaucoma in 50%
• Associated with aniridia, PFV, retinal detachment,
microcornea
• Type 1: iridocorneal adhesions in non-vascularized
corneal opacity, mutations of PITX2, FOXC1, CYP1B1,
PAX6
• Type 2: lens touch cornea of vascularized corneal
opacity; failure of lens vesicle to separate from surface
ectoderm; mutation of FOXE3

133
Q

What is Peters plus syndrome?

A

• Peters anomaly with the addition of systemic defects:
congenital brain defect, heart defects, craniofacial
anomalies

134
Q

What is the dosing of tetracyclines (doxycycline) for blepharitis?

A

• Dosing for MGD: 100 mg PO BID x 3-4 weeks then
50-100 mg daily based on clinical response
• Use with caution in the following: women of
childbearing age, women who are nursing, hx of liver
disease, taking warfarin, <8 years old
• Cause permanent discoloration of teeth and bones if
<8 years age or exposure during pregnancy
• Other side effects: photosensitization, GI upset,
oral/vaginal candidiasis, reduce efficacy of oral
contraceptives

135
Q

What are the different types corneal iron lines?

A

• “Ferry’s line” = leading edge of filtering bleb
• “Fleischer ring or line” = base of cone in keratoconus
• “Stocker’s line” = leading edge of pterygium
• “Hudson-Stahli line” = upper border of normal tear
lake (elderly pts)

136
Q

What is the immune privilege of the cornea?

A

• Responsiveness to foreign antigens is relatively
suppressed due to the following
• Absence of blood vessels and lymphatics
• Expression of immunosuppressive factors
• Increased expression of Fas ligand (CD95)
• Down regulation of MHC molecules

137
Q

What is microcornea?

A

• Autosomal dominant
• Clear cornea
• Normal thickness
• Horizontal diameter < 10 mm
• Hyperopic (cornea is relatively flat)
• More prone to angle closure glaucoma due to flat
cornea
• 20% can develop open angle

138
Q

What is Terrien marginal degeneration?

A

• Unilateral or asymmetrically bilateral
• Cornea starts to thin superiorly and thinning spreads
circumferentially
• Epithelium intact
• Pannus traverses the area of corneal thinning
• End of pannus is a line of lipid deposition
• Perforation is rare
• If perforation occurs - lamellar transplantation
• Starts in 2nd or 3rd decade of life

139
Q

What is the threshold tear meniscus below which is considered abnormal and a sign of dry eye?

A

• 0.3 mm

140
Q

What is the corneal vertex?

A

• Point located at the intersection of the line of fixation
and corneal surface. For refractive surgery, center your
ablation around corneal vertex.

141
Q

What is posterior polymorphous corneal dystrophy?

A

• Diffuse abnormality of Descemet’s membrane
• Multi-laminated appearance
• Recur in graft in PK
• Prognosis of PK or endothelial keratoplasty depends on
presence/absence of PAS and management of
glaucoma
• Mild localized swelling managed with anterior stromal
micropuncture

142
Q

What are the criteria for a donor cornea?

A

• Endothelial cell count 2000 or more
• Death-to-preservation time 12-18 hours
• Age of donor between 2 years to 70 years
• Exclusion criteria: death of unknown cause, active
septicemia, HIV/hepB/hepC, active ocular
inflammation

143
Q

What are diabetic corneal findings?

A

• Hypoesthesia
• Poor adherence of epithelium to stroma
• Delayed healing time with removal of epithelium at
the time of surgery

144
Q

What is congenital hereditary stromal dystrophy

A

• Rare
• Presents at birth
• Bilateral opacification of central stroma (white flakes)
• Peripheral cornea is clear
• Moderate-severe visual loss
• Non progressive/slowly progressive
• Thickened cornea
• Mutation in decorin gene on chromosome 12

145
Q

What is the gene defect in gelatinous drop like dystrophy?

A

● Defect in tumor associated calcium signal transducer 2

146
Q

What is an axial power map or “sagittal curvature” map?

A

• Based on reference axis through the line of sight
• Better estimation of central corneal power and less
accurate at measuring peripheral cornea

147
Q

What is instantaneous map, or tangential power map, or meridional power map?

A

• Based on best-fit spherical approximation at the point
of cornea being measured
• Better estimation of peripheral corneal power

148
Q

What is an epibulbar dermoid?

A

• Most commonly inferotemporal
• Can cause astigmatism
• Associated with Goldenhar syndrome - dental and
skeletal abnormalities and preauricular skin tags.
vertebral abnormalities include butterfly vertebrae,
hemivertebrae - secondary scoliosis, kyphosis, rib
abnormalities

149
Q

What are some examples of negative staining?

A

• SPK
• Pseudodendrites
• ABMD
• Thygeson superficial punctate keratitis

150
Q

What is dacryoadenitis?

A

• Most commonly secondary to sterile inflammatory
disease (orbital pseudotumor variant)
• EBV most common viral cause
• Multiple corneal infiltrates are associated with EBV

151
Q

What is Peters anomaly type 1?

A

• Iridocorneal adhesions in area of non-vascularized
corneal opacity
• Mutations in PITX2, FOXC1, CYP1B1, PAX6

152
Q

What is Peters anomaly type 2?

A

• Lens touch to area of vascularized corneal opacity
• Failure of lens vesicle to separate from surface
ectoderm
• Mutation in FOXE3

153
Q

What is the average thickness of corneal epithelium?

A

• 50 microns

154
Q

What is the average volume of the tear lake?

A

• 7-10 microliters

155
Q

Which corneal layer is most susceptible to UV radiation (i.e. welding, snow blindness)?

A

• Epithelium

156
Q

What is c-ANCA?

A

• Cytoplasmic antineutrophil cytoplasmic abs
• Cytoplasmic staining pattern
• Target antigen is proteinase 3
• Positive in Wegener’s granulomatosis

157
Q

What is p-ANCA?

A

• Peri-nuclear antineutrophil cytoplasmic abs
• Perinuclear staining pattern
• Target antigen is myeloperoxidase
• Positive in polyarteritis nodosa and IBD

158
Q

What is nanophthalmos?

A

• Small eye
• “N” normally organized (normal lens, cornea, etc)
• High hyperopia
• Short axial length 15-20 mm
• Crowded AC
• Thick/rigid sclera
• Choroidal detachments and hemorrhages

159
Q

What is microphthalmos?

A

• Small eye
• “M” messed up
• Disorganized eye
• Associated with trisomy 13, intellectual disability,
dwarfism

160
Q

What are the different forms of ichthyosis?

A

• Ichthyosis vulgaris - autosomal dominant, most
common
• X-linked ichthyosis - form that has corneal changes

161
Q

What is Tyrosinemia?

A

• Autosomal recessive
• Defect of tyrosine aminotransferase
• Excess tyrosine in blood and urine; normal
phenylalanine level
• Pseudodendrites
• Think of this in child with recurrent dendrites - may be
misdiagnosed as having recurrent HSV keratitis
• Treat with restricting dietary tyrosine and
phenylalanine

162
Q

What was the stromal keratitis arm of the HEDS study?

A

• Treated with PF q2h and trifluridine QID
• Topical antiviral used to prevent outbreak of epithelial
keratitis
• No benefit to adding oral acyclovir to topical
prednisone + trifluridine

163
Q

What are the three sphingolipidoses that cause corneal verticillata?

A

• Fabry
• Multiple sulfatase
• Generalized gangliosidosis

164
Q

What is chlamydia trachoma?

A

• Limbal follicles sequelae - Herbert pits
• Tarsal conjunctival scarring
• Vascular pannus most marked superiorly
• Conjunctival follicles most numerous on superior
tarsus

165
Q

What is olopatadine?

A

• Selective H1 receptor antagonist (rapid onset) and
inhibitor of mast cell degranulation (prolonged
duration)
• Therapeutic and prophylactic

166
Q

What is topical cyclosporine?

A

• Fungal metabolite that reduces ocular inflammation
• Inhibit Th2 lymphocytes proliferation, IL-2 production,
histamine release from mast cells
• Improves tear film stability
• Anti-inflammatory effects on meibomian glands
• Treats vernal and atopic keratoconjunctivitis

167
Q

What is oncocytoma?

A

• Slow-growing cystadenoma
• Originates from ductal and acinar cells of main and
accessory lacrimal glands

168
Q

What is cornea plana?

A

• Flat cornea with central corneal power < 43 D
• Cornea curvature similar to adjacent to sclera
• Isolated cases occur in Finnish individuals
• Seen in other ocular abnormalities like sclerocornea
and colobomas
• Associated with Ehlers-Danlos syndrome
• Open and chronic angle closure glaucoma can be
found

169
Q

What is the role of laser therapy in band keratopathy?

A

• Phototherapeutic keratectomy (PTK) is not
recommended because calcium ablate at slower rate
than the stroma. End up with irregular astigmatism
• Rather treat with epithelial debridement and then
application of disodium EDTA

170
Q

What are the exam findings in limbal stem cell deficiency?

A

• Loss of palisades of Vogt
• Peripheral pannus formation
• Late staining of epithelium (“wavelike” irregularity)
• Punctate epithelial keratopathy
• Persistent epithelial defects - lead to stromal loss
(ulcers), stromal scarring, corneal perforation
• Conjunctivalization - conjunctiva grows onto the
cornea to fill epithelial defects

171
Q

What is alkaptonuria?

A

• Inability to metabolize tyrosine and phenylalanine
• Deposition of pigmented material near medial and
lateral rectus muscle insertions
• Urine turns dark if left standing, due to elevated
urinary homogentisic acids
• Treated with high dose vitamin C to improve
arthropathy

172
Q

What is cystinosis?

A

• Autosomal recessive
• Most common in French speaking Canadians
• Three forms: infantile (most common), adolescent and
adult
• Crystals in anterior stroma
• Severe renal impairment, patchy depigmentation of
RPE, generally do not have vision loss

173
Q

What are different parts of the orbicularis muscle and their function?

A

• Orbital portion: responsible for voluntary eyelid
closure
• Pretarsal and preseptal: responsible for unconscious
blinking of eyelids

174
Q

What are the common cornea complications of hard CL?

A

• Central epithelial edema → treat with discontinuing
lens
• Corneal warpage

175
Q

What is a common corneal complication of soft CL?

A

• Micropannus of 1-2 mm
• Treatment with lens holiday or switch to lens with
higher oxygen transmissibility

176
Q

What is superior limbic keratoconjunctivitis?

A

• Caused by mechanical trauma of upper eyelid on
superior limbal area
• Commonly in adult women
• Asymmetrically bilateral
• Papillary reaction on palpebral conjunctiva
• Hypertrophy of superior conjunctiva
• Punctate epithelial erosions on superior conjunctiva
and cornea, superior corneal pannus
• Associated with thyroid abnormalities
• Obtain TSH, free T4
• Treatment: aggressive lubrication, resection of
conjunctiva, large diameter soft CLs, cauterization of
conjunctiva, Restasis

177
Q

What are the most common etiologies of post refractive surgery infectious keratitis?

A

• Within 10 days - gram positive bacteria
• More than 10 days after surgery - atypical
mycobacteria

178
Q

What is the most accurate imaging modality for measuring sulcus-to-sulcus distances?

A

• High-frequency ultrasound (UBM)
• Structures posterior to iris are imaged with great
accuracy

179
Q

What is a Scheimpflug camera (Pentacam)?

A

• Mounted on rotating arm
• Takes multiple images of the cornea while rapidly
rotating around
• Images generate anterior and posterior curvature
maps, pachymetry maps, anterior chamber depth
• Accurate for measuring posterior corneal curvature

180
Q

What is a scanning-slit topographer (Orbscan)?

A

• Mathematically derived posterior curvature maps

181
Q

What is a keratometer?

A

• Measures anterior corneal curvature and assumes
posterior corneal curvature to be fixed constant

182
Q

What is the meaning of vernal?

A

• Spring

183
Q

What is vernal conjunctivitis?

A

• Allergic phenomena
• Children within in first 2 decades of life during spring
or fall
• Giant papillary reaction
• Horner-Trantas dots - jelly like limbal nodules
representing eosinophils
• Shield ulcer - corneal epi defect upper half of cornea

184
Q

What are the risk factors for fungal keratitis?

A

• Trauma with plant or vegetable matter
• CL wearer
• Prior corneal surgery (PKP and RK)
• Chronic keratitis
• Topical steroids

185
Q

What is filamentous fungal keratitis?

A

• Common etiology: aspergillus and fusarium
• Gray-white infiltrate with feathery margin
• Multifocal or satellite lesions. Anterior lesion may
elevate surface of cornea, rough/dry/gritty
appearance
• Treat with Natamycin 5% (commercially produced)
until cultures are back
• If Aspergillus, then treat with amphotericin B
(compounding pharmacy)
• In United States, occur most commonly in Southern
areas, secondary to Fusarium

186
Q

What is Yeast keratitis?

A

• Most common etiology: Candida
• Anterior raised colonies, remains superficial
• Culture with blood, Sabouraud, brain-heart infusion
• Treat with amphotericin B (compounding pharmacy)

187
Q

What is lisch epithelial corneal dystrophy?

A

• X-linked dominant
• Densely-crowded epithelial microcysts in band-like or
feathery pattern
• Between bands, epithelial is clear
• Treatment not needed unless bands cross visual axis,
then epithelium can be scraped
• Do not have epithelial erosions
• Most closely resembles Meesmann corneal dystrophy
(both have intraepithelial microcysts)
• Difference between Meesman and Lisch is that
Meesman has diffuse evenly spaced cysts. Lisch has
broad, band-shaped feather lesions in whorled
patterns that more densely crowded together

188
Q

What are the systemic and corneal findings in congenital syphilis?

A

• Interstitial keratitis, presents late in 1st decade,
immune-mediated manifestation
• Dental deformities (notched incisors, mulberry
molars)
• Saddle nose, saber skins, frontal bossing, perforation
of palate
• Deafness
• Mental retardation

189
Q

What are the ocular findings in acquired syphilis?

A

• Much less likely to develop interstitial
keratitis compared to congenital syphilis
• If interstitial keratitis occurs, unilateral 60% of time
• Uveitis and retinitis more common sequelae in
acquired than congenital

190
Q

What is acute hydrops in keratoconus?

A

• Spontaneous rupture of Descemet’s membrane
• Passage of fluid into stroma
• I-S values >1.4 associated with keratoconus (“I-S”
value compares keratometric reading inferior cornea
to superior cornea)
• Treat with topical hypertonic saline drops, patching,
cycloplegia, aqueous suppressant, BCL while awaiting
Descemet membrane repair itself, takes 6-12 weeks
• Also treat with injection of air or gas (C3F8, SF6) into
anterior chamber, speeds up resolution of edema.
“Pneumatic descemetopexy”, does not influence final
visual outcomes or need for corneal transplantation

191
Q

What is the endothelial coefficient of variation and hexagonality?

A

• Coefficient of variation: how variable endothelial cell
size. >0.4 is abnormal, increased risk for postoperative
edema
• Hexagonality: <50% is abnormal, called pleomorphism,
increased risk of postoperative edema
• View endothelium with specular microscopy

192
Q

When does endothelium act like epithelium?

A

• ICE - unilateral, no inherited
• PPMD - bilateral, autosomal dominant
• Both have corectopia, glaucoma, endothelial
dysfunction

193
Q

What is the location of conjunctival involvement in adult inclusion conjunctivitis?

A

• Typically involves inferior palpebral conjunctiva

194
Q

What type of conjunctival reaction is seen in neonatal inclusion conjunctivitis (ophthalmia neonatorum disease)?

A

• Papillary reaction (not follicular)

195
Q

What is fleck dystrophy?

A

• Autosomal dominant
• Dandruff-like deposits throughout stroma
• Spare epithelium and endothelium
• Vision does not decrease

196
Q

What are the risk factors for corneal decompensation after intraocular surgery?

A

• > 640 microns central corneal thickness
• Endothelial cells <1,000

197
Q

What is familial dysautonomia (Riley day syndrome)?

A

• Ashkenazi family
• Skin blotching
• Neurotrophic keratopathy
• Decreased tearing when crying
• Enlarged corneal nerves

198
Q

What is the rate of pterygium recurrence?

A

• Highest rate of recurrence with bare sclera, leaving
involved area open; 40-75% rate of recurrence
• With simple closure, amniotic membranes, or
conjunctival autograft, rate of recurrence is 3-5%

199
Q

What are the clinical findings in congenital glaucoma?

A

• Photophobia
• Corneal edema
• Corneal horizontal diameter >12 mm
• Horizontal tears in Descemet’s membrane = Haab
striae

200
Q

What is the most common cause of explosive endophthalmitis after penetrating eye trauma?

A

• Bacillus cereus - spores, found in soil/vegetative
material
• Species are motile
• Treated with intravitreal vancomycin or clindamycin
• 25% of post traumatic endophthalmitis

201
Q

At what corneal thickness does corneal epithelial edema occur?

A

• 700 microns or more

202
Q

What is the inheritance pattern and ocular findings in Hunter syndrome?

A

• X-linked recessive
• Pigmentary retinopathy

203
Q

What is Fraser syndrome?

A

• Autosomal recessive
• Associated with cryptophthalmos
• Malformations of genitals, nose, ears, larynx and renal
system
• Mutations in FRAS1, codes for extracellular matrix
protein

204
Q

What is infectious crystalline keratopathy?

A

• White, branching stromal deposits resembling
snowflakes with no or minimal inflammatory signs
• History of PKP, chronic topical steroids
• Bacteria gain access via epithelial ingrowth through
suture track
• Most common: strep viridans (alpha hemolytic strep)
• Treat with topical fortified vancomycin or cefazolin,
stop steroids, broad spec systemic antibiotics
• If resistant to treatment then repeat PKP

205
Q

What were the results of the HEDS trial?

A

• Topical trifluridine and topical steroids expedite
resolution of stromal inflammation in HSV stromal
keratitis
• Adding oral acyclovir did not provide additional
improvement
• Long term oral antiviral prophylaxis reduces
recurrences of HSV keratitis (recommend if >1 episode
of HSV keratitis)
• This trial did not test whether topical trifluridine +
topical steroids is better than oral acyclovir
• General consensus: oral antiviral with topical steroid is
good alternative (compared to topical trifluridine +
topical steroids)
• Antiviral agent used in isolated HSV stromal keratitis to
prevent epithelial keratitis while on steroid drops

206
Q

Recurrent dendrites in a child is seen with which systemic metabolic condition?

A

• Seen with tyrosinemia, these patients do not have true
dendrites, rather, they have pseudodendrites

207
Q

What is Rizzuti sign?

A

• Conical reflection on the nasal cornea when penlight is
shone temporally
• Seen in keratoconus

208
Q

What are the screening serum markers and ocular effect of Sjogren’s syndrome?

A

• Screening: ANA, SS-A, SS-B
• Lymphocytic infiltration of lacrimal gland
• Topical beta blocker and Diamox worsen dry eyes

209
Q

What is the difference between DMEK an DSEK?

A

• DMEK - transplant just Descemet membrane and
endothelium
• DSEK - transplant Descemet membrane/endothelium
and portion of posterior stroma

210
Q

What is disciform keratitis?

A

• Overlying stroma and epithelium have edema in round
pattern
• Secondary to endotheliitis
• Treat with oral acyclovir (penetrate deeper cornea
tissues via aqueous) + topical trifluridine or ganciclovir
• Most commonly due to HSV and VZV, both present the
same

211
Q

Which medications cause corneal verticillata?

A

• Amiodarone (most common)
• Chloroquine
• Hydroxychloroquine
• Chlorpromazine
• Subconj gentamicin
• Ibuprofen
• Indomethacin
• Naproxen
• Tamoxifen

212
Q

What is the risk of developing glaucoma and uveal melanoma in ocular melanocytosis?

A

• 10% - glaucoma
• 1/400 - uveal melanoma (much greater than sporadic
risk in general population)

213
Q

What is the a platinum kimura spatula most useful for?

A

• Obtaining bacterial cultures

214
Q

What is a Dacron swab most useful for?

A

• Obtaining viral cultures

215
Q

What is the difference between megalocornea versus congenital glaucoma?

A

• Megalocornea - nonprogressive, bilateral, X-linked
recessive, horizontal diameter >13 mm, normal IOP, A
scan with normal axial length and deep AC
• Congenital glaucoma - Haab striae (break in Descemet
membrane), elevated IOP, elongated axial length

216
Q

What are the indications for anterior chamber washout in an eye with hyphema?

A

• IOP ≥ 60 mmHg for ≥ 48 hours
• Hyphema does not decrease ≥ 50% by 8 days
• IOP ≥ 25 mmHg with total hyphema for ≥ 5 days
• IOP 24 mmHg for ≥ 24 hours (or any transient increase
IOP 30 mmHg) with sickle cell trait/disease
• Signs of corneal blood staining
• Children at risk for amblyopia
• Significant visual impairment

217
Q

What is the most common cause of chronic blepharoconjunctivitis?

A

• Staph aureus

218
Q

What are the branches of CNV1?

A

• Frontal
• Lacrimal
• Nasociliary

219
Q

Involvement of which branch of CNV1 has the highest risk of ocular involvement?

A

• Nasociliary branch

220
Q

What is the treatment of HZO?

A

• Valacyclovir 1g TID or acyclovir 800 mg 5x/day or
famciclovir 500 mg TID for 7-10 days
• If retinal or choroidal or optic nerve or cranial nerve
involvement → intravenous acyclovir 10 mg/kg IV q8h
for 7 days

221
Q

What is Terrien’s marginal degeneration?

A

• T: Thinning cornea
• T: Top (starts superiorly)
• T: age is in the Thirties
• T: Treatment Transplantation (crescent shaped
lamellar)

222
Q

What mimics Terrien’s marginal degeneration and is seen in children?

A

• Fuchs superficial marginal keratitis

223
Q

What is Kaposi sarcoma?

A

• Herpesvirus/human herpesvirus 8
• Secondary to malignant transformation of vascular
endothelium
• Can cause subconjunctival hemorrhage
• Associated with HIV

224
Q

What is the osmolarity, lysozyme composition, and lactoferrin composition of tears in dry eye syndrome?

A

• Increased osmolarity
• Decreased lysozyme and lactoferrin
• This test is not necessarily diagnostic of dry eye in
isolation
• There can be variable results at the same appointment
• Results should be considered in context of clinical signs

225
Q

What is Marfan syndrome?

A

• Autosomal dominant
• Abnormal fibrillin
• Rule out aortic root dilation and aneurysm
• Zonules are brittle
• Superotemporal ectopia lentis (50-80%)

226
Q

What is homocystinuria?

A

• Patients are tall and 50% have intellectual disability
• Inferonasal dislocation of lens
• Brittle zonules
• Prone to thromboembolic events with general
anesthesia
• Treat with dietary restrictions with low methionine
and high cysteine

227
Q

Which fungi are filamentous?

A

• Fusarium
• Aspergillus

228
Q

Which fungi are septate?

A

• Aspergillus

229
Q

Which fungi are non-septate?

A

• Mucor
• Rhizopus

230
Q

How soon can limbal stem cell transplantation be performed after chemical injury?

A

• 2 weeks
• Reducing inflammation prior to transplantation
increases grafts odds of survival because inflammation
leads to cell death
• Same goes for corneal transplant

231
Q

What are Hassall-Henle bodies?

A

• AKA peripheral endothelial guttae
• Small, wart-like, transparent peripheral excrescences
• Found in descemet membrane
• Common in elderly → normal aging change →
thickening of Descemet membrane that happens
throughout life
• Composed of collagen
• Represent overactive hyaline production by
endothelial cells
• Best seen with specular reflection with the slit lamp
• Pathologic when these appear in central cornea →
called cornea guttae → Fuchs endothelial dystrophy

232
Q

What are the causes of ectopia lentis?

A

• Marfan syndrome
• Homocystinuria
• Aniridia
• Congenital glaucoma
• Ehlers-Danlos
• Hyperlysinemia
• Sulfite oxidase deficiency
• Weill-Marchesani disease
• Isolated anomaly
• Ectopia lentis et pupillae
• Pseudoexfoliation syndrome
• Trauma
• Microspherophakia

233
Q

What are diagnostic tools that can be used to analyze the posterior corneal surface?

A

● Scheinflug tomography
● Pentacam
● Galilei

234
Q

What virus and which serotypes causes Epidemic Keratoconjunctivitis?

A

• Adenovirus serotypes 8, 19, 37
• Subgroup D

235
Q

What are the differences between Diffuse Lamellar Keratitis and Infectious Keratitis?

A

● Diffuse Lamellar Keratitis
○ Within 24 hours of surgery
○ Begins at flap periphery
○ More intense inflammation in periphery
○ Minimal to no anterior chamber reaction
● Infectious Keratitis
○ 2-3 days postoperatively
○ Anywhere under flap
○ Focal inflammation around infection
○ Mild to moderate anterior chamber reaction

236
Q

What wavelength of light can cross-link collagen and what is it used for?

A

• 365 nm with concomitant administration of topical
riboflavin
• Treats corneal ectasia

237
Q

What is Epithelial Basement Membrane Dystrophy?

A

• No documented inheritance pattern
• Abnormality in epithelial turnover, maturation, and
production of the basement membrane
• Thickened basement membrane with microcysts or
fibrillar material between basement membrane and
Bowman layer
• Often with abnormal hemidesmosomes
• 6-18% of population

238
Q

What does a handheld esthesiometer (Cochet-Bonnet) measure?

A

• Contact device that measures corneal sensation

Ophthalmology Boards Review (10 decks)

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