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Block 15 > Anterior Seg Disease > Flashcards

Anterior Seg Disease Flashcards

1
Q

Most common cause of infectious K blindness in developed countries

A

Herpes simples keratitis

HSV-1

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2
Q

Most common cause of infectious k blindness in underdeveloped countries

A

Trachoma

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3
Q

How is HSV primary infection spread?

A

Via respiratory droplets

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4
Q

Primary infection of HSV

A

Uncommon during first 6 months of life due to maternal antibodies
Subclinical or mild fever/upper respiratory tract infection

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5
Q

How can you treat primary infections of HSV if they are eye/skin lesions?

A

Topical antiviral ung(ointment)/cream

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6
Q

Recurrent Infections of HSV

A

Latent virus within sensory dermatome (trigeminal ganglion) re-activated by various stressors: fever, hormone changes, UV, etc
Virus replicates and moves along sensory nerve to periphery
Recurrence rates vary, but the more you’ve had, the more you’re likely to have again in the future (can be hundreds over a lifetime)

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7
Q

HSV epithelial keratitis occurs with what?

A

‘’Active” viral replication (dendritic or geographic)

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8
Q

Symptoms of HSV epithelial keratitis

A

Mild/moderate discomfort, redness, photophobia, watering

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9
Q

Signs of HSV epithelial keratitis

A

Swollen/opaque epithelial cells —> dendritic ulceration
Decreased K sensation
Ulcer may enlarge to geographic/amoeboid appearance with steroid use
Mild subepithelial haze typical
May see: mild AC rxn, follicular conj., vesicular lid lesions, increased IOP - affecting the outflow of the trabecular meshwork (check non-involved eye first and disinfect)

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10
Q

When staining for HSV epithelial keratitis, what stains are used to stain what?

A

NaFl stains the bed of the ulcer

Rose bengal stains the margins of the ulcer

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11
Q

HSV dendritic ulcer

A

Branching pattern with end bulbs

Will probably go away on it’s own if no treatment, b/c immune system will catch up with it

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12
Q

What can happen if you put a patient on a topical steroid if they have HSV corneal ulceration?

A

It can make it worse and the ulcer can take on the geographic appearance

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13
Q

HSV geographic ulcer

A

Occurs due to a patient with HSV being treated with steroids, causing an even larger ulcer than just the dendrites

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14
Q

Corneal sensitivity testing checks for what?

A

Pt can lose sensation due to the sensory nerves being affected from HSV
Brushing against the cornea can show if their issue is definitive for the herpes simplex virus instead of bacterial or sometimes viral

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15
Q

Diagnosis for HSV epithelial keratitis

A

Clinical (can culture, do PCR, or stain as well)

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16
Q

Treatment of HSV epithelial keratitis

A

Most will heal without treatment, but that can increase the pt’s risk of scarring
Anti-viral gel on ung(ointment) 5 x day (typical treatment)
Tablets (for kinds or immunodeficiency pt’s)
Debribement (rub ulcer away)
Aciclovir cream 5 x day for skin vesicles
Antibiotics prophylactically
IOP lowering medications (NOT PROSTAGLANDIN DERIVATIVES)

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17
Q

Why do you not want to prescribe the IOP lowering medications, prostaglandin derivatives, to a patient who is suffering from HSV epithelial keratitis?

A

Prostaglandin derivatives are pro-inflammatory; the reason the IOP is elevated is because the trabecular meshwork is inflamed. Using these would just add to the inflammation, and make the IOP worse.

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18
Q

Prognosis for HSV epithelial keratitis

A

Virtually all ulcers heal within 2 weeks (but we like to speed this up with topical medications like aciclovir gels/ung to decrease scarring)
Avoid steroids (tobradex = combination of antibiotic and steroid)
Mild subepithelial haze often lingers for weeks after ulcer heals
Persistent haze may increase with each recurrence, eventually compromising vision

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19
Q

What response may and HSV stromal keratitis issue represent?

A

Either an immune-mediated response or an “active” viral replication (within stroma)

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20
Q

Symptoms of HSV stromal keratitis

A

Blurring of vision (due to some opacification

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21
Q

Signs of HSV stromal keratitis

A

Infiltration of stroma (usually without accompanying dendritic ulceration) that may be diffuse or focal
Anterior chamber reaction with KP’s (penetrating keratoplasty) underlying area of infiltration
Stromal (interstitial) scarring (opacification), thinning, and vascularization may ensue

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22
Q

Treatment for HSV stromal keratitis

A

Topical steroids with antiviral cover (often oral)

Best managed by a corneal specialist

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23
Q

Appearance of mild HSV stromal keratitis

A

Eye is red
Don’t stain b/c epithelium is intact
Do cross-section, an notice place in stroma (focal stromal infiltration) where it has a grayish color

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24
Q

Appearance of marked HSV stromal keratitis

A

Graying through the stroma, coving part of vision
Has neovascularization
Will affect vision
Can lead to scarring

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25
Q

Appearance of significant scarring from HSV stromal keratitis

A

White circular opacification-like spot right on the center of the pupil, located within the stroma of the cornea
Significant scar due to stromal herpetic simplex
Very common cause of vision loss

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26
Q

Disciform endotheliitis (or disciform keratitis)

A

Frequent form of recurrent HSV keratitis thought to be an immune reaction rather than infection of the endothelial cells

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27
Q

Symptoms of disciform endotheliitis (keratitis)

A

Gradual blurring of vision with “haloes around lights”

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28
Q

Signs of disciform endotheliitis (keratitis)

A

Central zone of stromal edema in a circular (disc-like) pattern
Underlying KP’s
Surrounding immune (Wessely) ring of deep stromal haze

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29
Q

History of disciform endotheliitis (keratitis)

A

Don’t always have clear history of prior HSV epithelial ulcer, but decreasing corneal sensitivity may assist diagnosis

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30
Q

Treatment of disciform endotheliitis (keratitis)

A

Topical steroids with antiviral cover

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31
Q

Outcome for vision in patients with disciform endotheliitis (keratitis)

A

Visual loss is usually reversible with steroid drops (since the edema can be treated, the vision can come back)

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32
Q

Appearance of HSV disciform keratitis

A

Won’t stain b/c no topical viral infiltration present
Disc-like, typically in the center, due to endothelialitis
Large circular white opacification in the cornea

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33
Q

Associated condition with HSV keratitis

A

Neurotrophic keratopathy

Iriddocyclitis

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34
Q

What treatment can make HSV keratitis worse?

A

Antiviral drops b/c it is not an active viral disease

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35
Q

Treatment for neurotrophic keratopathy

A

Lubricants, etc. with judicious use of steroids for any inflammatory component

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36
Q

Decompensation of epithelium due to loss of sensation

A

Neurotrophic keratitis

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37
Q

Issues arising from neurotrophic keratopathy

A

Corneal hypoesthesia or complete anesthesia from damage to corneal nerves, possibly leading to persistent non-healing corneal epithelial defects (stromal scarring, corneal perforation, or secondary bacterial infection)

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38
Q

Issues arising from iridocyclitis

A

May present without signs of active keratitis
Acute trabeculitis may result in an acute rise in IOP
Uveitis associated with HSV mandates a thorough fundoscopic exam to exclude concomitant acute retinal necrosis

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39
Q

Treatment for iridocyclitis

A

Steroids (and often oral antiviral cover)

Must differentiate from IOP spike due to steroid treatment

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40
Q

Prophylaxis for HSV keratitis

A

Cuts recurrence rate of epithelial/stromal keratitis in half
Indicated for frequent, severe recurrences or monocular patients
Common regimen is 400 mg oral aciclovir bid x years

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41
Q

Complications of HSV keratitis

A 
Secondary infections (most often bacterial)
Glaucoma (due to trabeculitis or chronic steroid use, both causing an increase in IOP)
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42
Q

What is sometimes the end result for HSV keratitis?

A

Keratoplasty

  • recurrent HSV keratitis common
  • rejection common
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43
Q

Herpes zoster ophthalmicus (HZO)

A

Shingles involving the ophthalmic division of trigeminal (CN V) nerve
Reactivation when immunity fades
Follows initial infection (HSV) of chickenpox

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44
Q

Hutchinson’s sign

A

In HZO, if pt presents with nose rash involved, the eye will likely be involved as well

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45
Q

How is the cornea affected by HZO?

A 
Direct infection (epithelial keratitis)
Secondary infection (stroma, endothelium)
Nerve damage (hypo-aesthesia which may lead to neurotrophic keratopathy)
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46
Q

Typical age of patient’s to get HZO

A

50-60’s (when immunity fades from the chickenpox virus)

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47
Q

How does singles present?

A

Prodrome (fever, malaise, HA) for 3-5 days

Painful rash respecting midline —> vesicles, crust/heal over weeks —> scarring/depigmentation

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48
Q

Diagnosis of shingles

A

Clinical, aided by PCR, microscopy, etc.

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49
Q

Treatment for shingles

A 
Oral antivirals (ex. 800 mg aciclovir 5x daily for 5-7 days)
Prompt treatment (within 72 hours) decreases the severity/duration and likelihood of post-herpetic neuralgia and late ocular complications (x 50%)
IV antivirals for severe presentations or immunodeficient pt’s
Contagious - can spread chickenpox (avoid those pregnant or immunodeficient)
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50
Q

Skin reactivation of VZV infection

A

Shingles

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51
Q

If there is a singles rash on the abdomen, does it still equal HZO?

A

No; the eyes won’t be affected

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52
Q

If there is a shingles rash on the face, including Hutchinson’s sign, can this equal HZO?

A 
Yes! Is still shingles, but this zoster has the subset of shingles
CN 5 (ophthalmic branch)
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53
Q

Half of pt’s with HZO develop what soon after the rash?

A

Dendritic epithelial ulcerations (smaller/finer than with HSV and usually self-resolve) = pseudodendrites - don’t have end bulbs an don’t stain quite as well

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54
Q

What are some ocular inflammation issues that can occur with HZO?

A 
Stromal (interstitial) keratitis
Anterior uveitis common (can elevate IOP)
Disciform keratitis (left often with HSV)
Posterior uveitis  = PRN (posterior retinal necrosis)/ARN (acute retinal necrosis), so must do DFE (dilated fundus exam)
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55
Q

HZO infection that can show pseudodendrites

A

HZO epithelial keratitis

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56
Q

HZO infection that is the leading form of blindness in this country, causing scarring, is what kind of infection?

A

HZO stromal (interstitial) keratitis

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57
Q

Infections that cause interstitial keratitis

A 
Syphilis
Herpetic viruses (more common in simplex than zoster)
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58
Q

Non-infectious things that can cause interestitial keratitis

A

Sarcoidosis

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59
Q

Non-viral things that can cause interstitial keratitis

A

Tuberculosis

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60
Q

If pt’s acquire interstitial keratitis at birth, what are the side-effects?

A

Lesion is in the stroma, leading to lots of inflammation and neovascularization in the cornea

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61
Q

What is HZO?

A

Shingles with ocular involvement

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62
Q

What are some potential issues of HZO?

A

Neurotrophic keratitis (half) - not typically severe
Scleritis, if chronic, can lead to patchy atrophy
Lid scarring —> ptosis, exposure (incomplete closure), trichiasis
Post-herpetic neuralgia = pain long after rash heals

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63
Q

Post-herpetic neuralgia is most commonly associated with what?

A

HZO
Pain greater than a month after the shingles rash heals
More likely with increased age (over 70)
Can be very sever and best dealt with by a pain specialst

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64
Q

Can you give HZO pt’s a vaccine?

A

Once you acquire the virus, you can’t eradicate the organism, but you can give them a booster to decrease their likelihood of developing the reactivation of shingles later on.
Doesn’t treat shingles, but helps to avoid shingles in the first place.

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65
Q

CASE:
22 yo, CL wearer, suspected to have acanthomoeba; descemet’s membrane shows folds = edema (swelling); you notice circular graying of the cornea. What do you do?
What do you suspect?

A

Stain to see if it’s in the stroma or the epithelium
This is disciform scarring (edema) - will reabsorb and vision should better
Treatment with steroid drops (prednisone QID)

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66
Q

CASE:
44 yo, has been taking medications; after staining the eye with sodium fluorescein, you notice multiple large lesions on the surface of the cornea very well.
What layer of the cornea is likely involved?
What lesion do you think this could be?
What do you think this could be caused by?

A

Most likely the epithelium
Geographic ulcerations, caused by taking steroid medications after already having corneal involvement of herpes (dendritic ulcers)
Herpes simplex virus

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67
Q

CASE:
On SLE, you notice some type of elevated, mounted up, raised looking bubbles that don’t really have the appearance of an ulcerations on a pt’s cornea that don’t stain real well; pt has no history of red eye; this is noticed a few days after a pt has come down with a rash on their face.
What do you think it could be?
What would you do to treat it?

A

Epithelial involvement of zoster reactivation
They are probably already on aciclovir for the rash, and you probably don’t want to give them any topical drops b/c it won’t help.

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68
Q

CASE:
75 yo develops redness, tearing, light sensitivity, and blurred vision in the right eye (20/400); looks like there may be an ulceration in his central vision, with some neovascularization around the outer edge of the cornea; he has a history of recurrent corneal simplex keratitis, with his last episode being about 6 months ago; he has substantial denervation due to constant recurrence, and he’s on topical antivirals for treatment.
What do you think this could be?
How do you treat this patient?

A

Neurotrophic epithelial keratitis
Stop all drops/medications immediately (no preservatives -artificial tears); may need to go to amniotic membrane or flap or graft to heal this up; need to treat with lubrication before they develop secondary bacterial corneal infections; send pt to specialist

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69
Q

What does meta-herpetic mean?

A

Associated with herpes, but non-healing epithelial ulcerations

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70
Q

Corneal sensitivity testing has two methods. One is the qualitative method and the other is the quantitative method. Describe the qualitative method.

A

If they feel it much more on one eye than the other, you know there is corneal desensitization on one eye = corneal hypo-asthesia
Herpetic diseases are most common cause of this

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71
Q

Corneal sensitivity testing has two methods. One is the qualitative method and the other is the quantitative method. Describe the quantitative method.

A

Thin filament you touch to the eye; keep shortening the filament until they feel it (more resistance the shorter it gets)
Helps to decide the magnitude of sensitivity loss

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72
Q

What test do you use to rule out HSV keratitis?

A

Corneal sensitivity test

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73
Q

How can you use rigid dental floss to test for corneal sensitivity, which checks for HSV keratitis?

A

First, touch the unaffected eye with the floss. The pt can grad the sensitivity on a scale of 1-10.
Then, touch the other eye and see if they sensitivity is low or non-existent.

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74
Q

61 yo femal pt presents with itchy eyes, dryness, and occasional burning. She has seen other doctors and gets improvement for 2-4 weeks, but no resolution. She has previously used lid scrubs and tobradex. The location of her itchiness is more at the lash margin. You don’t notice any discharge or grittiness, but there is a clear sleeve around the base of the lashes.
What do you think this pt has?
How do you treat them?

A 
Demodex blepharitis (if the pt presented with itchiness in the nasocanthal corner of the eye, then you would suspect allergies)
Tx: Tea tree oil
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75
Q

57 yo female pt presents with itching and irritated eye lids, occurring over 2 years on and off. She has tried numerous OTC products with no relief. You notice dandruff/flaking/scales in the lashes, with nothing at the base, and suspect it’s coming from the skin instead.
What do you think is the issue wit this patient?
How do you treat this pt?

A

Seborrheic dermatitis

Tx: tramcinolone dermatological prep (steroid cream) and can use OcuSoft lid scrub plus

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76
Q

Pt presents with frothy tear film.

What do you suspect immediately?

A

MGD = most common cause of evaporative dry eye

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77
Q

Pt is a CL wearer, who has dry eye. What is the key to treat their dry eye?

A

Treat the underlying MGD (meibomian gland deficiency)/DED (dry eye deficiency)

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78
Q

You stain a pt’s eye with NaFL dye who you suspect might have dry eye. Corneal staining indicates what?

A

Late indicator of disease

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79
Q

How do you treat a pt with neurotrophic dry eye (someone with shingles)?

A

It’s good to use punctal occlusion first to treat the dry eye

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80
Q

What is known as the top level of dry eye management?

A

Scleral lenses

81
Q

Acanthamoeba keratitis

A

Ubiquitous Protozoa of soil, water, and URT (upper respiratory tract)

82
Q

Disease often associated with CL’s rinsed with tap water in the USA?

A

Keratitis (acanthamoeba keratitis)

83
Q

Symptoms of acanthamoeba keratitis

A

Blurred vision

Discomfort/pain —> clinical picture (helps differentiate from HSV)

84
Q

Signs of acanthamoeba keratitis

A

Grayish irregular K surface —> infiltrates
Slowly progressive stromal opacification/vascularization
Corneal melt may occur at any stage

85
Q

Different types of infiltrates found in acanthamoeba keratitis

A

Perineural = ‘radial keratoneuritis’ virtually pathognomonic

Focal/diffuse anterior stromal gradually coalesce and enlarge - often forming ring abscess

86
Q

Whiteish (WBC’s) around the corneal nerve that’s pathognomonic for acanthamoeba keratitis

A

Radial keratoneuritis

87
Q

Diagnosis of acanthamoeba keratitis

A

Difficult and often delayed
Consider whenever there’s limited response to antibiotics
Stains and/or cultures - of corneal scrapes
PCR and in vivo confocal microscopy
Biopsy

88
Q

Treatment for acanthamoeba keratitis

A

The earlier the better!!!
Debribement - facilitates gtt penetration
Topical amoebicides (initially hourly, then dec., can take weeks to clear, and often continued for months)
Pain control (oral NSAIDs) - ibuprofen
Adjunctive low-dose steroids IF necessary
May require PK (penetrating keratoplasty) for resistance, late scarring, or perforation

89
Q

Do we try to treat or prescribe for acanthamoeba keratitis?

A

No; it’s difficult to treat, so get a corneal specialist to do it

90
Q

Onchocerciasis keratitis

A

River blindness
Transmitted by black fly bite and worm transmitted to the cornea
The body kills the worm, and then bacterial infection if what causes so many issues into the cornea (hypersensitivity reaction)
Found mainly in equatorial Africa (fast moving rivers)

91
Q

Marginal keratitis

A

Hypersensitivity to staphylococcal exotoxins and cell wall proteins

92
Q

What kind of infiltration does marginal keratitis have?

A

Lymphocytic infiltration, not infectious

93
Q

Signs of marginal keratitis

A

Peripheral ‘marginal’ K infiltrates (outer margins)
Adjacent conjunctival hyperemia
Typically only a small, in any, overlying epithelial defect
Multiple infiltrates may coalesce/enlarge circumferentially (crescent shape around the cornea)

94
Q

Symptoms of marginal keratitis

A

No pusy/ropey discharge
Mild discomfort
Redness
Tearing

95
Q

Treatment for marginal keratitis

A

Often self-resolving over week
Occasionally with residual superficial scarring/pannus (vascularization)
**Treat any associated blepharitis
Sometimes a weak topical steroid +/- antibiotic given QID x 1-2 weeks

96
Q

Phlyctenular keratitis

A

Nodular inflammation of cornea resulting from hypersensitivity reaction to a foreign antigen/bacteria (staph aureus, mycobacterium tuberculosis, etc.)

97
Q

Symptoms of phlyctenular keratitis

A

Photophobia
Lacrimation
Blepharospasm

98
Q

Who commonly gets phlyctenular keratitis?

A

Primarily in children from 6 months to 16 years old

99
Q

Signs of phlyctenular keratitis

A

White limbal nodule, that may extend further onto cornea, with associated intense local conjunctival hyperemia

100
Q

Disease that is less common, but more severe than marginal keratitis

A

Phlyctenular keratitis

101
Q

Treatment for phlyctenular keratitis

A

Usually spontaneously resolve over weeks - often with scar, superficial vascularization and thinning
Can lead to ulceration

102
Q

What two things do you want to decrease when treating phlyctenular keratitis?

A

Inflammatory response (generally topical steroids +/- antibiotic)
Source of antigens
(Treat blepharitis or underlying infection - TB, chlamydia, etc.)

** not infectious

103
Q

Pt’s are generally more bothered by this more than marginal keratitits

A

Phlyctenular keratitis

104
Q

Rosacea

A

Common chronic condition of sun-exposed skin (face. And neck) characterized by telangiectasia (vessels that have always been there but not evident until swelling), papule/pustule formation, rhinophyma (nose gets bulbous/large on tip = meaty) and facial flushing

105
Q

Rosacea is a multifactorial etiology that involves defects where?

A

In the body’s immune response to pathogens (skin/GI) and vasoregulatory process

106
Q

Rosacea that is common and has eye involvement

A

Ocular rosacea

107
Q

Ocular rosacea includes what structures?

A

Lids - marginal telangiectasia and MGD
Conjunctiva - inflammation
Cornea

108
Q

What kind of things do you find with corneal involvement with ocular rosacea?

A

Punctate epithelial erosions inferiorly
Peripheral vascularization
Marginal keratitis (one of many causes)
Thinning which can progress to perforation
Scarring/vascularization may eventually develop

109
Q

Appearance of dermatological rosacea

A

Common facial pattern with papules and pustules; bilateral and symmetrical; chronic and long-term; can’t really cure

110
Q

Appearance of ocular rosacea

A

Pannus = blood vessels growing superiors into the cornea from the sclera
Cornea is becoming involved (thinned)
Potential opacification of cornea

111
Q

Management of ocular rosacea

A

Directed toward symptomatic control and disease prevention (avoid flare triggers) rather than cure

112
Q

When treating ocular rosacea, what kind of approach can be undertaken?

A

Stepwise approach

113
Q

In the stepwise approach to treat ocular rosacea, what is the first step?

A

Lid hygiene and artificial tears

114
Q

In the stepwise approach to treat ocular rosacea, what is the second step?

A

Anti-inflammatory medications (low dose doxycycline = controlled release form) - oral tetracyclines most common and effective regimen
Lower ones than used for antibiotic effect

115
Q

What does treating ocular rosacea with low-dose anti-inflammatories do for MGD treatment?

A

Improves meibomian gland secretions by decreasing bacterial lipase
Protects cornea from perforation by inhibiting collagenase (big part of corneal thinning - inhibiting helps stop perforation)

116
Q

In the stepwise approach to treat ocular rosacea, what is the last step?

A

Late surgical intervention if required

117
Q

Mooren’s ulcer

A

A rare poorly understood condition characterized by peripheral stromal ulceration that progresses circumferentially

118
Q

Location of Mooren’s ulcer

A

Focal (non-systemic) autoimmune disorder isolated to the eye

119
Q

Two forms of Mooren’s ulcer

A 
Older patients (usually one eye)
Younger patients (may be both eyes and more aggressive)
120
Q

Symptoms of Mooren’s ulcer

A

Pain
Photophobia
Blurred vision

121
Q

Signs of Mooren’s ulcer

A

Peripheral
Principally stromal
Ulceration

122
Q

Diagnosis of Mooren’s ulcer

A

Clinical and by exclusion of ocular infection or associated systemic autoimmune disorder
Seems to be associated with certain HLA alleles

123
Q

Treatment of Mooren’s ulcer

A

Corneal specialist

Frequent topical steroid gtts —> other immunosuppressants and collagenase inhibitors —> surgery

124
Q

PUK

A

Peripheral ulcerative keratitis

125
Q

PUK associated with systemic disease

A

May present before/after systemic autoimmune symptoms

126
Q

Systemic diseases commonly associated with PUK

A

RA > Wegener’s granulomatosis, polyarteritis nodosa, SLE, etc.

127
Q

Signs of PUK associated with systemic disease

A

Crescent shaped destructive lesion of the juxtalimbal corneal stroma
Usually with neighboring scleritis (unlike Mooren’s ulcer)

128
Q

Diagnosis of PUK associated with systemic disease

A

Based on history and physical exam

129
Q

Treatment for PUK associated with systemic disease

A

Goals are to minimize inflammation, prevent superinfection, and promote healing of the ulcer
Systemic immunosuppession often required to control ocular inflammation (rheumatology consult)
Surgery may be necessary (corneal specialist)

130
Q

Terrien’s marginal degeneration

A

Uncommon idiopathic from of peripheral thinning (degeneration?) of the cornea
Slowly progressive and non-inflammatory
Unilateral or asymmetrically bilateral

131
Q

Who usually gets terrien’s marginal degeneration?

A

Young adults onward

132
Q

Symptoms of terrien’s marginal degeneration

A 
Often none (discomfort uncommon)
Gradual blur may develop due to astigmatism
133
Q

Signs of terrien’s marginal degeneration

A

Results in peripheral gutter, but rarely perforated

Associate with superficial corneal vascularization, opacification and lipid deposition

134
Q

Since terrien’s marginal degeneration is not inflammatory, what won’t you see?

A

Infiltrates (WBC’s)

135
Q

Diagnosis of terrien’s marginal degeneration

A

Primarily clinical, based on history and slit lamp exam of the eye
Differential from other peripheral corneal thinning disorders
Collagen vascular diseases should be excluded

136
Q

What are some peripheral corneal thinning disorders that must be differentiated from terrien’s marginal degeneration

A

Lack of inflammation or epithelial defect
Linear deposition of lipid
Slow progressive course

137
Q

Treatment of terrien’s marginal degeneration

A 
Protective eyewear (as indicated)
Contact lenses (for irregular astigmatism
Surgery only when impending/actual perforation
138
Q

Peripheral ulceration/inflammation due to focal autoimmune rxn; usually treated wth frequent steroid drops initially

A

Mooren’s ulcer

139
Q

Severe peripheral ulceration/thinning, often with associated scleritis; usually requires systemic (oral/IV) steroids

A

PUK associated with systemic disease

140
Q

Slowly progressive peripheral thinning without ulceration/inflammation; generally does not require treatment

A

Terrien’s marginal degeneration

141
Q

Neurotrophic keratopathy

A

Epithelial breakdown and persistent ulceration may occur with loss of trigeminal innervation from any cause

142
Q

Diagnosis of neurotrophic keratopathy

A

Corneal sensation reduce
Non-healing epithelial defects tend to have thickened/rolled edges
Progressive stromal melting with minimal discomfort

143
Q

Treatment for neurotrophic keratopathy

A

If possible, discontinue all drops except non-preserved artificial tears
Perforation is a concern, so anti-collagenase meds sometimes used
Consult corneal specialist: may require tarsorrhaphy, BOTOX, keratoplasty

144
Q

Technique where they sew the upper lid to the lower lid for treatment of the cornea

A

Tarsorrhaphy

145
Q

Exposure keratopathy results from what?

A

Incomplete lid closure (lagophthalmos) due to many causes

146
Q

Examples of causes for exposure keratopathy

A

Facial nerve palsy (CN 7) - Bell’s Palsy
Parkinsonism (overall loss of muscle tone)
Proptosis
Post-blepharoplasty (cosmetic surgery)

147
Q

Symptoms of exposure keratopathy that help in diagnosis

A

Dry eye (burning, grittiness, FB sensation, etc.)

148
Q

Signs of exposure keratopathy

A

Punctate epithelial changes (pin pricks of areas with staining that we don’t pick up easily without staining) - preferentially across inferior 1/3 of cornea, which may progress to ulceration, second degree infection, scarring
Potentially with permanent vision loss

149
Q

Treatment of exposure keratopathy

A

Depends on severity and whether recovery anticipated

150
Q

If exposure keratopathy is reversible, what is the treatment?

A

Lubricants (Day and night)
Lid taping
BCL (bandage contact lens)
Etc.

151
Q

If not reversible exposure keratopathy, what is the treatment?

A

Surgically covered via tarsorrhaphy, conjunctival flap, etc.

152
Q

Proptosis appearance

A

Eyes are bulging forward
Lag ophthalmitis
Looks like the patient is surprise or shocked and raising their eyebrows, but they aren’t

153
Q

Thyroid eye disease

A

Orbital fat (EOM) become infiltrated and swell up; space in bony orbit is full, and it pushes the eyes forward

154
Q

Appearance of exposure keratopathy

A

When stained, the inferior portion of the cornea looks like it has multiple different tiny ulcerations, all filling with dye

155
Q

Thygeson’s SPK

A

Idiopathic, bilateral, disorder, characterized by the episodic appearance of corneal opacities causing irritation/blur

156
Q

Who usually gets thygeson’s SPK?

A

Onset commonly in young adulthood, but can arise at any age and last (on and off) for decades

157
Q

Symptoms of thygeson’s SPK

A

Recurrent bouts of irritation
Photophobia
Tearing
Blurred vision

158
Q

Signs of thygeson’s SPK

A

Multiple small, slightly elevate grayish epithelial irruption across the central cornea - with little if any associated conjunctival injection

159
Q

Management of thygeson’s SPK

A 
Lubricants (mild cases)
Topical steroids (low potently fluorometholone with prolonged taper)
EW bandage CL (symptomatic relief)
160
Q

Does thygeson’s SPK typically cause permanent damage?

A

Disease tends to wax and wane (flares up and comes and goes) over many years, before eventually disappearing without clinical sequelae (with no permanent damage)

161
Q

Recurrent corneal erosion syndrome

A

Epithelial erosions caused by abnormal attachment to underlying basement membrane

162
Q

What is recurrent corneal erosion syndrome typically associated with?

A 
Prior trauma (unilateral) or
Certain corneal dystrophies (bilateral)
163
Q

Symptoms of recurrent corneal erosion syndrome

A

Significant pain
Photophobia
Tearing
Difficulty keeping eye open

164
Q

Signs of recurrent corneal erosion syndrome

A

Epithelial defect not always evident at exam

Basement membrane irregularities include: microcysts, swirls, etc.

165
Q

Management of recurrent corneal erosion syndrome

A 
Lubricants
Prophylactic antibiotics (if epithelium compromised)
Oral or topical NSAIDs for pain relief (if needed) (topical = diclofenac)
Bandage CL (symptoms in select cases)
Procedures for frequent recurrent cases
166
Q

Recent studies have shown that what drugs reduce the frequency of recurrent corneal erosion?

A

Combination of doxycycline 50 mg bid and a topical corticosteroid (such as prednisolone acetate 1%, or fluorometholone 0.1%) bid or tid x 3 weeks

167
Q

Procedures for frequent recurrent corneal erosion syndrome cases include:

A

Anterior stromal puncture
Diamond blur polishing
PTK (phototherapeutic keratoplasty)

168
Q

Filamentary keratopathy

A

Common uncomfortable condition in which strands of mucus and cellular debris attach to epithelial surface

169
Q

Causes of filamentary keratopathy

A

Aqueous deficient dry eye
SLK (superior limbic keratitis - sometimes related to thyroid eye disese - Superior margin filaments)
RCE (Recurrent corneal erosion)
Toxicity to various eye drops

170
Q

Symptoms of filamentary keratopathy

A

FB sensation

Sometimes with photophobia

171
Q

Treatment of filamentary keratopathy

A

Elimination of underlying cause
Removal of filaments provides immediate (but temporary) relief to some extent
Acetylcysteine (mucolytic) drops break up mucus strands/plaques on eye and lessen formation

172
Q

What stain works best on filamentary keratopathy?

A

Rose bengal

173
Q

Xerophthalmia

A

Refers to the constellation of ocular signs and symptoms associated with Vitamin A deficiency (as a late manifestation of such)

174
Q

What is xerophthalmia usually associated with?

A

Malnutrition, but can occur due to malabsorption and metabolic abnormalities

175
Q

The World Health Organization (WHO) estimated that about how many children have Vitamine A deficiency and how many have xerophthalmia?

A

254 million have vitamine A deficiency

2.8 million have xerophthalmia

176
Q

The most common cause of childhood blindness

A

Xerophthalmia

177
Q

Where is the most likely place you’ll find someone with vitamin A deficiency and xerophthalmia?

A

Children from South and South East Asia

178
Q

Why is vitamin A important for the eye?

A

Maintains the integrity and proliferation of the epithelium of the conjunctiva and cornea (deficiency can cause conjunctival and corneal xerosis = dryness, corneal ulcers, keratomalacia, and corneal scarring)
Precursor to rhodopsin (rods are much more sensitive to vitamin A deficiency than cones, such that defective vision in dim light (nyctalopia) occurs first

179
Q

Nyctalopia

A

Defective vision in dim light

180
Q

Systemic treatment for xerophthalmia

A

Vitamin A supplementation (oral or injection initially)

-underlying diseases such as liver disease an inflammatory bowel disease must also be managed in non-dietary cases

181
Q

Ocular treatment for xerophthalmia

A

Intense lubrication (while guarding against perforation)

182
Q

Bitot spots are specific to what condition?

A

Xerophthalmia

183
Q

Keratoconus

A

Progressive thinning and anterior protrusion of a portion of the paracentral cornea

184
Q

What is keratoconus associated with?

A

Various connective tissue disorders and eye rubbing

185
Q

Presentation of keratoconus usually occurs when?

A

During teens/20’s unilaterally, becoming bilateral over time

186
Q

Symptoms of keratoconus

A

Blurred vision due to irregular astigmatism - sometimes with CL intolerance
If descemet’s membrane ruptures (acute hydrops) —> pain, photophobia, decreased vision

187
Q

If descemet’s membrane ruptures, what is this known as? If in keratoconus, what symptoms will they have?

A

Acute hydrops

Pain, photophobia, decreased vision

188
Q

Signs of keratoconus

A

“Oil droplet” reflex with ophthalmoscopy
“Scissoring” reflex with retinoscopy
Vogt striae = vertical stress lines in deep stroma
Fleischer’s ring = epithelial iron deposition at base of “cone” best seen with cobalt filter
“Cone” observable from side or against lower lid upon downgaze (Munson sign)

189
Q

Confirmation/quantification of keratoconus

A

Keratometry - steep readings, often upwards of 50 D

Corneal topography - demonstrates contours of anterior protrusion

190
Q

Treatment of keratoconus

A 
Avoid eye rubbing
Use protective eyewear
Specialty CL fitting (RGPs, sometimes scleral)
Corneal cross-linking
Intracorneal implants (Intax)
Keratoplasty (often DALK)
191
Q

What is contraindicated in pt’s with keratoconus?

A

LASIK (refractive surgery candidates) b/c cornea is already so thin

192
Q

Topography appearance of keratoconus

A

Deep red lower/inferiorly, and paracentrally (this is where the cone is)

193
Q

Acute hydrops with keratoconus

A

Sudden significant stromal edema due to a tear in descemet’s membrane
-may occur with any corneal ectasia/thinning (either spontaneously or with trivial trauma)

194
Q

Symptoms of acute hydrops with keratoconus

A

Sudden onset pain and photophobia with decreased BCVA

195
Q

Signs of acute hydrops with keratoconus

A

Severe corneal edema

196
Q

Prognosis for acute hydrops with keratoconus

A

Most cases of acute corneal hydrops spontaneously resolve over 2-4 months, with resolution of edema, but often with variable degrees of scarring

197
Q

Two different types of management for acute hydrops associated with keratoconus

A

Conservative treatment

Surgery

198
Q

Conservative treatment for acute hydrops associated with keratoconus

A 
Cycloplegia
Hydronic saline
Topical antibiotic for prophylaxis
Bandage CL
Anti-glaucoma medications
Corticosteroids or non-steroidal anti-inflammatory agents
199
Q

Surgery management for acute hydrops associated with keratoconus

A

Injection of anterior chamber air or gas may accelerate recovery; reduce scarring
Penetrating keratoplasty if indicated (for underlying ecstatic disorder or scarring)

Block 15 (4 decks)

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