Transitions Ophthalmology Flashcards

1
Q

Conjunctival hemorrhage

A
  • Self-resolves, completely non-urgent
  • “Like having a bruise, but on the eye there is no skin”
  • Especially common w/ patients on blood thinners
  • Usually spontaneous w/ no trauma involved, but if there is Hx for significant trauma an ophthalmologic exam is indicated to assess for hemorrhage in other areas of the eye too.
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2
Q

Conjunctavitis

A
  • Conjunctiva covers the eye ball and base of eyelid
  • Mucoserous discharge and swollen paranasal tear glands usually indicates viral etiology
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3
Q

DDx and hints to etiology of a conjunctavitis

A
  • Viral conjunctavitis
    • Adenovirus
    • Enterovirus
    • Herpetic (often w/ Herpetic red vesicles on eyelid)
    • Molluscum (often w/ umbilicated, pearly vesicles on eyelid)
  • Allergic conjunctavitis
    • Seasonal
    • Environmental
    • Topical medications
  • Bacterial
    • Staph aureus
    • Strep (including pneumococci)
    • H. influenzae
    • Chlamydia (sexual Hx, yellowish serious discharge may be present)
    • Gonococcal (sexual Hx, thick purulent discharge)
  • Toxic
    • Topical medications (again)
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4
Q

Treatment for conjunctavitis

A

Usually self limited, non-urgent, treatment if any is just supportive. Typically lasts ~14 days, highly contagious by contact, often gets worse before it gets better. Stay home from work.

  • Warm or cool compress
  • Artificial tears of dry
  • Topical antihistamine or decongestant
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5
Q

Conjunctiva regions

A

Bulbar = on the eye, sparing the sclera

Palpebral = Tarsal = conjunctival reflection on the lower eyelid

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6
Q

Bacterial conjunctavitis

A
  • Usually copious mucopurulent discharge and pain rather than itching
  • Erythromycin-contianing ointment or 10% sulfacetamide drops for 5 days are first line
  • Culture/gram stain is not performed unless eye is “hyperpurulent”
    • In this case take sexual history to rule out chlamydia or gonococci
    • Chlamydial or gonococcal eye infections may be present in newborn if mother is colonized
    • Gonoccocus secretes an enzyme which can perforate the globe
    • If gonococci present, treat w/ systemic ceftriaxone
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7
Q

Chalazion

A
  • Focal area of inflammation within the eyelid related to obstruction of a meibomian gland
  • Resolution is slow; painless swelling may persist for months owing to the formation of a granuloma.
  • Non-urgent. This is usually a self-limited process that is never sightthreatening.
  • Treatment is typically conservative at first with daily warm compresses.
    • Persistent chalazia can be treated with incision and drainage, particularly if they are disfiguring or induce astigmatism
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8
Q

Hordeolum

A
  • Aka a stye
  • Looks almost the same as a chalazion, but is acute and painful while chalazion is chronic and nonpainful
  • Acute inflammation of the meibomian gland with associated pain, swelling and erythema focally in the lid
  • Sometimes local Staphylococcus is contributory, so treatment of styes with antibiotic ointment such as Ilotycin (Erythromycin) BID for 1 week is reasonable
    • Do not respond to incision and drainage
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9
Q

A recurrent, non resolving chalazion or hordeolum should be evaluated . . .

A

. . . histopathologically for neoplasm

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10
Q

Blepharitis

A
  • Flaky crusting of lashes, without discharge
  • Possible etiologies: seborrhea, staphylococci, rosacea
  • Non-urgent, not sight threatening
  • Warm compresses and/or lid hygiene (w/ baby shampoo) and/or erythromycin ointment BID for two weeks.
    • If condition does not respond, patient should be referred to ophthalmologist
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11
Q

Herpes simplex keratitis

A
  • The “cold sore” of the eye
  • Grayish opacity over cornea
    • Dendritic for Herpes simplex
    • Linear for bacterial
  • Referral to ophthalmologist within 1-2 days
  • Expression of HSV latent in the trigeminal ganglion
  • Self-limited, but anti-viral treatment (oral or topical) can shorten the duration of the eruption and the shedding of live virus.
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12
Q

Bacterial keratitis with hypophon

A
  • Hypophon = layering of white cells between and iris
    • Sign of severe anterior segment inflammation
  • Emergent referral to ophthalmology same day
    • They will decide whether to treat empirically or do culture/stain
    • Seen every day until response is noted
  • If untreated, can lead to corneal ulceration with scarring, perforation, and loss of the eye as possible sequelae
  • If contact lens wearer, Pseudomonas is common etiology
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13
Q

Acute angle closure glaucoma

A
  • Diffuse injection, dilated pupil, cornea rim hazy from epithelial edema.
  • Emergent. Ophthalmologist should be called immediately. Can threaten vision within 24 hours
  • Often presents with one-sided headache and photophobia
  • Diagnosis is confirmed by measurement of intra-ocular pressure, which can be estimated by palpation and comparison with eye
  • Initial topical therapy: 2% pilocarpine (stop fluid production) along w/ topical beta blocker and alpha agonist (increase alpha tone, reduce pressure). Sometimes acetazolomide may be give orally.
    • Definitive treatment is therapeutic laser iridotomy which is ideally performed within 24 hours, with fellow eye treated prophylactically within a few days.
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14
Q

Hypopyon

A

White cell infiltration into the cornea. They tend to settle at the bottom due to gravity and form a small pool of pus.

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15
Q

Fluorescein staining in ophthalmology

A

Used to highlight epithelial abrasions on visual exam

Shown is a dendritic herpes simplex keratitis lesion highlighted by fluorescein

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16
Q

Acanthamoeba keratitis

A
  • Uncommon amoebic cause of keratitis
  • Classically, the patient’s symptoms are out of proportion to the signs on ophthalmologic exam. These patients are in a lot of pain.
  • Inquire about fresh-water swimming in Hx.
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17
Q

Ddx for hypopyon without keratitis

A
  • Post-operative endophthalmitis
  • Endogenous endophthalmitis
  • Sterile hypopyon from Behcet’s disease
  • All also emergent conditions, get seen by ophthalmology w/in 24 hours
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18
Q

Behcet’s disease

A
  • Rare disorder that causes blood vessel inflammation throughout your body
  • Etiology is unknown
  • Recurrent sterile oral and anogenital ulcers, and uveitis presenting as hypopyon w/o keratitis
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19
Q

Why is the pupil static in acute angle closure glaucoma?

A

Ischemia causes a temporary local loss of function of pupillary muscle causing fixed, mid-dilated pupils

If the pupil is reactive, it’s not angle closure

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20
Q

After you perform iridotomy on a patient for acute angle closure, you are not done. What do you need to do next?

A

Prophylactic treatment of the OTHER eye.

It is very likely to happen again in the other eye at some point and so it is better to avoid an acute scenario by treating ahead of time.

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21
Q

Corneal light reflex

A
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22
Q

Infantile esotropia

A
  • Common presentation of strabismus in infants
  • Can differentiate from abducens palsy by covering the nonaffected eye and witnessing some correction in the affected eye
  • Followup with ophthalmology indicated within a few weeks
  • Likely needs to be corrected by surgery on extraocular muscles to align the eyeball properly (usually stengthening or resection of medial and lateral rectus, we try to leave the obliques alone). Perfect alignment is not always achievable.
  • Cover unaffected eye with a patch to prevent the development of amblyopia in the meantime
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23
Q

Strabismus

A
  • A condition in which the eyes do not properly align with each other when looking at an object. The eye that is focused on an object can alternate. The condition may be present occasionally or constantly.
  • Can be esotropic, exotropic, hypertropic, or hypotropic.
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24
Q

Amblyopia

A
  • “Lazy eye” colloquially
  • Decreased eyesight due to abnormal visual development.
  • Amblyopia occurs in early childhood. When nerve pathways between the brain and an eye aren’t properly stimulated, the brain favors the other eye.
  • Ultimately, it is an adaptive neurologic process secondary to strabismus or another process. Once it has set in, because it is a structural neurologic feature, it cannot easily be reversed.
  • Symptoms include a wandering eye, eyes that may not appear to work together, or poor depth perception. Both eyes may be affected.
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25
Q

Internuclear ophthalmoplegia diagram

A
  • Remember that the signal fires first from the CN6 nucleus, splitting into the CN6 axon and MLF. Then, it reaches the CN3 nucleus and axon via the MLF.
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26
Q

A full “down and out syndrome”, with dilation of pupil, is ___ until proven otherwise.

A

A full “down and out syndrome”, with dilation of pupil, is cerebral aneurysm until proven otherwise.

Particularly posterior communicating artery. The anatomical relationship is shown below.

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27
Q

Pupillary vs muscular CN3 palsies

A
  • Pupillary fibers are the most superficial and superior within CN3, and tend to be the first affected by compression of the nerve (such as by PcA aneurysm)
  • Motor fibers are the most deep and inferior within CN3 and tend to be the frist affected by ischemia of the nerve (such as thrombosis within the vasa nervosum)
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28
Q

If a patient presents w/ Horner’s syndrome, what additional tests should you perform on physical exam?

A
  • Full neurological workup (could this be medullary Horner’s?)
  • Examine skin overlying carotids and listen for carotid bruit (could this be carotid dissection?)
  • Listen carefully to lung apices (could this be apical lung cancer compressing sympathetic fibers before they reflect?)
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29
Q

Leukochoria

A
  • ALWAYS CONCERNING
  • Tumor, infantile cataract (just infantile is emergent – because they can cause amblyopia in kids), Toxocariasis canis (infection of eye in children associated with dog exposure), persistent hyperplastic primary vitreous, or retinopathy of prematurity (underdeveloped retina in premies)
    • Remember that retinoblastoma is a tumor of childhood
  • Urgent, refer to ophthalmologist within days
  • If bilateral, it is a pRb mutation.
    • Autosomal dominant cancer syndrome. Indicates examination of siblings and genetic counseling.
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30
Q

White spots on fundoscopy

A

Lipid deposits

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31
Q

Cotton wool spots on fundoscopy

A

Focal areas of ischemia

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32
Q

Treatments for diabetic retinopathy

A
  • Blood sugar control (baseline)
  • First line: VEGF inhibitors
  • Second line: Laser photocoagulation
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33
Q

To an ophthalmologist, “the eyes are the windows to ___”

A

To an ophthalmologist, “the eyes are the windows to the vascular beds throughout the body

What you can see on fundoscopy within the eye is probably what is happening in capillaries everywhere else.

34
Q

What is going on in this individual’s eye?

A

This patient has had panretinal photocoagulation, probably for diabetic or hypertensive retinopathy. It appears that the treatment has been successful as the rest of the vasculature now appears normal.

It decreases peripheral vision slightly in order to protect central foveal vision. Patients often don’t even notice the difference in peripheral vision.

35
Q

Uveitis

A
  • Looks similar to conjunctavitis from the outside, but the below will be seen on fundoscopy and the patient will also be photophobic
    • These are keratic precipitates on the inner surface of the cornea, indicative of white blood cells in the eye (intraocular inflammation)
      *
36
Q

What is going on in this patient with presumed uveitis?

A
  • Synechia
  • Note the deformity of the pupillary shape
  • This case of anterior chamber uveitis was complicated by scarring of the iris and attachment of the iris to the lens
  • Not much can be done about this once it has occured, but it can be prevented by keeping the pupil dilated (keeping the iris and lens apart) while the uveitis is ongoing.
37
Q

When using topical occular steroids, just like systemic steroids, you need to . . .

A

. . . taper once you are done.

You also need to keep an eye on the intraocular pressure, as steroids may raise the pressure after a few weeks and can potentially threaten glaucoma.

38
Q

HLA B27 syndromes

A
  • Ankylosing spondylitis
  • Psoriatic arthritis
  • Reactive arthritis (Reiter’s syndrome)
  • Uveitis
  • IBD
39
Q

Treatment of V1 Herpes Zoster

A

Urgently treat with acyclovir or valacyclovir

DO NOT DEFER TREATMENT pending ophthalmologic consult, but you should probably consult ophth urgently too.

Both cyclovirs used are very benign, so don’t worry about being wrong either. If it’s on the differential just do it.

40
Q

How can you tell orbital cellulitis apart from viral or allergic conjunctavitis?

A

Presence of additional signs on exam: Difficulty moving the eye, proptosis, and relative afferent pupillary defect are the two big ones.

41
Q

If patient with apparent orbital cellulitis fails to respond to antibiotics, what alternative diagnosis should you consider?

A

Orbital rhabdomyosarcoma

Sometimes masquerades as orbital cellulitis. Orbital biopsy is indicated for diagnosis.

42
Q

Patient being worked up for Grave’s disease has 20/50 on the R eye and 20/20 on the L eye. Previous eye exam was 20/20 on R eye.

What is the pathophysiology causing this vision deficit? What should you do?

A

The proptosis in Grave’s disease is caused by swelling of the extraocular muscles, for reasons we don’t really understand. Chronically, muscles can fibrose and grow up to 8x in size.

When they are sufficiently swollen, they can compress the optic nerve – and damaged caused to the optic nerve is usually permanent. So, this is an emergency, requiring urgent evaluation by an ophthalmologist.

Even in the absence of apparent vision loss, new Grave’s patients should receive baseline ophthalmologic examination within a few weeks of diagnosis. Don’t forget to check visual fields too.

43
Q

Orbital decompression surgery

A

Removal of bone to expand the space available for eye and associated structures.

Done for advanced Grave’s patients with severe proptosis.

44
Q

Exposure keratitis

A

Basically dry eye. It is a common concern in patients who 1) have trouble blinking for whatever reason and 2) have proptosis from Grave’s.

Can cause some permanent damage and scarring if it goes on for too long, and is generally very uncomfortable for the patient. Treatment is simply with lubricating eye drops.

45
Q

Restrictive stribismus

A
  • May be seen in advanced Grave’s patients due to muscle thickness and strength changes
  • Requires surgery, but in order for surgery to be done accurately and restore proper muscle movement and eye position, it must be done when the patient’s muscle mass and composition is stable
    • This means that the patient must be fully treated for Grave’s first and have had normal anti-TSHR antibody levels for 6 months before they are a surgical candidate.
46
Q

Optic nerve “cup”

A

The area at the center of the optic nerve on fundoscopy which appears white

This is the portion of the optic nerve not made up of axons (the axons are the dark striations which take a right turn and form the red ring surrouding the cup)

If the cup is enlarged, as below, it suggests fewer axons, and therefore death of ganglion cells.

47
Q

Open angle glaucoma

A
  • Progressive visual field loss in arcuate pattern w/ preserved acuity due to chronically increased intraocular pressure
  • Optic nerve cup widening on fundoscopy
  • Much more chronic than closed angle glaucoma. Open angle indicates a non-urgent consult, while closed-angle is an ophthalmologic emergency.
  • First line therapy – eye drops to lower pressure (prostaglandins, beta blockers, alpha agonists)
  • Second line – oral carbonic anhydrase inhibitors (prevent fluid formation in eye)
  • Third line – trabeculoplasty or other surgery
    • Trabeculoplasty opens up spongy trabecular tissue near the cornea to relieve pressure
48
Q

DDx for age-related progressive vision loss

A
  • Age-related macular degeneration (wet and dry, but especially dry)
  • Open angle glaucoma
  • Cataracts
  • Myopia/hyperopia (sometimes you just need glasses!)
49
Q

Drusen

A

Yellowish, lipoid deposits seen in, among other things, age-related macular degeneration

50
Q

Atrophy vs drusen

A

Drusen on L. Note that they are wider, softer, and fade into the background

Atrophy on the R. Note that it is punctate and clearly defined borders

51
Q

What is the #1 thing you should counsel patients with age-related macular degeneration on?

A

If they keep smoking, they will go blind

52
Q

“Dry” ARMD vs “Wet” ARMD

A

Dry is slow, progressive w/ drusen and atrophy in the foveas on a greenish background. Non-urgent, refer to ophth within weeks. Treat w/ risk reduction (vitamin supplementation, smoking cessation)

Wet (often happening in the setting of preexisting dry) is acute hemorrhage into the fovea and sudden loss of or decline in vision. Patients may also complain of “blurriness and wavy lines” because the retina often wrinkles in wet ARMD due to subretinal bleeding/fluid. Emergent, refer to ophth immediately. Treat w/ VEGF inhibitors (ranibizumab, bevacizumab). Second-line highly selective photocoagulation in abnormal arteries.

53
Q

“Blurriness and wavy lines” in vision

A

Indicates wrinkling of the retina, usually due to fluid below retina. Many possible etiologies for this including wet ARMD, edema, chronic steroid use, acute changes in blood pressure, etc.

54
Q

Differentiating monocular and binocular double vision

A

Have the patient cover each eye one at a time and see if that resolves the double vision.

55
Q

Occulo-cardiac reflex

A

When you pull on eye muscles, you cause bradycardia

If you pull enough, you can cause complete heart block

Sometimes this happens when there is a sinus fracture and muscle entrapment, especially with the inferior rectus muscle.

56
Q

The pupil often ___ after acute trauma to the eye. Why is this the case? What syndrome is this associated with?

A

The pupil often dilates after acute trauma to the eye.

Trauma causes hemorrhage, which in turn causes mild ischemia. The result is muscle shock of the pupillary muscles, and the net effect of this is constant pupillary dilation. The pupil will often be slightly misshapen as well.

This syndrome is referred to as hyphema. In these cases, blood cells may clog the angle of the iris and trabecular meshwork, causing effective closed angle glaucoma. This is an ophthalmologic emergency.

Note, hyphemas may be microscopic (microhyphema).

57
Q

In general, subconjunctival hemorrhage is completely benign and resolves on its own without therapy. In what cases is it more concerning?

A
  1. If the patient is on anticoagulation – in which case you should work them up and see if their INR is too high
  2. If there is still a foreign body present – in which case there may be other damage such as corneal abbrasion
58
Q

Where are the meibobian glands located?

A

Just posterior to the eyelashes

When one is blocked, you develop a chalazion (a granulomatous response) to the oil that builds up. That is why heating it up helps relieve it – it mobilizes the oil more, leading to decongestion.

59
Q

Central Retinal Artery Occlusion

A
  • The cherry red spot is seen at the fovea while the surrounding retina is pale due to infarction, edema,and opacification of the inner retinal layers
  • Acute blockage of the retinal artery, due to stroke or giant cell arteritis
  • Emergent – refer to ophtho immediately
60
Q

Retinal detachment

A
  • Urgent referral to ophthalmology (w/in one week). Emergent if fovea not involved (to prevent its involvement).
  • Floaters and photopsias (sensation of flashing lights) are very common
  • Often described as a “dark curtain” over part of the visual field
  • Treatment options include LASER barricade, cryotherapy, pneumatic retinopexy, scleral buckle, and vitrectomy
61
Q

What is going on in this patient’s eye?

A

This is a retinal scar left by LASER barricade therapy, indicating that this patient has previously been treated for retinal detachment.

62
Q

Arteritic Anterior Ischemic Optic Neuropathy (AAION)

A
  • Often the initial presentation of visual symptoms with giant cell arteritis
  • Emergent referral to medicine (not ophtho) to treat GCA. Start presumptive steroids immediately
  • Blurry, chalky-white optic disc
  • Positive relative afferent pupillary defect
  • Usually in context of polymyalgia rheumatica, temporal headache, and jaw claudication
  • Almost universally related to GCA, but can rarely be caused by Wegner’s
63
Q

AAION, ANION, and Papilledema table

(Exam and symptoms, disc appearance, and associated conditions)

A
64
Q

Senile cataract

A
  • Age-related degeneration of the lens that impairs vision
  • Non-urgent ophthalmologic surgical referral
  • Most commonly present with symptoms of painless, progressive, gradual visual decline as well as difficulty with glare and compromised contrast sensitivity.
  • May present initially as night blindness since low-light exacerbates visual deficit.
65
Q

Relative afferent pupillary defect

A
66
Q

If there is eye pain present on ophthalmologic evaluation for vision change, you can be certain that it is not. . .

A

. . . just the retina.

The retina has no pain receptors.

67
Q

Why does panretinal photocoagulation work in diabetic retinopathy?

A

It basically kills off all of the “slowly dying” peripheral tissue to reduce its VEGF production – thereby decreasing angiogenesis and preserving the function of macular tissue.

68
Q

Stellate cataract

A
  • Blunt trauma-induced cataract
  • Pathognomonic star-shaped or flower-shaped appearance
69
Q

What is going on in this patient’s eye?

A

Lisch nodules

Indicative of neurofibromatosis type I

70
Q

Steroid-induced cataract

A
  • Posterior subcapsular cataract
  • More focal than age-related
71
Q

Anticholinergic-induced cataract

A
  • Anterior subcapsular cataract
    • Note, anterior is anticholinergic, posterior is steroid
72
Q

Vitamin cocktail for dry age-related macular degeneration

A
  • Reduces rate of progression of dry AMD by ~25%
  • Includes:
    • Vitamin C
    • Vitamin E
    • Lutein
    • Zeaxanthin
    • Zinc
    • Copper
73
Q

Tonometry

A

Fancy word for measuring the pressure within the eye

74
Q

Gold standard for diagnosing acute angle closure glaucoma

A

Gonioscopy

A technique that lets you see magnifications of the person’s iris angles. Literally looking directly at the angle that is closed.

But of course, who the fuck has one of these things? Tonometry is the more practical way to diagnose acute glaucoma, cause you need to treat it fast.

75
Q

Preseptal vs Orbital cellulitis

A
76
Q

Vision blurring with “halos” around lights is highly suggestive of. . .

A

. . . cataracts

77
Q

Trachoma summary

A
  • Caused by C. trachomatis
  • Characterized by follicular conjunctavitis, often with concommitant rhinorrhea and pharyngitis
  • Diagnose by examination of tarsal conjunctivae. Giemsa stain of scrapings will show intracellular organisms.
  • Oral azithromycin is curative, but those with chronic changes will need surgery to correct them
78
Q

First-line therapy for open angle glaucoma

A
  • Prostaglandin analogues:
    • latanoprost
    • bimatoprost
79
Q

Sjogren’s ophthalmologic manifestations

A
  • Dry eye/mouth and foreign body sensation
  • Decreased visual accuity
  • Increased risk of infection
  • Corneal irritation and ulceration
80
Q

“Grid” test

A

To patients with macular degeneration, lines in a grid appear wavy and non-linear