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NBEO Part 2 > NBEO Part 2 > Flashcards

NBEO Part 2 Flashcards

1
Q

Episcleritis

A
  • Benign, self-limiting inflammation of the episclera
  • Most common in young adults 20-40yo
  • Idiopathic, RA, Lupus, Idiopathic, UCRAP
  • Blanches with phenylephrine 2.5% (alpha 1 agonist)
  • Tx: Mild topical ophthalmic steroid QID
    • Mild: cool compresses, ATs
    • Moderate: FML QID or Ibuprofen 200-600mg or Combination steroid/NSAID for 5-10 days
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2
Q

Phlyctenular Keratoconjunctivitis

A
  • Type 4 - Delayed T-cells
  • Tx:
    • Ophthalmic decongestant
    • Topical ophthalmic steroid
    • Combo steroid/antibiotics
    • Restasis/cyclosporine - inibits T cells
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3
Q

Superior Limbic Keratoconjunctivitis

A
  • Velvety papillae
  • Superior SPK with fluorescein
  • Causes: thyroid disease, CL wear, dry eye
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4
Q

Pinguecula

A
  • degeneration of collagen fibrils caused by UV exposure
  • NO neovascularization (don’t confused with CIN)
    *
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5
Q

Scleritis

A
  • Severe boring pain
  • Non-necrotizing
  • Necrotizing scleritis
    • with inflammation - worst form
    • without inflammation - scleromalacia perforans 2’ RA: blue sclera
  • Non-necrotizing can be diffuse or nodular
    • Diffuse - most common 60^ of all anterior scleritis cases
    • Nodular - immobile
  • Necrotizing without inflammation - caused by RA
    • Scleromalacia perforans (bilateral blue sclera)
    • Minocycline can cause blue sclera
  • Tx:
    • ​need ORAL NSAID (do NOT give topical)
      • Ibuprofen 400-600mg QID
      • Indomethacin 25mg TID
      • naproxen 250-500mg BID
    • Immunosuppressive (methotrexate)
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6
Q

What causes whorl keratopathy & risk of retinopathy

A
  • Whorl your CHAI-T - chloroquine, hydroxychloroquine, amiodarone, indomethacin, tamoxifen
  • The risk of retinopathy when taking the standard dose of Plaquenil (400 mg/day) increases if the pt weighs less than 135 lbs
  • The risk of crystalline retinopathy with tamoxifen tx increases with dosages > 6.5mg/kg.day for more than 5 years
  • The risk of corneal verticillata (whorl keratopathy) with amiodarone is minimal at 100-200 mg/day but inevitable at 400 mg/kg/day
    • may also cause anterior subcapsular crystalline lens within the visual axis (50% of pts taking > 60 mg/day after 6 months of treatment), and NAION (1-2% of cases)
    • Will see whorl keratopathy mostly from amiodarone
  • Fabry’s disease results in corneal verticillata in 90% of cases
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7
Q

Avoid steroids in which patients?

A
  • Pregnant
  • Peptic ulcers
  • DM
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8
Q

Ocular Albinism

A
  • Decreased number of melanosomes (NOT melanin)
  • Nystagmus does NOT cause poor acuity, usually its foveal hyperpigmentation (can cause nystagmus)
  • Most significant threat to vision with ectropion uveae - 2ndary angle glaucoma
  • Tx
    • Refer to hematology to rule out associated sx, b/c they are deaf you want to rule out chediak-Higashi and Hermansky pudlak syndrome
    • Not really any treatment for the eyes
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9
Q

What causes blue sclera?

A
  • Minocycline
  • Blue sclera
  • Scleritis
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10
Q

Ectropion Uveae

A
  • Rare congenital iris anomaly
    • Could be associated with neurofibromatosis
    • Could cause angle closure
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11
Q

Keratoconus

A
  • Bilateral, asymmetric, non-inflammatory progressive disorder in which the cornea assumes a conical shape secondary to loss of structure integrity
  • Hallmark signs: central or paracentral corneal stromal thinning, apical corneal protrusion, and the presence of irregular astigmatism, scissor reflex retinopathy, , oil droplet on direct-o, voggt striae (disappears with pressure), kayser-fleischer ring,
  • In advanced cases of keratoconus munson sign, ruptures in descemet’s membrane can occur, leading to an acute influx of aqueous into the cornea causing hydrops,
  • Corneal topography will show progressive inferior axial steepning and irregular astigmatism, with steep kerotometry values that are usually greater than 48D in mild cases and can be greater than 54D in both meridians in severe cases
  • Corneal pachy can show progressive corneal thinning responding to the area of conical protrusion
  • Tx: Corneal crosslinking (goal is to halt progression) - indicated in children and adolescent at the time of their diagnosis without the need of documented progression
    • The max corneal power that should be considered for CXL is 65D, as higher k values are associated with increased failure rates
    • Pts over the age of 35 and those with distance VA of 20/25 or better, have a greater risk of VA loss after CXL tx
    • In order to reduce the chance of UVA-induce corneal endothelial damage, a corneal thickness less than 400 um was an exclusion criterion for CXL using criterion for CXL
    • Best candidates are pts who are less than 35 or younger, eyes that show progression in adults or at the time of diagnosis in children, with mod keratoconus (max K value less than 65D), corneal thickness greater than 400 microns (prevent endothelial damage), and VA of 20/30 or worse
  • Contraindication in pts with a hx of herpetic infections - we want to avoid viral reactivation, concurrent infection, severe corneal scarring or opacification, hx of poor wound healing, severe ocular surface disease, hx of autoimmune disorders.
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12
Q

Pellucid Marginal Corneal Degeneration

A
  • Protrudes superior to teh area of corneal thinning.
  • HAllmark sign - kissing doves on corneal topography
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13
Q

Keratoglobus

A
  • abnormal corneal thinning occurs over the entire cornea
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14
Q

Terrien’s marginal degeneration

A
  • peripheral corneal thinning that can be localized or involved extensive portions of the cornea
  • Degeneration typically begins superiorly with anterior stromal opacities, leaving a clear area between the opacities and the limbus
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15
Q

Forme fruste keratoconus

A
  • corneal topography will display central or paracentral irregular astig
  • The pt will be asymptomatic
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16
Q

Digitalis

A
  • “Nak for getting someones digits”
  • Sodium potassium channel blocker to treat heart conditions
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17
Q

Sodium potassium channels in 2 places of the eye

A
  • Photoreceptors - entopic phenomenon
  • NPCE of the pars plicata - decrease VA
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18
Q

Furosemide (Lasix)

A
  • LasiK –> causes hypokalemia/loses potassium
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19
Q

CRVO/BRVO

A
  • Big threats
    • Look for neovascularization
    • Macular edema
    • 90 day glaucoma
  • Causes
    • Big 4 = HTN, DM, Cardio dz, POAG
    • HTN - artery to compress vein causing turbulent blood flow causing a thrombus –> releasing VEGF
    • Oral contraceptive
    • Protein S,C, antithrombin 3 - blood clotting issue
    • Factor 12 deficiency
  • Treatment
    • PRP to treat neo
    • intravitreal AntivegF to treat macular edema
    • FA - ischemic shows 10dd or worse on ischemia or 20/200 VA
  • Key points for vein occlusions
    • Vein drain = vein occlusions –> hemes/CWS/collaterals
    • Big 4 risk factors = HTN/DM/cardiovascular dz/open angle glc (poor NFL) –> BMI at 20 yrs for BRVO
      • HTN –> AV compression –> turbulent blood flow –> thrombus –> release VEGF –> NVI/NVA/NVD/NVE
  • Major concerns
    • NEO: CVOS/BVOS –> PRP
    • Macular Dz: CRUISE/COPERNICUS (CRVO) & BRAVO/VIBRANT (BRVO) –> antivegF
    • CRVO: Check BP in office, evaluate every month for 6 months with gonio at each visit. Refer to MED for eval HTN, DM, CHF
    • BRVO: check BP in office. Evaluate Q1-2 months then Q3-12 monrha rhwewDRWE. REFER TO MD to eval HTN, DM, CHF
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20
Q

CRAO/BRAO

A
  • Caused by HTN & DM
  • Throws embolus
  • CRAO = caused by a calcific plaque (larger)
  • BRAO = caused by a hollenhorst plaque (smaller)
  • Tx
    • Refer to MD for carotid and heart
    • acute CRAO = refer for MRI for concurrent stroke
  • Key points
    • Arteries supply = artery occlusions –> ishcemia/white/cherry red spot
    • Big 4 risk factors = HTN, DM, Cardiac valve dz –> amaurosis/TIA
      • Carotid –> Hollenhorst plaque –> embolus –> smaller plaque that classically results in BRAO
      • Heart –> calcific plaque –> embolus –> larger plaque classically results in CRAO
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21
Q

AAION/NAION

A
  • NAION caused by vascular issues (HTN, DM)
    • Usually unilateral
  • AAION
    • happen in older pts 60-70 yo
    • Swollen nerve starts in one eye and go into the other eye within 48 hours
    • Neck pain, jaw caludication, anorexia, scalp tenderness, temporal HAs
    • Order CBC, ESR, CRP
    • Temporal artery is a branch of the external carotid artery
    • Tx: steroids
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22
Q

Optic Neuritis

A
  • 30 yo with swollen optic nerve, unilateral
  • order MRI to rule out MS
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23
Q

Which method of visual acuity testing toddlers offers the. most accurate measurement?

A

Landolt C & tumbling Es

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24
Q

At what age is the patient able to draw a

  • Vertical line
  • Square
  • Diamond
A
  • 3 years old - vertical line
  • 4-5 years old - square/trinagle
  • 6-7 years old - diamond shape
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25
Q

Mucin balls

A

small, white, pearl-like debris that develops behind the posterior surface of CL. They generally occur with silicone hydrogel lenses that are too flat.

Keep the pt in same lens but refit into a steeper base curve

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26
Q

Dimple Veiling

A

Occurs when a gas perm CL is fit incorrectly, causing carbon dioxide bubbles to become trapped underneath the lens, leaving small circular indentations on the surface of the corneal. This condition can be managed by flattening the base curve of the lens or by decreasing the lens overall diameter

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27
Q

Posterior embryotoxon

A
  • Prominent and anteriorly displaced schwalbe’s line - can be seen in up to 15% of normal pts
  • No treatment needed, follow up in 1 year
  • No racial predilection
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28
Q

Axenfeld anomaly

A

appears as peripheral iris strands attached to posterior embryoton - these pts at risk for glaucoma

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29
Q

Rieger anomaly

A

present with findings of axenfeld anomal along with iris thinning & corectopia 50-60% of pts with this condition develop glaucoma

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30
Q

Peters anomaly

A
  • Abnormal neural crest cell migration during weeks 6-8 of pregnancy.
  • typically rare & bilateral
  • Display central corneal opacity
  • Lens may be displaced anteriorly creating a shallow ant chamber
  • lens may be adhered to corneal opacity
  • Glaucoma present in 50% of pts who suffer from peters anomaly.
  • present with a donut appearance due to corneal lens adherence
31
Q

ALT

A
  • Instillation of topical anesthetic and topical hypotensive agent (usually alpha-agonist) is the initial step
  • A gonioscopy lens is place don the eye with the sem-circular lens at 12 o’clock in order to view the inferior angle (easiest area to see)
  • Focus the aiming beam at the junction of pigmented & non pigmented TM
32
Q

Best’s disease (vitelliform disease)

A
  • Divided into 5 stages:
    • Pre-vitelliform - child is asymptomatic and fundus will appear normal but EOG reading will be abnormal
    • pre-vitelliform stage - occurs 1st or 2nd decade and may not minor decrease in vision. Fundus will reveal an egg-yolk like lesion;
    • Pseudohypopyon stage occurs 2nd - 3rd decade and is marked by a blister-like lesion in which liposfuscin may gravitate inferiorly
    • Vitellruptive stage - breaking apart of the “egg yolk” causing a decrease in VA
    • End stage - CNVM and/or geographic atrophy, which may result in retinal detachment. Acuity is classified as legally blind (20/200)
  • The lesion is caused by lipofuscin at the level of the RPE
  • Bilateral
  • No treatment for this condition - monitor with amsler grid
  • AD - gene locus is 11q13
  • Normal ERG, abnormal EOG
33
Q

Stargardt’s disease

A
  • Bilateral in 1st-2nd decade of life and causes varying degrees of VA
  • Fundus looks initially normal, then progresses and macula may appear mottled
  • Beaten bronze appearance often surrounded by yellowish flecks
  • bull’s eye pattern will occur = devastating loss of VA
  • AR with a gene locus of ABC4R on 1p21-22
34
Q

Fundus flavimaculatus

A
  • Variant of stargardt’s disease
  • Posterior pole is littered with yellow flecks of various shapes (linear, round, psiciform (fish tail =-like), or oval.
  • VA is mostly good as long as macula is unaffected and geographic atrophy is absent
35
Q

Familial drusen

A
  • AD - gene locus EFEMP1 on 2p16
  • harmless, small, hard drusen located in the macular region
  • Appear in 3rd decade of life
  • Moderate cases - multiple, large, soft drusen distributed throughout the entire posterior pole and the peripapillary region; may occur after 3rd decade
  • VA rarely affected in advanced cases
  • CNVM and geographic atrophy may occur in 5th decade of life
36
Q

Retinitis Pigmentosa

A
  • Associated with Usher syndrome
  • Rubbing can cause keratoconus
  • Triad: Waxy pallor, bone spicules, attenuated vessels
  • Affects Central vision: PSC cataracts, hyaline bodies of the optic nerve (drusen), CMV, ERM, Keratoconus
  • Perform ERG
37
Q

Gyrate Atrophy

A
  • rare, bilateral, AR chorioretinal degeneration due to deficiency in the mitochondrial enzyme ornithine aminotransferase
  • Classic clinical appearance: multiple, well-defined, scalloped areas of peripheral chorioretinal atrophy - in childhood the lesions begin in the mid periphery then coalesce to engulf most of the post pole with the macula being spared until the 4th to 7th decade
  • Sx prevalent in most by age 10 - nyctalopia, decreased vision and constricted VF
  • Decreased vision eventually occurs as a result of PSC, macular chorioretinal degeneration, or cystoid ME
  • Gyrate atrophy is also associated with high myopia and astigmatism
38
Q

Choroideremia

A
  • Very rare condition characterized by diffuse and progressive atrophy of the choriocapillaris and overlying retinal pigment epithelium
  • x-linked recessive = affects only males, females are carriers
  • Deficiency in rab geranylgeranyl transferase, an enzyme utilized in membrane metabolism
  • The most common initial sx is nyctalopia. By late child hood -pt will report photophobia and peripheral vision loss and will have constricted VF.
  • In males - nigh blindness occurs early in life & progresses to total night blindness within 10 years, in females the condition is benign and non-progressive
  • Initially appears diffuse and posteriorly (from ages 15-45) resulting in a scalloped appearance that is similar to gyrate atrophy
  • The macula is spared until later stages of the dz; legal blindness occurs by 50-60 yo
39
Q

Fundus albipunctatus

A
  • AR congenital disorder that causes stationary night blindness
  • characterized by numerous small, yellow-white dot-like lesions at the level of the RPE; lesions are in the mid-periphery and spare the macula
  • A variant of RP, retinitis punctate albescens, has a similar appearance to fundus albipunctatus, but differs in that it results in slow progression of night blindness
40
Q

Patch children below the age of __

A

12

41
Q

Findings for basic exophoria

A
  • equal exophoria at distance and near (within 5pd)
  • decreased PFV at both distance and near
  • low vergence facility with more difficulting using BO prism
  • decreased NRA
  • decreased binocular accommodative facility (with + power being more difficult to clear)
42
Q

Symptoms for basic exophoria

A

occasional diplopia at distance and near, headaches, asthenopia

43
Q

Convergence insufficiency

A
  • low exophoria or ortho at distance with a greater degree of exophoria at near (greater than 6pd)
  • exophoria fixation disparity at near
  • low AC/A ratio
  • reduced NPC
  • reduced NRA
  • decreased vergence facility (difficulty with BO prism)
  • decreased positive fusional vergence ranges at near
44
Q

Symptoms of convergence insufficiency

A
  • all sx are worse at the end of the day and with prolonged near work
  • words are moving around the page
  • pulling sensation of the eyes
45
Q

What is the most common vergence deficiency?

A

CI

46
Q

Divergence excess

A
  • higher degree of exophoria at distance compared to near (10pd difference)
  • high AC/A ratio
  • decreased PRA
  • poor second degree fusion at distance
47
Q

symptoms of divergence excess

A
  • suppression (asymptomatic)
  • covering or squinting an eye in bright light
  • asthenopia (eye strain/ocular fatigue)
48
Q

Basic esophoria

A
  • equal esophoria at distance and near (within 5pd)
  • average AC/A ratio
  • disparity at far and near
  • average AC/A ratio
  • decreased distance and near NFV
  • decreased vergence facility (difficulty with BI prisms)
  • lag on MEM
  • decreased PRA
  • Poor binocular accommodative facility (difficulty clearing minus-powered lens)
49
Q

Sx of basic esophoria

A
  • horizontal diplopia, blur, asthenopia
  • sx increased by the end of the day
50
Q

Accommodative insufficiency

A
  • decreased amplitude of accommodation
  • lag of accommodation on MEM
  • poor monocular facility (with minus-powered lenses being more difficult to clear)
  • decrease binocular accommodative facility (with minus lens being more difficult)
  • reduced PRA
51
Q

Symptoms of accommodative insufficiency

A

difficulty concentrating when reading, blurred vision, eye strain when reading

52
Q

What is the most common accommodation disorder? Second?

A
  1. accommodative insufficiency
  2. accommodative infacility
53
Q

Accommodative infacility

A
  • decreased monocular and binocular facility
  • decreased NRA and PRA
54
Q

Sx for accommodative infacility

A
  • reduced distance vision following sustained periods of near work
55
Q

How would you calculate a CL that would provide a predicted fluorescein pattern of apical alignment

A

Average K - 0.75

56
Q

How would you determine CL power?

A
  • Determine effect of the tear layer created btw the anterior corneal surface and back surface of the CL using the flat k and CL base curve values
  • If CL is flatter than K, a minus tear lens is created - therefore corresponding change in plus power is necessary
  • If CL is steeper than K, a plus tear lens is created - therefore a corresponding change in minus power is necessary
57
Q

When using a diagnostic lens fitting set, which available CL should you select to continue with your fitting?

A
  • If the CL you have calculated to provide the best fit and vision is not available - choose a lens with less desirable BC and/oor power
  • when fitting a gas perm CL - it is easier to quantify the amt of apical touch relationship of the lens and cornea compared to apical clearance
  • fudging flatter on the BC with diagnostic lenses will allow for better eval of the fluorescein pattern and more accurate calculation of the actual BC
  • IF correct CL power is not available - choose a lens that will provide a low minus over-refraction compared to either plus over refraction or large discrepancy in the expected and diagnostic CL power
58
Q

Conditions that falsely elevates A1c levels

A
  • Iron deficiency anemia
  • Any process that slows erythropoiesis increases a1c by maintaining an older erythrocyte cohort in the blood plasma (aplastic anemia)
  • Alcoholism
  • Hyperbilirubinemia
  • Certain meds (salicylates, chronic opioid use)
59
Q

Conditions that falsely lower A1c

A
  • Pregnancy
  • Hypertriglyceridemia
  • Certain meds (antiretrovirals, ribavirin, dapsone)
  • Vit C & E (inhibits glycosylation of glucose to hemoglobin)
  • Any process that shortens the life span of erythrocytes (hemolytic anemia, chronic kidney or liver dz)
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NBEO Part 2 (3 decks)

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