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neurology STEP 2 > ophthalmology > Flashcards

ophthalmology Flashcards

1
Q

viral vs bacterial conjunctivitis - transmissible? itchy? adenopathy, vision?

A

viral –> not itchy, easiy transmissible, PREAURICULAR adenopathy, normal vision
bacterial –> itchy, poorly transmissible, no adenopathy, normal vision

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2
Q

red eye (opthalmologic emergencies) - types and presentation

A
  1. conjunctivitis: itchy eyes with discharge
  2. uveitis autoimmune disease
  3. glaucoma: pain
  4. abrasion: trauma
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3
Q

red eye (opthalmologic emergencies) - types and eye findings

A
  1. conjunctivitis: normal pupil
  2. uveitis: photophobia
  3. glaucoma: fixed midpoint pupil
  4. abrasion: like sand in the eye
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4
Q

red eye (opthalmologic emergencies) - types and most accurate test

A
  1. conjunctivitis: clinical diagnosis
  2. uveitis: slit lamp examination
  3. glaucoma: tonometry
  4. abrasion: fluorescein stain
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5
Q

red eye (opthalmologic emergencies) - types and best initial therapy

A
  1. conjunctivitis: topical antibiotics
  2. uveitis: topical steroids
  3. glaucoma: acetazolamide, mannitol, pilocarpine, laser trabeculoplasty
  4. abrasion: no specific therapy, patch not clearly beneficial
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6
Q

chronic glaucoma - presentation / diagnosed by / confirmed by (findings)

A

diagnosed by routine screening

confirmation with tonometry –> extremely elevated intraocular pressure

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7
Q

chronic glaucoma - drugs

A
  1. prostaglading analogues: latanoprost, travoprost, bimatoprost
  2. topical beta blockers: timolol, carteolol, metipranolol, betaxolol, levobunolol
  3. topical carboic anhydrase inh: dorzolamide, brinzolamide
  4. alpha-2 agonists: apraclonidine
  5. pilocarpine
  6. laser trabeuloplasty (if medical treatment fail)
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8
Q

chronic glaucoma - prostagladin analogues - drugs and purpose

A

latanoprost, travoprost, bimatoprost

increase outflow of aqueous humor (uveoscleral flow)

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9
Q

chronic glaucoma - topical beta blockers - drugs and purpose

A

timolol, carteolol, metipranolol, betaxolol, levobunolol

decrease synthesis by nonpigmented epithelium on ciliary body

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10
Q

chronic glaucoma - topical carboic anhydrase inh - drugs and purpose

A

dorzolamide, brinzolamide

decrease synthesis by nonpigmented epithelium on ciliary body

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11
Q

chronic glaucoma - alpha-2 agonists - drugs and purpose

A

apraclonidine

decrease synthesis by nonpigmented epithelium on ciliary body

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12
Q

chronic glaucoma - pilocarpine - drugs and purpose

A

pilocarpine

increase outflow of aqueous humor (trabecular ouflow bu cilliary body contraction)

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13
Q

epinephrine (a1 agonist on glaucoma)

A

decreases aqueous humor synthesis via vasoconstriction

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14
Q

acute angle-closure glaucoma - clinical presentation

A
  • SUDDEN onset of an extremely painful
  • red eye that s hard to palpation
  • walking into a dark rook can precipitate pain because of pupillary dialation (SOS)
  • steamy cornea
  • non-reacting pupil
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15
Q

acute angle-closure glaucoma - diagnostic sign

A

the cup-to-disc ratio is greater than the normal 0.3

optic disc atrophy with charactersiting cupping (thinning of the outer rim of the optic nerve head vs normal

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16
Q

acute angle-closure glaucoma - the diagnosis is confirmed by

A

tonometry

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17
Q

acute angle-closure glaucoma - treat with (and why)

A
  1. IV acetazolamide
  2. IV mannitol: osmotic driving of fluid out of the eye
  3. Pilocarpie, beta-blockers and apracloinidine to constrict the pupil and enchance and enchance drainage)
  4. laser iridotomy
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18
Q

keratitis - definition / presentation

A

infection of the cornea

the eye may be very red, swollen and painful, but do not use steroids

19
Q

hepres keratitis - never use …. (why)

A

steroids –> make it worse / increase the production of the virus

20
Q

hepres keratitis - diagnosis

A

Fluorecein staining of the eye helps confirm the dendritic pattern seen on examination

21
Q

hepres keratitis - treatment

A

oral acyclovir, famciclovir or valacyclovir

topical anthepretic treatment is trifluridine and

22
Q

Cataracts - therapy

A
  • no medical therapy
  • surgically remove the lens and replace with a new intraocular lens. The lew lens may automatically have bifocal capability.
23
Q

Cataracts - diagnosis

A

early Cataracts: ophthalmoscope or slit lamp exam

advanced: visible on examination

24
Q

diabetic retinopathy - how to prevent / definition and types

A
  • annual screening (before serious visual loss)
    retinal damage due to chronic hyperclycemia:
    1. prolferative
    2. nonproliferative (or background)
25
Q

nonprolferative vs proliferative diabetic retinopathy - treatment

A

nonprolif: blood glucose control
prolif: laser photocoagulation and VEGF inh(to control neovascularization, surgery

26
Q

diabetic retinopathy - surgery

A

vitrectomy (remove the vitreous gel from the middle of the eye): to remove vitreal hemorrhage obstructing vision

27
Q

diabetic retinopathy - most accurate test

A

flurescein angiography

28
Q

retinal artery and vein occlusion - presentation

A

both conditions present with the sudden loss of monocular visual loss

29
Q

retinal artery and vein occlusion - diagnosis

A

cannot diagnose without retinal examination

30
Q

retinal examination - findings in retinal artery occlusion

A

the macula is described as “cherry red” because the retina is pale and macula is dark

31
Q

retinal examination - findings in retinal vein occlusion

A

extravasation of blood into retina

32
Q

retinal artery occlusion - treatment

A
  1. 100% O2
  2. ocular massage
  3. acetazolamide
  4. anterior chamber paracentiesis (decreased IOP)
  5. thrombolytics
  6. evaluate embolic source
33
Q

retinal vein occlusion - treatment

A

ranibizumab (VEGF-A inh)

34
Q

Retinal detachment - risks

A
  1. trauma of the eye
  2. extreme myopia that changes the shape of the eye
  3. diabetic retinopathy
    ANYTHING THAT PULLS THE RETINA CAN DETACH IT
35
Q

Retinal detachment - presentation

A

sudden onset of painless, unilateral loss of vision that is described as “A CURTAIN COMING DOWN”

36
Q

Reattachemen of retina is attempted …

A

with a number of mechanical methods such as:

  1. surgery 2. laser 3. cryotherapy
  2. injection of an expansile gas that pushes the retina back up against the globe of the eye
37
Q

The MCC of blindness in older person in the US

A

Macular degeneration

38
Q

causes of Macular degeneration / diagnosis

A

unknown

diagnosed only by visualization of the retina

39
Q

Macular degeneration - types

A
  1. atrophic (dry)

2. neovascular (wet)

40
Q

Macular degeneration - characteristics of visual loss

A
  1. far more common in older patients
  2. bilateral
  3. Normal external appearance of the eye
  4. loss of central vision
41
Q

Macular degeneration - atrophic dry vs neovascular regarding the progression and the severity (DESCRIBE)

A

neovascular is more rapid and more severe –> New vessels grow between the retina and the underlying Bruch membrane. The neovascular or wet type causes 90% of permanent blindness from macular desegregation

42
Q

atrophic dry Macular degeneration - treatment

A

no proven effective therapy

43
Q

neovascular or wet Macular degeneration - treatment

A

best initial: VEGF inh (ranibizumab, bevasizumab, aflibercept. Injected directly into the vitreous chamber every 4-8 wks.

44
Q

neovascular or wet Macular degeneration - results of the treatment

A
  1. over 90% of patients will expereience a halt (stop) of progression
  2. 1/3 will have improvement in vision

neurology STEP 2 (8 decks)

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