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Clin Med I Exam #2 > L6: Ophthalmology and vision loss > Flashcards

L6: Ophthalmology and vision loss Flashcards

1
Q

Define photopsias

A

Perceived flashes of light in the field of vision

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2
Q

Define hard exudates

A

Yellow-ish deposits of lipids in the outer layers of the retina (mostly macular area) from leakage due to damaged capillaries

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3
Q

Define drusen

A

Occurs naturally w/ age

yellow, fatty, protein and lipid deposits under the retina

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4
Q

Define scotoma

A

Area of partial alteration in field of vision w/ surrounding areas of normal visual acuity

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5
Q

Define metamorphopsia

A

Visual defect in which linear objects look curved or rounded

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6
Q

Define cotton wool spots (aka soft exudates)

A

Nerve fiber layer infarcts (ischemic event), pale, grayish white areas with ill-defined edges

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7
Q

What are the 5 conditions associated w/ ACUTE vision loss?

A
  • Retinal Detachment
  • Angle-closure glaucoma
  • Central retinal artery occlusion
  • Central retinal vein occlusion
  • Optic Neuritis

Think: RACCON (like rock-on)
The N comes from optic NEURITIS (helps differentiate from an O condition in chronic loss)

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8
Q

What are the 5 conditions associated w/ CHRONIC vision loss?

A
  • CATaract
  • Diabetic retinopathy
  • Open-angle glaucoma
  • Hypertensive retinopathy
  • Macular degeneration

Think: Cat DOHM (cat dome)

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9
Q

What are the 3 painful vision loss conditions?

A
  • Angle-closure glaucoma
  • Optic neuritis
  • Causes w/ red eye
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10
Q

What is the Amsler grid used for? What is an abnormal finding?

A
  • Monitors central vision loss (one eye at a time)

- Abnormal finding: pt sees wavy pattern (count how many squares are wavy as a measuring tool)

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11
Q

Describe an Afferent Pupillary Defect

A

-Lesion on CN II: Shine light in the affected eye, no pupillary reflex bilaterally
(Info travels from retina > optic nerve > CNS)

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12
Q

Describe an Efferent Pupillary Defect

A

-Lesion on CN III: Shine light in either eye, no pupillary constriction on affected side only
-Pupil is “fixed and dilated”
(Oculomotor nerve controls pupillary constrictor muscle)

Think: Efferent- CN thrEE

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13
Q

What is the result of a Relative Afferent Pupillary Defect (RAPD)? What is this phenomenon called?

A

Shine light in normal eye: both pupils constrict
Shine light in affected eye: no response; pupils remain dilated

AKA Marcus Gunn Pupil performed by “swinging flashlight test!***

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14
Q

What are the 3 primary components of glaucoma?

A
  • Intraocular pressure increase (urgent if >30mmHg)
  • Optic nerve damage
  • Visual field loss
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15
Q

_____ is the leading cause of irreversible blindness in the world.

A

Glaucoma

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16
Q

What is angle-closure glaucoma?

A

Acute rise of intraocular pressure (IOP) due to outflow obstruction

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17
Q

What is the cause of a primary angle-closure?

A

Anatomic predisposition

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18
Q

What is the cause of a secondary angle-closure?

A

Other causes such as scarring, inflammation, etc.

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19
Q

How would you test for a narrowed anterior chamber? What would an abnormal test show?

A

Pen light test

  • Shine light from lateral (temporal) aspect of eye towards nose
  • If narrowed chamber: shadow projects on nasal iris (crescent moon shape)
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20
Q

What is the clinical presentation of angle-closure glaucoma?

A
  • HALOS AROUND LIGHTS
  • MID-DILATED PUPIL 4-6 mm (reacts poorly to light)
  • PAIN!
  • Nausea, vomiting
  • Acutely decreased vision
  • Steamy, cloudy cornea
  • Firm globe
  • Ciliary flush
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21
Q

What is the gold standard for dx of angle-closure glaucoma?

A

Gonioscopy (can measure angle)

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22
Q

How do you treat angle-closure glaucoma?

A
  • OPTHO EMERGENCY! REFER!
  • Topical ocular anti-hypertensive meds: Beta-blockers, Alpha 2 agonists
  • Oral/IV osmotic agents (mannitol)
  • Laser peripheral iridotomy (where they poke a hole to relieve pressure)
  • Surgical trabeculectomy
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23
Q

What should you NEVER use to treat angle-closure glaucoma?

A

Cycloplegics (dilating drops)

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24
Q

What is open-angle glaucoma?

A
  • Optic neuropathy

- Increased aqueous production and/or decreased outflow can lead to increased IOP

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25
Q

What is the clinical presentation of open-angle glaucoma?

A

Early: asymptomatic
Late: CHRONIC, PAINLESS VISUAL FIELD LOSS (peripheral first, central later)

  • Increased IOP usually, but not always
  • INCREASED CUP/DISC RATIO
  • May have afferent pupillary defect
  • Visual field loss cannot be recovered once it occurs :-(
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26
Q

How do you treat open angle glaucoma?

A
  • Ophto referral (not AS emergent as angle closure)
  • Topical ocular anti-hypertensive meds: Beta blockers, Alpha-2 agonists
  • Laser trabeculoplasty
  • Surgical trabeculectomy

Goal: to reduce risk of progression

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27
Q

What is a cataract?

A

Opacity secondary to breakdown and clumping of proteins with the lens

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28
Q

List some contributing factors of cataracts.

A
  • Age >60 but can occur younger
  • Poor nutrition
  • Excessive exposure to sunlight
  • Some meds (like glucocorticoids)
  • Smoking/alochol
  • DM
  • HIV/AIDs
  • Trauma
  • Congenital
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29
Q

What is the clinical presentation of a cataract?

A
  • Gradual, chronic painless loss of vision
  • Variable in pace of progression
  • Usually sx are bilateral
  • DIFFICULTY W/ NIGHT DRIVING; GLARE FROM HEADLIGHTS
  • Decreased visual acuity
  • Yellow/opalescent changes to the lens on exam
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30
Q

What is the tx for cataracts?

A
  • Ophtho referral
  • Rx glasses for changes in vision
  • No criteria for surgery based on visual acuity
  • Surgery indicated if pt struggles with ADT (great prognosis for those with NO ocular comorbidities)
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31
Q

What is the #1 cause of central legal blindness in the Western world?

A

Age-Related Macular Degeneration (ARMD)

32
Q

What is macular degeneration

A

Degenerative disease of the posterior aspect of the retina (macula)

33
Q

What are the risk factors for macular degeneration?

A
  • > 50
  • Smoking/heavy alcohol use
  • Diet
  • FH
  • Meds: Nitroglycerin, oral beta blockers, aspirin
34
Q

What are the 2 types of ARMD?

A
  • Dry (atrophic)
  • Wet (neurocascularization or exudative)

*Dry AMD progresses to wet in some patients

35
Q

What is the general presentation for ARMD (both types)

A
  • Gradual or acutely blurred vision
  • Metamorphpsia
  • Central scotoma
  • Amsler grid distortion
36
Q

What are the unique characteristics of dry ARMD?

A
  • Early may be asymptomatic
  • Drusen deposits (fatty deposits around retina)
  • PIGMENT MOTTLING (loss of retinal pigment)
  • Geographic atrophy (thinning and loss of tissue in macula)
  • Vision loss SLOW/GRADUAL
  • Can be in one OR both eyes
  • Better preservation than wet ARMD!
37
Q

What are the unique characteristics of wet ARMD?

A
  • SUBRETINAL NEOVASCULAR (abnormal vessel growth)
  • Subsequent degeneration = leaky vessels
  • Fribrosis/scarring
  • RAPID VISION DISTORTION
  • Most commonly in ONE EYE
38
Q

How do you treat ARMD?

A
  • Ophtho referral (especially for wet)
  • Vitamins
  • Stop smoking!
  • Daily Amsler grid
  • Low vision aids
  • Stop offending drugs
39
Q

What other more specific tx would you use for wet ARMD?

A
  • Photocoagulation
  • Photodynamic therapy
  • Intravitreal steroid/monoclonal antibodies
40
Q

What is retinal detachment?

A
  • Separation of retina from the underlying epithelial layer and choroid
  • Causes ischemia and rapid degeneration of photoreceptors!
41
Q

What are the risk factors for retinal detachment?

A
  • HX OF MYOPIA (near-sightedness)
  • Complication of cataract surgery
  • Current use of fluoroquinolones (antibiotic)
  • FH of detachment
42
Q

What are the 2 types of retinal detachment?

A
  1. Rhegmatogenous RD
  2. Nonrhegmatogenous RD

Traumatic RD is uncommon and Exudative RD exists but is hella rare so we mostly DGAF

43
Q

Describe Rhegmatogenous RD

A
  • Full-thickness tear in the retina, most likely due to posterior vitreous detachment (PVD)
  • PVD happens when the VITREOUS SHRINKS OVER TIME and eventually pulls away
  • Can take a week to months for complete development
44
Q

Describe Nonrhegmatous RD

A

-Caused by VITREOUS TRACTION PULLING ON RETINA AND TEARING IT (scarring causes adherence to retina which eventually rips it away)

45
Q

Which type of retinal detachment is associated with DM?

A

Nonrhegmatogenous

  • Fibrosis from neurovascularization adherent between retina and vitreous
  • Retina pulled away from back of eye by vitreous
46
Q

What is the general presentation for a retinal detachment?

A
  • Painless, can rapidly progress
  • Floaters/PHOTOPSIAS
  • Loss of vision (complete or parital)
    • Progressive scotoma
    • CURTAIN-LIKE (top to bottom) *most common
    • May be peripheral only
  • Raised, whitish retina
  • Bilateral 20% of time (so always check both eyes)
  • Rate of progression dependent on size of retinal break
  • May have afferent pupillary defect (if unilateral w/ significant detachment)
47
Q

What conditions of the eye may result in an afferent pupillary defect?

A
  • Retinal detachment
  • Open angle glaucoma
  • CRAO
  • Sometimes CRVO
48
Q

How do you treat a retinal detachment?

A
  • W/o tx, most RD progress to involve entire retina
  • Pt with sudden onset, floaters, photopsias, visual loss:
    • Urgent ophtho referral
    • Laser photocoagulation (small tear)
    • Surgery (frank retinal detachment)
      • Scleral Buckle
      • Vitrectomy: Replaced with gas, silicone
49
Q

What is hypertensive retinopathy?

A

-Retinal vascular changes due to chronic, systemic hypertension
(95% are asymptomatic; 5% mild vision changes)

50
Q

What is the clinical presentation of hypertensive retinopathy

A
  • Copper wiring: arteriolar narrowing
  • Silver wiring: arteriolar sclerosis
  • A:V nicking: A:V crossing changes
  • Cotton-wool spots
  • Retinal hemorrhages
  • Retinal and disc edema
51
Q

How do you help treat hypertensive retinopathy?

A
  • SYSTEMIC BLOOD PRESSURE CONTROL

- Ophtho referral (laser photocoagulation of retinal hemorrhage)

52
Q

What is the primary cause of impaired vision in diabetic pts ages 25-75?

A

Diabetic retinopathy

*Risk decreased with good glycemic control!

53
Q

Why do pts with DR experience vision loss?

A
  • Macular edema
  • Retinal thickening
  • Hemorrhage from neurovascularization
  • Retinal detachment
54
Q

What are the 2 types of DR?

A
  • Proliferative

- Nonproliferative

55
Q

Describe proliferative DR

A
  • NEUROVASCULARIZATION
  • PRERETINAL AND VITREOUS hemorrhage w/ subsequent fibrosis (can cause sudden blindness)
  • Traction retinal detachment
  • Retinal thickening
  • Macular edema
56
Q

Describe nonproliferative DR

A
  • Blurred vision
  • RETINAL hemorrhage
  • Retinal and macular edema
  • VENOUS DILATION
  • HARD EXUDATES

Nonproliferative (no new vessel formation)

57
Q

How do you manage DR?

A
  • Blood sugar control
  • Ophtho referral
  • Laser photocoagulation
  • Virectomy
58
Q

What is the major difference between CRAO and CRVO?

A

CRAO: Embolic (traveling clot)
CRVO: Thrombotic

59
Q

Which of the two (CRAO or CRVO) is more rare?

A

CRAO

CRVO is an important cause of vision loss for older adults

60
Q

What is the most common risk factor associated with CRAO?

A

Carotid artery artherosclerosis

Other risk factors:

  • Hypertension
  • Smoking
  • Hyperlipidemia
  • Diabetes
61
Q

What are the risk factors for CRVO?

A
  • Older age
  • Hypertension
  • Diabetes
  • Smoking
  • Obesity
  • HYPERCOAGULABLE STATE
  • GLAUCOMA
62
Q

What is the common presentation for CRAO?

A
  • Acute, TOTAL, painless loss of vision
  • Pts might say “BLACK AS NIGHT”
  • No light perception
  • CHERRY RED SPOT
  • Ischemic retinal whitening
63
Q

What is the common presentation for CRVO?

A
  • Acute, VARIABLE, painless loss of vision
  • Scotoma w/ blurred vision
  • May have visual field loss
  • BLOOD AND THUNDER RETINAL APPEARANCE
64
Q

When I say: CHERRY RED SPOT!!! You say:

A

CRAO!!!!

65
Q

When I say: BLOOD AND THUNDER RETINAL APPEARANCE!!!! You say:

A

CRVO!!!!

66
Q

Which of the 2 central vascular occlusions has a poor prognosis

A

CRAO

Ocular emergency!

67
Q

How do you manage a pt with CRAO?

A
  • Immediate ophtho referral bc emergency!
  • No effective treatment :-( poor prognosis
  • Evaluate etiology (prevent future strokes)
    • Carotid plaques
68
Q

How do you manage a pt with CRVO?

A
  • Refer to ophtho
  • Aspirin to help thin blood
  • Observation
  • Tx for retinal edema or ischemia
  • Evaluate for etiology if young (why are they clotting?)
69
Q

What is optic neuritis?

A
  • Acute inflammatory DEMYELINATION OF OPTIC NERVE

- Causes vision loss over hours-days; peaks at 1-2 weeks

70
Q

What age range is most affected by optic neuritis?

A

20-40 years old

2/3 are female

71
Q

What disease do pts with optic neuritis usually develop later?

A

Multiple Sclerosis

30% get this 5 years later, 50% get this 15 years later

72
Q

What is the clinical presentation for optic neuritis?

A
  • Central scotoma (>90%)
  • PAINFUL!!; WORSE WITH EOMs
  • +/- abnormal color vision
  • +/- photopsias
  • Optic disc edema
  • OPTIC NERVE PALE AND SHRUNKEN
73
Q

How do you manage optic neuritis?

A
  • Order MRI brain and orbits with contrast
  • IV methylprednisone for severe vision loss or >/= 2 white matter brain lesions on MRI
    • More rapid recovery but similar visual acuity at year one w/ no tx
    • May delay onset of MS in year 1-2 but similar outcomes by year 5
74
Q

Is there treatment for optic neuritis?

A

No :-(

  • Improvement in 2-3 weeks
  • Typically 20/40 vision by one year
  • 35% recurrence at 10 years
75
Q

Who is the best group ever?!

A

Lab ladiezzz <3

Clin Med I Exam #2 (6 decks)

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