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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
What is the clinical presentation of open-angle glaucoma?
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 :-(
26
How do you treat open angle glaucoma?
- 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
27
What is a cataract?
Opacity secondary to breakdown and clumping of proteins with the lens
28
List some contributing factors of cataracts.
- Age >60 but can occur younger - Poor nutrition - Excessive exposure to sunlight - Some meds (like glucocorticoids) - Smoking/alochol - DM - HIV/AIDs - Trauma - Congenital
29
What is the clinical presentation of a cataract?
- 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
30
What is the tx for cataracts?
- 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)
31
What is the #1 cause of central legal blindness in the Western world?
Age-Related Macular Degeneration (ARMD)
32
What is macular degeneration
Degenerative disease of the posterior aspect of the retina (macula)
33
What are the risk factors for macular degeneration?
- >50 - Smoking/heavy alcohol use - Diet - FH - Meds: Nitroglycerin, oral beta blockers, aspirin
34
What are the 2 types of ARMD?
- Dry (atrophic) - Wet (neurocascularization or exudative) *Dry AMD progresses to wet in some patients
35
What is the general presentation for ARMD (both types)
- Gradual or acutely blurred vision - Metamorphpsia - Central scotoma - Amsler grid distortion
36
What are the unique characteristics of dry ARMD?
- 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
What are the unique characteristics of wet ARMD?
- SUBRETINAL NEOVASCULAR (abnormal vessel growth) - Subsequent degeneration = leaky vessels - Fribrosis/scarring - RAPID VISION DISTORTION - Most commonly in ONE EYE
38
How do you treat ARMD?
- Ophtho referral (especially for wet) - Vitamins - Stop smoking! - Daily Amsler grid - Low vision aids - Stop offending drugs
39
What other more specific tx would you use for wet ARMD?
- Photocoagulation - Photodynamic therapy - Intravitreal steroid/monoclonal antibodies
40
What is retinal detachment?
- Separation of retina from the underlying epithelial layer and choroid - Causes ischemia and rapid degeneration of photoreceptors!
41
What are the risk factors for retinal detachment?
- HX OF MYOPIA (near-sightedness) - Complication of cataract surgery - Current use of fluoroquinolones (antibiotic) - FH of detachment
42
What are the 2 types of retinal detachment?
1. Rhegmatogenous RD 2. Nonrhegmatogenous RD Traumatic RD is uncommon and Exudative RD exists but is hella rare so we mostly DGAF
43
Describe Rhegmatogenous RD
- 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
Describe Nonrhegmatous RD
-Caused by VITREOUS TRACTION PULLING ON RETINA AND TEARING IT (scarring causes adherence to retina which eventually rips it away)
45
Which type of retinal detachment is associated with DM?
Nonrhegmatogenous - Fibrosis from neurovascularization adherent between retina and vitreous - Retina pulled away from back of eye by vitreous
46
What is the general presentation for a retinal detachment?
- 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
What conditions of the eye may result in an afferent pupillary defect?
- Retinal detachment - Open angle glaucoma - CRAO - Sometimes CRVO
48
How do you treat a retinal detachment?
- 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
What is hypertensive retinopathy?
-Retinal vascular changes due to chronic, systemic hypertension (95% are asymptomatic; 5% mild vision changes)
50
What is the clinical presentation of hypertensive retinopathy
- 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
How do you help treat hypertensive retinopathy?
- SYSTEMIC BLOOD PRESSURE CONTROL | - Ophtho referral (laser photocoagulation of retinal hemorrhage)
52
What is the primary cause of impaired vision in diabetic pts ages 25-75?
Diabetic retinopathy | *Risk decreased with good glycemic control!
53
Why do pts with DR experience vision loss?
- Macular edema - Retinal thickening - Hemorrhage from neurovascularization - Retinal detachment
54
What are the 2 types of DR?
- Proliferative | - Nonproliferative
55
Describe proliferative DR
- NEUROVASCULARIZATION - PRERETINAL AND VITREOUS hemorrhage w/ subsequent fibrosis (can cause sudden blindness) - Traction retinal detachment - Retinal thickening - Macular edema
56
Describe nonproliferative DR
- Blurred vision - RETINAL hemorrhage - Retinal and macular edema - VENOUS DILATION - HARD EXUDATES Nonproliferative (no new vessel formation)
57
How do you manage DR?
- Blood sugar control - Ophtho referral - Laser photocoagulation - Virectomy
58
What is the major difference between CRAO and CRVO?
CRAO: Embolic (traveling clot) CRVO: Thrombotic
59
Which of the two (CRAO or CRVO) is more rare?
CRAO | CRVO is an important cause of vision loss for older adults
60
What is the most common risk factor associated with CRAO?
Carotid artery artherosclerosis Other risk factors: - Hypertension - Smoking - Hyperlipidemia - Diabetes
61
What are the risk factors for CRVO?
- Older age - Hypertension - Diabetes - Smoking - Obesity - HYPERCOAGULABLE STATE - GLAUCOMA
62
What is the common presentation for CRAO?
- Acute, TOTAL, painless loss of vision - Pts might say "BLACK AS NIGHT" - No light perception - CHERRY RED SPOT - Ischemic retinal whitening
63
What is the common presentation for CRVO?
- Acute, VARIABLE, painless loss of vision - Scotoma w/ blurred vision - May have visual field loss - BLOOD AND THUNDER RETINAL APPEARANCE
64
When I say: CHERRY RED SPOT!!! You say:
CRAO!!!!
65
When I say: BLOOD AND THUNDER RETINAL APPEARANCE!!!! You say:
CRVO!!!!
66
Which of the 2 central vascular occlusions has a poor prognosis
CRAO | Ocular emergency!
67
How do you manage a pt with CRAO?
- Immediate ophtho referral bc emergency! - No effective treatment :-( poor prognosis - Evaluate etiology (prevent future strokes) - Carotid plaques
68
How do you manage a pt with CRVO?
- 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
What is optic neuritis?
- Acute inflammatory DEMYELINATION OF OPTIC NERVE | - Causes vision loss over hours-days; peaks at 1-2 weeks
70
What age range is most affected by optic neuritis?
20-40 years old | 2/3 are female
71
What disease do pts with optic neuritis usually develop later?
Multiple Sclerosis | 30% get this 5 years later, 50% get this 15 years later
72
What is the clinical presentation for optic neuritis?
- Central scotoma (>90%) - PAINFUL!!; WORSE WITH EOMs - +/- abnormal color vision - +/- photopsias - Optic disc edema - OPTIC NERVE PALE AND SHRUNKEN
73
How do you manage optic neuritis?
- 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
Is there treatment for optic neuritis?
No :-( - Improvement in 2-3 weeks - Typically 20/40 vision by one year - 35% recurrence at 10 years
75
Who is the best group ever?!
Lab ladiezzz <3

Clin Med I Exam #2 (6 decks)

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