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Clinical Med I > HEENT - Vision Loss - Exam 2 > Flashcards

HEENT - Vision Loss - Exam 2 Flashcards

1
Q

What is photopsias?

A

Perceived flashes of light in the field of vision

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2
Q

What are hard exudates?

A

Yellowish-white deposits of lipids in outer layers of retina (mostly macular area) from leakage due to damaged capillaries

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3
Q

What is drusen?

A

Yellow, fatty, protein and lipid deposits under retina (occur naturally with age)

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4
Q

What is a scotoma?

A

An area of partial alteration in field of vision with surrounding areas of normal visual acuity

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5
Q

What is metamorphopsia?

A

Visual defect in which linear objects look curved or rounded

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6
Q

What are cotton wool spots also known as?

A

Soft exudates

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7
Q

What are cotton wool spots?

A

Pale, grayish white areas with ill-defined edges

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8
Q

What is the Amsler grid used for?

A

Monitor central vision loss

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9
Q

What is considered an abnormal finding on the Amsler grid test?

A

Wavy pattern when looking at the grid

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10
Q

What should pupils be evaluated for?

A

PERRLA- pupils equal, round, reactive to light and accommodation

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11
Q

What CN’s does the pupillary light reflex require? Which one is afferent/ efferent?

A

CN II = afferent

CN III = efferent

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12
Q

What is considered a normal pupillary reflex?

A

Shine light in unaffected eye, bilateral pupils constrict

*abnormal = no reflex bilaterally = afferent pupillary defect

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13
Q

If there is a lesion in CN II, what will be present upon exam?

A

Afferent

Sine light in affected eye, no pupillary reflex bilaterally

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14
Q

What type of relative afferent pupillary defect (RAPD) will be seen upon performing the “swinging flashlight test”?

A

Marcus Gunn pupil

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15
Q

What are the 3 primary components of glaucoma?

A
  1. Intraocular pressure increase (urgent if >30mmHg)
  2. Optic nerve damage
  3. Visual field loss
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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

How is angle-closure glaucoma identified on exam?

A

Shine light from lateral (temporal) aspect of eye towards the nose > if shadow projects on nasal iris, the chamber is narrow

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18
Q

What is the presentation of angle-closure glaucoma?

A 
Acutely decreased vision
Halos around lights
Ciliary flush
Steamy, cloudy cornea
Mid-dilated pupil 4-6mm, reacts poorly to light
Firm globe
Severe eye pain
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19
Q

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

A

Gonioscopy (can measure angle)

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20
Q

What should NOT be used in the management of angle-closure glaucoma?

A

Cycloplegics (dilating drops)

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21
Q

What is included in the management of angle-closure glaucoma?

A 
Ophthalmologic emergency!
Topical ocular anti-hypertensive meds (beta blockers, alpha-2 agonists)
Oral/ IV osmotic agents (mannitol)
Laser peripheral iridotomy 
Surgical trabeculectomy
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22
Q

What are the causes of open-angle glaucoma?

A

Optic neuropathy
Increased aqueous production/ decreased outflow > IOP
(Pathogens not clear)

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23
Q

What is the presentation of open-angle glaucoma?

A 
Increased IOP (usually)
Increased cup/ disc ratio
Afferent pupillary defect
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24
Q

What are early vs late symptoms of open-angle glaucoma?

A

Early- asymptomatic

Late- chronic painless visual field loss (peripheral first)

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25
Q

What is included in the management of open-angle glaucoma?

A

Ophthalmologic referral
Topical ocular anti-hypertensive medications
Laser trabeculoplasty
Surgical trabeculectomy

Goal is to reduce risk of progression

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26
Q

What is a cataract?

A

Opacity secondary to breakdown and clumping of proteins within the lens

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27
Q

Do cataracts usually present with unilateral or bilateral symptoms?

A

Bilateral

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28
Q

How do cataracts present clinically?

A

Gradual, chronic, painless vision loss
Difficulty with night driving
Decreased visual acuity

29
Q

What would be seen on an exam of a patient with cataracts?

A

Yellowing/ opalescent changes to the lens

30
Q

When should management of cataracts be considered?

A

If a patient struggles with ADL due to vision changes > possible prescription glasses

31
Q

What are surgical options for cataracts?

A

Extracapsular cataract extraction

Intraocular lens implant

32
Q

What is the prognosis for a patient with cataracts?

A

Excellent (with no ocular comorbidity)

33
Q

What are the 2 categories of macular degeneration?

A

Dry- strophic

Wet- neovascularization or exudative

34
Q

What is the general presentation of macular degeneration?

A

Blurred vision
Metamorphopsia (Amsler grid distortion)
Central scotoma

35
Q

What presentation of ARMD is unique to the dry subtype?

A

Drusen deposits
Pigment mottling (loss of retinal pigment)
Geographic atrophy (thinning/ loss of tissue in macula)
Vision loss slow/ gradual

36
Q

What presentation of ARMD is unique to the wet subtype?

A

Subsequent degeneration = “leaky vessels”
Fibrosis/ scarring
Rapid vision distortion

37
Q

What is included in the management of both dry and wet ARMD?

A 
Referral
Vitamins/ omega 3 fatty acids
Stop smoking
Daily Amsler grid
Low vision aids
38
Q

What is included in the management of only wet ARMD?

A

Photocoagulation
Photodynamic therapy
Intravitreal steroid/ monoclonal antibodies

39
Q

What does retinal detachment result in?

A

Ischemia and rapid degeneration of photoreceptors

40
Q

What is the main risk factor for retinal detachment?

A

History of myopia (near sightedness)

41
Q

What are the 3 types of RD?

A

Rhegmatogenous, nonrhegmatogenous and exudative (rare)

42
Q

What are the most common causes of a rhegmatogenous RD?

A

Full-thickness tear
Posterior vitreous detachment (PVD)
Traumatic RD

43
Q

What is posterior vitreous detachment (PVD)?

A

PVD normally adhered to retina but shrinks/ liquifies with age > pulls away from retina resulting in tears

44
Q

What is the cause of nonrhegmatogenous RD?

A

Vitreous traction pulling on retina and tearing it

Associated with diabetes

45
Q

How does diabetes related to nonrhegmatogenous RD?

A

Fibrosis from neovascularization adherent between retina and vitreous

46
Q

How does RD present?

A 
Painless
Floaters/ photopsias 
Loss of vision (curtain-like) 
Raised, whitish retina 
May have afferent pupillary defect
47
Q

What is the management for a RD?

A

If sudden onset of symptoms:
Urgent referral
Laser photocoagulation (small tear)
Surgery (frank RD)

48
Q

What is included in the surgical treatment of a RD?

A

Scleral buckle

Vitrectomy- replaced with gas, silicone oil

49
Q

What is hypertensive retinopathy?

A

Retinal vascular changes due to chronic, systemic hypertension

50
Q

Is hypertensive typically symptomatic or asymptomatic?

A

Asymptomatic (95%)

51
Q

What are the characteristic ophthalmic changes seen with hypertensive retinopathy?

A 
Arteriolar narrowing - copper wiring
Arteriolar sclerosis - silver wiring
A:V crossing changes - nicking 
Cotton wool spots
Retinal hemorrhages
52
Q

What is included in the management of hypertensive retinopathy?

A

Systemic BP control
Referral
Laser photocoagulation if retinal hemorrhage

53
Q

What are the 2 classifications of DR?

A

Non-proliferative and proliferative

54
Q

What are the characteristics of non-proliferative DR?

A 
Blurred vision
Retinal hemorrhage
Cotton wool spots
Venous dilation
Hard exudates
55
Q

What are the characteristics of proliferative DR?

A

Neovascularization
Preretinal and vitreous hemorrhage
Traction RD
Retinal thickening

56
Q

What is involved in the management of DR?

A

Blood sugar control
Referral
Laser photocoagulation
Vitrectomy

57
Q

What are the 2 types of vascular occlusion and how is each classified?

A

Central Retinal Artery Occultion (CRAO) = embolic

Central Retinal Vein Occlution (CRVO) = thrombotic

58
Q

What is included in the presentation that is unique to CRAO?

A 
Acute, TOTAL, painless loss of vision
Often "no light perception" - "black as night"
Afferent pupillary defect 
Ischemic retinal whitening 
"Cherry red spot"
59
Q

What is included in the presentation that is unique to CRVO?

A

Acute, VARIABLE, painless loss of vision
Scotoma with blurred vision (possible visual field loss)
+/- afferent pupillary defect
“Blood and thunder” retinal appearance

60
Q

What is involved with the management of vascular occlusion that is unique to CRAO?

A

Ocular emergency
No effective treatment/ poor prognosis
Evaluate etiology - carotid plaques

61
Q

What is involved with the management of vascular occlusion that is unique to CRVO?

A

Aspirin
Observation
Treatment for retinal edema/ ischemia
Evaluate etiology if young- hypercoagulable state

62
Q

What is optic neuritis?

A

Acute inflammatory demyelination of the optic nerve

63
Q

Does optic neuritis typically in one or both eyes?

A

One - mononuclear vision loss = 90%

64
Q

How does vision loss associated with optic neuritis present?

A

Vision loss over hours to days, peaks at 1-2 weeks

65
Q

What disease is associated with optic neuritis?

A 
Multiple sclerosis (MS)
30% at 5 years, 50% at 15 years
66
Q

How does optic neuritis present?

A

Central scotoma
Painful (worse with EOM)
Abnormal color vision
Photopsias

67
Q

What is involved in the management of optic neuritis?

A

MRI brain and orbits with contrast

IV methylprednisone

68
Q

When is IV methylprednisone used specifically for treatment of optic neuritis?

A

Severe vision loss or 2+ white matter brain lesions on MRI (more rapid but short term treatment, may delay onset of MS short term)

Clinical Med I (24 decks)

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