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CLIN MED 3 - HEENT > Refractive errors, Glaucoma and Cataracts - waldron > Flashcards

Refractive errors, Glaucoma and Cataracts - waldron Flashcards

1
Q

what is the leading cause of blindness and low vision in the US

A

primarily age related:
Age-related macular degeneration (AMD)
Cataract
Diabetic retinopathy
Glaucoma

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2
Q

what are refractive errors

A

most frequent eye problems in the US
myopia, hyperopia, astigmatism, presbyopia
most can be corrected by classes, contacts, or surgery

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3
Q

what is Myopia

A

near sightedness
point of focus is in front of retina: cornea too steeply curved, axial length of eye too long, or both
distant objects are blurred

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4
Q

what is hyperopia

A

far - sightedness
point of focus is behind the retina: cornea too flatly curved, axial length too short or both
adults: both near and distant objects blurred

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5
Q

what is astigmatism

A

distorted vision at all distances
non-spherical (variable) curvature of cornea or lens causes light rays of different orientations to focus at different points

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6
Q

what is presbyopia

A

loss of ability to focus up close i.e. reading
loss of lens’ ability to change shape to focus on near objects due to aging
typically becomes noticeable upon reaching early-mid 40s

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7
Q

how do you correct myopia

A

concave (minus) lens

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8
Q

how do you correct hyperopia

A

a convex (plus) lens

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9
Q

how do you correct astigmatism

A

cylindrical lens (a segment cut from a cylinder)

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10
Q

how do you correct Presbyopia

A

a convex (plus) lens is used for correction when viewing near objects
lenses may be supplied as separate glasses or built into a lens as bifocals or variable focus lenses

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11
Q

What is anisometropia

A

significant different between refractive errors of the 2 eyes (usually > 3 diopters)
when corrected with glasses, a different in image size is produced

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12
Q

what is aniseikonia

A

difference in image size

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13
Q

what are the symptoms of refractive errors

A

primary is blurred vision for distant objects, near objects or both
headaches: excessive ciliary muscle done, prolonged squinting and frowing with ocular use
eye irritation, itching, visual fatigue, FB sensation, rendess
percieved imabalance, dizziness, stumbling

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14
Q

what is difference in image size

A

aniseikonia

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15
Q

how do you diagnose and work up refractive errors

A

visual acuity
refraction: should be done every 1-2 years. screening children visual acuity helps detect refractive errors before interfering with learning
comprehensive eye exam: ophthalmologist/optometrist

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16
Q

what are the treatment for refractive errors in the eye

A

glasses, contacts, refractive surgery

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17
Q

what are the numbers of corrective lens prescriptions

A

first number: power (magnitude) of spherical correction required (- for myopia; + for hyperopia)
second number: power of cylindrical correction required (+ or -)
third: axis of cylinder

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18
Q

What is amblyopia

A

lazy eye

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19
Q

what is a functional reduction in visual acuity of an eye caused by disuse during visual development

A

amblyopia

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20
Q

What is strabismus

A

misalignment of eyes resulting in different retinal images being sent to visual cortex
-childs brain can pay attention to only one eye at a time, input from other eyes is suppressed - results in diplopia rather than suppression of one image

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21
Q

what is anisometropia

A

different focus of retinal images. with image from eye with greater refractive error being less well focused

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22
Q

what is obstruction of the visual axis

A

at some point between the surface of eye and retina something interferes with or completely prevents formation of retinal image affected eye

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23
Q

what is the clinical presenation of amblyopia

A

often asymptomatic, commonly discovered on routine vision screening
child rarely complains of unilateral vision loss, but may squint or cover one eye
if strabismus is cause, deviation of gaze may be noticeable to others
cataracts causing occlusion of visual axis may go unnoticed

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24
Q

how can stabismus be confirmed

A

with alternate cover test or cover-uncover test

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25
Q

how do opthamoloists confirm anisometriopia

A

doing a refraction on each eye

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26
Q

what is the treatment of amblylopia

A

eyeglasses or contact lenses
cataract removal
patching atropine drops
treatment of strabismus if present

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27
Q

what is the most common cause of irreversible central vision loss in older patients

A

age-related macular degeneration (AMD)

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28
Q

what is the diagnostic test for AMD

A

dilated fundoscopic findings

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29
Q

what is the treatment of AMD

A

dietary supplements, intravitreal injection of anti-vascular endothelial growth factor drugs, laser photocoagulation, photodynamic therapy, low-vision devices

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30
Q

what are risk factors for AMD

A

age
genetic variants
family hx
smoking
CVD/HTN
obesity
sun exposure
diet low in omega-3 fatty acids and dark green leafy vegetables

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31
Q

what are the forms of AMD

A

dry (non-exudative or atrophic) - all starts here
wet (exudative or neovascular)

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32
Q

What is dry AMD

A

causes changes of retinal pigment epithelium, typically visible as dark pinpoint areas
accumulation of waste products from rods and cones results in drusen, which appear as yellow spots

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33
Q

What is Wet AMD

A

new abnormal blood vessels develop under the retina: choroidal neovascularization
localized macular edema or hemorrhage may elevate an area of the macula or cause a localized retinal pigment epithelial detachment

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34
Q

what can untreated neovascularization cause

A

disciform scar under the macula

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35
Q

what is the clinical presentation of Dry AMD

A

loss of central vision occurs over years and is painless
central blind spots (scotomas) usually occur late and can become severe
symptoms are usually bilateral

36
Q

what is seen on fundoscopic exam with dry AMD

A

changes in retinal pigment epithelium
Drusen
Areas of chorio-retinal atrophy

37
Q

What is the clinical presentation of Wet AMD

A

rapid vision loss, usually over days to weeks
first sx usually visual distortion (i.e. central blind spots (scotoma) or curving sraight lines (metamorphopsia))
peripheral vision and color vision generally unaffected - may become legally blind if not treated
often unilateral

38
Q

what is the criteria for legally blind

A

< 20/200 vision

39
Q

What are the fundoscopic changes with Wet AMD

A

subretinal fluid, appearing as localized retinal elevation
retinal edema
gray-green discoloration under the macula
exudates in or around macula
detachment of retinal pigment epithelium
subretinal hemorrhages in or around the macula

40
Q

Define scotomas

A

centrally blind spots

41
Q

how is AMD diagnosed/worked up

A

fundoscopic exam: will dx both forms
color fundus photography: suspect wet AMD
fluorescein angiography: suspect wet AMD
optical coherence tomography (OCT)
visual changes can be detected with Amsler grid

42
Q

What is the treatment of dry AMD

A

no way to reverse damage
can reduce risk of wet AMD by taking zinc, copper, vitamin C, vitamin E, Lutein
reduce CV risk factors, eating flood high in omega-3 fatty acids and dark green leafy vegetables

43
Q

what is the treatment of wet AMD

A

unilat: daily nutritional supplements as recommended for dry AMD (reduce risk of AMD-induced vision loss in other eye)
choice of tx depends on size, location and type of neovascularization
intravitreal injection of anti-vascular endothelial growth factor drugs

44
Q

what are the supportive measures for AMD

A

low vision devices: magnifiers, high-power reading glasses, large computer monitors, telescopic lenses
software can display computer data in large print or read information aloud
low-vision counseling is advised

45
Q

what are Cataracts

A

clouding of the lens
“looking through a steamed-up window”
congenital or degenerative opacity of the lens; several possible locations

46
Q

what is the leading cause of blindness worldwide, leading cause of vision loss in the US

A

cataracts

47
Q

what are the possible locations of cataracts

A

central lens nucleus (nuclear cataract)
beneath posterior lens capsule (posterior subcapsular cataract)
on side of the lens (cortical cataract)

48
Q

what are the main symptoms of cataracts

A

gradual, painless vision blurring

49
Q

how do you diagnose cataracts

A

opthalmoscopy and slit-lamp examination

50
Q

what is the treatment of cataracts

A

surgical removal and replacement of an intraocular lens

51
Q

what are risk factors of cataracts

A

trauma (may present years later)
smoking
alcohol use
exposure to x-ray
heat from infrared exposure
systemic disease
uveitis
systemic drugs
undernutrition
chronic UV light exposure

52
Q

what are the clinical presentations of cataracts

A

usually develop slowly over years
early symptoms: loss of contrast, glare, need more light to see well, problems distinguishing dark blue from black
painless blurring

53
Q

what are the clinical presentation of nuclear cataracts

A

distance vision worsens; near vision may improve in early stages temporarily; presbyopic patients may be temporarily able to read without classes (second sight)

54
Q

what is the clinical presentation of posterior subcapsular cataract

A

reduced visual acuity when pupil constrics; more likely to cause loss of contrast and glare, esp. from bright lights or from car headlights at night

55
Q

how are cataracts diagnosed/worked up

A

opthalmoscopy followed by slit-lamp examination
dx best made with pupil dilated
appear as gray, white or yellow-brown opacities in lens

56
Q

what are the treatment options for cataracts

A

frequent refractions and corrective lens prescription changes may help maintain useful vision during cataract development
indirect lighting while reading minimizes pupillary constriction and may optimize vision for close tasks
sx removal or cataract - placement of intraocular lens
phacoemulsification (extracapular cataract extraction)

57
Q

what is phacoemulsification

A

type of extracapuslar cataract extraction
hard central nucleus is dissolved by ultrasound and then soft cortex is removed in multiple small pieces
preferred procedure

58
Q

what is the second most common cause of blindness worldwide and 2nd most common cause of blindness in the US and leading casue of blidness for AA and hispanics

A

glaucoma

59
Q

what is POAG

A

primary, open-angle glaucoma

60
Q

what is glaucoma

A

group of eye disorders characterized by progressive optic nerve damage; key component is a relative increase in IOP
acquired loss of retinal ganglion cells and axons within the optic nerve, that results in a characteristic optic nerve head appearance and corresponding progressive loss of vision

61
Q

what is “angle”

A

angle formed by junction of iris and cornea at periphery of anterior chamber
where >98% of aqueous humor exits eye via either trabecular meshwork and schlemm canal (major pathway, particularly in elderly) or ciliary body face and choroidal vasculature

62
Q

what is primary glaucoma

A

cause of outflow resistance or angle closure is unknown

63
Q

what is secondary glaucoma

A

outflow resistance result from a known disorder

64
Q

what is angle-closure glaucoma

A

associated with physically obstructed anterior chamber angle, chronic or acute
acute: sever ocular pain and redness, decreased vision, colored halos around lights, headache, N/V
IOP elevated

65
Q

what is the treatment of angle-closure glaucoma

A

immediate tx of acute condition with multiple topical and systemic drugs is required to prevent permanent vision loss, followed by definitive treatment - iridotomy

66
Q

what causes angle-closure glaucoma

A

factors that either pull or push iris up to angle physically blocking drainage of aqueous and raising IOP
elevated IOP damages optic nerve
may be primary or secondary to another condition (acute, subacute or chronic)

67
Q

what is primary angle-closure glaucoma

A

as age, lens continues growth; growth can push iris forward, narrowing angle
risk factors for narrowing angles: Fhx, advanced age, ethnicity
pressure from continued secretion of aqueous into posterior chamber pushes peripheral iris anteriorly, closing angle
ophthalmic emergency requiring an immediate treatment

68
Q

what is the presentation of Acute primary angle closure

A

pupillary dilation (mydriasis) can push iris into angle and precipitate angle-closure glaucoma in any person with narrow angles
severe ocular pain and redness, decreased vision, colored halos around lights, headache, N/V
systemic complaints may be so severe that misdiagnosed as neurologic or GI problem

69
Q

what are the types of primary angle-closure

A

intermittent angle-closure glaucoma: if episode of pupillary block resolves spontaneously after several hours, usually after sleeping supine
chronic angle-closure glaucoma: if angle narrows slowly, allowing scarring btwn peripheral iris and trabecular meshwork; IOP elevation is slow

70
Q

what is secondary angle-closure

A

mechanical obstruction due to coexisting condition
-proliferative diabetic retinopathy (PDR)
-ischemic central vein occlusion
-uveitis epithelial down-growth
contraction of neovascular membrane or inflammatory scarring can pull iris into angle

71
Q

what is seen on examination of acute angle closure

A

conjunctival hypermia, “hazy” cornea, fixed mid-dialted pupil, anterior chamber inflammation
vision is decreased
IOP usually 40-80mmHg
optic nerve difficult to visualize due to corneal edema ; visual field testing not done because of discomfort

72
Q

what is seen on clinical exam with chronic angle closure

A

manifests like open-angle
may have ocular redness, discomfort, blurred vision, headache that lessens with sleep
angle is narrow and periopheral anterior synechiae (PAS)
IOP may be normal but usu higher in affected eye

73
Q

how are angle closure glaucomas diagnosed/worked up

A

acute: measurement of IOP and clinical findings
chronic: Gonioscopy showing periopheral anterior synechiae and characterisitic optiv nerve and visual fild abnormaliteis

74
Q

what is the treatment of Acute angle-closure glacucoma

A

tx immediately
multi-drug regimen: timolol, pilocarpine, brimonidine, acetazolamide, osmotic agent
response is evaluated by measuring IOP

75
Q

what is the definitive treatment of acute angle-closure glaucoma

A

laser peripheral iridotomy (LPI)
opens another path to pass fluid from posterior to anterior chamber

76
Q

what is the treatment of chronic angle-closure glaucoma

A

chronic, subacute or intermittent: LPI

77
Q

what is primary open-angle glaucoma

A

syndrome of optic nerve damage associated with open anterior chamber angle and elevated or sometimes avg IOP

78
Q

how do you diagnose POAG

A

opthalmoscopy, gonioscopy, visual field examiation, measurement of central corneal thickness, IOP

79
Q

what is the treatment of POAG

A

topical drugs (prostaglandin analogs, beta blockers); often requires laser or incisional surgery to increase aqueous drainage

80
Q

what are risk factors of POAG

A

older age
Fhx
African ethnicity
thinner central corneal thickness
HTN
DB
myopia

81
Q

what is normal pressure glaucoma or low-pressure glaucoma

A

IOP within average range, but optic nerve damage and visual field loss typical of glaucoma are present
higher incidence of vasospastic disease
average-range IOP more common among asians

82
Q

what is the clinical presentation of Open angle glaucoma

A

early primary symtpoms are uncommon
usu. aware of visual field loss only when optic nerve atrophy is significant; typically, asymmetric deficits contribute to dleay in recognition
unobstructed open angle on gonioscopy and characteristic optic nerve appearance and visual field defects

83
Q

what is seen on fundoscopic with open angle

A

increased cup to disk ration (increasing ration over time)
thinning of neurosensory rim
pitting or notching of rim
nerve fiber layer hemorrhage that crosses disk margin (splinter hemorrhages)
vertical elongation of cup
quick angulations in course of exiting blood vessels (bayoneting)

84
Q

how is open angle diagnosed/worked up

A

visual field testing
ophthalmoscopy
measurement of central corneal thickness and IOP
exclusion of other optic neuropathies
diagnosis of POAG is suggested by examination)

85
Q

what is the treatment of open angle

A

goal to prevent further optic nerve and visual field damage by lowering IOP
topicals are preferred (prostaglandin analogs - latanoprost, tafluprost) then beta- blockers (timolol))
surgery: selective laser trabeculoplasty (SLT), Argon laser trabeculoplasty (ALT)
guarded filtration procedure, partial-thickness procedures

CLIN MED 3 - HEENT (8 decks)

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