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week 1 PC 2 > adult eyes stuff > Flashcards

adult eyes stuff Flashcards

1
Q

what is considered low vision?

A

20/70 or worse

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2
Q

what is considered legally blindness?

A

20/200 or worse

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3
Q

major causes of vision loss in older adults

A

age related cataracts, glaucoma, macular degeneration, diabetic retinopathy, refractive error

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4
Q

what are cataracts?

A

refers to the opacification of the crystalline lens of the eye

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5
Q

cause of cataracts?

A

result from oxidative damage, thickening and opacification of lens

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6
Q

risk factors for cataracts

A

increasing age, tobacco use, UV exposure, systemic corticosteroid use, diabetes, HTN, CKD, HIV, hx of eye trauma, ETOH use

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7
Q

presentation of cataracts

A

typically bilateral; may complain of clouded, blurred or hazy, or dim vision; difficulty with nighttime driving and sensitivity to light/glare, halos around lights, glare from headlights; may present for frequent changing of prescription

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8
Q

how do you evaluate for cataracts?

A

-perform full eye and neuro exam
-test visual acuity
-there should be NO CONJUNCTIVAL REDNESS OR PAIN
-pupil exam is normal
-abnormal red reflex- dull, extinct or shady
-may have hazy visualization of optic nerve

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9
Q

management of cataracts

A

-early changes can be managed with adjustment of prescription (glasses and contact lenses) and avoid nighttime driving
-THERE ARE NO MEDS OR DROPS THAT REVERSE CHANGES
-consider referral to ophthalmology for consideration of surgery if greatly affecting visual acuity or functioning
-surgery generally considered low-risk –> lens is emulsified into tiny fragments, removed and replaced with artificial lens

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10
Q

pre-op med review is very important…why?

A

alpha adrenergic antagonists such as Tamsulosin (Flomax) may cause Floppy Iris Syndrome

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11
Q

post op education

A

avoiding heavy lifting or straining, consistent eye drop administration, need for sunglasses, reasons to seek urgent medical attention (ex: eye pain, sudden vision changes, etc)

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12
Q

macular degeneration

A

chronic process that involves damage to the macula and retina

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13
Q

macular degeneration: risk factors

A

age, tobacco use, family hx, HTN, HLD

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14
Q

dry (non-exudative) macular degeneration

A

-retinal atrophy and buildup of druse below the retina
-can lead to scarring/thinning of retina and gradual central vision loss

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15
Q

wet (exudative or neovascular) macular degeneration

A

-may develop in pts with dry form
-new blood vessels form and may cause swelling and bleeding into the retina
-may cause sudden or gradual vision loss

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16
Q

s/s of macular degeneration

A

-change in CENTRAL VISION
-difficulties adapting to dark
-dark spots in vision
-distorted straight lines
-colors may appear less vivid or darker

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17
Q

evaluation of macular degeneration

A

-perform full eye and neuro exam
-test visual acuity
-amsler grid can identify central vision defects and used for monitoring
-for this with family hx of early age-related macular degeneration, encourage to see ophthalmology

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18
Q

management of dry (non-exudative) macular degeneration

A

-referral and regular follow-up with ophthalmology
-risk modification: tobacco cessation, UV protection, BP and lipid control
-AREDs or AREDs2 for non-smokers
-vision aides

19
Q

management of wet (exudative or neovascular) macular degeneration

A

-referral and regular follow-up with ophthalmology
-intravitreous injections with VEGF inhibitors
-photodynamic therapy
-laser photocoagulation treatments
-risk modification: BP control
-AREDs or AREDs2 for non smokers
-vision aides

20
Q

glaucoma

A

-conditions that cause progressive damage to optic nerve resulting in vision loss
**may cause permanent peripheral and central vision loss
-primary open angle and primary angle closure are the most common forms
-most pts have increased intraocular pressure, but nerve damage can also occur with normal pressure

21
Q

glaucoma: risk factors

A

increasing age, family hx, tobacco use, HTN, nearsightedness, increased IOP

22
Q

glaucoma: management

A

-managed through regular visits with ophthalmology
-routine testing of visual acuity, measuring IOP, and visual fields testing
-medicated eye drops to lower IOP
-laser tx
-surgery–trabeculectomy which creates a shunt to allow drainage

23
Q

medicated eye drops to lower IOP

A

-prostaglandin analogs (ex: Latanoprost)
-beta blockers (ex: Timolol)
-combo products

24
Q

acute angle closure glaucoma

A

acute occlusion of the anterior chamber angle, preventing drainage of aqueous humor –> increased IOP and optic nerve damage

25
s/s of acute angle closure glaucoma
pts present with redness, EYE PAIN, vision loss, headache, halos
26
is acute angle closure glaucoma considered a vision emergency?
YES!!!!!! must be evaluated by ophthalmology within hours
27
short term tx of acute angle closure glaucoma
drops and systemic meds to decrease IOP. if unsuccessful--> iridotomy to reduce pressure (small hole in the iris to allow drainage of aqueous humor))
28
long term tx of acute angle closure glaucoma
eye drops to decrease IOP
29
open angle glaucoma
MOST COMMON TYPE -gradual decrease in IOP due to dysfunctional drainage--> peripheral and eventually central vision changes -commonly bilateral -DOES NOT CAUSE EYE PAIN
30
diabetic retinopathy
-disease of the vessels of the eyes related to the chronic effects of DM -as the A1c increases, the risk for diabetic retinopathy increases as the years go on
31
contributing factors of diabetic retinopathy
poor glycemic control, duration of dx, HTN, HLD, pregnancy
32
s/s diabetic retinopathy
-may be asymptomatic -vision loss or fluctuating vision -floaters or flashes of light -defects in visual fields -may present with sudden vision loss in proliferative diabetic retinopathy if hemorrhage occurs
33
evaluation of diabetic retinopathy
-diagnosed on fundal exam -in office technology for retinal scanning -exam findings: microaneurysms, dot blot hemorrhages, cotton wool spots
34
eval of non proliferative diabetic retinopathy
-mild, earlier stages -damaged blood vessels caused by hyperglycemia *microaneurysms *hemorrhages *blockages *dilation of larger vessels *macular edema -no new blood vessel growth
35
proliferative diabetic retinopathy
-more advanced -presence of new growth, abnormal blood vessels *abnormal vessels more likely to leak--increased risk of hemorrhage *increases development of scar tissue on retina *increased risk of retinal detachment *increased fluid leads to glaucoma *increased risk of damage to optic nerve -can lead to blindness!
36
management of diabetic retinopathy
prevention-- control of DM, HTN, and HLD early detection--screening eye exams; individuals with type 2 DM should have ophthalmologic exam at time of dx and annually
37
treatment of diabetic retinopathy
-continue to address contributing factors such as poor glycemic control -Fenofibrate can slow progression -Pan-retinal photocoagulation -limited evidence of tx with VEGF -intravitreal administration of corticosteroids, either by injection or implant, is another treatment option for macular edema
38
dry eye syndrome
characterized as abnormalities in the tear film; multifactorial disorder across lifespan
39
40
dry eye syndrome: patho
tear film relies on interactions from lacrimal glands and ducts, cornea, eyelids and meibomian glands; nourishes and lubricates ocular surface and provides protection
41
two categories of dry eye syndrome (though often a combo)
aqueos deficient: Sjogren's, hyposecretion evaporative dry eye: meibomian gland dysfunction, poor eyelid closure, insufficient blinking
42
dry eye syndrome: s/s
pts may self treat before seeking help may complain of: -dryness -foreign body sensation -burning or stinging -itchiness -ocular fatigue -blurriness relieved by blinking symptoms often worsened in context of extended periods of visual concentration and low humidity environments
43
eval of dry eye syndrome
-complete eye and neuro exam (which is often revealing) -also consider more complete PE (skin, joints, etc) to assess for systemic causes -fluorescein dye to assess for corneal abrasion -complete ROS -assess for symptoms of autoimmune conditions (lupus, RA) -review med hx (diuretics, anithistamines, TCAs may contribute to dry eyes) -specialized testing (through ophthalmology, such as Shirmer Test)
44
management of dry eye syndrome
-non pharm: avoid extended periods of visual concentration; avoid direct drying effect of AC or fan; lid hygiene -pharm: artificial tears 4-6x a day (avoid vasoconstrictors); consider fish oil, vitamin D; discontinue systemic meds that may be contributing (diuretics, TCAs, antihistamines); other tx managed by specialist: short course topical steroid, cyclosporine ophthalmic emulsion, low dose oral abx

week 1 PC 2 (3 decks)

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