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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
Q

s/s of acute angle closure glaucoma

A

pts present with redness, EYE PAIN, vision loss, headache, halos

26
Q

is acute angle closure glaucoma considered a vision emergency?

A

YES!!!!!! must be evaluated by ophthalmology within hours

27
Q

short term tx of acute angle closure glaucoma

A

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
Q

long term tx of acute angle closure glaucoma

A

eye drops to decrease IOP

29
Q

open angle glaucoma

A

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
Q

diabetic retinopathy

A

-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
Q

contributing factors of diabetic retinopathy

A

poor glycemic control, duration of dx, HTN, HLD, pregnancy

32
Q

s/s diabetic retinopathy

A

-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
Q

evaluation of diabetic retinopathy

A

-diagnosed on fundal exam
-in office technology for retinal scanning
-exam findings: microaneurysms, dot blot hemorrhages, cotton wool spots

34
Q

eval of non proliferative diabetic retinopathy

A

-mild, earlier stages
-damaged blood vessels caused by hyperglycemia
*microaneurysms
*hemorrhages
*blockages
*dilation of larger vessels
*macular edema
-no new blood vessel growth

35
Q

proliferative diabetic retinopathy

A

-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
Q

management of diabetic retinopathy

A

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
Q

treatment of diabetic retinopathy

A

-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
Q

dry eye syndrome

A

characterized as abnormalities in the tear film; multifactorial disorder across lifespan

39
Q
A
40
Q

dry eye syndrome: patho

A

tear film relies on interactions from lacrimal glands and ducts, cornea, eyelids and meibomian glands; nourishes and lubricates ocular surface and provides protection

41
Q

two categories of dry eye syndrome (though often a combo)

A

aqueos deficient: Sjogren’s, hyposecretion
evaporative dry eye: meibomian gland dysfunction, poor eyelid closure, insufficient blinking

42
Q

dry eye syndrome: s/s

A

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
Q

eval of dry eye syndrome

A

-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
Q

management of dry eye syndrome

A

-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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