Senescence and dysfunction of the retinal pigment epithelium (RPE), accompanied by sub retinal drusen deposits, and occasional choroidal neovascularization
Vision loss due to dysfunction of photoreceptors (receive nutrients from choroid along w/ RPE)
2 types: dry and wet (exudative) AMD
Symptoms: blurry vision, mostly in central vision (central scotoma)
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3
Q
Dry AMD
A
90% of AMD cases
Drusen deposits accumulate btwn RPE and bruch’s membrane near macula
Atrophy of RPE results in visual loss (photoreceptor dysfunction), areas of atrophy result in coalescing “geographic atrophy” around macula
Rx: antioxidants, regular exams, stem cell Rx in the works
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4
Q
Wet AMD
A
10% of AMD cases
New abnormal vessels grow from choroidal circulation into subretinal space
These form choroidal neovascular membranes (CNVM)
Subretinal fluid accumulates and subretinal hemorrhage and scaring occurs
All lead to loss of photoreceptors and vision
Rx: anti-VEGF, lasers
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5
Q
Glaucoma
A
Increase in intraocular pressure (IOP) that eventually leads to damage to ganglion cell axons at the optic nerve head and resultant vision loss
Results from an obstruction of flow for the aqueous humor (usually around the canal of schlemm)
2 types: primary open angle (POAG) and acute closed angle (ACAG)
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6
Q
Primary open angle glaucoma (POAG)
A
Slow progression (chronic), asymptomatic until late stage
Due to blockage of schlemm or trabecular meshwork leading to inability to drain aqueous humor
Increase IOP, damages ganglion cells and vascular supply
Generally bilateral
Symptoms: visual field loss and blurry vision, halos around lights
Can also increase outflow by using cholinergics and prostaglandin analogs
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7
Q
Acute closed angle glaucoma (ACAG)
A
Acute and abrupt blockage of aqueous outflow
Shallow anterior chamber predisposes to this, since iris is in close proximity to cornea
Pupillary dilation can precipitate an attach because it increases tightness of contact btwn iris and lens
Fluid must flow btwn lens and iris, around iris, then btwn iris and cornea. A blockage anywhere in this path results in ACAG
Symptoms: nausea, vomiting, pain
Rx: cholinergics to constrict pupil, osmotic agents (glycerol, mannitol) to decrease IOP, laser iridectomy to increase outflow
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8
Q
Cataracts 1
A
Due to lens opacities that impede vision
Cortical degeneration: opacities that radiate around the periphery of the lens, caused by swelling and liquefaction of younger cortical fiber cells
Nuclear sclerosis: opacity of central area of lens often w/ lens discoloration, caused by deterioration of older lens fibers
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9
Q
Cataracts 2
A
May result from systemic diseases (diabetes) and are correlated w/ UVB exposure
Present w/ blurry vision and glare, double vision (monocular diplopia), near-sightedness (myopia), and second sight (need for reading glasses disappears due to myopia)
Management: extraction of lens and replacement when severe and affecting daily lives
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10
Q
Diabetic retinopathy (DR)
A
Diabetes affects retinal vasculature (specifically the venous side of retinal capillary beds), and is a venous occlusive disease
The resulting damage to retina leads to visual loss
2 types: proliferative and non-proliferatvie
Both are chronic diseases
Sx: blurry vision, dark floaters, visual field loss, poor night vision
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11
Q
Non-proliferative DR
A
Venous dilation accompanied by micro aneurysms in venous capillaries (+ exudate)
Microaneurysms result in dot-blot appearance of retina as veins are deep in the retina (AV nicking)
Cotton wool spots: patches of lost retina
Macular edema (loss of central vision, lost vision can be in patches)
Rx: controlling diabetes/HTN, lasers
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12
Q
Proliferative DR
A
Areas of retinal neovascularization which extend into vitreous and bleed
Vitreous scaffolds areas of neovascularization
Accompanied by exudates
Retinal detachment may occur
Also may get recurrent vitreous hemorrhage
Rx: anti-VEGF and lasers, along w/ controlling diabetes