Visual/Sensory Issues Flashcards
Hordeolum (sty)
Infection of the oil-producing gland in the lid margin
Usually caused by bacteria Staph aureus
Hordeolum (sty) sympotms
Area of the eye is red, swollen, tender
Hordeolum (sty) treatment
Usually self-limiting; warm compresses 3-4 times a day; teach: do not squeeze or pop the sty bc that can spread the infection
Conjunctivitis (pink eye)
Infection or inflammation of the conjunctiva
Conjunctivitis etiology
Bacterial, viral, chlamydia, irritants (allergies)
Bacterial conjunctivitis treatment
Usually self-limiting; antibiotic drops can shorten the course
Viral conjunctivitis treatment
Topical steroids provide temporary relief for itching; antivirals are ineffective
BUT viral keratitis (herpes) treat with antiviral eye drops
Chlamydia conjunctivitis treatment
PO antibiotics; however, some infections are resistant
Allergic conjunctivitis treatment
Artificial tears, topical antihistamines, steroids
Keratitis
Inflammation/infection of the cornea — the clear, dome-shaped tissue on the front of your eye that covers the pupil and iris; may also involve the conjunctiva
Keratitis-bacteria
Contact lens wearers higher risk
Treat with antibiotics (topical, injection, IV)
Keratitis-amoeba
Caused by the contaminated contact lens
Treat with antifungal drops (often resistant)
Keratitis-viral
Caused by herpes virus
Treat with antiviral eye drops
Keratitis complication
Corneal ulcer
Corneal ulcer
Extremely painful
Constant feeling of something in your eye
Photophobia, discharge, redness
If untreated can lead to blindness
Keratoconjunctivitis sicca
Dry eye disorder
Dry eye disorder etiology
Aging, Sjogren’s syndrome (SLE), other systemic diseases
Sjogren’s syndrome (SLE)
Body’s immune system attacks its own healthy cells that produce saliva and tears
Dry eye disorder complaint
“Sand in my eye”
Dry eye disorder treatment
May need artificial tears
Cyclosporine eye drops can also be helpful
Cataracts
Cloudy lens
Gradual onset of PAINLESS blurry vision
If left untreated, may result in blindness
Cataracts treatment
Laser surgery
No medications
Cataract risk factors
Older age Eye trauma Congenital risk Diabetes Corticosteroid use Smoking/ ETOH consumption
Cataract symptoms
PAINLESS Uni- OR bilateral vision changes Blurry vision Halo around lights Altered color perceptions Glare issues at night Decreased accommodation
Cataract mechanism
Blocks some light from passing through the lens and scatters the light, preventing crisp focus on the retina
Nonproliferative DR
Capillary microaneurysms, retinal swelling, hard exudate
Macular edema: plasma leaks from macular blood vessels (common complication of DR)
Capillaries rupture, leading to “dot or blot” hemorrhaging
Proliferative DR
Advanced DR
All symptoms of NPDR + new blood vessels are fragile and leaky
Proliferative DR characteristics
Growth of abnormal blood vessels
Nonproliferative DR characteristics
Aneurysm, hard exudate, hemorrhage
NPDR-don’t memorize/for context
Hyperglycemia results in damage to retinal capillaries. This weakens the capillary walls and results in small outpouchings of the vessel lumens, known as microaneurysms. Microaneurysms eventually rupture to form hemorrhages deep within the retina, confined by the internal limiting membrane (ILM). Because of their dot-like appearance, they are called “dot-and-blot” hemorrhages. The weakened vessels also become leaky, causing fluid to seep into the retina. Fluid deposition under the macula, or macular edema, interferes with the macula’s normal function and is a common cause of vision loss in those with DR.
PDR-don’t memorize/for context
As mentioned earlier, the retina has a high metabolic requirement, so with continued ischemia, retinal cells respond by releasing angiogenic signals such as vascular endothelial growth factor (VEGF). Angiogenic factors, like VEGF, stimulate growth of new retinal blood vessels to bypass the damaged vessels. This is referred to as neovascularization. In PDR, the fibrovascular proliferation extends beyond the ILM. This may sound like a good idea, but the new vessels are leaky, fragile, and often misdirected. They may even grow off the retina and into the vitreous.
Hypertensive retinopathy etiology
Untreated high blood pressure creates BLOCKAGES in retinal blood vessels
Hypertensive retinopathy symptoms
Initially: no vision changes
Sustained: severe HTN can cause sudden visual loss related to swelling of the optic disc/ nerve
Normal vision is restored with the treatment of the HTN
Detached retina
Retina has a tear or leak –> vitreous humor flows behind the retina –> rapid, progressive detachment from the choroid
Detached retina
Usually spontaneous
Detached retina risks
Myopia (nearsightedness; close clear/far blurry)
Age >40
Traumas to the head
Eye tumors
Complication or history of cataract surgery
Detached retina symptoms
SUDDEN, unilateral vision loss Painless Floaters Flashes of light “Scene coming in”
Macular degeneration
Most common cause of irreversible vision loss in people > 60 in the US
Macular degeneration etiology
Retinal aging
Macula
Area near the center of the retina where cones are; cones: color vision, visual acuity
Dry macular degeneration
Yellow deposits (drusen) in the retinal pigment epithelium Most common (90% of cases)
DRy DRusen
Dry macular degeneration
Non-exudative
Wet macular degeneration
Growth of new, leaky blood vessels in an abnormal location of the retina
New hemorrhages
Less common (10%)
Wet macular degeneration
Exudative
Macular degeneration risk factors
Family history, genetics, UV light, hyperopia (farsightedness), smoking, light-colored eyes
Macular degeneration prevention
Dark green, leafy vegetables have protective properties
Macular degeneration symptoms
Asymptomatic in early stages Blurred, darkened vision Blind spots (scotomas) Distorted vision (metamorphopsia) Vision does not improve
Macular degeneration treatment
Treatment is limited
One option: medications injected into the eye
Glaucoma
Elevated intraocular pressure (IOP) with vision changes OR optic nerve damage
Glaucoma
Chronic condition
Glaucoma
Usually involves bilateral eyes
Open-angle glaucoma patho
Outflow obstruction of aqueous humor at the trabecular meshwork or canal of Schlemm even with adequate space for drainage
Reduced drainage of aqueous humor into canal of Schlemm
Imbalance between inflow and outflow
Results in increased IOP –> damage to optic nerve –> vision problems
Open-angle glaucoma patho
Blockage of the trabecular meshwork slows drainage of the aqueous humor, which increases IOP
Open-angle glaucoma risk factors
Elevated IOP Older age Race: African-Americans 3-4x higher risk Family history Myopia Diabetes HTN Migraines
Open-angle glaucoma symptoms
Initially asymptomatic Progressive loss of sight Vague eye pain Halos around lights Tunnel vision
Closed-angle glaucoma patho
Displacement of the iris toward the cornea with obstruction of the trabecular meshwork and obstruction of outflow of aqueous humor from the anterior chamber
Closed-angle glaucoma patho
Abnormal angle between the iris and later cornea
Outflow is blocked when the pupil is DILATED
Closed-angle glaucoma AKA
Acute angle-closure glaucoma (AACG)
Narrow-angle glaucoma
Closed-angle vs. open-angle glaucoma
Closed-angle is much less common
Closed-angle glaucoma risk factors
Asian American ethnicity Females Hyperopia Family history Older age
Acute angle-closure glaucoma
Medical emergency; outcome based on onset time to treatment
Acute angle-closure glaucoma
Triggered by anticholinergic drugs
Anticholinergics
Drugs that block the action of acetylcholine
Acetylcholine stimulates the PNS (rest/digest)
Acute closed-angle glaucoma: clinical manifestations
Typically UNILATERAL (but other eye is at risk) SEVERE eye pain Nausea and vomiting Blurry vision Halos Reddened eyes Dilated pupil– non-reactive to light Cloudy cornea
Glaucoma and blindness
Open-angle glaucoma long-term leads to blindness
Untreated acute angle-closure can lead to blindness
Glaucoma and blindness
Due to the increased IOP –> more pressure on inner eye structures –> decreased blood flow to optic nerve –> nerve fiber death –> blindness
Open-angle glaucoma pharm
Drugs that DECREASE aqueous humor production AND/OR INCREASE aqueous humor drainage
Acute angle-closure glaucoma pharm
Surgery
timolol (non-selective beta blocker)
DECREASES aqueuous humor production
betaxolol (selective beta blocker)
DECREASES aqueuous humor production
brimonidine (alpha-2 adrenergic agonist)
DECREASES aqueous humor production
MAYBE INCREASES aqueous humor drainage
latanoprost (prostaglandin analogs)
INCREASES aqueous humor drainage
Aqueous humor
Clear fluid filling the space in the front of the eyeball between the lens and the cornea.
Administering optical topical agents
Use nasolacrimal pressure with instillation
Helps prevent systemic effects/ensures localization
Hold pressure for 2 minutes
timolol
non-selective beta blocker
betaxolol
beta-1 selective blocker
timolol, betaxolol MOA (beta-blockers)
Block SNS stimulation of beta receptors
DECREASES aqueuous humor production
timolol, betaxolol indications
Open-angle glaucoma maintenance treatment
If acute-angle closure– need drops ASAP and other interventions
timolol, betaxolol (beta-blockers) SE
Transient burning & discomfort
If allowed to go systemic- can have systemic effects
timolol, betaxolol (beta-blockers) contraindications
timolol, bc nonselective, contraindicated for patients with asthma, COPD, bradycardia, etc.
timolol, betaxolol (beta-blockers) patient teaching
Must take– otherwise will progress to blindness
Apply nasolacrimal pressure with instillation
latanoprost (Xalatan) class
Prostaglandin analogs
latanoprost (Xalatan) MOA
INCREASES outflow drainage of aqueous humor
INCREASES aqueous humor drainage
latanoprost (Xalatan) indications
Open-angle glaucoma
Ocular hypertension
latanoprost (Xalatan) SE
Well-tolerated
brimonidine (Alphagan) class
Alpha-adrenergic agonist
brimonidine (Alphagan) MOA
DECREASES aqueous humor production
MAYBE INCREASES aqueous humor drainage/outflow
brimonidine (Alphagan) indication
Open-angle glaucoma
Increased intraocular pressure
brimonidine (Alphagan) SE
Burning/stinging Dry mouth Fatigue H/A Blurred vision Hypotension
dorzolamide (Trusopt) class
Carbonic anhydrase inhibitor
dorzolamide + timolol
Cosopt
dorzolamide (Trusopt) indication
Second-line treatment
Open-angle glaucoma
Increased IOP
dorzolamide (Trusopt) MOA
DECREASES production of aqueous humor
dorzolamide (Trusopt) SE
Stinging
Bitter taste
Allergic reactions (conjunctiva or lid reactions)
Meniere’s Disease
Endolymphatic hydrops
Episodic disorder of the middle ear
Can occur at any age; more common between 20-40
Can be unilateral or bilateral
Endolymph: fluid that fills the hearing/balance structures of inner ear
Fluctuation in endolymph –> distension –> disruption of hearing and balance
Excessive endolymph and pressures in the membranes disrupt vestibular (balance) and hearing function
Meniere’s Disease symptoms
Recurring episodes of vertigo [usually with nausea & vomiting], hearing loss, ringing in the ears (tinnitus), and feeling of fullness
Meniere’s Disease treatment
Symptomatic treatment
Some pharm treatment but none widely available; no meds affecting the endolymph-just helps the vertigo
Meniere’s Disease diet changes
Disease can be triggered by high salt, caffeine, alcohol, MSG, stress, allergies
Most patients require sodium restriction
