Visual/Sensory Issues Flashcards
1
Q
Hordeolum (sty)
A
Infection of the oil-producing gland in the lid margin
Usually caused by bacteria Staph aureus
2
Q
Hordeolum (sty) sympotms
A
Area of the eye is red, swollen, tender
3
Q
Hordeolum (sty) treatment
A
Usually self-limiting; warm compresses 3-4 times a day; teach: do not squeeze or pop the sty bc that can spread the infection
4
Q
Conjunctivitis (pink eye)
A
Infection or inflammation of the conjunctiva
5
Q
Conjunctivitis etiology
A
Bacterial, viral, chlamydia, irritants (allergies)
6
Q
Bacterial conjunctivitis treatment
A
Usually self-limiting; antibiotic drops can shorten the course
7
Q
Viral conjunctivitis treatment
A
Topical steroids provide temporary relief for itching; antivirals are ineffective
BUT viral keratitis (herpes) treat with antiviral eye drops
8
Q
Chlamydia conjunctivitis treatment
A
PO antibiotics; however, some infections are resistant
9
Q
Allergic conjunctivitis treatment
A
Artificial tears, topical antihistamines, steroids
10
Q
Keratitis
A
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
11
Q
Keratitis-bacteria
A
Contact lens wearers higher risk
Treat with antibiotics (topical, injection, IV)
12
Q
Keratitis-amoeba
A
Caused by the contaminated contact lens
Treat with antifungal drops (often resistant)
13
Q
Keratitis-viral
A
Caused by herpes virus
Treat with antiviral eye drops
14
Q
Keratitis complication
A
Corneal ulcer
15
Q
Corneal ulcer
A
Extremely painful
Constant feeling of something in your eye
Photophobia, discharge, redness
If untreated can lead to blindness
16
Q
Keratoconjunctivitis sicca
A
Dry eye disorder
17
Q
Dry eye disorder etiology
A
Aging, Sjogren’s syndrome (SLE), other systemic diseases
18
Q
Sjogren’s syndrome (SLE)
A
Body’s immune system attacks its own healthy cells that produce saliva and tears
19
Q
Dry eye disorder complaint
A
“Sand in my eye”
20
Q
Dry eye disorder treatment
A
May need artificial tears
Cyclosporine eye drops can also be helpful
21
Q
Cataracts
A
Cloudy lens
Gradual onset of PAINLESS blurry vision
If left untreated, may result in blindness
22
Q
Cataracts treatment
A
Laser surgery
No medications
23
Q
Cataract risk factors
A
Older age Eye trauma Congenital risk Diabetes Corticosteroid use Smoking/ ETOH consumption
24
Q
Cataract symptoms
A
PAINLESS Uni- OR bilateral vision changes Blurry vision Halo around lights Altered color perceptions Glare issues at night Decreased accommodation
25
Cataract mechanism
Blocks some light from passing through the lens and scatters the light, preventing crisp focus on the retina
26
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
27
Proliferative DR
Advanced DR
| All symptoms of NPDR + new blood vessels are fragile and leaky
28
Proliferative DR characteristics
Growth of abnormal blood vessels
29
Nonproliferative DR characteristics
Aneurysm, hard exudate, hemorrhage
30
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.
31
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.
32
Hypertensive retinopathy etiology
Untreated high blood pressure creates BLOCKAGES in retinal blood vessels
33
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
34
Detached retina
Retina has a tear or leak --> vitreous humor flows behind the retina --> rapid, progressive detachment from the choroid
35
Detached retina
Usually spontaneous
36
Detached retina risks
Myopia (nearsightedness; close clear/far blurry)
Age >40
Traumas to the head
Eye tumors
Complication or history of cataract surgery
37
Detached retina symptoms
```
SUDDEN, unilateral vision loss
Painless
Floaters
Flashes of light
“Scene coming in”
```
38
Macular degeneration
Most common cause of irreversible vision loss in people > 60 in the US
39
Macular degeneration etiology
Retinal aging
40
Macula
Area near the center of the retina where cones are; cones: color vision, visual acuity
41
Dry macular degeneration
```
Yellow deposits (drusen) in the retinal pigment epithelium
Most common (90% of cases)
```
DRy DRusen
42
Dry macular degeneration
Non-exudative
43
Wet macular degeneration
Growth of new, leaky blood vessels in an abnormal location of the retina
New hemorrhages
Less common (10%)
44
Wet macular degeneration
Exudative
45
Macular degeneration risk factors
Family history, genetics, UV light, hyperopia (farsightedness), smoking, light-colored eyes
46
Macular degeneration prevention
Dark green, leafy vegetables have protective properties
47
Macular degeneration symptoms
```
Asymptomatic in early stages
Blurred, darkened vision
Blind spots (scotomas)
Distorted vision (metamorphopsia)
Vision does not improve
```
48
Macular degeneration treatment
Treatment is limited
| One option: medications injected into the eye
49
Glaucoma
Elevated intraocular pressure (IOP) with vision changes OR optic nerve damage
50
Glaucoma
Chronic condition
51
Glaucoma
Usually involves bilateral eyes
52
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
53
Open-angle glaucoma patho
Blockage of the trabecular meshwork slows drainage of the aqueous humor, which increases IOP
54
Open-angle glaucoma risk factors
```
Elevated IOP
Older age
Race: African-Americans 3-4x higher risk
Family history
Myopia
Diabetes
HTN
Migraines
```
55
Open-angle glaucoma symptoms
```
Initially asymptomatic
Progressive loss of sight
Vague eye pain
Halos around lights
Tunnel vision
```
56
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
57
Closed-angle glaucoma patho
Abnormal angle between the iris and later cornea
| Outflow is blocked when the pupil is DILATED
58
Closed-angle glaucoma AKA
Acute angle-closure glaucoma (AACG)
| Narrow-angle glaucoma
59
Closed-angle vs. open-angle glaucoma
Closed-angle is much less common
60
Closed-angle glaucoma risk factors
```
Asian American ethnicity
Females
Hyperopia
Family history
Older age
```
61
Acute angle-closure glaucoma
Medical emergency; outcome based on onset time to treatment
62
Acute angle-closure glaucoma
Triggered by anticholinergic drugs
63
Anticholinergics
Drugs that block the action of acetylcholine
| Acetylcholine stimulates the PNS (rest/digest)
64
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
```
65
Glaucoma and blindness
Open-angle glaucoma long-term leads to blindness
| Untreated acute angle-closure can lead to blindness
66
Glaucoma and blindness
Due to the increased IOP --> more pressure on inner eye structures --> decreased blood flow to optic nerve --> nerve fiber death --> blindness
67
Open-angle glaucoma pharm
Drugs that DECREASE aqueous humor production AND/OR INCREASE aqueous humor drainage
68
Acute angle-closure glaucoma pharm
Surgery
69
timolol (non-selective beta blocker)
DECREASES aqueuous humor production
70
betaxolol (selective beta blocker)
DECREASES aqueuous humor production
71
brimonidine (alpha-2 adrenergic agonist)
DECREASES aqueous humor production
| MAYBE INCREASES aqueous humor drainage
72
latanoprost (prostaglandin analogs)
INCREASES aqueous humor drainage
73
Aqueous humor
Clear fluid filling the space in the front of the eyeball between the lens and the cornea.
74
Administering optical topical agents
Use nasolacrimal pressure with instillation
Helps prevent systemic effects/ensures localization
Hold pressure for 2 minutes
75
timolol
non-selective beta blocker
76
betaxolol
beta-1 selective blocker
77
timolol, betaxolol MOA (beta-blockers)
Block SNS stimulation of beta receptors
DECREASES aqueuous humor production
78
timolol, betaxolol indications
Open-angle glaucoma maintenance treatment
| If acute-angle closure– need drops ASAP and other interventions
79
timolol, betaxolol (beta-blockers) SE
Transient burning & discomfort
| If allowed to go systemic- can have systemic effects
80
timolol, betaxolol (beta-blockers) contraindications
timolol, bc nonselective, contraindicated for patients with asthma, COPD, bradycardia, etc.
81
timolol, betaxolol (beta-blockers) patient teaching
Must take– otherwise will progress to blindness
| Apply nasolacrimal pressure with instillation
82
latanoprost (Xalatan) class
Prostaglandin analogs
83
latanoprost (Xalatan) MOA
INCREASES outflow drainage of aqueous humor
| INCREASES aqueous humor drainage
84
latanoprost (Xalatan) indications
Open-angle glaucoma
| Ocular hypertension
85
latanoprost (Xalatan) SE
Well-tolerated
86
brimonidine (Alphagan) class
Alpha-adrenergic agonist
87
brimonidine (Alphagan) MOA
DECREASES aqueous humor production
| MAYBE INCREASES aqueous humor drainage/outflow
88
brimonidine (Alphagan) indication
Open-angle glaucoma
| Increased intraocular pressure
89
brimonidine (Alphagan) SE
```
Burning/stinging
Dry mouth
Fatigue
H/A
Blurred vision
Hypotension
```
90
dorzolamide (Trusopt) class
Carbonic anhydrase inhibitor
91
dorzolamide + timolol
Cosopt
92
dorzolamide (Trusopt) indication
Second-line treatment
Open-angle glaucoma
Increased IOP
93
dorzolamide (Trusopt) MOA
DECREASES production of aqueous humor
94
dorzolamide (Trusopt) SE
Stinging
Bitter taste
Allergic reactions (conjunctiva or lid reactions)
95
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
96
Meniere's Disease symptoms
Recurring episodes of vertigo [usually with nausea & vomiting], hearing loss, ringing in the ears (tinnitus), and feeling of fullness
97
Meniere's Disease treatment
Symptomatic treatment
| Some pharm treatment but none widely available; no meds affecting the endolymph-just helps the vertigo
98
Meniere's Disease diet changes
Disease can be triggered by high salt, caffeine, alcohol, MSG, stress, allergies
Most patients require sodium restriction
