Chapter 19: Eyes Flashcards
Extraocular Muscles
Oculomotor (CN III)
Trochlear (CN IV)
Abducens (CN VI)
Vitamin A
Nerve impulses and retinal function
Production of rods and cones
Need for low-light and moisture
Vitamin A Deficiencies
Dry eyes
Nyctalopia (night blindness)
Foods high in Vitamin A
papaya, cantaloupe, squash, milk, sweet potatoes, dark leafy vegetables, carrots
Vitamin C and E
strong antioxidants that protect the eye against damage from free radicals (associated with macular degeneration and cataracts)
Vitamin C rich foods
oranges, spinach, strawberries, broccoli/cauliflower, tomatoes, lemons, blackberries
Vitamin E rich foods
nuts and seeds, sunflower seeds and oil, spinach/greens, peanuts, pumpkin, red bell pepper
Beta-Carotene
precursor of Vitamin A
50% of Vitamin A comes from conversion of beta-cartotene
Foods rich in beta-carotene
yellow, green, and orange leafy fruits and vegetables
carrots, spinach, lettuce, tomatoes, sweet potatoes, broccoli, cantaloupe, squash
Lutein
protects eye from harm UV rays
may improve dim light vision and prevent glare
may hold off macular degeneration
Foods rich in lutein
kale, spinach, broccoli, corn, lettuce, peas, zucchini, tangerines, carrots, celery, tomatoes, oranges
Ptosis
eyelid droop - weakness of levator muscle
can be muscular or r/t CN III damage
Entropion
turning IN of the lid margins
can normally occur with aging
can cause corneal irritation, abrasion or infection
Ectropion
turning OUT of the lid margin
most frequent eyelid condition
usually d/t CN VII weakness
see tearing
Posterior Blepharitis
inflammation of the meibomian glands
see frothy, oily tears
Hordeolum (Sty)
infection of the sebaceous glands of the eye lid
internal - obstruction of meibomian gland
external - obstruction of hair follicle
painful
Chalazion
Meibomian cyst
small, firm, nontender nodules on upper and lower lid
may need to be surgically removed
Dacryocystitis
obstruction of the lacrimal duct that causes the nasolacrimal sac to be inflamed
pain, swelling, redness, purulent drainage
Dacryoadenitis
inflammation of the lacrimal gland
pain, redness, swelling to upper outer third of eye
Seen in Mumps, Measles, and Mono
Enopthalamos
“sunken” posterior displacement of eye
most often caused by atrophy of orbital fat
Exopthalamos
“bulging” anterior displacement of eye
seen in hyperthyroidism and Grave’s dx
Hypoglobus
inferior displacement of eye
seen in fractures of the orbit
Hyperglobus
superior displacement
seen also in fractures
Conjunctivitis
“pink eye” - injected conjunctiva (redness)
Allergic Conjunctivitis
IgE-mediated hypersensitivity
redness, itching, watery eyes
Bacterial Conjunctivitis
Hyperacute (N. gonorrhea) will threaten vision = purulent discharge
Acute (S. aureus, H. influenzae) eyes will be stuck together; foreign body sensation
Viral Conjunctivitis
usually self-limiting
caused by adenovirus and herpes simplex
watery drainage, photosensitivity
Keratitis
inflammation of the cornea
Bacterial Keratitis
can ulcerative (chlamydia, staph, strep) or nonulcerative (lupus, syphilis)
Herpes Simplex Keratitis
middle layer of cornea can become scarred leading to corneal blindness
80% from HSV1
neonates are exposed to HSV2
Varicella Zoster Opthalmicus
lies dormant and becomes activated at the ophthalmic division of the trigeminal nerve
treated with high dose antivirals
Arcus Senilis
bilateral benign corneal degeneration as people age, seen as thin grayish white arc around periphery of cornea
no vision changes
does not indicate hyperlipidemia
Uveitis
inflammation of the entire uveal tract (iris, choroid, and ciliary body)
can be bacterial, autoimmune, or malignant
Glaucoma
classified as an optic neuropathy vs disease of elevated IOP
can be primary or secondary
can be open-angle or angle-closure
Tonometer
measures IOP
normal IOP = 10 - 21
Primary Glaucoma
occurs w/o evidence of preexisting ocular or systemic disease
Secondary Glaucoma
results from inflammatory processes that affect the eye
Glaucomatous Cupping
optic nerve axons atrophy = optic disc pallor and increases depth of the optic cup
can result in transient or permanent vision loss
Open-Angle Glaucoma
gradual loss of peripheral vision
usually affects both eyes
usually occurs d/t abnormality of flow of aqueous humor in Canal of Schelmm
Risk Factors for Open-Angle Glaucoma
>40 years black myopia HTN, Type II DM, hyperthyroidism migraine HAs OSA first-degree family hx
Treatment for Open-Angle Glaucoma
topical medications to increase outflow of fluid Laser trabeculopathy (inner trabecular meshwork is burned to widen the Canal of Sclemm
Angle-Closure Glaucoma
Narrow-Angle Glaucoma
result of an inherited anatomic defect causing narrow angle of the anterior chamber d/t iris enlargement
Risk Factors for Narrow-Angle Glaucoma
Asian (preexisiting shallow anterior chambers) Older adults (lens thickened and iris becomes anteriorly displaced)
Acute Angle-Closure Glaucoma Attack
medical emergency
eye pressure rises quickly - often precipitated by pupillary dilation
Signs/Symptoms of Acute ACG Attack
sudden eye pain blurred, halos, iridescent vision tunnel vision unilateral HA pupil may be fixed symptoms subside with pupillary constriction
Treatment for Narrow-Angle Glaucoma
meds to reduce pressure
iridotomy (creates permanent opening between the anterior and posterior chambers)
Hyphema
blood that collects in the anterior chamber d/t blunt trauma or spontaneous hemorrhage
Hypopyon
purulent matter in the anterior chamber usually d/t iritis and inflammation of the chamber itself
Eye Refraction
measurement based on how much the lens of the eye has to bend light rays to process visuall stimuli
how power of eye glasses or contacts is calculated
Myopia
near-sightedness
objects focus IN FRONT of the retina
(convex)
Hyperopia
far-sightedness
objects focus BEHIND the retina
(concave)
Astigmatism
abnormally shaped cornea or lens blurry vision (near and/or far)
Presbyopia
far-sighted due to aging
lens thickens and becomes more rigid = difficulty focusing on near objects (changing shape of lens)
Miosis
pupillary constriction
improves clarity of vision for near objects
Mydriasis
pupillary dilation
improves the clarity of vision for far objects
Cycloplegia
paralysis of the ciliary muscles
loss of accomodation
Cataracts
clouding of the lens = interferes with the transmission of light
most common cause of age-related vision loss
an absent red reflex may be noticed
Traumatic Cataracts
caused by injury from a foreign body, blunt trauma to the eyes, or overexposure to UV radiation
Congenital Cataracts
present at birth
caused by genetics, toxins, viruses (rubella), or maternal diabetes
Senile Cataracts (Nuclear)
central opacity
Senile Cataracts (Peripheral Cortical)
white, wedge-like opacities that start in the periphery and work their way to the center of the lens in a spoke-like fashion
little effect on vision initially
Senile Cataracts (Subcapsular Cataracts)
opacities occur in front of the posterior capsule
associated with prolonged, steroid use, DM, obesity, or trauma
near vision is affected w/ inc sensitivity to glare
Color Blindness
inherited X-linked disorder of the cones (green, red, and blue vision) - photopigment missing or deficient
not considered a clinical disease
Ishihara cards
polychromatic pictures/figures used to screen for color blindness
Papilledema
edema of the optic papilla caused by increased IOP = collapse retinal artery/veins = back flow and inc capillary permeability
Causes of Papilledema
cerebral tumor
subdural hematoma
hydroecephalus
malignant HTN
Hypertensive Retinopathy
longstanding HTN = thickened arteriole walls
appear pale and more opaque (copper wiring)
MICH - microaneurysms, intraretinal hemorrhages (flame-like), hard exudates, cotton wool spots
optic disc swelling
Diabetic Retionopathy
most common cause of blindness
can be proliferative or non-proliferative
Nonproliferative Diabetic Retinopathy
background retinopathy
confined to the retina
see microaneurysms, cotton wool spots, exudates
macular edema = dec vision and sensation of glare
Proliferative Diabetic Retinopathy
more several retinal changes
characterized by the neovacularization and can result in retinal detachment
Retinal Detachment
Retina becomes separated from nerve tissues and blood supply
emergency that will result in permanent vision loss if untreated
Clinical Manifestations of Retinal Detachment
painless
sudden appearance of floaters/flashes of light
“curtain” across vision
altered red reflex
Exudative (Serous) Retinal Detachment
caused by accumulation of fluid in the subretinal space
HTN, neoplasm, inflammation
usually resolves well
Traction Retinal Detachment
detachment due to pulling force
scar, fibrous tissue, or inflammation
Rhegmatogenous Retinal Detachment
most common form
vitreous humor leaks through hole or tear, separating the receptors from their blood supplier (choroid) = vision loss
Macular Degeneration
degenerative changes in the central portion of the retina (macula)
age-related (AMD) most common cause of reduced vision worldwide
Risk Factors for Macular Degeneration
>50 years female caucasian smoking CVD poor nutrition genetics
Atrophic Macular Degeneration
“Dry Form”
Drusen (yellow fatty deposits) develop beneath the retina
slow onset with mild vision loss
no established treatment
Exudative Macular Degeneration
“Wet Form”
neovascularization occurs and vessels leak and bleed = edema, fibrosis and scarring
loss of central vision occurs
Treatment: photodynamic therapy, corticosteroids or VEGF
Amsler Grid
screening tool for macular degeneration
identify visual distortions
used with early diagnosis
Anopia
blindness in one eye
Hemianopia
half of the visual field in one eye is lost
can be homonymous (same side) or heteronymous (different)
Homonymous Quadrantic Defect
quarter of the visual field is lost
usually caused by a partial lesion of the optic tract
Bitemporal Anopia
loss of temporal vision
central (nasal) vision maintained
Amblyopia
decrease in visual acuity resulting from abnormal visual development in infancy or early childhood
