Eye 2 Flashcards

1
Q

Thyroid Orbitopathy AKA Thyroid Eye Disease

General

A

Usually an immune-mediated disorder
most commonly presents in association with hyperthyroidism in Graves disease but sometimes seen in euthyroid or hypothyroid pts.
Orbitopathy may precede the actual thyroid disease
female-to-male ratio of 4:1 and a peak in the fourth to fifth decade
It is the most common cause of bilateral or unilateral proptosis
Bilateral involvement is the most frequent presentation
deposition of mucopolysaccharides, namely hyaluronic acid, within the extraocular muscles. Results in a classic imaging appearance of fusiform muscle enlargement with sparing of the muscular tendon

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2
Q

Uveitis

S/Sx and complications

A

Emergency inflammation of uveal tract (choroid, ciliary body, iris)
Can cause blindness

Painful, red, photophobia- these are less common when posterior uveitis but posterior is very uncommon anyway
Distorted/blurred vision

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3
Q

Uveitis

General

A

Sudden onset with no easy cause to explain symptoms
Usually acute and less than 3 months duration but can be recurrent or chronic
Can be unilateral or bilateral
Easy to confuse with glaucoma
Sometimes occurs in patients with adult RA/JRA, sarcoidosis, MS, syphilis, Lyme dz, CMV, HSV, TB, ankylosing spondylitis, and other inflammatory diseases
Sometimes can be drug induced (especially with certain antibiotics and antivirals)

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4
Q

Uveitis

types

A
  1. Anterior: anterior chamber structures
  2. Posterior: retina, choroid
  3. Intermediate= vitreous body only;
    4.Panuveitis= EVERYTHING
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5
Q

Uveitis

PE

A

Physical Exam:
Small or constricted pupil
Pupil reacts poorly to light (iris is stuck to anterior lens capsule)
Iris sometimes difficult to see (because of corneal edema and protein in aqueous humor)
Redness
Photophobia
WBCs settled in the bottom of the anterior chamber
Sometimes decreased IOP

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6
Q

Uveitis

Slit lamp findings

A
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7
Q

Uveitis

Tx

A

Needs immediate referral to ophthalmology
Can be exacerbated if given drugs for treating glaucoma
Usually given steroids first but this can cause other diseases on the differential list to worsen

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8
Q

Uveitis

Complications

A

19% to 60% of patients have visual loss (depending on population)
Cyst-like formations on/in macula
Glaucoma can be caused by disease AND treatment
Cataracts can be caused by using steroids for treatment

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9
Q

Episcleritis

general and causes

A

Inflammation of the episclera (thin layer of vascular elastic tissue between the sclera and conjunctiva)
Pretty rare
Most common in 40s
Usually idiopathic but can happen with trauma, vasculitis and collagen-vascular diseases (marfan)

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10
Q

Episcleritis

PE

A

Red, vascular injection of conjunctiva with enlarged blood vessels beneath the conjunctiva
Pain is mild and only in area of inflammation
Can be diffuse or nodular inflammation

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11
Q

Episcleritis

Tx

A

Refer to ophthalmology
Warm compresses
Steroids (topical)
NSAID drops if worried about glaucoma
Oral NSAIDs

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12
Q
A
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13
Q

Nystagmus

General

A

Involuntary rhythmic eye motion/oscillation
Results from dysfunction in vestibular system, brainstem, or cerebellum
MANY types, next few slides are only a few examples

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14
Q

Vestibular nystagmus

patho

A

Vestibular nystagmus results from dysfunction of the labyrinth (Ménière’s disease), vestibular nerve, or vestibular nucleus in the brainstem.

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15
Q

vestibular nystagmus

S/Sx

A

nausea and vertigo
Possibly associated tinnitus and hearing loss
*Sudden shifts in head position may provoke or exacerbate symptoms.

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16
Q

Jerk Nystagmus

general

A

This is characterized by a slow drift off the target, followed by a fast corrective movement. Jerk nystagmus can be downbeat, upbeat, horizontal (left or right), and torsional. Some patients will be oblivious to their nystagmus. Others will complain of blurred vision or a subjective to-and-fro movement of the environment (oscillopsia) corresponding to the nystagmus.

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17
Q

Up/Downbeat nystagmus

General

A

Downbeat nystagmus results from lesions near the craniocervical junction (Chiari malformation, basilar invagination). It also has been reported in brainstem or cerebellar stroke, lithium or anticonvulsant intoxication, alcoholism, and multiple sclerosis.

Upbeat nystagmus is associated with damage to the pontine tegmentum from stroke, demyelination, or tumor.

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18
Q

Gaze evoked nystagmus

general

A

When the eyes are held eccentrically in the orbits, they have a natural tendency to drift back to primary position. The subject compensates by making a correction to maintain the deviated eye position. Many normal patients have mild gaze-evoked nystagmus. Exaggerated gaze-evoked nystagmus can be induced by drugs (sedatives, anticonvulsants, alcohol); muscle paresis; myasthenia gravis; demyelinating disease; and cerebellopontine angle, brainstem, and cerebellar lesions.

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19
Q

Strabismus

general

A

visual axes of the eyes are not aligned
misalignment may be constant or intermittent, and it may vary depending on the gaze direction
2% of population
Most common in childhood

caused by problems with eye muscles, the nerves that transmit information to the muscles, or the control center in the brain that directs eye movements

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20
Q

strabismus

RF

A

Risk factors for developing strabismus include:
Family history of strabismus.
Refractive error. People who have a significant amount of uncorrected farsightedness (hyperopia) may develop strabismus because of the additional eye focusing they must do to keep objects clear.
Medical conditions. Down syndrome, cerebral palsy & those who have suffered a stroke or head injury are at a higher risk

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21
Q

Strabismus

Emergent causes

A

Emergent causes can be orbital fractures, cellulitis, tumors (primary or metastatic), meningitis, or elevated IOP

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22
Q

Strabismus

A
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23
Q

Strabismus

S/Sx

A

Associated with diplopia, suppression, amblyopia - related to whether strabismus is present during development of visual system, which occurs up to age 7/8.

24
Q

Diplopia

general

A

Each fovea receives a different image.Diplopiaoccurs when the image of the object falls on fovea of the fixing eye and the object is localized straight ahead, and the same image falls on an extrafoveal retinal area in the deviating eye. The object is perceived to be in two places.

25
Q

Strabismus

Suppression

A

Common sensory adaptation in childhood strabismus - diminished sensitivity within visual field of the deviating eye under binocular viewing in order to avoid diplopia.

26
Q

strabismus

A
27
Q

strabismus

Accommodative esotropia

A

due to uncorrected farsightedness (hyperopia) which causes the eyes to turn inward.
Symptoms include seeing double, closing or covering one eye when doing close work, and tilting or turning the head.

28
Q

Strabismus

Intermittent exotropia
General/Sx

A

may develop when a person cannot coordinate both eyes together.

People with intermittent exotropia may experience headaches, difficulty reading and eye strain.

They also may close one eye when viewing at distance or in bright sunlight.

29
Q
A
30
Q

Strabismus

Clinical Diagnosis

A

Tests will be done to determine how much the eyes are out of alignment.

Corneal light reflex
Cover/uncover test
Retinal exam
Standard ophthalmic exam
Visual acuity

31
Q

Emergent Strabismus

A

If you suspect an emergent reason for strabismus (such as elevated IOP):
Orbital CT
Ocular infiltrative process
Tumors
Abscess
Cellulitis
Brain MRI
Evaluate CN roots and brainstem

32
Q

Strabismus

Tx

3

A

Congenital strabismus may spontaneously resolve in infancy as the extraocular muscles strengthen

Prism lenses: These special lenses have a prescription for prism power in them. The prisms alter the light entering the eye and reduce how much turning the eye must do to view objects. Sometimes the prisms can eliminate the eye turning.

Vision therapy: Your optometrist might prescribe a structured program of visual activities to improve eye coordination and eye focusing. Vision therapy trains the eyes and brain to work together more effectively. These eye exercises can help problems with eye movement, eye focusing and eye teaming and reinforce the eye-brain connection. Treatment can occur in your optometrist’s office as well as at home.

Eye muscle surgery: Surgery can change the length or position of the muscles around the eye so they appear straight. Often, people who have eye muscle surgery will also need vision therapy to improve eye coordination and to keep the eyes from becoming misaligned again.

33
Q

Amblyopia

A
34
Q

Amblyopia

patho

A

“lazy eye”
Amblyopia is the lack of development of clear vision in one or both eyes for reasons other than an eye health problem that cannot be improved with glasses alone.
The brain cannot effectively combine the two images and it suppresses, or “turns off,” one of them. The constant suppression of an image from one eye can lead to the development of amblyopia in that eye.
In cases where the images of both eyes are affected, the brain never develops the ability to see clearly with both of the eyes.

35
Q

Amblyopia

general

A

“lazy eye”
Occurs at a young age from disuse when an eye doesn’t see well.
Child’s visual nervous system is still developing until age 7/8. If during this developmental period, one eye has poorer vision, the “brain wiring” for that eye does not form as strongly as the better eye.

36
Q

Amblyopia

causes

A

Causes: early strabismus, early myopia or presbyopia,or visual problems such as congenital cataract.

37
Q

Amblyopia

Ocular Misalignment

A

Definition: Ocular Misalignment

May have a normal variant of misalignment that will improve without any intervention by 3-4 months. This improvement will occur as strength of the extraocular muscles improve.

38
Q

Amblyopia

Tx

A

Occlusion/patching is the gold standard
Patching the good eye closed, the lazy eye is forced to work and reform its wiring
Better eye is covered with a patch for 2 - 14 hours daily to stimulate the amblyopic eye.
Occlusion treatment is continued as long as visual acuity improves.
If treatment is started early enough, substantial improvement or complete normalization of visual acuity can be achieved.
Child peeking around a patch or inadequate enforcement of therapy by the parents may limit results.
There is no way to fix it in adulthood since brain wiring has already formed

In conjunction with patching and/or prescribing glasses,vision therapyshould be considered to develop eye teaming skills and improve functional vision to prevent regression.

39
Q

Strabismus versus Amblyopia

A

Strabismusis a problem with eye alignment, in which both eyes do not look at the same place at the same time.
(Often called crossed eyes)

Amblyopiais a problem with visual acuity, or eyesight. Even with prescription glasses, a person with amblyopia cannot see an image clearly in one or both eyes.
(Often called lazy eye)

40
Q

GLAUCOMA

General

A

Abnormal flow of fluid around lens that causes increases in pressure and then damages the optic nerve causing diminished vision and eye irritation

2 types are angle-closure and open-angle

Increased pressure in the eye, loss of blood flow to optic nerve. Nerve fibers begin to die.
Cup becomes larger in comparison to the optic disc, since support structure is not there.

41
Q
A
42
Q

Glaucoma

Chronic

A

Chronic angle-closure glaucoma and chronic open-angle glaucoma are usually asymptomatic.

In all forms of glaucoma, foveal acuity is spared until end-stage disease is reached. For these reasons, severe and irreversible damage can occur before either the patient or the physician recognizes the diagnosis.

Screening of patients for glaucoma by noting the cup-to-disc ratio on ophthalmoscopy and by measuring intraocular pressure is vital.

43
Q

Glaucoma

Epidemiology

A

One of leading causes of irreversible blindness in US
Prevalence increases with age
African Americans risk 3-4x > Caucasians
Family history increases risk
Chronic open is most common

44
Q

Open angle Glaucoma

General

A

In chronic open-angle glaucoma, primary or secondary, intraocular pressure is elevated due to reduced drainage of aqueous fluid through the trabecular meshwork.

45
Q

Open angle glaucoma

Tx goals

A

Tx: reduce the pressure by reducing the amount of fluid with medications or clear up the blockage with surgery so fluid can drain

46
Q

Open angle (chronic) glaucoma -

Essentials of Dx

A

No symptoms in early stages.
Insidious progressive bilateral loss of peripheral vision, resulting in tunnel vision but preserved visual acuities until advanced disease.
Pathologic cupping of optic discs.
Intraocular pressure usually elevated.

*evidence suggests loss of central vision can also be a symptom of glaucoma, so keep a broad differential in vision loss

47
Q

Angle-closure Glaucoma

predisposing factors and patho

A

The predisposing factors are shallow anterior chamber, which may be associated with farsightedness or short stature (or both); enlargement of the lens with age; and inheritance, such as among Inuits and Asians.

Closure of the angle is caused by pupillary dilation.

This is an unusual but frequently misdiagnosed cause of a red, painful eye. May also have headache.

Diagnosis is made by measuring IOP during an acute attack or by performing gonioscopy, a procedure that allows one to observe a narrow chamber angle with a mirrored contact lens.

48
Q

angle closure glaucoma

general
Complications

A

Untreated acute angle-closure glaucoma results in severe and permanent visual loss within 2–5 days after onset of symptoms. Affected patients need to be monitored for development of chronic glaucoma.

Patients with acute glaucoma usually seek treatment immediately because of extreme pain, redness, and blurred vision.

Typically, the blurred vision is associated with halos around lights.
Nausea and abdominal pain may occur.

49
Q

Angle-closure Glaucoma

PE

A

PE: The eye is red, the cornea cloudy, and the pupil moderately dilated and nonreactive to light.
PE: Intraocular pressure is usually over 50 mm Hg, producing a hard eye on palpation.

50
Q

angle closure glaucoma

Tx (3)

A

All patients with primary acute angle-closure should undergo prophylactic laser peripheral iridotomy to the unaffected eye

single 500-mg intravenous dose of acetazolamide,

pilocarpine is used to reverse the underlying angle closure

The definitive treatment is laser peripheral iridotomy or surgical peripheral iridectomy. Cataract surgery is a possible alternative

51
Q

glaucoma

Timolol

A

Blocks b1 and b2 adrenergic receptors

Interferes with cyclic adenosine monophosphate (cAMP, used to produce aqueous humor in the ciliary of the eye)
reduces aqueous humor
reduce IOP

Can absorb systemically – avoid use in patients with HF, AV block , bradycardia

Timolol (Timoptic)

52
Q

Topical Prostaglandin Agonists

MOA

glaucoma

A

MOA: selective agonists of a prostaglandin receptor
increase outflow of aqueous humor and decrease IOP
Latanoprost (Xalatan)
Bimatoprost (Lumigan)
Travoprost (Travatan Z)

53
Q

Screening Guidelines
American Academy of Ophthalmology

A

Everyone at age 40
Age 40-60 no risks: every 3-5 years
Age 40-60 risks: every 1-2 years
Age > 60: every 1-2 years

54
Q

Glaucoma

Tx open vs closed

A
55
Q

glaucoma

Alpha-2 Adrenergic Agonist

A

Mimic action of epinephrine on dilator muscle of iris
cause iris/pupil to dilate (mydriasis)
facilitates aqueous flow into trabecular meshwork
lowers IOP
Brimonidine (Alphagan)

56
Q

Glaucoma

Carbonic Anhydrase Inhibitors

A

Carbonic anhydrase inhibitors decrease aqueous humor volume
decrease IOP
Brinzolamide (Azopt)
Dorzolamide (Trusopt)
Acetazolamide (Diamox – oral)