Exam SG Flashcards

(216 cards)

1
Q

Categories of systemic diseases that affect eye

A
  • Mnemonic = PD Vitamin C
  • Psychiatric/functional, Drugs/toxins, Vascular, Infectious, Traumatic, Autoimmune/allergy, Metabolic/endocrine, Idiopathic/iatrogenic, Neoplastic, Congenital
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2
Q

Muscle and CN that closes eye

A
  • Orbicularis oculi – CN VII. Mnemonic = 7 is like a hook that closes the eye
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3
Q

Muscle and CN that opens the eye

A
  • Levator palpebrae superioris – CN III. Mnemonic = III looks like columns (in Greek times) that holds the eyes open
  • Note: Muller’s muscle (aka superior tarsal muscle) also helps. This muscle innervated by SNS.
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4
Q

Review anatomy of eye

A

Review anatomy of eye

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5
Q

T/F. Damage to corneal epithelium generates scar.

A
  • False. Damage to layers beneath leaves scar. Epithelial damage regenerates.
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6
Q

What produces and secretes aqueous humor in eye? To what structure does this drain?

A
  • Ciliary body

- Drains to trabecular meshwork (Schlemm’s canal)

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7
Q

Blood supply to the retina

A
  • Inner 1/3rd from central retinal artery

- Outer 2/3rd from choroid (which gets its blood supply from posterior ciliary arteries off ophthalmic artery off ICA)

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8
Q

Define scotoma

A
  • Area of reduced or absent vision. Aka a blind spot.
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9
Q

Define hemianopia

A
  • Loss of ½ of visual field

- Bitemporal, binasal or left/right homonymous hemianopia

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10
Q

Define homonymous hemianopia

A
  • Left or right of visual fields, but the same in both eyes.

- Eg. Left hemianopia: vision on temporal left eye missing with nasal right eye.

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11
Q

Where is the lesion if there is vision loss to the left eye (monocular) completely?

A
  • Left optic nerve anterior to chiasm
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12
Q

Where is the lesion if there is a bitemporal hemianopia?

A
  • Optic chiasm. Typical with pituitary tumor.
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13
Q

Where is the lesion if there is a left or right homonymous hemianopia?

A
  • Left homonymous hemianopia: right side of brain posterior to chiasm
  • Right homonymous hemianopia: left side of brain posterior to chiasm
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14
Q

What is the name of the location on the retina where central (fine) vision is picked up?

A
  • Macula. No blood vessels are present here.
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15
Q

Describe lens metabolism and clinical significance of this

A

**

  • Glucose enters lens from aqueous humor and is rapidly metabolized. When hyperglycemic state (> 200-250) exists and low levels of hexokinase shunts glucose to sorbitol pathway using aldose reductase. Sorbitol is not able to diffuse out of lens and osmotic gradient brings water into lens causing lens edema. This results in loss of lens fibers and transparency leading to acute refractive changes.
  • Sorbitol is slowly converted to fructose which can diffuse out of lens normalizing the shape. This takes up to 6 weeks. Therefore someone doesn’t need glasses or change to rx.
  • Chronic occurrences of hyperglycemia leads to cataract formation in diabetics (via cell rupture, release of AAs and K)
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16
Q

What provides the refractive power in the eye?

A
  • Cornea = 2/3rd

- Lens = 1/3rd

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17
Q

Define astigmatism

A
  • Distorted vision because the refractive power of cornea/lens is different in one meridian than in another. Essentially an irregular shape.
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18
Q

Define accommodation

A
  • Ability of ciliary muscle to contract or relax zonules allowing lens to focus at near
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19
Q

Define hyperopia and myopia

A
  • Myopia: nearsighted

- Hyperopia: farsighted

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20
Q

Define presbyopia

A
  • Decreased ability to focus at near (manifests in early 40s) with age requiring reading glasses. Cannot be halted or mitigated with refractive surgery such as Lasix.
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21
Q

Define legal blindness

A
  • 20/200. Means that you need to be 20 feet away from something to read it whereas most people can read it at 200 feet away.
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22
Q

3 complaints (ROS) of eye

A
  1. Disturbances in vision
  2. Pain/discomfort in or about eyes
  3. Abnormal eye secretions
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23
Q

Define amaurosis fugax

A
  • Sudden partial/total loss of vision
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24
Q

Floaters/flashing lights (aka photopsia) think…

A
  • Retinal detachment
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25
How to distinguish between monocular vs binocular diplopia
- Cover up eyes - Monocular: if you see with just one when other covered up - Binocular: if you see with both eyes and when covering eye it goes away
26
Define epiphora
- Overflow tearing
27
What does purulent vs mucous vs serous say about the etiology of abnormal eye secretions?
- Purulent: bacterial - Mucous: allergic - Serous: viral
28
Photophobia think…
- Iritis or migraine/HA
29
When is the only time a visual acuity is not done as part of eye exam?
- Burn
30
Visual acuity is based off of best monocular vision or binocular vision?
- Best corrected monocular vision
31
What is the order of checking visual acuity?
1. Chart 2. Finger counting 3. Hand motion 4. Light perception 5. No light perception
32
How to test visual fields?
- Confrontation test. Gross test. Stand 1 meter apart.
33
Scintillating scotomas as most commonly associated with what?
- Last 5-25 mins preceding migraines.
34
Types of pupillary testing
- Direct: size, equal (or anisocoria), round, central, reactive to light (NOT PERRLA) - Swinging flashlight looking for afferent reflex
35
Define a Marcus-Gunn afferent pupillary defect
- Defective afferent pathway (ocular nerve lesion or severe retinal injury) is seen with pupil consistently dilating as light is shone on it during swinging light test.
36
When is it important to check EOM?
- Diplopia, paresis/palsy, nystagmus | - 9 cardinal positions
37
EOM innervation
- SO4LR6 rest 3
38
Best test for eye alignment
- Cover/uncover, not eye light reflex
39
Test to assess anterior chamber depth
- Side penlight test
40
What CN is being tested with corneal sensitivity?
- CN V
41
What is arcus coneae? Indicative of what?
- Blue ring surrounding cornea | - Under 30: think dyslipidemia. Over: don’t be concerned.
42
How to test for corneal epithelial defects (abrasions, ulcers etc.)?
- Fluorescein staining
43
What is papilledema?
- Disc edema d/t increased ICP | - NOTE: Disc edema doesn’t = papilledema. Can get disc edema d/t other causes other than increased ICP.
44
Normal IOP (intraocular pressure)
- 10-21 mmHg
45
Refractive media of the eye from anterior to poster
- Tear film, cornea, anterior chamber, lens, vitreous humor
46
When to refer to ophthalmology?
- VA 22
47
Corneal edema. Describe it. What is the most common cause?
- Description: dull, ground glass appearance | - Cause: commonly = increased IOP. Less commonly: corneal dystrophies, ulcers and surgery
48
Acute angle closure glaucoma. a. Timing of onset b. Sx c. PE findings
a. Acute b. Severe eye pain, blurred vision, haloes around lights, HA, nausea and vomiting c. Mid-dilated fixed pupil, rock hard when pressing on it (increased IOP)
49
What is hyphema? Cause?
- Blood in anterior chamber. | - Cause: Generally secondary to blunt trauma, less commonly d/t neovascularization or iris
50
Etiology of vitreous hemorrhage
- 50% d/t diabetic retinopathy with neovascularization | - Others = retinal break/detachment, posterior vitreous detachment, trauma
51
Sx with vitreous detachment
- Floaters
52
Common etiologies of vitreous detachment
- Myopia, > 45 yo, cataract surgery, trauma, inflammatory dz
53
Hallmark sx with retinal detachment
- Flashes of light (aka photopsia) and floaters, often followed by a shade in visual field
54
Leading causes of blindness in USA
1. Diabetes (25-75) 2. Macular degeneration 3. Glaucoma
55
Types of macular degeneration
- Dry (aka atrophic) | - Wet (aka exudative)
56
What is macular degeneration?
- Deterioration of macula / central vision
57
Differentiate between sx of wet vs dry macular degeneration
- General: difficulty reading/driving, straight lines crooked. Advanced: central blind spot. Note: peripheral vision remains good. - Dry: gradual loss of vision (as above) - Wet: progressed to sudden loss of vision (subretinal neovascularization/bleeding)
58
Key findings on funduscopic exam for dry macular degeneration? Wet?
- Dry: drusen | - Wet: neovascularization/hemorrhage
59
What is amaurosis fugax? What should be included in workup when evaluating this?
- Sudden, transient loss of vision d/t temporary obstruction of artery to retina - Evaluation: CV system, cerebrovascular, ophthalmologic, migraine (classic vs ophthalmic). Evaluation done as the most common cause is embolism of some kind.
60
Visual sx with migraine
- Scintillating scotoma, amaurosis fugax, transient cortical blindness, homonymous hemianopia
61
Sx of central retinal artery occlusion (CRAO)? PE findings?
- Sx: sudden, painless visual loss - PE (depends on timing): a. Visual acuity: light perception or worse b. Pupil: RAPD c. Retina: opaque with cherry red spot
62
Tx of CRAO
- Medical emergency | - Tx = digital massage (10 seconds, release, etc. for 5 mins), glaucoma meds, emergent page to ophthalmologist
63
Etiology of BRAO (branched retinal artery occlusion)
- Emboli (cardiac, talc, fat, vasculitis)
64
Sx of BRAO
- Scotoma depending on size/location, visual acuity variable
65
CRVO (central retinal vein occlusion). a. Onset b. Sx c. PE findings
a. Subacute b. Severe vision loss, typically older patient c. Retina: “blood & thunder” appearance – disc swelling, diffuse retinal hemorrhages, venous engorgement, cotton wool spots
66
Etiologies of CRVO
- HTN, arteriovascular dz, DM, glaucoma, hyperviscosity syndromes, smoking
67
Optic disease associated with MS
- Optic neuritis
68
Classic sign for optic neuritis
- RAPD
69
Tx for optic neuritis
- Parenteral steroids
70
2 subgroups of optic neuritis? PE findings?
- Papillitis: lesion at optic nerve papilla (disc). PE: disc edema (d/t swollen optic nerve), RAPD, poor vision, hyperemia of disc, tortuosity of vessels - Retrobulbar: lesion in optic nerve prior to disc. PE: no disc edema, pain on EOM, RAPD
71
Young adult w/monocular progressive loss of vision over hours to day with pain on ocular movement and RAPD. What is the diagnosis?
- Retrobulbar neuritis
72
Compare and contrast papillitis and papilledema in terms of: vision, pupillary responses, optic nerve findings, presence of hemorrhages and etiology
- Papillitis: reduced vision, RAPD, swollen optic nerve, hemorrhages present, inflammatory etiology - Papilledema: normal vision, normal pupillary responses, swollen optic nerve, hemorrhages present, raised ICP. Other = hyperemia of disc, tortuosity of vessels.
73
Ischemic optic neuropathy. a. Which patient group is affected? b. Sx c. PE findings
a. > 55 yo usually b. Sudden monocular loss of vision (can be bilateral), cephalalgia (aka HA), scalp tenderness, jaw claudication (hurts with chewing), malaise, weight loss, low grade fever, arthralgias (limb girdle pain). One of causes = giant cell arteritis (HA, scalp tenderness, jaw claudication, polymyalgia rheumatica) c. RAPD, pale swollen optic nerve and altitudinal visual field defect?
74
Lab tests positive in anterior ischemic optic neuropathy
- Elevated ESR, CPR and platelet count | - Temporal artery biopsy (don’t wait for results before treating)
75
Tx for anterior ischemic optic neuropathy
- High dose systemic steroids
76
Most frequent cause of blindness in AAs?
- Glaucoma (primary open angle)
77
Triad of glaucoma
- Elevated IOP (> 21-22), optic nerve damage (increased cup to disc ratio), visual field loss
78
Normal IOP
- 10-21
79
Cup to disc ratio that is normal?
-
80
When comparing horizontal to vertical cup to disc ratio, which do you hope is bigger if they are not the same?
- Horizontal > Vertical = better prognosis | - Vertical > horizontal = worse prognosis
81
Types of glaucoma. Which is most common?
1. Primary open angle glaucoma (most common): clogging in trabecular meshwork. Risk factors = > 50, family hx, AA, myopic 2. Angle closure 3. Congenital 4. Secondary
82
SSx of primary open angle glaucoma
- Chronic gradual / insidious progression of vision loss, normal pupil, no haloes, no nausea, essentially asymptomatic
83
Tx of primary open angle glaucoma
- Meds to increase drainage or decrease aqueous humor production - BBs, adrenergics, cholinergics, CAIs, PG analogues - Surgery
84
Precipitating factors for acute angle closure glaucoma
- Physical / emotional stress, natural dilation of pupil (blocks off trabecular network), dilating drops, sympathomimetic drugs (decongestants etc.)
85
Tx for acute angle closure glaucoma
- *** Initial treatment: pilocarpine 15 mins x 2, acetazolamide, oral glycerine or isosorbide, IV mannitol (key to breaking attack) - Refer when: IOP > 21, IOP not elevated by difference of > 5 mmHg between eyes, cup/disk > 0.5, cup/disk different > 0.2 between eyes, sx of glaucoma - Ophthalmologist can do laser iridotomy
86
If you see a cloudy big eye in a neonate/young child, what do you suspect?
- Should suspect congenital glaucoma
87
Sx of cataracts
- Slight blur initially, increased myopia (aka second sight where one can read without glasses), diplopia / multiple images and starbursts, decreased color
88
Is there RAPD in cataracts?
- No
89
Leading cause of blindness in patient > 50 yo
- Macular degeneration
90
Risk factors for macular degeneration? Which are modifiable?
- Age, smoking, hyperopia, blue eyes, family hx | - Modifiable = smoking only!
91
Tx for macular degeneration (dry and wet)
- SMOKING CESSATION. Control CV dz - Dry: low vision aid lights, magnifiers, talking books, electronic TVs, MOTIVATION, various types of surgeries and other meds. Notable: AREDS study suggested lutein, zeaxanthin and omega 3. Also vitamin supplementation: vit C, zinc oxide, beta-carotene, vitamin E, cupric oxide. - Wet: destroy/inactivate abnormal blood vessels via thermal laser, photodynamic therapy, intravitreal injections
92
Primary indication for cataract extraction is?
- Interference with daily activities of living
93
When should glaucoma be suspected?
- Cup to disc ratio difference between eyes > 0.2 or asymmetry
94
When should red eyes be referred to ophthalmo?
- Red eye with decreased vision
95
Compare and contrast between pre-septal cellulitis and orbital cellulitis (aka post-septal) in terms of SSx
- Pre-septal cellulitis is that in the lid vs further into orbit - Both: red eye, swollen eye lid - Orbital: impaired eye movement with pain, proptosis (+/-), +/- RAPD, disc edema (d/t swelling) and decreased vision if optic nerve involvement
96
Tx of pre-septal cellulitis
- Warm, moist compresses | - Outpatient systemic abx
97
Tx of orbital cellulitis
- Hospitalization with eye, ENT consult. Why? Complications include cavernous sinus thrombosis, meningitis, brain abscess and death - Culture (nasopharynx, blood and conjunctiva) - Imaging (CT of sinuses preferred) - IV abx - Surgical debridement if mucor or Rhizopus - Surgery if unresponsive to abx
98
Sx and PE findings for herpes zoster ophthalmicus
- Sx: intense pain/discomfort, itching, photophobia (if uveitis) - PE: vesicles, crusting with exudate, spares midline, conjunctivitis, keratitis, uveitis, glaucoma
99
Tx of congenital nasolacrimal duct obstruction
- Up to 90% spontaneously resolve after ~ 8 months. - Depending on manifestations (amniotocele, mucocele, dacryocystitis, tearing, mattering), use: topical abx, massage tear sac daily, systemic abx if infected, probing/irrigation?
100
Define blepharitis? Types? Sx? Tx?
- Chronic inflammation of lid margin - Types: staph, seborrheic or combo - Sx: FB sensation, burning, mattering (discharge) - Tx: proper lid hygiene, warm moist compresses, cleansing with non-irritating shampoo (J&J baby). Rx abx solution and ointment for night use.
101
What is ocular surface disease?
- Aka dry eye syndrome | - Either an evaporative compromised lipid layer or aqueous tear deficiency
102
Sx of aqueous tear deficiency
- Burning, FB sensation, grittiness, photophobia, tearing reflex
103
Most common manifestation of CT disease
- Aqueous tears deficiency (dry eye syndrome)
104
Etiology of aqueous tears deficiency
- Aging, RA, systemic meds. Note: more common in women d/t loss of male hormones as they age.
105
Presentation of Sjogren’s syndrome
- Dry eyes, dry mouth and +/- CT disorder
106
Tx of dry eye syndrome (ocular surface dz)
- Artificial tears, lubricating ointment at night, omega 3, lid hygiene (warm compresses and lid scrubs), topical anti-inflammatories, azithromycin (not as abx, but lowers melting point of oils to allow them to flow), serum tears
107
Stye vs chalazion
- Stye: acute inflammation of glands of eyelid | - Chalazion: chronic generally sterile inflammation of glands of eyelid
108
Tx of stye/chalazion
- Same. Goal to promote drainage. - Warm compress & abx solution. - I&D if no response. - Persistent: do biopsy to r/o serious carcinomas
109
Sx of ectropion and entropion? Tx
- Ectropion: burning, tearing, mattering, keratitis, ulcers - Entropion: FB sensation, tearing, mattering, abrasion, ulcers - Tx = abx solution and ointment. Surgery for ectropion.
110
Describe discharge seen in allergic, bacterial and viral conjunctivitis
- Allergic: stringy, white mucus - Bacterial: purulent - Viral: clear (sometimes purulent). Associated with pre-auricular LAD.
111
Presentation of allergic conjunctivitis
- Bilateral eyes: itchy, redness, lid edema/puffiness, conjunctival swelling (aka chemosis), burning/stinging/tearing, white stringy discharge - Other sx: hay fever, asthma, eczema
112
Tx of allergic conjunctivitis
- Attempting to avoid allergens (difficult) | - Tears, decongestants, antihistamines, mast cell stabilizers, NSAIDs, steroids (we shouldn’t use them, only ophthalmo)
113
Presentation of viral conjunctivitis
- Watery discharge, irritation, redness, palpable pre-auricular LN. Other sx related to URI, pharyngitis, fever common. Usually travels from one eye to other ***. Decreased vision secondary to corneal infiltrates.
114
Most common etiology for viral conjunctivitis
- Adenovirus
115
Tx of viral conjunctivitis
- Avoid close contact/sharing, symptomatic relief: antihistamines, abx, cool compresses, ?antivirals and povidone iodine, opthalmo can use topical steroids
116
PE findings of blepharoconjunctivitis d/t HSV. Tx?
- Vesicles on skin/eyelid margin, conjunctival rxn, epithelial keratitis, pre-auricular LAD. - Tx: antivirals
117
Sx of bacterial conjunctivitis
- Bilateral eye involvement, mucopurulent discharge, lid crusting
118
Most common causes of bacterial conjunctivitis? Tx?
- Staph, strep, hemophilus, pseudomonas | - Tx: topical abx solution and ointment at night, cleansing, warm moist compresses
119
Conjunctivitis in neonate has what etiology?
- This is neonate is STD until proven otherwise
120
Tx of bacterial ulcers
- Non-cultured ulcers are treated with fluoroquinolones | - Refer to ophthalmo
121
Corneal ulcer in a contact lens wearer is more likely what etiology
- Pseudomonas | - Note: any contact lens wearer who develops ocular sx should be evaluated by ophthalmo
122
Leading cause of infectious corneal blindness in USA
- Herpetic infections
123
Pathognomic findings for herpes simplex corneal infection
- Branching dendritic pattern with terminal end bulbs is ALWAYS herpes simplex virus
124
Tx of corneal herpes infection
- Avoid topical steroids (exacerbates keratitis, IOP increase leading to steroid responsive glaucoma, cataract formation if prolonged use) - Antivirals (acycl, fam, vala) - Refer to ophthalmo for tx
125
Tx of conjunctival hemorrhage
- Spontaneous resolution, reassure patient
126
Etiology of inflamed pinguecula and pterygium? Tx?
- Excessive UV & wind exposure | - Tx: artificial tears, topical vasoconstrictors/antihistamines, refer if severe
127
Presentation of episcleritis/scleritis
- Red eye in sector of eye, hurts to move eye as underneath this is muscle insertion - Scleritis often associated with collagen vascular dz often an indication of an exacerbation of disease
128
Common sx in iritis/uveitis. Tx?
- Photophobia - Others = circumcorneal injection, pain, decreased vision, miotic pupil - Tx: steroids!
129
T/F. Topical anesthestics should never be prescribed.
- True. Why? Inhibit growth/healing of epithelium and may cause severe allergic rxns.
130
T/F. VA is acutely and significantly reduced in conjunctivitis
- False
131
Define lagophthalmos
- Inability to close eye
132
Which is more a serous chemical burn to eye – alkali or acid?
- Alkali
133
Tx of chemical burns to eye
- Instill topical anesthetic, check for FBs, institute copious irrigation (liters) with any type of fluid (water, NS, LR) - Following irrigation: topical cycloplegic agent, topical abx, pressure patch. Refer to opthalmo
134
Corneal abrasion Sx
- FB sensation, intense pain, tearing, photophobia
135
Tx for corneal abrasion
- Topical abx solution, topical NSAID, oral analgesics, pressure patch (DON’T PATCH CONTACT LENS WEARERS, IF DENDRITIC/STELLATE EPITHELIAL DEFECTS PRESENT OR POOR HISTORIANS). TOPICAL ANESTHETICS CONTRAINDICATED D/T CORNEAL TOXICITY. - Refer to opthalmo if not healed in 24 hrs, abrasion related to contact lens, white corneal infiltrate (this is an ulcer)
136
Mgmt. of hyphema
- Assume globe ruptured, shield and refer to ophthalmo | - Complications: rebleeding into anterior chamber, glaucoma
137
Tx of globe rupture or laceration
- Stop exam, shield eye/don’t patch, give tetanus Prophy and refer to opthalmo
138
Presentation of severe orbital hemorrhage? Tx?
- Sx: bullous subconjunctival hemorrhage, proptosis, corneal exposure - Tx: emergent lateral canthotomy consultation (otherwise blindness)
139
Sx and PE findings for orbital fracture. Tx?
- Sx: diplopia, hypoesthesia (numbness) under eye/upper cheek (d/t infraorbital nerve involvement) - PE: Periorbital edema, ecchymosis, subcutaneous emphysema, entrapment of EOM (unable to move to all cardinal points) - Tx: surgery indicated if persistent diplopia, poor cosmesis
140
Exposure hx of UV keratitis
- UV, Welder’s burn
141
Sx of UV keratitis
- Photophobia, FB sensation, tearing pain
142
Tx of UV keratitis
- Cycloplegics, topical analgesics
143
PE findings for penetrating injury to eye
- Teardrop pupil (pointing towards area of laceration) and flat anterior chamber
144
T/F. Never rx a topical anesthetic
- True
145
Define amblyopia and strabismus
- Amblyopia: decreased vision eye d/t brain and eye not working properly together in absence of detectable organic dz (can be with strabismus). Aka lazy eye. Brain selects better eye and suppresses blurred/conflicting image from lazy eye. - Strabismus: misalignment of eye(s). - Both can be present.
146
When is amblyopia detection and treatment best?
- Earlier in life, the better. Tx should begin before age 5. If not detected and treated early, can cause visual impairment for entire lifetime d/t atrophy in parts of brain.
147
Etiologies of amblyopia
- Strabismic (slight) - Refractive issue (difference in power between eyes) - Form-deprivation (media become opaque): cataracts, corneal scarring and occlusion
148
Define concomitant strabismus
- Angle of deviation/misalignment remains same (constant) in all gaze positions, where non-concomitant it changes depending on gaze position.
149
Presentation of amblyopia
- Failed vision test, strabismus, parental concern
150
How is amblyopia detected?
- Assess red reflex - Determine visual acuity - Evaluate ocular alignment
151
How is strabismus detected?
- General inspection of gaze in cardinal position, epicanthi and facies - Corneal light reflex at 2ft - Cover/uncover to distinguish pseudostrabismus from true
152
Leukocoria as far as we are concerned are always what?
- Retinoblastoma
153
Describe how exam differs for amblyopia and strabismus in newborn, infant to 2 yo patient, 2-5 yo, child
- Newborn: corneal light reflex, red reflex, pupillary reflex (normal to be sluggish) - Infant to 2 yo: able to fixate and follow to check EOM, cover good eye and see how child reacts - 2-5 yo: E game/Allen pictures, cover/uncover, photo screen - Child: Snellen, E game, cover/uncover
154
What should be corrected first, amblyopia or strabismus?
- Amblyopia
155
Tx for amblyopia
1. 1st strategy: optimize retinal image a. Clear visual pathway: cataract, ptosis surgery b. Correct refractive error: glasses/contacts 2. 2nd strategy: intensify neural image to visual cortex a. Occlusion therapy: cover good eye (10 years) b. Penalization: use cycloplegic agent (eg. Atropine) to better eye. This eye cannot accommodate to near, but can see far and therefore the child is using the amblyopic eye whenever near.
156
Tx for strabismus
1. Glasses: can correct some forms 2. EOM surgery ** Note: tx amblyopia before treating strabismus
157
When to refer child for ophthalmo immediately for ocular concerns?
- Poor red reflex in one or both eyes - Concern about vision by parent/doctor - Asymmetric or diminishing VA - Constant or acute-onset strabismus
158
Why is diplopia not present in children?
- Brain will turn bad eye off.
159
Adie’s Tonic Pupil (benign ciliary ganglionopathy). What is it? Who does it affect? Sx? Diagnosis+
- It is a benign idiopathic ciliary ganglion (PSNS) defect that leads to tonically dilated pupil (80% unilateral) that is poorly reactive to light. - Predominantly seen in females - Sx: blurred vision near, periocular discomfort, decreased depth perception - Diagnosis: Poorly reactive to light. Use 0.1% pilocarpine. Normal pupil will not constrict, while lesioned eye will.
160
What is Horner’s syndrome? Sx? Etiology?
- SNS pathway lesion that leads to classic triad: - Sx: ptosis, miosis, facial anhidrosis - Etiologies: congenital or acquired (lesion at multiple locations including Pancoast tumor, subclavian artery, etc.)
161
Describe diagnosis of Horner’s syndrome?
- Apraclonidine. It reverses anisocoria
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How to distinguish between congenital or acquired Horner’s syndrome?
- SNS required to darken iris in development. Normally born with lighter eyes. If patient presents with triad consistent with Horner’s and heterochromia, this would indicate congenital as affected eye didn’t darken.
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What is Argyll Robertson pupil? Diseases this is associated with?
- Pupils accommodate, but don’t react to light. Pupils are irregular and small bilaterally usually. Associated with syphilis (prostitute’s pupil), DM, alcoholism.
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Diplopia during heavy exercise could indicate?
- Aneurysm as etiology
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Diplopia when fatigued could indicate?
- Myasthenia
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Diplopia associated with headache and retro-orbital pain could indicate?
- Aneurysm
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PE findings for CN III paresis/palsy. Type of diplopia present?
- Pupil: dilated (aneurysm of PCA until proven otherwise) or normal (known as pupil sparing) if DM & HTN - Ptosis - EOM: abducted (why? LR is next strongest muscle that takes over) and down (down and out) - Diplopia: horizontal and vertical diplopia
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Etiology of CN III paresis/palsy
- IC aneurysm, vascular dz (HTN and DM), trauma, brain tumor
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Why is there pupil sparing with CN III paresis/palsy d/t vascular dz (HTN and DM) whereas the pupil isn’t spared in aneurysm?
- Aneurysm compresses pupillary fibers which are found on the outer area of CN III - Vascular dz leads to infarct of central nerve fibers, sparing the outer area where the pupillary fibers are
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55 yo male with hx of DM, HTN and CAD presents with new onset right ptosis, exotropia and hypotropia with fixed right dilated pupil. What is diagnosis?
- CN III paresis/palsy d/t PCA aneurysm until proven otherwise. Do catheter angiogram or MRI/MRA.
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PE findings for CN IV palsy/paresis. Type of diplopia present?
- SO isn’t working - Pupil: normal - Diplopia: vertical with compensatory head tilt to opposite shoulder (to affected eye)
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Etiology of CN IV paresis/palsy
- Vascular dz (DM, HTN). If bilateral, closed head trauma.
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PE findings for CN VI palsy/paresis. Type of diplopia present?
- LR isn’t working - Pupil: normal - EOM: loss of abduction - Diplopia: horizontal
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Etiologies of CN VI paresis/palsy
- IC tumors, head trauma, vascular diseases, increased ICP (pseudotumor cerebri), demyelinated dz (MS)
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When checking for weakness in patient’s smile or ability to close eye while attempting to open them, what CN is being tested?
- CN VII
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Myasthenia gravis ocular manifestations. How is diagnosis made?
- Ptosis/diplopia with no pupillary abnormalities. Can mimic any EOM problem. Exhibits fatigability, worse at end of day. - Diagnosis: use edrophonium, will make sx better.
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Types of nystagmus
1. Benign a. End-gaze (3-4 beats, then dampens) b. Drug induced: dilantin, barbs, sedatives c. Congenital: searching pendular 2. Pathological a. MS b. Intracranial mass c. CNS degenerations
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21 yo w/acute bitemporal vision loss (bitemporal hemiano w/severe HA and eye pain. PE: PERRLA, but did have a +ve RAPD. Fundus is normal. What is the diagnosis?
- Pituitary tumor/apoplexy
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Blurred disc could mean?
- Congenital abnormality (pseudopapilledema) - Papilledema (ICP increased) - Papillitis
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Etiology of papilledema
- 50% d/t brain tumors/space occupying lesions | - Other = idiopathic intracranial HTN, cerebral trauma or hemorrhage, dural sinus thrombosis
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Can you know by looking at fundus whether or not it is papilledema or disc edema?
- No. Look at symptoms. Get CT.
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What is idiopathic intracranial HTN (pseudotumor cerebri)? Which patient group? Sx? PE? Tx?
- Neurological disorder characterized by increased ICP in absence of tumor or other dz. - Group: 20-40 yo females with obesity/weight gain - Sx: headaches, visual obscurations, pulsatile tinnitus, horizontal diplopia (6th CN palsy), pain on EOM - PE: papilledema - Tx: weight loss, CAI (acetazolamide), VP shunt, optic nerve fenestration
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Sx of optic neuritis
- Decreased vision, unilateral, red desaturation (decreased red visual detection), visual field defects
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Most common etiology of optic neuritis?
- MS (50%) | - Other = ischemia, infiltration, postviral, sarcoidosis, Lyme, CTD?
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Tell difference between papilledema and optical neuritis
- Papilledema: no RAPD, normal vision | - Optical neuritis: RAPD, abnormal vision
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Pallor of optic nerve, think…
- Optic atrophy
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Common causes of optic nerve atrophy
- Previous optic neuritis (multiple episodes), long-standing papilledema, compression of optic nerve (meningioma, thyroid), ischemia damage (GCA), glaucoma, previous trauma, toxins (ethambutol, methanol)
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Funduscopic finding in optic nerve atrophy
- Bright light shining at you from disc
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Charles Bonnet syndrome. Presentation? Which patient group is affected?
- Visual hallucinations with significant visual loss (
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When to check CN V and VII for eye issues?
- If abnormal EOM and suspect CN palsy
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What do you suspect with slowly progressive visual loss or CN palsy?
- Compressive lesion (tumor or aneurysm)
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What do you suspect with abrupt vision loss or diplopia?
- Vascular dz (ischemia GCA or vasospasm)
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What are the ocular manifestations of diabetes?
- Refractive error changes (sorbitol pathway), cataracts, retinopathy
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Factors that correlate with severity of diabetic retinopathy
- Duration of dz, HTN, high A1C, smoking
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What is the pathogenesis of DM retinopathy?
- High BGL = VEGF = neovascularization/increased capillary permeability
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Subgroups of diabetic retinopathy? What are the funduscopic findings?
1. Non-proliferative (NPDR) - Microaneurysms, leakage of intravascular fluids (hard exudates), intraretinal hemorrhages, retinal ischemia (cotton wool spots) 2. Proliferative (PDR): NPDR findings + neovascularization (wispy vessels), vitreous hemorrhage (scabbing contracts and can leading to retinal detachment), fibrous proliferation
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When are NPDR patients at imminent risk for PDR?
- Cotton wool spots, capillary dropout, venous beading (sausaging)
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Sx of vitreous hemorrhage
- Floaters/cobwebs, sudden loss of vision
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Is ischemic maculopathy from DM reversible?
- No
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Tx of diabetic retinopathy
- Note: early tx may prevent blindness (leading cause in USA) - Ischemic maculopathy not treatable - Laser (kills off neovascular tissue, preventing further proliferation and reduces risk for collateral damage to other good parts) or injection - Vitrectomy in cases of vitreous hemorrhage or retinal detachment
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Does PDR increase risk in DM patient for other complications?
- Yes. Risk increased for MI, CVA, amputation, diabetic nephropathy and death.
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How often should diabetics receive ophthalmo exams?
- Annually at least. If advanced dz, more frequently.
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Funduscopic characteristic changes seen with HTNsive retinopathy
- Early: attenuation of arterioles (copper wiring, silver wiring) = AV nicking - Later: above + hard exudates, cotton wool spots and hemorrhages. Highest grade = + disc edema
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Eye changes seen in pregnancy
- Refractive error changes, dry eyes, transient loss of accommodation, retinopathy (with pregnancy-induced HTN), rarely retinal detachments. If DM patient, progression of retinopathy.
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Eye features in Graves’ dz
- Enlargement of EOM (spindle-shaped on CT) = exophthalmos, lid retraction, lid lag, conjunctival congestion, drying/friability of cornea d/t inability to close lid, disc edema d/t EOM compression
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Most common cause of uni/bilateral exophthalmos in adult
- Graves’ dz | - Note: can progress after thyroid function returned to normal
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Tx of thyroid ophthalmology
- Temporizing: artificial tears, steroids, orbital irradiation - Ultimately: surgery (EOM or decompression)
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Eye exam findings for iritis
- White cells (snow globe) in anterior chamber
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Ocular findings in sarcoidosis
- Key points: AA, photophobia, iritis/uveitis
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Most common ocular manifestation in RA
- Dry eye syndrome | - Other: episcleritis/scleritis (not conjunctivitis), severe corneal ulcers
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Ocular findings in juvenile RA
- Iritis asymptomatic and chronic (no photophobia). If unrecognized may lead to cataracts, glaucoma, corneal calcification
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Chemotherapeutic drugs with toxicity to eye
- Cytosine arabinoside (superficial keratitis) - Vincristine (optic neuropathy) - BCNU (carmustine) – CRAO with carotid artery injection
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Ocular manifestations of AIDS
1. AIDS retinopathy: Cotton-wool spots d/t ag-ab complexes 2. CMV retinitis: leading cause of visual loss in AIDS 3. Kaposi’s sarcoma affecting eyelids 4. Others
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Tx for CMV retinitis
- Gangiclovir, foscarnet, cidofovir
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Tx for herpes zoster ophthalmicus
- Acyclovir, famacyclovir, valacyclovir | - Capsaicin for PHN
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Meds with irreversible toxic retinopathies
- Hydrochloroquine, ethambutol