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Ophthalmology > Exam SG > Flashcards

Exam SG Flashcards

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
Q

How to distinguish between monocular vs binocular diplopia

A
  • 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
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26
Q

Define epiphora

A
  • Overflow tearing
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27
Q

What does purulent vs mucous vs serous say about the etiology of abnormal eye secretions?

A
  • Purulent: bacterial
  • Mucous: allergic
  • Serous: viral
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28
Q

Photophobia think…

A
  • Iritis or migraine/HA
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29
Q

When is the only time a visual acuity is not done as part of eye exam?

A
  • Burn
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30
Q

Visual acuity is based off of best monocular vision or binocular vision?

A
  • Best corrected monocular vision
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31
Q

What is the order of checking visual acuity?

A
  1. Chart
  2. Finger counting
  3. Hand motion
  4. Light perception
  5. No light perception
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32
Q

How to test visual fields?

A
  • Confrontation test. Gross test. Stand 1 meter apart.
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33
Q

Scintillating scotomas as most commonly associated with what?

A
  • Last 5-25 mins preceding migraines.
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34
Q

Types of pupillary testing

A
  • Direct: size, equal (or anisocoria), round, central, reactive to light (NOT PERRLA)
  • Swinging flashlight looking for afferent reflex
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35
Q

Define a Marcus-Gunn afferent pupillary defect

A
  • 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.
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36
Q

When is it important to check EOM?

A
  • Diplopia, paresis/palsy, nystagmus

- 9 cardinal positions

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37
Q

EOM innervation

A
  • SO4LR6 rest 3
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38
Q

Best test for eye alignment

A
  • Cover/uncover, not eye light reflex
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39
Q

Test to assess anterior chamber depth

A
  • Side penlight test
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40
Q

What CN is being tested with corneal sensitivity?

A
  • CN V
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41
Q

What is arcus coneae? Indicative of what?

A
  • Blue ring surrounding cornea

- Under 30: think dyslipidemia. Over: don’t be concerned.

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42
Q

How to test for corneal epithelial defects (abrasions, ulcers etc.)?

A
  • Fluorescein staining
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43
Q

What is papilledema?

A
  • Disc edema d/t increased ICP

- NOTE: Disc edema doesn’t = papilledema. Can get disc edema d/t other causes other than increased ICP.

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44
Q

Normal IOP (intraocular pressure)

A
  • 10-21 mmHg
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45
Q

Refractive media of the eye from anterior to poster

A
  • Tear film, cornea, anterior chamber, lens, vitreous humor
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46
Q

When to refer to ophthalmology?

A
  • VA 22
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47
Q

Corneal edema. Describe it. What is the most common cause?

A
  • Description: dull, ground glass appearance

- Cause: commonly = increased IOP. Less commonly: corneal dystrophies, ulcers and surgery

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48
Q

Acute angle closure glaucoma.
a. Timing of onset

b. Sx
c. PE findings

A

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)

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49
Q

What is hyphema? Cause?

A
  • Blood in anterior chamber.

- Cause: Generally secondary to blunt trauma, less commonly d/t neovascularization or iris

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50
Q

Etiology of vitreous hemorrhage

A
  • 50% d/t diabetic retinopathy with neovascularization

- Others = retinal break/detachment, posterior vitreous detachment, trauma

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51
Q

Sx with vitreous detachment

A
  • Floaters
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52
Q

Common etiologies of vitreous detachment

A
  • Myopia, > 45 yo, cataract surgery, trauma, inflammatory dz
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53
Q

Hallmark sx with retinal detachment

A
  • Flashes of light (aka photopsia) and floaters, often followed by a shade in visual field
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54
Q

Leading causes of blindness in USA

A
  1. Diabetes (25-75)
  2. Macular degeneration
  3. Glaucoma
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55
Q

Types of macular degeneration

A
  • Dry (aka atrophic)

- Wet (aka exudative)

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56
Q

What is macular degeneration?

A
  • Deterioration of macula / central vision
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57
Q

Differentiate between sx of wet vs dry macular degeneration

A
  • 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)
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58
Q

Key findings on funduscopic exam for dry macular degeneration? Wet?

A
  • Dry: drusen

- Wet: neovascularization/hemorrhage

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59
Q

What is amaurosis fugax? What should be included in workup when evaluating this?

A
  • 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.
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60
Q

Visual sx with migraine

A
  • Scintillating scotoma, amaurosis fugax, transient cortical blindness, homonymous hemianopia
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61
Q

Sx of central retinal artery occlusion (CRAO)? PE findings?

A
  • 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
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62
Q

Tx of CRAO

A
  • Medical emergency

- Tx = digital massage (10 seconds, release, etc. for 5 mins), glaucoma meds, emergent page to ophthalmologist

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63
Q

Etiology of BRAO (branched retinal artery occlusion)

A
  • Emboli (cardiac, talc, fat, vasculitis)
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64
Q

Sx of BRAO

A
  • Scotoma depending on size/location, visual acuity variable
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65
Q

CRVO (central retinal vein occlusion).
a. Onset

b. Sx
c. PE findings

A

a. Subacute
b. Severe vision loss, typically older patient
c. Retina: “blood & thunder” appearance – disc swelling, diffuse retinal hemorrhages, venous engorgement, cotton wool spots

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66
Q

Etiologies of CRVO

A
  • HTN, arteriovascular dz, DM, glaucoma, hyperviscosity syndromes, smoking
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67
Q

Optic disease associated with MS

A
  • Optic neuritis
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68
Q

Classic sign for optic neuritis

A
  • RAPD
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69
Q

Tx for optic neuritis

A
  • Parenteral steroids
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70
Q

2 subgroups of optic neuritis? PE findings?

A
  • 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
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71
Q

Young adult w/monocular progressive loss of vision over hours to day with pain on ocular movement and RAPD. What is the diagnosis?

A
  • Retrobulbar neuritis
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72
Q

Compare and contrast papillitis and papilledema in terms of: vision, pupillary responses, optic nerve findings, presence of hemorrhages and etiology

A
  • 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.
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73
Q

Ischemic optic neuropathy.
a. Which patient group is affected?

b. Sx
c. PE findings

A

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?

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74
Q

Lab tests positive in anterior ischemic optic neuropathy

A
  • Elevated ESR, CPR and platelet count

- Temporal artery biopsy (don’t wait for results before treating)

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75
Q

Tx for anterior ischemic optic neuropathy

A
  • High dose systemic steroids
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76
Q

Most frequent cause of blindness in AAs?

A
  • Glaucoma (primary open angle)
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77
Q

Triad of glaucoma

A
  • Elevated IOP (> 21-22), optic nerve damage (increased cup to disc ratio), visual field loss
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78
Q

Normal IOP

A
  • 10-21
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79
Q

Cup to disc ratio that is normal?

A

-

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80
Q

When comparing horizontal to vertical cup to disc ratio, which do you hope is bigger if they are not the same?

A
  • Horizontal > Vertical = better prognosis

- Vertical > horizontal = worse prognosis

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81
Q

Types of glaucoma. Which is most common?

A
  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
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82
Q

SSx of primary open angle glaucoma

A
  • Chronic gradual / insidious progression of vision loss, normal pupil, no haloes, no nausea, essentially asymptomatic
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83
Q

Tx of primary open angle glaucoma

A
  • Meds to increase drainage or decrease aqueous humor production
  • BBs, adrenergics, cholinergics, CAIs, PG analogues
  • Surgery
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84
Q

Precipitating factors for acute angle closure glaucoma

A
  • Physical / emotional stress, natural dilation of pupil (blocks off trabecular network), dilating drops, sympathomimetic drugs (decongestants etc.)
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85
Q

Tx for acute angle closure glaucoma

A
  • *** 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
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86
Q

If you see a cloudy big eye in a neonate/young child, what do you suspect?

A
  • Should suspect congenital glaucoma
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87
Q

Sx of cataracts

A
  • Slight blur initially, increased myopia (aka second sight where one can read without glasses), diplopia / multiple images and starbursts, decreased color
88
Q

Is there RAPD in cataracts?

A
  • No
89
Q

Leading cause of blindness in patient > 50 yo

A
  • Macular degeneration
90
Q

Risk factors for macular degeneration? Which are modifiable?

A
  • Age, smoking, hyperopia, blue eyes, family hx

- Modifiable = smoking only!

91
Q

Tx for macular degeneration (dry and wet)

A
  • 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
Q

Primary indication for cataract extraction is?

A
  • Interference with daily activities of living
93
Q

When should glaucoma be suspected?

A
  • Cup to disc ratio difference between eyes > 0.2 or asymmetry
94
Q

When should red eyes be referred to ophthalmo?

A
  • Red eye with decreased vision
95
Q

Compare and contrast between pre-septal cellulitis and orbital cellulitis (aka post-septal) in terms of SSx

A
  • 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
Q

Tx of pre-septal cellulitis

A
  • Warm, moist compresses

- Outpatient systemic abx

97
Q

Tx of orbital cellulitis

A
  • 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
Q

Sx and PE findings for herpes zoster ophthalmicus

A
  • Sx: intense pain/discomfort, itching, photophobia (if uveitis)
  • PE: vesicles, crusting with exudate, spares midline, conjunctivitis, keratitis, uveitis, glaucoma
99
Q

Tx of congenital nasolacrimal duct obstruction

A
  • 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
Q

Define blepharitis? Types? Sx? Tx?

A
  • 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
Q

What is ocular surface disease?

A
  • Aka dry eye syndrome

- Either an evaporative compromised lipid layer or aqueous tear deficiency

102
Q

Sx of aqueous tear deficiency

A
  • Burning, FB sensation, grittiness, photophobia, tearing reflex
103
Q

Most common manifestation of CT disease

A
  • Aqueous tears deficiency (dry eye syndrome)
104
Q

Etiology of aqueous tears deficiency

A
  • Aging, RA, systemic meds. Note: more common in women d/t loss of male hormones as they age.
105
Q

Presentation of Sjogren’s syndrome

A
  • Dry eyes, dry mouth and +/- CT disorder
106
Q

Tx of dry eye syndrome (ocular surface dz)

A
  • 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
Q

Stye vs chalazion

A
  • Stye: acute inflammation of glands of eyelid

- Chalazion: chronic generally sterile inflammation of glands of eyelid

108
Q

Tx of stye/chalazion

A
  • Same. Goal to promote drainage.
  • Warm compress & abx solution.
  • I&D if no response.
  • Persistent: do biopsy to r/o serious carcinomas
109
Q

Sx of ectropion and entropion? Tx

A
  • Ectropion: burning, tearing, mattering, keratitis, ulcers
  • Entropion: FB sensation, tearing, mattering, abrasion, ulcers
  • Tx = abx solution and ointment. Surgery for ectropion.
110
Q

Describe discharge seen in allergic, bacterial and viral conjunctivitis

A
  • Allergic: stringy, white mucus
  • Bacterial: purulent
  • Viral: clear (sometimes purulent). Associated with pre-auricular LAD.
111
Q

Presentation of allergic conjunctivitis

A
  • Bilateral eyes: itchy, redness, lid edema/puffiness, conjunctival swelling (aka chemosis), burning/stinging/tearing, white stringy discharge
  • Other sx: hay fever, asthma, eczema
112
Q

Tx of allergic conjunctivitis

A
  • Attempting to avoid allergens (difficult)

- Tears, decongestants, antihistamines, mast cell stabilizers, NSAIDs, steroids (we shouldn’t use them, only ophthalmo)

113
Q

Presentation of viral conjunctivitis

A
  • 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
Q

Most common etiology for viral conjunctivitis

A
  • Adenovirus
115
Q

Tx of viral conjunctivitis

A
  • Avoid close contact/sharing, symptomatic relief: antihistamines, abx, cool compresses, ?antivirals and povidone iodine, opthalmo can use topical steroids
116
Q

PE findings of blepharoconjunctivitis d/t HSV. Tx?

A
  • Vesicles on skin/eyelid margin, conjunctival rxn, epithelial keratitis, pre-auricular LAD.
  • Tx: antivirals
117
Q

Sx of bacterial conjunctivitis

A
  • Bilateral eye involvement, mucopurulent discharge, lid crusting
118
Q

Most common causes of bacterial conjunctivitis? Tx?

A
  • Staph, strep, hemophilus, pseudomonas

- Tx: topical abx solution and ointment at night, cleansing, warm moist compresses

119
Q

Conjunctivitis in neonate has what etiology?

A
  • This is neonate is STD until proven otherwise
120
Q

Tx of bacterial ulcers

A
  • Non-cultured ulcers are treated with fluoroquinolones

- Refer to ophthalmo

121
Q

Corneal ulcer in a contact lens wearer is more likely what etiology

A
  • Pseudomonas

- Note: any contact lens wearer who develops ocular sx should be evaluated by ophthalmo

122
Q

Leading cause of infectious corneal blindness in USA

A
  • Herpetic infections
123
Q

Pathognomic findings for herpes simplex corneal infection

A
  • Branching dendritic pattern with terminal end bulbs is ALWAYS herpes simplex virus
124
Q

Tx of corneal herpes infection

A
  • 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
Q

Tx of conjunctival hemorrhage

A
  • Spontaneous resolution, reassure patient
126
Q

Etiology of inflamed pinguecula and pterygium? Tx?

A
  • Excessive UV & wind exposure

- Tx: artificial tears, topical vasoconstrictors/antihistamines, refer if severe

127
Q

Presentation of episcleritis/scleritis

A
  • 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
Q

Common sx in iritis/uveitis. Tx?

A
  • Photophobia
  • Others = circumcorneal injection, pain, decreased vision, miotic pupil
  • Tx: steroids!
129
Q

T/F. Topical anesthestics should never be prescribed.

A
  • True. Why? Inhibit growth/healing of epithelium and may cause severe allergic rxns.
130
Q

T/F. VA is acutely and significantly reduced in conjunctivitis

A
  • False
131
Q

Define lagophthalmos

A
  • Inability to close eye
132
Q

Which is more a serous chemical burn to eye – alkali or acid?

A
  • Alkali
133
Q

Tx of chemical burns to eye

A
  • 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
Q

Corneal abrasion Sx

A
  • FB sensation, intense pain, tearing, photophobia
135
Q

Tx for corneal abrasion

A
  • 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
Q

Mgmt. of hyphema

A
  • Assume globe ruptured, shield and refer to ophthalmo

- Complications: rebleeding into anterior chamber, glaucoma

137
Q

Tx of globe rupture or laceration

A
  • Stop exam, shield eye/don’t patch, give tetanus Prophy and refer to opthalmo
138
Q

Presentation of severe orbital hemorrhage? Tx?

A
  • Sx: bullous subconjunctival hemorrhage, proptosis, corneal exposure
  • Tx: emergent lateral canthotomy consultation (otherwise blindness)
139
Q

Sx and PE findings for orbital fracture. Tx?

A
  • 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
Q

Exposure hx of UV keratitis

A
  • UV, Welder’s burn
141
Q

Sx of UV keratitis

A
  • Photophobia, FB sensation, tearing pain
142
Q

Tx of UV keratitis

A
  • Cycloplegics, topical analgesics
143
Q

PE findings for penetrating injury to eye

A
  • Teardrop pupil (pointing towards area of laceration) and flat anterior chamber
144
Q

T/F. Never rx a topical anesthetic

A
  • True
145
Q

Define amblyopia and strabismus

A
  • 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
Q

When is amblyopia detection and treatment best?

A
  • 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
Q

Etiologies of amblyopia

A
  • Strabismic (slight)
  • Refractive issue (difference in power between eyes)
  • Form-deprivation (media become opaque): cataracts, corneal scarring and occlusion
148
Q

Define concomitant strabismus

A
  • Angle of deviation/misalignment remains same (constant) in all gaze positions, where non-concomitant it changes depending on gaze position.
149
Q

Presentation of amblyopia

A
  • Failed vision test, strabismus, parental concern
150
Q

How is amblyopia detected?

A
  • Assess red reflex
  • Determine visual acuity
  • Evaluate ocular alignment
151
Q

How is strabismus detected?

A
  • General inspection of gaze in cardinal position, epicanthi and facies
  • Corneal light reflex at 2ft
  • Cover/uncover to distinguish pseudostrabismus from true
152
Q

Leukocoria as far as we are concerned are always what?

A
  • Retinoblastoma
153
Q

Describe how exam differs for amblyopia and strabismus in newborn, infant to 2 yo patient, 2-5 yo, child

A
  • 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
Q

What should be corrected first, amblyopia or strabismus?

A
  • Amblyopia
155
Q

Tx for amblyopia

A
  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
Q

Tx for strabismus

A
  1. Glasses: can correct some forms
  2. EOM surgery

** Note: tx amblyopia before treating strabismus

157
Q

When to refer child for ophthalmo immediately for ocular concerns?

A
  • Poor red reflex in one or both eyes
  • Concern about vision by parent/doctor
  • Asymmetric or diminishing VA
  • Constant or acute-onset strabismus
158
Q

Why is diplopia not present in children?

A
  • Brain will turn bad eye off.
159
Q

Adie’s Tonic Pupil (benign ciliary ganglionopathy). What is it? Who does it affect? Sx? Diagnosis+

A
  • 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
Q

What is Horner’s syndrome? Sx? Etiology?

A
  • 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
Q

Describe diagnosis of Horner’s syndrome?

A
  • Apraclonidine. It reverses anisocoria
162
Q

How to distinguish between congenital or acquired Horner’s syndrome?

A
  • 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.
163
Q

What is Argyll Robertson pupil? Diseases this is associated with?

A
  • Pupils accommodate, but don’t react to light. Pupils are irregular and small bilaterally usually. Associated with syphilis (prostitute’s pupil), DM, alcoholism.
164
Q

Diplopia during heavy exercise could indicate?

A
  • Aneurysm as etiology
165
Q

Diplopia when fatigued could indicate?

A
  • Myasthenia
166
Q

Diplopia associated with headache and retro-orbital pain could indicate?

A
  • Aneurysm
167
Q

PE findings for CN III paresis/palsy. Type of diplopia present?

A
  • 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
168
Q

Etiology of CN III paresis/palsy

A
  • IC aneurysm, vascular dz (HTN and DM), trauma, brain tumor
169
Q

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?

A
  • 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
170
Q

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?

A
  • CN III paresis/palsy d/t PCA aneurysm until proven otherwise. Do catheter angiogram or MRI/MRA.
171
Q

PE findings for CN IV palsy/paresis. Type of diplopia present?

A
  • SO isn’t working
  • Pupil: normal
  • Diplopia: vertical with compensatory head tilt to opposite shoulder (to affected eye)
172
Q

Etiology of CN IV paresis/palsy

A
  • Vascular dz (DM, HTN). If bilateral, closed head trauma.
173
Q

PE findings for CN VI palsy/paresis. Type of diplopia present?

A
  • LR isn’t working
  • Pupil: normal
  • EOM: loss of abduction
  • Diplopia: horizontal
174
Q

Etiologies of CN VI paresis/palsy

A
  • IC tumors, head trauma, vascular diseases, increased ICP (pseudotumor cerebri), demyelinated dz (MS)
175
Q

When checking for weakness in patient’s smile or ability to close eye while attempting to open them, what CN is being tested?

A
  • CN VII
176
Q

Myasthenia gravis ocular manifestations. How is diagnosis made?

A
  • 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.
177
Q

Types of nystagmus

A
  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
178
Q

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?

A
  • Pituitary tumor/apoplexy
179
Q

Blurred disc could mean?

A
  • Congenital abnormality (pseudopapilledema)
  • Papilledema (ICP increased)
  • Papillitis
180
Q

Etiology of papilledema

A
  • 50% d/t brain tumors/space occupying lesions

- Other = idiopathic intracranial HTN, cerebral trauma or hemorrhage, dural sinus thrombosis

181
Q

Can you know by looking at fundus whether or not it is papilledema or disc edema?

A
  • No. Look at symptoms. Get CT.
182
Q

What is idiopathic intracranial HTN (pseudotumor cerebri)? Which patient group? Sx? PE? Tx?

A
  • 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
183
Q

Sx of optic neuritis

A
  • Decreased vision, unilateral, red desaturation (decreased red visual detection), visual field defects
184
Q

Most common etiology of optic neuritis?

A
  • MS (50%)

- Other = ischemia, infiltration, postviral, sarcoidosis, Lyme, CTD?

185
Q

Tell difference between papilledema and optical neuritis

A
  • Papilledema: no RAPD, normal vision

- Optical neuritis: RAPD, abnormal vision

186
Q

Pallor of optic nerve, think…

A
  • Optic atrophy
187
Q

Common causes of optic nerve atrophy

A
  • Previous optic neuritis (multiple episodes), long-standing papilledema, compression of optic nerve (meningioma, thyroid), ischemia damage (GCA), glaucoma, previous trauma, toxins (ethambutol, methanol)
188
Q

Funduscopic finding in optic nerve atrophy

A
  • Bright light shining at you from disc
189
Q

Charles Bonnet syndrome. Presentation? Which patient group is affected?

A
  • Visual hallucinations with significant visual loss (
190
Q

When to check CN V and VII for eye issues?

A
  • If abnormal EOM and suspect CN palsy
191
Q

What do you suspect with slowly progressive visual loss or CN palsy?

A
  • Compressive lesion (tumor or aneurysm)
192
Q

What do you suspect with abrupt vision loss or diplopia?

A
  • Vascular dz (ischemia GCA or vasospasm)
193
Q

What are the ocular manifestations of diabetes?

A
  • Refractive error changes (sorbitol pathway), cataracts, retinopathy
194
Q

Factors that correlate with severity of diabetic retinopathy

A
  • Duration of dz, HTN, high A1C, smoking
195
Q

What is the pathogenesis of DM retinopathy?

A
  • High BGL = VEGF = neovascularization/increased capillary permeability
196
Q

Subgroups of diabetic retinopathy? What are the funduscopic findings?

A
  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
197
Q

When are NPDR patients at imminent risk for PDR?

A
  • Cotton wool spots, capillary dropout, venous beading (sausaging)
198
Q

Sx of vitreous hemorrhage

A
  • Floaters/cobwebs, sudden loss of vision
199
Q

Is ischemic maculopathy from DM reversible?

A
  • No
200
Q

Tx of diabetic retinopathy

A
  • 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
201
Q

Does PDR increase risk in DM patient for other complications?

A
  • Yes. Risk increased for MI, CVA, amputation, diabetic nephropathy and death.
202
Q

How often should diabetics receive ophthalmo exams?

A
  • Annually at least. If advanced dz, more frequently.
203
Q

Funduscopic characteristic changes seen with HTNsive retinopathy

A
  • Early: attenuation of arterioles (copper wiring, silver wiring) = AV nicking
  • Later: above + hard exudates, cotton wool spots and hemorrhages. Highest grade = + disc edema
204
Q

Eye changes seen in pregnancy

A
  • Refractive error changes, dry eyes, transient loss of accommodation, retinopathy (with pregnancy-induced HTN), rarely retinal detachments. If DM patient, progression of retinopathy.
205
Q

Eye features in Graves’ dz

A
  • 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
206
Q

Most common cause of uni/bilateral exophthalmos in adult

A
  • Graves’ dz

- Note: can progress after thyroid function returned to normal

207
Q

Tx of thyroid ophthalmology

A
  • Temporizing: artificial tears, steroids, orbital irradiation
  • Ultimately: surgery (EOM or decompression)
208
Q

Eye exam findings for iritis

A
  • White cells (snow globe) in anterior chamber
209
Q

Ocular findings in sarcoidosis

A
  • Key points: AA, photophobia, iritis/uveitis
210
Q

Most common ocular manifestation in RA

A
  • Dry eye syndrome

- Other: episcleritis/scleritis (not conjunctivitis), severe corneal ulcers

211
Q

Ocular findings in juvenile RA

A
  • Iritis asymptomatic and chronic (no photophobia). If unrecognized may lead to cataracts, glaucoma, corneal calcification
212
Q

Chemotherapeutic drugs with toxicity to eye

A
  • Cytosine arabinoside (superficial keratitis)
  • Vincristine (optic neuropathy)
  • BCNU (carmustine) – CRAO with carotid artery injection
213
Q

Ocular manifestations of AIDS

A
  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
214
Q

Tx for CMV retinitis

A
  • Gangiclovir, foscarnet, cidofovir
215
Q

Tx for herpes zoster ophthalmicus

A
  • Acyclovir, famacyclovir, valacyclovir

- Capsaicin for PHN

216
Q

Meds with irreversible toxic retinopathies

A
  • Hydrochloroquine, ethambutol

Ophthalmology (1 decks)

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