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2017 EENT Clin Med Group > Chronic Eye Diseases > Flashcards

Chronic Eye Diseases Flashcards

1
Q 
Keratoconjunctivitis sicca (Dry Eye)-
Etiology
A

Etiology

Decreased Tear Production

  • Sjogren syndrome
  • age-related duct obstruction
  • sarcoidosis, lymphoma, graft-vs-host (infiltrative dz)
  • contacts
  • DM

Increased evaporation loss

  • Meibomian gland dysfunction
  • decreased blinking
  • decreased eyelid integrity
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2
Q

Allergic Eye Disease-

Etiology

A

Etiology

  • usually occurs with allergic rhinitis, atopic dermatitis and asthma
  • IgE mediated hypersensitivity reaction
  • allergic conjunctivitis
  • acute, seasonal and year round subtypes
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3
Q

Age-Related Macular Degeneration-

Etiology

A

Etiology

  • degeneration of macula resulting in central vision loss
  • druses body accumulation in brunch membrane
  • Normal part of aging
  • sped up by risk factors
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4
Q

Open-Angle Glaucoma-

Etiology

A

Etiology

  • Progressive degeneration of optic nerve
  • cupping of optic disc with visual field defects from retinal ganglion loss
  • can occur with normal intraocular pressure
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5
Q

Open-Angle Glaucoma-

Epidemiology

A

Epidemiology

  • Second leading cause of irreversible blindness in US
  • only half aware they have disease
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6
Q

Open-Angle Glaucoma-

Pathophysiology

A

Pathophys

  • poor aqueous humor drainage at trabecular meshwork
  • pressure increases in anterior chamber and then rest of the globe
  • nerve damage due to intraocular pressure
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7
Q

Open-Angle Glaucoma-

Clinical Presentation

A

Clin Presentation

  • symptoms not until LATE in the disease
  • Hx eye pain or redness
  • multicolored halos visualized by pt
  • diminished peripheral
  • Headache
  • Previous ocular disease: cataracts, uveitis, diabetic retinopathy, vascular occlusions
  • Most of the time glaucoma found on IOP screening
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8
Q

Open-Angle Glaucoma-

Diagnosis

A

Diagnosis

  • Increasing cup to disc ratio
  • never fiber layer damage
  • perimetry
  • Scanning laser polarimetry
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9
Q

Open-Angle Glaucoma-

Management

A

Tx
-REFER to ophthalmologist
-Regular IOP screening and peripheral vision
-Control IOP
-Topical prostaglandins (increase Uber’s legal outflow)
Lumigan
Travatan
Xalatan
-Topical beta blockers (decrease aqueous humor production)
Timolol
-Laser or surgical trabedulectomy

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10
Q

Age-Related Macular Degeneration-

Risk Factors

A

Risk Factors

  • over 75
  • caucasians
  • females
  • family Hx
  • high BMI, CVD, inflamm conditions
  • Smoking
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11
Q

Age-Related Macular Degeneration-

Clinical Presentation

A

Clin Presentation

  • gradual onset blurred central vision
  • drusen body accumulation around macula (diff from hard exudates = diabetic retinopathy)
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12
Q

Age-Related Macular Degeneration-

Diagnosis

A

Diagnosis

  • dilated eye exam with slit lamp
  • optical coherence tomography (dry/wet AMD)
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13
Q

Age-Related Macular Degeneration-

Management

A 
Tx 
-Amsler grid (if asymptomatic)
-Stop smoking
-healthy lifestyle
-vitamin/mineral supplements
-advanced 
      vascular endothelial growth factor inhibitors (injection)
      Photodynamic therapy
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14
Q

Cataracts-

Etiology

A 
Etiology
-Lenses start out clear but gradually become opaque
-Subtypes
      Nuclear sclerotic (MOST COMMON)
      Posterior subcapular (DM or chronic steroid use)
      Congenital
      Traumatic
      Posterior capsular pacification
      Lens dislocation
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15
Q

Cataracts-

Clinical Presentation

A 
Clin Presentation 
-Gradual decrease in vision
-Glare
     Contrast sensitivity
     Daytime glare
     Difficulty driving at night
-Second sight (myopic shift)
     Claim to have improved vision after long-time use reading glasses
     Enlarging lens becomes more round
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16
Q

Cataracts-

Pathophysiology

A

Pathophys

-Gradual pacification of lens that obstructs vision

17
Q

Cataracts-

Management

A

Tx

  • Surgical therapies are only real success
  • Lens extraction
18
Q

Diabetic Retinopathy-

Etiology

A

Etiology

  • LEADING cause of complete blindness in the US
  • Chronic hyperglycemia
  • hypertension
  • hypercholesterolemia
  • Smoking
19
Q

Diabetic Retinopathy-

Clinical Presentation

A

Clin Presentation

Non-Proliferative

  • Dot/blot hemorrhaging
  • Hard exudates
  • Cotton-wool spots
  • Flame hemorrhages
  • mircoaneurysms
  • venous dilation

Proliferative
-neovascularization of optic disc
-vitreous hemorrhage
(proliferative presentation = closer to blindness)

20
Q

Diabetic Retinopathy-

Management

A

Tx

  • optimized glucose control
  • regulation of blood pressure
  • laser photocoagulation
  • vitrectomy

SEVERE DISEASE IS PERMANENT

21
Q

Hypertensive Retinopathy-

Etiology

A

Etiology

-Acute or accelerated hypertension greatest risk

22
Q

Hypertensive Retinopathy-

Clinical Presentation

A

Clin Presentation

  • Arteriolar narrowing
  • copper or silver wiring of retinal vasculature
  • flame shaped hemorrhages
  • cotton wool spots
  • hard exudates
  • AV nicking (atherosclerosis)
23
Q

Papilledema-

Etiology (Don’t worry too much about this one)

A

Etiology
-Increased intracranial pressure

  • malignant hypertension
  • hemorrhagic strokes
  • acute subdural hematoma
  • pseudotumor cerebri (idiopathic intracranial hypertension)
24
Q

Papilledema-

Clinical Presentation

A

Clin Presentation
-Pt may be asymptomatic or complain of transient visual alterations that last seconds

Early Fundoscopic Exam

  • Disc margins are blurred
  • disc hyperemia (discoloration)
  • small precapillary hemorrhages
  • loss venous pulsation

Late Fundoscopic Exam

  • vessels are obliterated within disc
  • very blurry disc margins
  • disc elevation
  • venous congestion with small hemorrhages, exudates and cotton wool spots

Frisen Scale
Used to measure 5 different progressive stages of papilledema
-Grade 1: C-shaped halo with temporal gap
-Grade 2: Halo becomes circumferential
-Grade 3: loss of major vessels as they LEAVE the disc
-Grade 4: Loss of major vessels ON the disc
-Grade 5: Partial or TOTAL obscurantism of vessels of the disc

25
Q

Papilledema-

Management

A

Tx

-Therapy for underlying cause

26
Q

Optic Neuritis-

Etiology

A

Etiology

  • Occurs in younger, white women from northern climates
  • 90% of pts with MS will develop optic neuritis
27
Q

Optic Neuritis-

Pathophysiology

A

Pathophys

  • Inflammation of the nerve, often demyelinating
  • Lesions occurring at different times and places that hit the optic nerve
  • Pts with optic neuritis sometimes progress to develop MS
28
Q

Optic Neuritis-

Clinical Presentation

A

Clin Presentation

  • Sudden vision loss
  • Decreased contrast and color sensitivity
  • pain with eye movement
  • optic nerve head edema
  • afferent pupillary defect
29
Q

Optic Neuritis-

Management

A

Tx
-MRI of brain and orbits (looking for enhancing lesions)
-IV steroids (NO ORAL - increases reoccurrence of MS)
-refer to neurology (for advanced lesions)
Interferon Tx (Avonex) to decrease progression

30
Q

Allergic Eye Disease-

Epidemiology

A

Epidemiology

-up to 20% of population (more common in young)

31
Q

Allergic Eye Disease-

Pathophysiology

A

Pathophys

- Mast cells - histamine release - vasodilation, vasopermeability - itching

32
Q

Allergic Eye Disease-

Clinical Presentation

A

Clin Presentation

  • BILATERAL
  • Excess tear production (diff from dry eye disease)
  • ITCHY, RED, BURNING (diff from bacterial conjunctivitis = not itchy)
  • Kemosis (doughnut formation - edema between conjunctiva and sclera)
33
Q

Allergic Eye Disease-

Differential Diagnosis

A

Differential

  • dry eye
  • viral conjunctivitis
  • keratitis (esp if unilateral)
  • blepharitis
  • toxic exposure
  • acute angle closure glaucoma
  • episcleitis (if eye pain)
34
Q

Allergic Eye Disease-

Management

A

Tx

  • Don’t rub eyes
  • cool compress
  • artif tears
  • discontinue contacts
  • allergen avoidance
  • topical antihistamines/mast cell stabilizers
35
Q 
Keratoconjunctivitis sicca (dry eye)-
Clinical Presentation
A

Clin presentation

  • Loss of luster
  • posterior blepharitis
  • Punctate epithelial lesions (fluorecin dye)
  • Injection neovascularization
  • corneal scarring (hazy area)
  • Burning
  • Blurry vision
  • photophobia
  • red
  • gritty eyes
36
Q 
Keratoconjunctivitis sicca (dry eye)-
Diagnostic Tests
A

Diagnostic tests

Low tear production

  • shirmers test
  • corneal sensation

Evaporative

-tear break up time

37
Q 
Keratoconjunctivitis sicca (dry eye)-
Differential Diagnosis
A

Differential diagnosis

  • Blepharitis (more crusting Presentation)
  • conjunctivitis (more acute onset - dry eye more chronic)
  • Allergic eye disease (Hx of allergies/allergen present)
38
Q 
Keratoconjuncivitis sicca (dry eye)-
Management
A

Tx

  • artificial tears is most used therapy
  • topical cyclosporine (if pts fail OTC artif tears)
  • improvement during and right after shower
39
Q 
Keratoconjunctivitis sicca (dry eye)-
Prevention
A

Prevention

  • blink more
  • avoid air currents to eyes
  • humidifier

2017 EENT Clin Med Group (13 decks)

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