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The Eye > Chronic Eye Disease - 9/1 > Flashcards

Chronic Eye Disease - 9/1 Flashcards

1
Q

What is the common name for Keratoconjunctivities Sicca?

A

Dry Eye

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2
Q

Dry Eye (KS) - Epidemiology

A
  • very common (5-30%)
  • Elderly
  • Female
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3
Q

Dry Eye (KS) - DDX

A
  • blepharitis
  • conjunctivitis
  • allergic eye disease
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4
Q

Dry Eye (KS) - Treatment/Management

A
  1. Non-pharmacologic
    • blink more often
    • avoid ac/heating
    • use humidifier (esp. at night)
    • moisture chamber glasses/goggles
  2. Artificial Tears - Mainstay (OTC)
  3. Restasis (topical cyclosporine) - prescription with immunosuppressive char. Must fail OTC artificial tears. Doesn’t work for everyone and really expensive (donut hole)
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5
Q

Dry Eye - Diagnosis and Tests

A
  • tear break-up time (E)
  • Schirmer’s tear test - (LP)
  • corneal sensation (LP) - low sensitivity
  • tear hyperosmolarity (non-specific)
  • ocular surface inflammatio (non-specific)
  • Questionnaires (non-specific)
    • ocular surface disease index (OSDI)
    • impact of dry eye on everyday life (IDEEL)
    • Salisbury eye evaluation questionnaire (SEE)

(E) = evaporative

(LP) = low production

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6
Q

Dry Eye - Etiology (2 causes)

A
  1. Decreased tear production
  2. Increased evaporative loss of tears (can be from quality of tear film or exposure)
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7
Q

Dry Eye - Clinical Presentation

Symptoms

Signs

A
  1. Symptoms:
    • irritation
    • feeling of grittiness or sand
    • redness
    • photophobia
    • burning
    • blurry vision
  2. Signs:
  • conjunctival injection
  • loss of luster
  • mebomian gland dysfunction
  • punctate epithelial lesions
  • neovascularization
  • corneal scarring
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8
Q

Dry Eye - Decreased Tear Production

Pathophysiology

A
  • Sjogren Syndrome - autoimmune disease that cuases decreased fluid secretion
  • Age-related duct obstruction
  • infiltrative disease (attacks lacrimal gland) - sarcoidosis, lymphoma, graft-vs-host
  • contact lens use (reflexive decrease in tears)
  • DM

Decreased tear production–>hyperosmolar tear film–>inflammation of ocular surface cells on cornea

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9
Q

Dry Eye - Increased Evaporative Loss

Etiology/Pathophys

A
  • meibomian gland dysfunction (aka posterior blepharitis) - decreased lipid in tears, so they evaporate faster
  • decreased blinking - staring at a computer screen
  • decreased eyelid integrity (TED, entropian)
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10
Q

Allergic Eye Disease - Definition and subtypes

A

Allergic conjunctivitis

acute allergic conjunctivitis

  • exposure to allergen
  • rapid (less than one hour) onset

seasonal allergic conjunctivitis (Hay Fever)

Outdoor environmental allergen

  • spring = tree pollens
  • summer = grass pollens
  • late summer/early fall = weed pollens
  • slow onset, constant through season

perennial allergic conjunctivitis - year-round symptoms to ubiquitous allergens (mold, dust mites, etc.)

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11
Q

Allergic Eye Disease - Epi

A
  • 20% of the population
  • more common in young
  • decreasing prevalence with age
  • commonly co-occurs with other allergic disorders
    • allergic rhinitis
    • atopic dermatitis
    • asthma
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12
Q

Allergic Eye Disease - Pathophys.

A

IgE mediated hypersensitivity reaction

Mast cells cause histamine release which in turn, causes vasodilation, vasopermeability, itching

attracts, eosinophils, basophils and neutrophils

then monocytes and lymphocytes

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13
Q

Allergic Eye Disease - Clinical Presentation

A
  • itchy
  • burning
  • red

bilateral

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14
Q

Allergic Eye Disease - DDX

A
  • dry eye
  • viral conjunctivitis
  • keratitis (esp. if unilateral)
  • blepharitis
  • toxic exposure
  • acute angle closure glaucoma
  • episcleritis - layer on top of sclera inflammed (if eye pain)
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15
Q

Allergic Eye Disease - Management and Treatment

A
  • don’t rub eyes
  • cool compresses
  • artificial tears
  • discontinue contact lens use
  • allergen avoidance
  • antihistamines/mast cell stabilizers (goal is vasoconstriction)
    • visine-A (antihistamine/vasoconstric)
    • alaway - (antihistamine/mast cell stab.)
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16
Q

Age-Related Macular Degeneration (AMD)

Definition

A
  • degeneration of the macula resulting in central vision loss
  • normal part of aging
  • can be accelerated by certain risk factors
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17
Q

AMD - Epi

A
  • Age - 40% of 75+ have some form
  • white>Asian>Hispanic>Black
  • F>M
  • Genetics - Ask about FH
  • Disease-related factors
    • High BMI
    • CV Disease
    • inflammatory conditions
  • Smoking (2x more likely) - progress from dry to wet faster
18
Q

AMD - Clinical Presentation

A

Symptoms - gradual onset of blurred central vision in one or both eyes

Signs - Drusen body accumulation around the macula (dist. from hard exudates).

Amsler grid distortion

19
Q

AMD - Pathophysiology

A

Vascular Endothelial Growth Factor (VGEF) - produced in excess in eye promotes neovascularization but the vessels do not reach maturity. They are friable and bleed and leak.

Leaking vessels is more prominent in wet, which is advanced form. Most are dry (80%) and stay dry.

20
Q

AMD - Treatment and Management

A
  • quit smoking
  • vitamin and mineral supplements (lutein in particular)
  • Advanced disease - injectable VEGF inhibitors (4-8 weeks)
  • photodynamic therapy
21
Q

Primary Open-Angle Glaucoma (POAG)

Definition

A

Progressive degeneration of the optic nerve with cupping of the optic disc and visual field defects.

NB: CAN OCCUR WITH NORMAL IOP

22
Q

POAG - Pathophysiology

A
  • poor drainage of aqueous humor at trabecular mesh network
  • increases anterior chamber pressure
  • translation of pressure to rest of globe
  • nerve damage due to IOP increase

but, there’s issues with this model (because IOP can be normal)

23
Q

POAG - Epi

A
  • 1/2 of people aware they have disease
  • cited as second leading cause of irreversible blindness
  • 2.25 over 40 in U.S. have POAG
24
Q

POAG - Clinical Presentation

A
  • hx of eye pain or redness
  • halos around lights (rainbows)
  • diminshed peripheral vision
  • headache (elevated IOP)
  • previous ocular disease
25
Q

POAG - Diagnosis (Testing)

A
  • usually found on routine eye exam (most are covered every 2 years)
    • normal IOP is 12-22 mmHg
    • ocular hypertension >22 mmHg with no evidence of glaucoma
  • Increasing cup:disk ratio (greater than 0.5)
  • Photograph retina to tell extent of nerve damage
  • Perimetry - available in ophtho.
26
Q

POAG - Rx and Prevention

A
  • Regular screening of IOP and peripheral vision
  • medications (topical protaglandins increase uveoscleral outflow) - the “prosts” (Bimatoprost/Lumigan; Travoprost/Travatan; Latanoprost/Xalatan)
  • topical Beta Blockers (decrease aqueous humor production) - Timolol (Timoptic)
  • Laser trabeculoplasty
  • surgical trabulectomy
    • last two focus on improving drainage
27
Q

Cataracts - Definition

A
  • opacification of the lens
28
Q

Cataracts - Types

A
  1. Nuclear sclerotic cataract (most common)
    • aging lens becomes larger and more dense
    • gradual opacification that obstructs vision
    • potential for iris and lens to touch - POAG
  2. posterior subcapsular cataract
    • opacification of the posterior capsule
    • DM or chronic steriod use causes
  3. congenital
  4. traumatic
  5. posterior capsular opacification (side effect of cataract surgery - ironic)
  6. lens dislocation
29
Q

Cataracts - Clinical Presentation

A
  • People complain of decline in vision, but it is really color vision and sharpness that goes
  • glare - daytime glare/night driving
  • second sight (aka myopic shift) - presbyopia disappears because of “tired” lens changing shape
  • cloudiness on the lens during exam
30
Q

Cataract - Treatment

A
  • sunglasses for glare
  • avoid night driving
  • surgical replacement with artificial lens
31
Q

Diabetic Retinopathy - Definition

A

Disease of the retina from persistent hyperglycemia. Leads to destruction of the retina and blindness.

32
Q

Diabetic Retinopathy - Epidemiology

A
  • Type I - 3-5 years after onset of systemic disease
  • Type II - DR usually present at the time of diagnosis of DM
  • Can occur with GD
  • Risk factors:
    • chronic hyperglycemia
    • hypertension
    • hypercholesterolemia
    • smoking
33
Q

Diabetic Retinopathy - Clinical Presntation

A

Fundoscopic Exam:

Non-Proliferative

  • Dot and Blot hemmorrhages
  • hard exudates (lipid deposition)
  • microaneurysms
  • cotton wool spots
  • flame hemorrhages - within superficial nerve fiber layer

Proliferative

  • neovascularization
  • vitreous hemorrhage (due to new blood vessels that are friable permeating into humor)
34
Q

Diabetic Retinopathy - Rx

A
  • Treat DM
  • Then, for non-proliferative DR:
    • Anti-VEGFs
    • intravitreal corticosteriod implants
    • focal photocoagulation therapy
    • vitrectomy
  • For proliferative
    • panretinal laser photocoagulation
35
Q

Papilledema - Definition

A

swelling of the optic nerve and disc

36
Q

Papilldema - Causes

A
  • tumors
  • space-occupying lesions of the CNS
  • subarachnoid hemorrhage
37
Q

Papilledema (Clinical Presentation)

A
  • Early
    • blurred disc margins
    • disc hyperemia
    • small peripapillary hemorrhages
    • loss of venous pulsation
  • Late
    • very blurry disc margins
    • elevation of disc
    • venous congestion with small hemorrhages, exudates, cotton wool spots
38
Q

Papilledema - Frisen Scale

A
  • O = normal
  • Stage 1 = C=shaped halo of disc edema with preservation of the temporal disc
  • Stage 2 = papilledema is a circumferential halo of edema on the disc
  • Stage 3 = elevation of disc with partial obstruction of one or more segments of the blood vessels at the disc margin
  • Stage 4 = characterized by almost complete obscuration of the major blood vessels on the disc
  • Stage 5 = partial or total obscuration of all blood vessels on the surface of the disc
39
Q

Hypertensive Retinopathy - Definition

A
  • Damage to the retina resulting from elevated systemic hypertension
40
Q

Hypertensive Retinopathy - Path

A
  • High pressure causes
    • damage to the endothelial lining of vessels in retina
      • weakens endothelium
      • endothelium breaks
    • vasoconstriction of retinal vessels to reduce flow and pressure
      • damages to smooth muscles (fatigue)
      • microaneurysms
      • endothelium breaks
    • Hemorrhages
    • Plasma leaks into vessel wall
    • plasma clots in vessel wall
    • wall thickens, lumen narrows
    • areas of ischemic damage (cotton wool spots)
41
Q

Hypertensive Retinopathy - Clinical Presntation

A
  • arterial narrowing
  • AV nicking
  • copper or silver wiring
  • flame shaped hemorrhages
  • cotton wool spots
  • hard exudates
42
Q

Hypertensive Retinopathy - RX

A
  • Treat the underlying HTN
  • Then:
    • laser therapy
    • intravitreal corticosteriod injection
    • anti-VEGF

The Eye (3 decks)

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