Block 7 Ophtho Flashcards

1
Q

Cataract

A

Degradation of optical quality of crystalline lens

Nuclear cataract: central opacification; progress slowly; affect distance vision

Cortical cataract: central or peripheral; symptom is glare

Posterior subcapsular cataract: visual impairment if affect axial region of lens; in younger patients; symptoms are glare and poor vision with bright light; near vision more affected

Mixed cataract: predominant type; some of many types

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2
Q

Treatment of cataract

A

Once vision starts declining, no chance of recovery unless there is surgical intervention

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3
Q

Glaucoma

A

Damage to the optic nerve in a characteristic pattern

Usually associated with increased intraocular pressure (IOP)

Open angle (no symptoms until vision loss) or closed angle (halos around lights, blurry vision, pain, headache)

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4
Q

Treatment of glaucoma

A

No cure at this time

Goal is to lower eye pressure

Medications, laser surgery or incisional surgery

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5
Q

Age-related macular degeneration

A

Gradual destruction of macula (central part of retina) causing central vision loss

Usually in people age 50 and older

Risk factors: smoking, caucasian, family history (genetic risk)

Diagnosed with dilated eye exam

Symptoms: early on no symptoms, then difficulty adjusting to lights at night, distortion of central vision, late symptoms are blurred central vision then central dark spot

Symptoms are gradual for dry form and sudden/rapid for wet form

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6
Q

Dry vs. Wet AMD

A

Either form can cause severe vision loss

Almost all who have wet form had dry form first

Dry: 90% (more common), slow break down of cells in macula slowly blurs central vision, drusen (yellow deposits under retina), pigment disturbances, pigment epithelial detachments, geographic atrophy

Wet: 10%, advanced AMD, when new blood vessels under macula leak blood and fluid (choroidal neovascular membranes cause disciform scars), treat with drug injections, photodynamic therapy, laser therapy

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7
Q

Thyroid eye disease (TED)

A

AKA Grave’s ophthalmopathy, Grave’s orbitopathy, Dysthyroid orbitopathy, Thyroid-associated orbital disease

Autoimmune inflammatory disease

2 phases: active/dynamic and static/inactive

Clinical diagnosis

Thyroid function may be normal, hyper or hypo (TED can arise before or after thyroid disease manifests)

Severe effects on visual function (5% go blind), appearance: proptosis, periorbital swelling, double vision, sight threatening (corneal ulceration, compressive optic neuropathy), fibrosis

Treatment: corticosteroids (oral or injection)

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8
Q

Staged surgical management of TED

A

1) Orbital decompression: remove bone and fat from behind eye or medial wall of orbit
2) Extraocular muscle surgery: remove muscle then suture back together
3) Eyelid repositioning
4) Soft tissue redraping: cosmetic rejuvenation

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9
Q

Diabetic retinopathy

A

With Type I, get DR 3-5 years after onset of DM

With Type II, get vision loss/DR as presenting symptom

Long term hyperglycemia is a cause

HTN is risk factor

Pathophysiology of blood vessel disease: microaneurysms, capillary BM thickening, neovascularization, VEGF

Macular edema, central macular ischemia, proliferative DR (treat with panretinal photocoagulation)

Summary: poor glycemic control –> capillary occlusion/permeability –> retinal ischemia –> increased VEGF –> vitreous hemorrhage, traction retinal detachment lead to vision loss; macular edema due to VEGF causes vision loss too

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10
Q

Eye examination for diabetes

A

Type I: get first eye exam 5 years after onset; yearly follow-up

Type II: get eye exam at time of diagnosis; yearly follow-up

During pregnancy w/diabetes: get eye exam before pregnancy for counseling then early in first trimester, then each trimester or even more frequently; 3-6 months post partum follow-up

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11
Q

Eye disease and syphilis

A

Interstitial keratitis

Uveitis: anterior uveitis and subretinal plaques

Jarisch-Herxheimer reaction: inflammation after beginning antibiotics when spirochetes are dying

Argyll-Robertson pupil

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12
Q

Eye disease and gonorrhea

A

Natural pathogen means can affect mucus membrane even when epithelium is intact (goes thru intact epithelial barriers)

Copious purulent discharge

Requires systemic treatment

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13
Q

Inclusion conjunctivitis

A

Chlamydia trachomatis serotypes D-K

Always associated with GU infection

Requires systemic treatment

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14
Q

HLA-B27 acute anterior uveitis (AAU)

A

Most common intraocular inflammation (uveitis)

Sudden onset, one eye, lasts 1 month but is recurrent

Gut disease (mucosal): subclinical colitis

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15
Q

Vitamin A deficiency

A

Vitamin A needed for absorption of light (rhodopsin)

Mutations in genes for enzymes cause some forms of retinitis pigmentosa

Night blindness (nyctalopia)

Dry eye (bitots spots, corneal damage, secondary infection)

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16
Q

Posterior segment manifestations of collagen vascular diseases

A

Retinal vasculitis

Occlusive retinal vasculopathy

Exudative retinal detachment

17
Q

Anterior segment manifestations of collagen vascular diseases

A

Keratoconjunctivitis sicca (Secondary Sjogren’s Syndrome)

Scleritis

Corneal involvement, especially peripheral corneal ulcers

Treatment complications

18
Q

Dry eye

A

Keratoconjunctivitis sicca

2 types fo dry eye: evaporative and aqueous deficiency (don’t produce aqueous from lacrimal gland; most associated with CVD)

Symptoms: dryness, soreness (scratchy or gritty sensation), photophobia, worsens over course of day, vision disturbance

Signs: conjunctival hyperemia, staining of cornea and conjunctiva, eyelid manifestations

Treatment: artificial tears (w/ or w/o preservatives), eyelid hygiene, punctal plugs, restasis, ointments

19
Q

Immune-mediated eye disorders

A

Allergic conjunctivitis: hay fever conjunctivitis, vernal keratoconjunctivitis, atopic keratoconjunctivitis, contact lens-associated giant papillary conjunctivitis

Stevens-Johnson syndrome

Ocular mucous membrane pemphigoid

Thygeson superficial punctate keratitis

Episcleritis

Scleritis