Ophthomology Clin Med Flashcards
Describe the epidemiology and pathophysiology of cataracts
epidemiology: leading cause of visual impairment + blindness in the WORLD
- prevalence increases with age
- F > M
pathophysiology: clouding of the ocular lens
can be acquired
- age =-related > 90%
- ocular diseases: DM, renal insufficiency
- drug induced: glucocorticoids
- traumatic: bruises
can also be congenital < 1 % of cases
What is the clinical presentation, diagnosis and treatment for cataracts?
clinical presentation
- develops gradually
- reduced visual acuity: blurred, clouded, or dim vision that’s worse at night
- impaired vision: painless, often bilateral
- severity and location determine impairment
diagnosis - primarily clinical
- fundoscopy: changed red reflex: opacities, darkening, absent or decreased
- slit lamp exam: clouded lens - gray, white, yellow or brown
treatment: surgery to remove the lens
What is the epidemiology of glaucoma?
second leading cause of blindness in the US
- only behind age-related macular degeneration
- 2.3 million cases in US
Describe the normal physiology of aqueous humor
produced by the ciliary body on the iris
- flows from the posterior chamber through the pupil into the anterior chamber
- drains back in the the venous system via trabecular meshwork in the angle of the anterior chamber
aqueous humor has an intraocular pressure of 10-21 mmHg
Describe the pathophysiology of open angle glaucoma
bilateral, progressive loss of optic nerve fibers with open chamber angles + increased IOP
- secondary clogging of the trabecular meshwork OR reduced drainage = increased IOP
- increased IOP causes vascular compression = ischemia to the optic nerve
What is the clinical presentation for open angle glaucoma?
often asymptomatic
- nonspecific: headache, impaired adaptation to darkness
- bilateral, progressive visual field loss
- arcuate scotoma: arch shaped scotoma that starts from the blind spot (see picture)
Describe the diagnosis for open angle glaucoma
slit lamp exam: normal anterior chamber angle
tonometry: used to measure IOP
- increased in 40%
- not required for diagnosis
fundoscopy:
- cupping/pallor of optic disc
- disc hemorrhage
- narrowing of optic disc rim
perimetry: to detect blind spot (scotoma)
Describe the treatment of open angle glaucoma
meds - first line: topical prostaglandin analogs: latanoprost, travoprost
alts:
- beta blockers (timolol)
- alpha-2 agonists (brimonidine)
- topical anhydrase inhibitors (brinzolamide)
interventional therapy: lowers IOP via drainage of aqueous humor
- laser trabeculoplasty
- surgical trabeculectomy
- tube shunt surgery
lower IOP by decreasing aqueous humor production: cyclodestructive surgery
Describe the epidemiology of age-related macular degeneration
leading cause of blindness in individuals > 65 in developed countries
onset usually > 55
F > M
describe the pathophysiology of age-related macular degeneration (wet and dry)
definition: progressive degenerative changes in the central part of the retina (macula) = visual impairment
Dry AMD ~ 90%
- deposition of yellow-white material (lipids + proteins) retinal pigment epithelium between it and the Brusch membrane
- causes slow, progressive atrophy of the local retinal pigment epithelium
Wet AMD ~ 10%
- choroidal neovascularization between retinal pigment epithelium and Bruch’s membrane
- leakage of intravascular serous fluid and blood causes sudden localized elevation of macula + detachment of the retinal pigment epithelium
What is the clinical presentation of age-related macular degeneration?
painless central or peri central visual impairment
- reduced visual acuity
- difficulty adapting to changes in lighting
- scotoma
- metamorphasia: visual lines appear wavy
- dry: slow, progressive, uni/bilateral
- wet: acute/insidious onset, manifests in one eye first
Describe how to diagnose dry AMD and what are the findings?
Amsler grid: detects metamorphasias and scotomas
fundoscopy:
- Drusen (yellow-white flecks around macula)
- retinal pigments epithelium atrophy/hypertrophy
fluorescence angiography:
- well-defined hyper fluorescence of the altered retinal pigment epithelium
Describe how to diagnose wet AMD and what are the findings?
amsler grid: detects metamorphopsias and scotomas
fundoscopy
- gray green retinal discoloration
- serous detachment of retina + pigment epithelium
- sub retinal and intraretinal hemorrhage and/or exudate
- fibrous disci form scars
fluorescence angiography: neovascularization and exuding in macular region
color fundus photography: evaluation of disease progression
optical coherence tomography
- detection of intraretinal/subretinal fluid retention
- helps confirm diagnosis of wet AMD
What is the treatment for age-related macular degeneration?
no curative treatment
supportive
- visual + reading aids
- antioxidant therapy: vitamin A, C, E, beta-carotene, zinc
- improve diet: higher in leafy veggies + fish
Wet AMD
first line: injection of VEGF inhibitors - bevacizumab
second line
- laser coagulation
- photodynamic therapy: causes thrombosis of sub retinal neovascularization
Describe the epidemiology and pathophysiology of giant cell arteritis?
F > M
Peak incidence 70-90
pathophysiology: thought to be due to cell-mediated immune response to endothelial injury
- possible a mechanism of inflammation, local vascular damage, and stimulation of vascular wall proliferation
What is the clinical presentation for giant cell arteritis?
non-specific: constitution, symptoms of anemia, musculoskeltal pain + morning stiffness in shoulders + neck
extra cranial branches of the common carotid, internal carotid, and external carotid
hardened tender temporal artery
jaw claudication - jaw pain with chewing
vision loss - occlusion/inflammation of ophthalmic artery
- scintillating scotoma: arch shaped blind spot
- amaurosis fugax - permanent loss of vision
What would you see in the labs of someone who has giant cell arteritis? What is the gold standard for diagnosing GCA?
inflammatory markers: increased ESR, CRP
CBC - thrombocytosis
GOLD STANDARD - temporal artery biopsy
- arteritis of large and medium arteries
- proliferation of the intima
- necrosis of the media
Duplex US - firs line imaging for suspected GCA
- edema + thickening of vessel wall
What is the treatment for giant cell arteritis?
glucocorticoids - HIGH DOSE
- mostly to prevent worsening or spreading to other eye
Describe the clinical presentation, pathophysiology, and diagnosis of a corneal abrasion
pathophysiology: defects in epithelial surface caused by trauma
- direct injury, foreign body, trachoma
clinical presentation:
- foreign body sensation
- eye pain
- epiphora - excessive tears
- photophobia
- blurred vision
- conjunctival injection
diagnosis
- clinical
- slit lamp exam with fluorescein staining
Describe the pathophysiology, clinical presentation, diagnosis and management of corneal ulcer?
pathophys: defect of corneal epithelium + underlying stroma that occurs secondary to infection/inflammation
clin man: foreign body sensation, pain, tears, photophobia, blurred vision, conjunctival injection
- DISCHARGE FROM EYE
diagnosis: slit lamp exam + fluorescein stain
tx:
- bacterial keratitis - antibiotics
- herpes simplex/zoster - antivirals
What are clinical manifestations and management of chemical eye injuries?
signs:
- erythematous/whitened conjunctiva
- cloudy cornea
- swelling and burns to eyelid
symptoms:
- intense pain
- blepharospasms (eyelid twitch) + involuntary eyelid closure
- photophobia + epiphora (eye watering)
- visual impairment
management: IMMEDIATE LARGE GOLUME IRRIGATION
- topical anesthetic
- measure pH of fornixes: must be 7-7.5
What is endophtalmitis and what is its pathophysiology?
pathophysiology: inflammation of the vitreous humor
infectious:
exogenous entry: surgery, injections
endogenous: hematogenous spread
- bacteria
What are the clinical manifestations of acute endophtlamitis?
endophthalmitis: inflammation of vitreous humor
