Ophthalmology
Eye Anatomy
Cornea, lens, retina — how light becomes vision
The eye is a 24 mm sphere that focuses light onto the retina. The cornea provides about 65% of refractive power; the lens fine-tunes via accommodation by ciliary muscle contraction. The pupil controls light through iris muscles (sphincter parasympathetic, dilator sympathetic). Aqueous humor is made by ciliary body, drains through the trabecular meshwork at Schlemm's canal — IOP normally 10-21 mmHg. The vitreous fills the posterior cavity. The retina contains rods (~120 million, scotopic, peripheral) and cones (~6 million, photopic, central) — with the fovea at the macula center for sharpest vision. The optic nerve carries 1.2 million axons to the lateral geniculate nucleus and visual cortex. The retina has no pain fibers; pathology is silent.
- Eye diameter~24 mm axial length
- Refractive powerCornea ~43 D; lens ~19 D; total ~60 D
- Normal IOP10-21 mmHg
- Photoreceptors~120 million rods, ~6 million cones
- Aqueous turnover2.5 µL/min; full turnover ~100 minutes
- Optic nerve1.2 million axons (CN II)
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Why eye anatomy matters
- Sudden vision loss. Localizes the lesion — cornea, vitreous, retina, optic nerve, cortex.
- Diabetic care. Annual dilated exam screens for retinopathy.
- Hypertension. Fundus shows AV nicking, hemorrhages, papilledema.
- Stroke localization. Visual field defects pinpoint the brain lesion.
- Increased intracranial pressure. Papilledema is a key sign.
- Drug toxicity. Hydroxychloroquine, ethambutol, amiodarone, digoxin all hit vision.
- Pediatric red reflex. Absent reflex screens for retinoblastoma and cataract.
Common errors
- Dilating pupils in suspected acute angle-closure. Triggers crisis.
- Treating red eye with steroids before slit lamp. Worsens herpetic dendrites and bacterial keratitis.
- Patching a bacterial corneal abrasion. Promotes infection — treat with topical antibiotic, no patch.
- Calling diplopia migraine. Could be CN III palsy, posterior communicating aneurysm, MS, myasthenia.
- Skipping fundus in headache. Misses papilledema and idiopathic intracranial hypertension.
- Ignoring flashes and floaters. Posterior vitreous detachment may herald retinal tear or detachment.
Frequently asked questions
How does the eye focus?
Cornea provides fixed refraction (~43 D). Lens accommodates — ciliary muscle contracts, zonules relax, lens becomes more spherical, refractive power increases for near vision. Presbyopia develops after age 40 as lens stiffens, requiring reading glasses. Myopia (nearsighted) — eye too long or refractive power too high; corrected with concave lens. Hyperopia (farsighted) — opposite. Astigmatism — irregular corneal curvature. LASIK reshapes cornea; cataract surgery replaces clouded lens with intraocular lens.
What is glaucoma?
Optic neuropathy with progressive visual field loss, often with elevated IOP. Open-angle glaucoma — slow trabecular outflow obstruction; painless peripheral vision loss; second leading cause of blindness worldwide. Treat with prostaglandin analogs (latanoprost), beta blockers (timolol), alpha agonists (brimonidine), carbonic anhydrase inhibitors (dorzolamide), surgery. Acute angle-closure — sudden severe pain, halos, fixed mid-dilated pupil; emergency — pilocarpine, timolol, acetazolamide, mannitol, then laser peripheral iridotomy.
What's diabetic retinopathy?
Microvascular damage from chronic hyperglycemia. Non-proliferative — microaneurysms, dot-blot hemorrhages, hard exudates, cotton wool spots. Proliferative — neovascularization with risk of vitreous hemorrhage and tractional retinal detachment. Macular edema causes most vision loss. Treat — glucose control (HbA1c <7%), blood pressure control, anti-VEGF injections (ranibizumab, aflibercept, bevacizumab), focal laser, panretinal photocoagulation. All diabetics need annual dilated exam.
How does the retina work?
Light traverses inner retinal layers to reach photoreceptors at the back. Rods contain rhodopsin — high sensitivity, no color, dominant in scotopic vision. Cones contain three opsins (S 420 nm, M 530 nm, L 560 nm) — photopic, color vision. Phototransduction — light isomerizes 11-cis retinal to all-trans, activating transducin G-protein, PDE, hydrolyzing cGMP, closing Na channels, hyperpolarizing the cell. Signal traverses bipolar then ganglion cells; ganglion axons form the optic nerve.
What is macular degeneration?
Leading cause of blindness in elderly Western populations. Dry AMD (90%) — drusen deposits, slow central vision loss; AREDS2 vitamins (vitamin C, E, zinc, copper, lutein, zeaxanthin) slow progression. Wet AMD (10%) — choroidal neovascularization, sudden distortion (Amsler grid metamorphopsia), rapid central vision loss; treat with intravitreal anti-VEGF every 4-8 weeks. Risk factors — age, smoking, family history, light skin/eye color.
What does pupillary exam reveal?
Anisocoria — unequal pupils. Worse in light suggests parasympathetic defect (CN III palsy, Adie tonic pupil); worse in dark suggests sympathetic defect (Horner syndrome — ptosis, miosis, anhidrosis). Marcus Gunn pupil (afferent defect) — swinging flashlight test shows dilation when light moves to affected eye, suggests optic neuritis or large retinal lesion. Fixed dilated pupil with eye pain — angle-closure glaucoma. Bilateral fixed dilated — brainstem disaster.
What's a retinal detachment?
Separation of neurosensory retina from RPE. Symptoms — flashes (photopsias), floaters, curtain or shadow over vision. Rhegmatogenous (most common) — retinal tear with fluid through. Tractional — diabetic, sickle cell. Exudative — tumor, inflammation. Emergency — refer same day. Treat with pneumatic retinopexy, scleral buckle, or pars plana vitrectomy with gas or silicone tamponade. Macula-on detachment has better prognosis than macula-off.