The American Board of Ophthalmology (ABO) board certification process is one of the most rigorous in medicine, requiring mastery of ocular anatomy and physiology, diagnosis and management of major ophthalmic conditions, surgical indications, ophthalmic pharmacology, and clinical examination techniques. Candidates must pass a Written Qualifying Examination (WQE) and an Oral Examination, with the oral component testing clinical reasoning and surgical decision-making under direct questioning from senior examiners.
This free printable PDF covers high-yield ABO board topics across all major domains. Work through the questions offline during commutes, between clinical duties, or in any study environment where screen time is impractical. Use it alongside our online ophthalmology board practice tests to build the full breadth and depth the ABO exams demand.
The anterior segment extends from the cornea to the posterior lens capsule. The cornea has five layers (epithelium, Bowman's layer, stroma, Descemet's membrane, endothelium), with the endothelial pump function critical for transparency maintenance — endothelial cell loss below ~500 cells/mm² leads to bullous keratopathy. The trabecular meshwork sits at the iridocorneal angle and provides the primary outflow pathway for aqueous humor; dysfunction here is the mechanism in open-angle glaucoma. The crystalline lens is suspended by zonules (zonules of Zinn) attaching to the ciliary body; loss of zonular integrity is a key surgical complication consideration in phacoemulsification.
The retina has ten histological layers; the most clinically important for board purposes are the retinal nerve fibre layer (RNFL, lost in glaucoma and detected by OCT), the ganglion cell layer, and the photoreceptor layer (rods in the periphery, cones concentrated in the fovea). The optic disc lacks photoreceptors (the physiological blind spot) and is the site of axonal exit through the lamina cribrosa. Cup-to-disc ratio (CDR) assessment is a primary clinical measure in glaucoma monitoring — a CDR above 0.6 or asymmetry between eyes warrants investigation. The vitreous attaches most firmly at the vitreous base (anterior), the optic disc, and the macula — the posterior vitreous detachment (PVD) process and its complications (retinal tear, detachment) are high-yield board topics.
Primary open-angle glaucoma (POAG) is characterised by IOP elevation, optic nerve cupping, and visual field loss with an open iridocorneal angle on gonioscopy. The target IOP in treatment is typically 30% below baseline, though the concept of "normal tension glaucoma" (optic nerve damage at IOP ≤21 mmHg) reinforces that IOP is not the sole pathophysiological factor. Primary angle-closure glaucoma (PACG) involves pupillary block causing iris bowing anteriorly, appositional or synechial angle closure, and acute IOP spikes that can exceed 50 mmHg — an ophthalmic emergency requiring immediate IOP lowering (IV acetazolamide, topical beta-blocker, pilocarpine) followed by laser peripheral iridotomy (LPI).
Three main morphological types appear on board exams: nuclear sclerotic cataracts (most common, age-related, central lens yellowing causing myopic shift and reduced contrast sensitivity), cortical cataracts (spoke-like opacities radiating from the equator, associated with UV exposure and diabetes), and posterior subcapsular cataracts (PSC) — the most visually disabling type per unit opacity because they sit at the nodal point, causing glare, haloes, and near-vision reduction disproportionate to Snellen acuity. PSC is strongly associated with corticosteroid use and diabetes. Surgical indication is primarily visual function impairment; phacoemulsification with intraocular lens (IOL) implantation is the standard technique.
Non-proliferative diabetic retinopathy (NPDR) features microaneurysms, dot-blot haemorrhages, hard exudates, cotton-wool spots, and intraretinal microvascular abnormalities (IRMA). Clinically significant macular oedema (CSMO) can occur at any DR stage and is the primary cause of vision loss in diabetic patients. Proliferative diabetic retinopathy (PDR) is defined by neovascularisation — new vessels at the disc (NVD) or elsewhere (NVE) — driven by VEGF release in response to retinal ischaemia. Untreated PDR leads to vitreous haemorrhage and tractional retinal detachment. Treatment: anti-VEGF intravitreal injections (ranibizumab, bevacizumab, aflibercept) for CSMO; panretinal photocoagulation (PRP) for high-risk PDR.
Dry AMD features drusen accumulation (hard drusen: small, discrete; soft drusen: larger, confluent, higher risk of conversion) and geographic atrophy of the RPE. Wet (neovascular) AMD involves choroidal neovascularisation (CNV) growing through Bruch's membrane into the subretinal space, causing rapid central vision loss. OCT is the primary imaging tool — subretinal fluid and intraretinal fluid are key activity markers. Treatment for wet AMD: monthly or treat-and-extend intravitreal anti-VEGF (bevacizumab/Avastin, ranibizumab/Lucentis, aflibercept/Eylea). No approved pharmacological treatment for dry AMD; AREDS2 supplementation (vitamins C/E, zinc, copper, lutein, zeaxanthin) slows progression in intermediate AMD.
Prostaglandin analogs (latanoprost, travoprost, bimatoprost) are first-line IOP-lowering agents — they increase uveoscleral outflow and reduce IOP by 25–35%. Side effects include iris pigmentation changes, eyelash growth (hypertrichosis), and periorbital fat atrophy with long-term use. Beta-blockers (timolol, betaxolol) reduce aqueous production and lower IOP by 20–25%; betaxolol is cardioselective and preferred in patients with pulmonary disease, but timolol is more effective. Carbonic anhydrase inhibitors (dorzolamide topically, acetazolamide systemically) also reduce aqueous production; systemic acetazolamide is used in acute angle-closure emergencies. Alpha-2 agonists (brimonidine) both reduce production and increase outflow, with the added benefit of neuroprotective properties under investigation. Rho kinase inhibitors (netarsudil) increase trabecular outflow — a newer class with good IOP-lowering and a distinct redness side-effect profile.
Three anti-VEGF agents dominate retinal practice: bevacizumab (Avastin — off-label, low cost, full-length antibody), ranibizumab (Lucentis — Fab fragment, on-label for wet AMD, CSMO, RVO), and aflibercept (Eylea — VEGF trap, higher VEGF-A and PlGF affinity, longer dosing interval). All three are administered by intravitreal injection at 4-week intervals initially, then by treat-and-extend or PRN protocols. Faricimab (Vabysmo), a bispecific antibody targeting both VEGF-A and Ang-2, offers potential for extended dosing intervals up to 16 weeks in wet AMD and CSMO. The choice between agents in board exam questions often hinges on cost-effectiveness, dosing interval, and specific label indications.
Slit-lamp biomicroscopy is the core anterior segment examination tool — mastery of diffuse illumination, direct focal illumination, retroillumination, and specular reflection is expected. Gonioscopy (direct with Koeppe lens, indirect with Goldmann or Zeiss four-mirror lens) visualises the iridocorneal angle and is mandatory for glaucoma classification. Visual field testing on the Humphrey Field Analyser (HFA) produces pattern deviation probability plots — board-relevant patterns include arcuate scotomas (glaucoma), bitemporal hemianopia (chiasmal compression), homonymous hemianopia (retrochiasmal lesion), and central scotoma (macular or optic nerve disease). OCT provides cross-sectional imaging of the retina, macula, and optic disc — RNFL thickness maps and ganglion cell analysis are standard in glaucoma monitoring; subretinal and intraretinal fluid maps are standard in macular disease.
Phacoemulsification (cataract surgery) is indicated when visual impairment from lens opacity significantly affects daily function. The procedure uses ultrasound energy to emulsify the nucleus, aspirate cortex, and implant a foldable IOL into the capsular bag. Trabeculectomy creates a partial-thickness scleral flap and a guarded sclerostomy to allow aqueous drainage into a subconjunctival bleb; mitomycin C (MMC) is applied to reduce fibrosis and maintain bleb function. Intravitreal injection technique requires aseptic preparation, povidone-iodine conjunctival preparation, and injection 3.5–4 mm posterior to the limbus in the inferotemporal quadrant. Laser peripheral iridotomy (LPI) uses Nd:YAG laser to create a full-thickness hole in the peripheral iris, eliminating pupillary block in angle-closure glaucoma and prophylactically in narrow-angle eyes.