Glaucoma Study Guide

📖 Core Concepts Glaucoma – a group of eye diseases that damage the optic nerve, often silently, leading to progressive vision loss. Intra‑ocular pressure (IOP) – the fluid pressure inside the eye; the main modifiable risk factor. Normal ≤ 21 mm Hg. Open‑angle vs. angle‑closure – Open‑angle: trabecular meshwork obstruction, painless IOP rise. Angle‑closure: iris blocks the trabecular meshwork, causing rapid IOP elevation and pain. Optic‑nerve cupping – enlargement of the optic‑disc cup‑to‑disc ratio, seen on fundus exam; hallmark of glaucomatous damage. Visual‑field loss pattern – peripheral (Bjerrum’s area) defects appear first; classic arcuate scotomas, nasal steps, tunnel vision. --- 📌 Must Remember IOP thresholds – > 21 mm Hg is abnormal; > 24 mm Hg markedly increases risk. Risk hierarchy – Age ↑ → ethnicity (African‑American, Latino, Asian) ↑ → family history (2‑4×) ↑ → steroid use ↑. First‑line drug – Prostaglandin analogues (latanoprost, bimatoprost) ↑ uveoscleral outflow. Laser options – SLT ≈ eye‑drops for IOP control; ALT is older, higher side‑effect profile. Surgical gold standard – Trabeculectomy with antimetabolites for advanced disease. Key trial outcomes – TAGS: similar vision/QoL for drops vs trabeculectomy; LiGHT: SLT often eliminates need for drops. Screening age – Begin at 40 yr, earlier if risk factors present. --- 🔄 Key Processes Aqueous humor flow Produced by ciliary body → posterior chamber → pupil → anterior chamber → drains via trabecular meshwork → Schlemm’s canal. Open‑angle IOP rise Trabecular meshwork degeneration/obstruction → ↓ outflow → chronic IOP elevation. Angle‑closure IOP rise Iris apposes trabecular meshwork → iridocorneal angle closes → acute blockage → rapid IOP spike. Medication mechanism Prostaglandins: ↑ uveoscleral outflow. Beta‑blockers: ↓ ciliary body aqueous production. Alpha‑2 agonists: ↓ production + ↑ outflow. Carbonic anhydrase inhibitors: ↓ aqueous synthesis. Laser trabeculoplasty (SLT/ALT) Apply laser spots to trabecular meshwork → cellular remodeling → enhanced outflow. --- 🔍 Key Comparisons Prostaglandin analogues vs. Beta‑blockers – ↑ outflow vs. ↓ production; prostaglandins are first‑line due to greater IOP drop and once‑daily dosing. SLT vs. ALT – Low‑energy selective (SLT) → fewer complications, repeatable; thermal (ALT) → higher inflammation, less repeatable. Open‑angle vs. Angle‑closure glaucoma – Chronic painless IOP rise vs. Acute painful attack with mid‑dilated pupil and halos. Trabeculectomy vs. Glaucoma drainage implant – Trabeculectomy: fistula, high success in early disease; implants: preferred when scarring risk high or previous surgery failed. --- ⚠️ Common Misunderstandings “Normal‑tension glaucoma” means no treatment – IOP may be normal, but optic‑nerve damage still requires IOP‑lowering therapy. All glaucoma patients need surgery – Most start with topical meds; surgery reserved for uncontrolled IOP or adherence issues. IOP alone predicts progression – Vascular and neurodegenerative factors also contribute; visual‑field testing is essential. Angle‑closure only occurs in Asians – Higher prevalence, but can affect any ethnicity; women are at higher risk. --- 🧠 Mental Models / Intuition “Water‑pipe model” – Think of the eye as a pipe: production (pump) = ciliary body, drainage (drain) = trabecular meshwork. Blocked drain → pressure builds. “Spot‑the‑hole” – In optic‑nerve head, the lamina cribrosa’s pores are like tiny holes; high pressure squeezes axons, like a clogged filter, leading to ganglion‑cell death. “Early field loss in the periphery” – Imagine the visual field as a dartboard; glaucoma knocks out the outer rings first (Bjerrum’s area). --- 🚩 Exceptions & Edge Cases Normal‑tension glaucoma – IOP ≤ 21 mm Hg but still progressive; consider vascular insufficiency, neurodegeneration. Steroid‑induced glaucoma – May develop high IOP even with normal anatomy; stop steroids if possible. Neovascular glaucoma – Driven by retinal ischemia (e.g., proliferative diabetic retinopathy); requires anti‑VEGF + IOP‑lowering therapy. --- 📍 When to Use Which Mild‑moderate POAG, good adherence → Start prostaglandin analogue. Contra‑indication to prostaglandins (e.g., uveitis) → Beta‑blocker or carbonic anhydrase inhibitor. Poor adherence or intolerable drops → Consider SLT (first‑line laser) or trabeculectomy for advanced disease. Acute angle‑closure attack → Immediate miotic (pilocarpine), systemic carbonic anhydrase inhibitor, then laser iridotomy/iridoplasty. Failed trabeculectomy or high scarring risk → Glaucoma drainage implant or MIGS (iStent, Xen). --- 👀 Patterns to Recognize Peripheral visual‑field loss + optic‑nerve cupping → classic POAG. Mid‑dilated, non‑reactive pupil + halos + corneal edema → acute angle‑closure. Rapid IOP rise after steroid use → steroid‑induced secondary glaucoma. Neovascularization on retina + very high IOP → neovascular glaucoma. --- 🗂️ Exam Traps Choosing “ALT” over “SLT” as first‑line laser – SLT is the evidence‑based first‑line; ALT is outdated. Assuming normal IOP rules out glaucoma – Normal‑tension glaucoma disproves this. Believing prostaglandins are contraindicated in all uveitis – Some prostaglandins can be used cautiously; the key is avoiding exacerbation of inflammation. Confusing “open‑angle” with “high‑tension” only – Open‑angle can be high‑ or normal‑tension; the angle status, not pressure level, defines the subtype. ---