CLINICAL METHODS IN DIAGNOSIS OF POAG OPTIC DISC million axons/ 5000 loss/year 10% Magnocellular 90% Parvo- SIZE AND SHAPE DD: 1.5mm Surface: mm2 (π/4xHDxVD) AGE: no change after 3-10 years RACE: African>Asian>Mexican>Caucasian REFRACTIVE ERROR:independent [–5-+5DS] Positive correlation to rim and cup size

Vertically oval (VDmax>HDmin by 10%) Abnoral shape or tilted: corneal astigmatism- amblyopia RIM SIZE AND SHAPE Related to disc size (+) ISNT rule (vert. oval disc/ Horizontal oval cup) Positive correlation to ret. arteriole diameter IT-ST-HT- IN-SN (predilection, mainly DIFFUSE loss) ST: sharp border cup-rim IT: some sloping (but NFL normal) Pallor: ? Non-glaucomatous (increased cup size)

OPTIC DISC CUP Increases with disc size Horizontally oval Depth:  with disc size (deepest: JPOAG, Shallowest: high myopic type of POAG)- negative correlation to PPA CD RATIO H>V hence H/V>1.0 but in early to medium G <1.0 Normal range: Independent of optic media magnification HCD/VCD: independent of cup and disc size

RNFL Ganglion cells axons+astrocytes+ Muller cell processes Visibility: unevenly distributed/  with age IT>ST>SN>IN>S>I>HT>HN Correlates with rim thickness, retinal artery caliber and foveolar location Sandwich arrangment Red –free/ wide beam Achromatic white light

Clinical examination Direct ophthalmoscope Indirect ophthalmoscope Slit lamp Red-free No stereo- Young children Uncooperative High myopes Opacities 90D 78D 60D FCL

DISC CHANGES IN POAG GENERALIZED Large cup Cup asymmetry Progressive  in cup size Saucerisation FOCAL Notching Vertical elongation Cupping of rim margin Regional pallor Splinter haemorrhage(  specificity, early-med advanced, IT-ST, Progression, NTG)

LESS SPECIFIC Exposed lamina cribrosa Nasal displacement Baring of circumlinear vessels/ constriction of arterioles PP crescent (spatial correlation with NRR loss) Shunt vessels of optic disc (advanced stage) RNFL CHANGES Focal defects wedge shaped (disc border-broad base to temporal raphe) 20%, always pathologic but not pathognomonic v:  from early to medium advanced G and  very advanced Associated with notching, haem, PPA in that sector/NTG 50% loss of thickness: visible Diffuse (commoner, more difficult to see) Sequence of sectors regarding RNFL visibility Retinal vessels( clearer- sharper)

RECORDING OF FINDINGS 1.CD ratio: poor description 2.NRR: colour, contour, width 3.Diagram 4.PHOTO (stereo+ magnification)

AQUEOUS HUMOUR DYNAMICS GOLDMAN EQUATION: IOP= (F/C)+P PRODUCTION Rate: 2-3 μl/min (1% turnover/min) Pigmented+non-pigmented cells Active transport (70%) Ultrafiltration (20%) Osmosis (10%) OUTFLOW μl/min /mmHg Trabecular (90%) Uveoscleral (10%) EPISCLERAL VENOUS PRESSURE 10mmHg

IOP Mean 16mmHg SD:3mmHg (10-22mmHg) Non Gaussian distribution, skew to R (>40y) Diurnal variation/ Seasonal (W>S) Heart beat/ respiration Exercise/ Posture Fluid intake Medication (systemic, topical, alcohol, caffeine, cannabis)) Age F>M after 40y Genetically influenced

IOP MEASUREMENT 1.Applanation tonometry (Imbert-fick: P= F/A) Goldmann, Perkins Airpuff (overestimate) Tonopen (scar, oedema) 2.Indentation: Schiotz 3.Digital pressure

SOURCES OF ERROR Squeezing Valsalva Pressure on globe Tight collars Calibration EOM force to restricted globe  FL:  IOP and vice versa  corneal astigmatism corneal oedema  scar  CL  Central corneal thickness (LASIK, PRK) Post scleral buckling 