Primary Open Angle Glaucoma (POAG) Flashcards
What is the aetiology and risk factors of POAG?
Aetiology: Optic Nerve Head Damage
Risk Factors: Age, Hypertension, Family Hx, Ethnicity Hyperopia
What are the two pathogenesis theories for POAG?
Mechanical Theory: High IOP mechanically forces the lamina cribrosa and axons on the ONH resulting in nerve fibre damage.
Vascular Theory: IOP causes ischaemia of nerve axons due to reduction of blood flow.
What are the two pathogenesis theories for POAG?
Mechanical Theory: High IOP mechanically forces the lamina cribrosa and axons on the ONH resulting in nerve fibre damage.
Vascular Theory: IOP causes ischaemia of nerve axons due to reduction of blood flow.
What are the signs of POAG?
CUP: deeper cup, larger C:D, asymmetry >0,2, lamina cribrosa.
NRR: Loss of ISNT, thinning
Vascular: Baring, Bayonetting, Disc haemorrhages, nasalisation of vessels
IOP (if >24mmHg):
Central cornea thickness greater than 550microns.
VF: Paracentral scotoma, Arcuate scotoma, Macula sparing (should all respect horizontal midline)
What are the symptoms of POAG?
Asymptomatic
What investigations would you do with a px with suspected POAG?
- VF
- OCT
- Fundus photo
- IOP
- Direct/indirect ophthalmoscopy
- Van Herrick’s
What is the management for a px with POAG?
If IOP < 30 = routine referral or advice/monitor
If IOP > 30 = Urgent Referral
What are the treatments for POAG?
If IOP < 30: Corticosteroid, Prostaglandins
If IOP > 30: Laser treatment i.e peripheral iris iridotomy or laser trabeculoplasty or surgery o.e. trabeculectomy
What are the differential diagnosis for POAG?
Ocular hypertension Tilted Discs Physiological cupping Pigment dispersion glaucoma Pseudoexfoliation glaucoma Steroid-induced glaucoma Myopia