L5: Glaucoma Flashcards
What is glaucoma?
Progressive optic neuropathy
- Mostly caused by high IOP, but can have normal IOP and just have increased sensitivity to changes in pressure
- Characteristic damage to optic nerve
- Associated visual field loss
Leading cause of preventable irreversible blindness
Glaucoma: sneak thief of sight?
Insidious disease –> develops very slowly & usually not noticed until 50% of vision lost
Unless PACG: headache, nausea, malaise in short-term
Aqueous production & outflow - where?
Produced in ciliary processes into anterior chamber
Primary drainage through trabecular meshwork; some through uveoscleral pathway
Pathophysiology - mechanical theory
Increased IOP
- -> Direct compression of optic nerve fibres
- -> Interruption of axoplasmic flow
- -> Loss of cell bodies & nerve fibres
Pathophysiology - vascular/ischaemic theory
Decreased perfusion at optic nerve
- -> Disturbance of vascular autoregulation
- -> Changes in systemic haemodynamics
Risk factors
High IOP/normal IOP with increased sensitivity to pressure changes
Elderly
Family history –> genetic mutations
Myopia
Diabetes –> retinopathy
IOP
Average: 15-16mmHg
High: 21mmHg or higher
IOP fluctuates throughout the day –> indicative of glaucoma if big fluctuations
- Highest at night
What are the main mechanisms of action of glaucoma drugs?
Decrease aqueous production
- Beta blockers
- Carbonic anhydrase inhibitors
Increase aqueous drainage
- Prostaglandin analogues
- Miotics (parasympathetic agonists)
Both
- Alpha agonists
Corticosteroids
Different people respond to different extents
High responders = higher increase in IOP
Risk factors for being high responder to corticosteroids
Glaucoma patients Family history of glaucoma Elderly patients Children High myopia Diabetes