Glaucoma 2 - Presentation and Pathogenesis Flashcards
Primary Open Angle Glaucoma/Normal tension Glaucoma (POAG/NTG) Signs and Symptoms?
SIGNS
• Raised or normal intra-ocular pressure
• Open angle or deep anterior chamber
• Abnormal optic disc cupping
• Abnormal visual field
SYMPTOMS
• None until advanced or paracentral visual field defect
Chronic Angle Closure Glaucoma (CACG) Signs and Symptoms?
SIGNS
•Raised or normal IOP
Open but narrow angle or moderate/deep AC
• Abnormal optic disc cupping
• Abnormal visual field
• Shallow AC
•3+ quadrants of ITC on gonioscopy
•Hypermetropia
SYMPTOMS
•None as per POAG
Intermittent Angle Closure Glaucoma (IACG) Signs and Symptoms:
SIGNS
• Raised or normal IOP
• Narrow angle
• +/-Abnormal optic disc cupping
• +/- Abnormal visual field
• Shallow AC
• 3+ Quadrants ITC on gonioscopy
• Hypermetropia
SYMPTOMS
• Intermittent brow ache
•HALOES
Acute Angle Closure Glaucoma (AACG) : Signs and symptoms:
SIGNS
•Red Eye
•Fixed mid-dilated pupil
• Hazy blue/green cornea
• Iritis
• IOP >40 mmHg
• Shallow AC
SYMPTOMS
• Brow ache/headache
•Blurred vision/haloes
• Nausea
Pathogenesis of POAG theories?
• Pressure theory
• Vascular theory
• Mixed mechanism
• Neurodegenerative and apotptosis
What does the pressure theory state?
•Trabecular dysfunction
- Trabecular meshwork gradually becomes less effective in allowing aqueous to pass through to Schlemm’s canal (increased outflow resistance)
Ocular Perfusion Supply:
• The posterior segment of the eye is supplied by 2 different circulatory systems
- Retina: Central retinal artery
- Choroid: Short posterior ciliary arteries
- Optic disc: both
• Vasoactive drugs can reach the optic nerve via the choroid
A reduced bloodflow to the optic nerve increases the eye’s sensitivity to IOP
Mixed Mechanism theory
•Combination of Pressure theory and Vascular Theory
Neurodegenerative and Apoptosis theory
•With time as px get older, the nerves get damaged
Mechanism of damage:
The exact mechanism in glaucoma is not understood completely:
•Loss of retinal ganglion cells
•Ischaemc changes at the ONH/free radicals
•Apoptosis
Pathogenesis Primary Angle Closure Glaucoma (PACG) (8 total)
Restricted access to trabecular meshwork
• Hypermetropia (eg + 2.00)
• Shallow anterior chamber
• Small eyes (short axial length)
• Anteriorly inserted iris
• Increase in lens size
• Dilatation of pupil
• Trabecular Dysfunction
• Narrow gonioscopic angle
What occurs during Angle Closure?
•Obstructed trabecular meshwork
•The angle between the iris and the cornea narrows or closes
•Iris pushing forward
•Cornea
PACG: ChronicAngle Closure (CAC):
• The Iris slowly comes into contact with an increasing area of TM, resulting in TM dysfunction and a gradual rise in IOP
PACG: Intermittent angle closure mechanism:
• The angle is narrow but open, but certain physiological states (producing dilation) lead to transient rises in IOP which resolve over variable periods of time
• This often produces transient symptoms of acute angle closure
PACG: Acute Angle Closure - Mechanism
•Dilation of the pupil (physiological or otherwise)leads to the angle becoming closed
• Marked rise in IOP due to:
• pupil block
• peripheral iris tissue occluding the angle (often both present simultaneously)