THE GLAUCOMAS 1
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Transcript of THE GLAUCOMAS 1
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THE GLAUCOMAS 1
Dr Russell J Watkins
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Anterior Chamber Anatomy Chamber volume is about 200l Chamber depth is about 3.2mm
Deeper in myopes Shallows with age
Schwalbe’s line marks end of DM Scleral spur receives insertion of the
longitudonal ciliary fibres - contraction opens TM spaces
TM lined by trabeculocytes which have contractile properties which may influence outflow resistance
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Anterior Chamber Anatomy Canal of Schlemm is oval in cross-section (200-
400m) Canal is lined by endothelial cells which on inner
wall have giant vacuoles Number & size of vacuoles varies with IOP
This is the mechanism of the bulk transfer of aqueous to Canal of Schlemm
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Anterior Chamber Anatomy With age, there is
2-3 fold thickening of trabecular sheets Loss of endothelial cellularity Increase in connective tissue Increased accumulation of TM debris Increased accumulation of GAGs
Such changes are exaggerated in OAG
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Autonomic Control of Aqueous Secretion
Cholinergic mechanisms probably not involved in control of IOP
Adrenergic (1, 1 2, & 2) receptors do regulate IOP receptor stimulation inhibits AC (IOP)
aqueous production PGF2
receptor stimulation activates AC (IOP) aqueous production
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Aqueous Humour Drainage ~90% aqueous leaves eye via trabecular
meshwork ~10% leaves eye via “unconventional” routes
most important = “uveoscleral” Trabecular meshwork modulated by GAGs & Ca2+
in ECM Inner wall endothelium of Schlemm’s canal
provides most of TM resistance to outflow Intrascleral & episcleral venous flow also
provides resistance to outflow
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Aqueous Outflow
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Classification All forms of glaucoma are classified into primary &
secondary forms based on Gonioscopic findings ONH findings VF defects
Major risk factors IOP (the major risk factor but not the whole story) Vascular risk factors
• Local• Systemic
Race
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Classification Associated conditions
Ocular Extraocular
Additional useful clinical data BP, pulse, blood glucose, blood lipids Migraine, cold hands/Raynaud’s Thyroid disease, neurological diseases History of blood loss, smoking FOH +ve for visual loss FOH +ve for glaucoma
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Glaucoma Classification
Primary Congenital Forms Primary Congenital
Glaucoma Primary Infantile
Glaucoma Glaucoma associated
with congenital anomalies
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Glaucoma Classification
Primary Open Angle Glaucomas Primary juvenile
glaucoma Primary open angle
glaucoma Normal tension
glaucoma Ocular hypertension
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Glaucoma Classification Secondary Open Angle Glaucoma
Pseudoexfoliation glaucoma Pigmentary glaucoma Lens-induced OAG Glaucoma associated with intraocular
haemorrhage Uveitic glaucoma et al ++
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Glaucoma Classification
Primary Angle Closure Glaucomas Pupillary block
mechanism Plateau iris mechanism Malignant glaucoma Chronic ACG
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Glaucoma Classification Secondary Angle Closure Glaucomas
Secondary ACG with pupil block Secondary ACG due to “pulling” of AC
• NVG• Aniridia• Inflammatory membrane• et al++
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Primary Congenital Forms Primary congenital glaucoma
Aetiology is angle dysgenesis Pathomechanism is aqueous outflow Onset from birth to second year of life Usually sporadic; 10% may be AR with
variable penetrance; specific chromosomal abnormalities (1p36 & 2q21)
1 in 10,000 live births M>F (65%:35%)
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Primary Congenital Forms Primary congenital glaucoma (cont.)
Photophobia, tearing, blepharospasm Eye rubbing, EUA for IOP unreliable Buphthalmos (cornea >11mm) Corneal oedema (±ruptures in DM Haab’s striae) ONH: pressure distension/uniform enlargement VCDR>0.3 Gonio: open angle but poorly differentiated structures;
trabeculodysgenesis; anterior iris insertion
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Primary Congenital Forms Primary infantile glaucoma
Probably late onset congenital glaucoma Same aetiology & pathomechanism as PCG Onset 3rd to tenth yr of life Similar genetics to PCG Pain unusual; no buphthalmos or corneal oedema Often presents late with symptomatic VF loss Peak IOP > 24mmHg without Rx ONH shows pressure distension & generalised cup
enlargement with diffuse rim damage Gonio as PCG
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Primary Congenital Forms Glaucoma associated with congenital anomalies
Aniridia Sturge Weber syndrome Neurofibromatosis Marfan syndrome Homocystinuria Goniodysgenesis
• Axenfeld-Rieger syndrome & Peter’s anomaly Rubella Microcornea PHPV et al.
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