MT 3
Glycogen
formation of glycogen in cornea vs no allowed in limbus
FIH-1: inhibiting enzyme
used when no O2
Closed eye
palp. conj + AH = source of O2
low O2 shifts to anaerobic glycolysis (increase lactate) + low pO2 due to high elevation
high lactate = swelling
Low pH = reduction in pump function
Edema - hypotonic tears and hypoxic metabolism
Lactate transport
lactate higher in stroma vs AH
lactate moves to AH via monocarboxylate cotransporters
Lactate cannot cross into tear film
Contact lenses
lowers O2 leading to anaerobic metabolism
74mmHg = minimum level of O2 exposure
Dk/t
diffusivity, solubility of O2, thickness
contact lenses act as a barrier to CO2 shifting bicarbonate equilibrium
CO2
Lactate is acid of eye
increase with anaerobic metabolism
Low pH
Acidosis
pump function decreased
reduce deturgescence
Diseases of Hypoxia
epithelial microcysts
epithelial thinning
Stromal striae
Endothelial blebs
Endothelial polymegethism
Neovascularization
imbalance of anti / pro angiogenic factor
Treatment: ranibizumab/ bevacizumab, VEGF antibodies, Corticosteroids/ NSAIDs
AH
AH drainage
through TM, into schlemm’s canal, collector channels, deep scleral/ intrascleral/ episcleral plexus, and episcleral vein
Across iris root, uveal meshwork, anterior face of ciliary muscle, through connective tissue, into suprachoroidal space
BAB
Non leaky tight junction of:
Non pigmented epithelium of ciliary body
Posterior Iris
Iris vasculature
Inner wall of schlemm’s canal
Non fenestrated blood vessels of the iris
AH Protein