Blood Aq Barrier And Formation Of Vitreous Flashcards
Are tight junctions present in NPCE or PCE
NPCE
Barrier to the movement of intermediate and high molecular weight substances such as protein
Blood aqueous barrier
Barrier protecting the eye from entry of toxic substances nad maintained the homeostatic control that underpins the ocular physiology
BAB
Explains why drugs administered ortally or IV can hardly reach therapeutic levels in intraocular tiussue
BAB
What constitutes an effective barrier to intermediate and high molecular weight substances such as proteins
Tight junctions between NPCE cells
Cells and flares in the anterior chamber
Uveitis
- inflammatory cells
- causes barrier breakdown and causes proteins to come in (flares)
Trauma and BAB
Hyphema
Breakdown of the barrier, so blood comes into anterior segment
Causes of BAB breakdown
Ocular injuries Ocular hypotony (low pressure)
Ocular injuries mechanisms of BAB breakdown
Inflammation
Ocular hypotony mechanism of BAB breakdown
Opening of the non-penetrated endothelial layer of the iris caps; and the tight junctions of the ciliary epithelium; increases epi scleral venous pressure
Clear gel which occupies the posterior compartment of the eye
Vitreous
Primary vitreous
3-4 gestational stage
- optic cup filled by system of fibrillation material
- VEGF causes hylaoid artery penetration
Secondary vitreous
6th week gestational weeks
- increasing of size
- antiVEGF causes hyoid to disappear
- cloquets canal formed
Tertiary vitreous
Controversial
-Secreted by NPCE of pars plans and persists in the adult as the suspensory ligament of the lens
Arises from the center of the optic disc, consitis of a small tuft of fibrous tissue and represents a remnant of the fetal hylaoid artyer
Bergmeister’s Papillae