Glaucoma, pathophysiology

Compare and contrast the pathophysiologic mechanisms responsible for open-angle glaucoma and acute angle-closure glaucoma. 

FIGURE 58-1. Anatomy of the eye. (From Lesar TS, Fiscella RG, Edward D. Glaucoma. In DiPiro JT, Talbert RL, Yee GC, et al, (eds.) Pharmacotherapy A Pathophysiologic Approach. 6th ed. New York McGraw-Hill 2005 1714, with permission.)... 

The crucial role played by GLTs in the pathophysiology of glaucoma is strengthened by the observed reduction of GLAST expression (Naskar et al., 2000) in conjunction with the induction of a splice variant of GLT-1 in RGCs (Sullivan et al., 2006) in glaucomatous eyes. 

Q7 What is glaucoma Comment on its pathophysiology, including the different types of glaucoma. 

Animal models for glaucoma have been used to study the pathophysiological basis of glaucoma. Animal based experiments are more representative than cell culture models particularly in the study of aqueous humor dynamics, the trabecular meshw ork-ciliary muscle complex, retinal ganglion cells, ONH axons, ONH framew ork and vascular flow dynamics in glaucoma subtypes (Weinreb and Lindsey, 2005). 

Ischemic injuries have been extensively studied in the brain in the context of stroke however, much remains to be learnt about the pathophysiological mechanisms. Excitotoxicity is an important contributing mechanism, especially in the areas where the blood supply is not critically reduced. In addition, ischemia affects cell bodies and the axons differently (Petty and Wettstein, 1999). These differences are important in understanding the pathophysiology of glaucoma, where the key events may be occurring in the ganglion cell axons rather than in the cell bodies. Ischemia could injure the neurons by several different mechanisms or their combinations. 

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