Causes

The exact cause of elevated IOP in POAG is not certain, although the role of accumulating
mucopolysaccharides in the trabecular meshwork beams continues to be a focus of research.
In general, the physiologic chain of events that leads to glaucomatous optic nerve damage from pressure or
other secondary mechanisms is unknown, although various theories, as described below, have been proposed.

Penyebab pasti dari peningkatan TIO di POAG tidak pasti, meskipun peran mengumpulkan
mucopolysaccharides di meshwork trabecular balok terus menjadi fokus penelitian.
Secara umum, rantai fisiologis peristiwa yang mengarah ke glaukoma kerusakan saraf optik dari tekanan atau
mekanisme sekunder lainnya tidak diketahui, meskipun berbagai teori, seperti yang dijelaskan di bawah ini,
telah diusulkan.
Other various theories have been advanced to explain the possible etiologic role of elevated IOP in
glaucomatous optic neuropathy.

The mechanical compression theory suggests that elevated IOP causes a backward bowing of the
lamina cribrosa, kinking the axons as they exit through the lamina pores. This may lead to focal ischemia,
deprive the axons of neurotrophins, or interfere with axoplasmic flow, triggering cell death.
The vascular theories propose that cell death is triggered by ischemia, whether induced by elevated
IOP or as a primary insult.
Other risk factors may play a role in the development of POAG, including a history of migraine
headaches (a condition associated with vasospasm), cardiovascular disease, diabetes, systemic
hypertension (leading to arteriosclerosis), and systemic hypotension (leading to decreased perfusion).
Genetic theories propose that cell death is triggered by genetic predisposition. Following the death of
individual axons, substances may be released into the environment that causes a secondary triggering of
apoptosis in neighboring cells, including glutamate (a neurotransmitter that may cause excitotoxicity),
calcium, nitric oxide, and free radicals.

a) Anamnesis
Pada glaukoma sudut tertutup akut, terdapat peningkatan mendadak tekanan intra okuler
dan mata terasa sangat nyeri serta fotofobia. Mata berair dan terjadi kehilangan penglihatan.
Pasien secara sistemikmungkin terlihat sakit dan mengalami nausea serta nyeri abdomen, gejala
yang membuat mereka pergi keinstalasi gawat darurat.
Glaukoma sudut tertutup primer intermiten terjadi ketika serangan akut menghilang
secara spontan. Pasien daoat mengeluhkan nyeri, mata kabur, dan melihat halo disekitar
cahaya.Gejala glaukoma tergantung dari kecepatan peningkatan tekanan intraokular. Glaukoma
sudut terbuka kronis dikaitkan dengan peningkatan perlahan tekanan dan ketiadaan gejala

kecuali pasien kemudian menjadi sadar akan adanya defisit penglihatan berat. Banyak pasien
terdiagnosis saat tanda glaukoma terdeteksi oleh ahli optometri.
Chronic glaucoma gradually reduces your peripheral vision. But by the time you notice it, permanent
damage may have already occurred. If your IOP remains high, the damage can progress until
significant loss of your peripheral vision develops, and you will be able to see only objects that are
straight ahead.
Left untreated, chronic glaucoma can lead to blindness.

http://www.allaboutvision.com/conditions/primary-open-angle-glaucoma.htm
Gary Heiting, 2014. Primary Open Angle Glaucoma.
Multiple theories exist concerning how IOP can be one of the factors that initiates glaucomatous
damage in a patient. Two of the major theories include the following: (1) onset of vascular
dysfunction causing ischemia to the optic nerve, and (2) mechanical dysfunction via cribriform
plate compression of the axons.
In addition to vascular compromise and mechanically impaired axoplasmic flow, contemporary
hypotheses of possible pathogenic mechanisms that underlie glaucomatous optic neuropathy
include excitotoxic damage from excessive retinal glutamate, deprivation of neuronal growth
factors, peroxynitrite toxicity from increased nitric oxide synthase activity, immune-mediated
nerve damage, and oxidative stress. The exact role that IOP plays in combination with these
other factors and their significance to the initiation and progression of subsequent glaucomatous
neuronal damage and cell death over time is still under debate; the precise mechanism is still a
hot topic of discussion.

Jerald, 2014. Primary Open-Angle Glaucoma. http://emedicine.medscape.com/article/1206147overview#aw2aab6b2b2aa

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