The pathophysiology of glaucoma: What you need to know

The article is professionally consulted by Specialist Doctor II Nguyen Thai Hung - Department of Medical Examination & Internal Medicine - Vinmec Danang International General Hospital.

Glaucoma is a medical condition caused by several mechanisms that cause increased pressure in the eye. If not treated properly, increased intraocular pressure can cause damage to the optic nerve. Pathological Glaucoma damage to the optic nerve is irreversible.

1.1. Mechanics Glaucoma is considered to be the causative factor in the initiation of a series of pathological changes at the cellular level of the optic nerve. The optic nerve consists of axons that begin at the VM ganglion cells (unmyelinated ganglia) and exit the eyeball (myelinated) through the sclera, a collagen-like structure.
Pressure on unmyelinated ganglion cells Increased intraocular pressure directly affects unmyelinated ganglion cells, including afferent axonal conduction activity, thereby causing ganglion cell death due to lack of nutritional factors Nerves originate in the brain. Prolonged hypoperfusion of the optic nerve leads to tissue ischemia leading to the accumulation of reactive oxygen species in the retina, resulting in damaged ganglion cells and undernutrition.
In Glaucoma, increased intraocular pressure is responsible for an activated response of optic nerve glial cells (microglial cells, astrocytes). Activated astrocytes synthesize molecules that cause degeneration and remodeling of the extracellular matrix and exert mechanical and biological effects on the optic nerve head and VM ganglion cells.

1.2. Immunity In terms of immunity, it is hypothesized that axonal cytoplasmic compression in the sclera sclera can prevent signal transduction from axons to ganglion cell bodies, leading to programmed cell death. This phenomenon includes activation of DNA-digesting enzymes in the nucleus and phagocytosis of cytoskeleton components by neighboring cells.
In the presence of stimuli induced by the pathological Glaucoma, the interaction between the apoptosis-inducing signals and the neurotrophic factors are determinants of ganglion cell survival VM.

1.3. Vascular Many studies have linked the progression of glaucoma to migraine and other vascular diseases such as hypertension and diabetes. Using flow survey techniques such as Pulsatile Ocular Blood Flowmeter, Scanning Laser Doppler Flowmetry, Color Doppler Imaging, the authors have detected hypoperfusion to many different locations of the eyeball including the optic nerve head, choroid, retina and posterior vascular system in glaucoma cases. In addition, studies have also shown a disorder in the ability to self-regulate blood flow (according to metabolic, hormonal, and neurological mechanisms) when there is hypoperfusion in the optic nerve.

2.1 Pathogenesis of Primary Angle-closure Glaucoma In eyes with a larger-than-normal crystalline structure, or where the lens protrusses more anteriorly than in normal individuals, then the anterior aspect of the lens is anterior. It will press against the back of the iris causing the pupil to block. The aqueous humor does not escape into the anterior chamber, it will be stasis in the posterior chamber and the posterior chamber pressure increases, the iris root is pushed forward against the corneal trabecular region, causing symptoms of angle closure. Water retention in the eyeball is the cause of glaucoma.
Anterior occlusion of the trachea - cornea (according to the mechanism of angle closure)
In eyes with small corneal structure, shallow anterior chamber, narrow anterior chamber angle, when the pupil dilates, the base of the iris thickens and adheres to the posterior surface of the cup. so the front room corner is closed. The aqueous humor does not escape through the trabecular area into the venous system, which causes the aqueous humor to accumulate in the eyeball, causing increased intraocular pressure.
Angle-closure glaucoma can occur without pupillary obstruction. In some cases, the iris surface is flat, and the central anterior chamber appears deeper than normal. This phenomenon is caused by a malformation of the iris, without a pupillary blockage. After the pupil is dilated, the iris circumferential area swells and occludes into the trabecular region, causing angle-closure glaucoma.

2.2. The pathogenesis of primary open-angle glaucoma is unknown. Glaucoma usually corresponds to optic nerve damage caused by disturbances in blood supply to the optic disc and glaucoma due to impaired circulation of vitreous in the trabecular region.
Glaucoma is quite dangerous disease and causes blindness. However, you can completely avoid this risk if the disease is detected early. Vinmec International General Hospital is currently providing Glaucoma Package that will perform comprehensive examinations and appoint surgery (if any) for customers with Glaucoma symptoms.
Specialist II Nguyen Thai Hung has 13 years of experience as an eye doctor at C Hospital Da Nang and Ngu Hanh Son General Hospital - Da Nang. Currently working as an Ophthalmologist at the Inter-specialty Clinic of Medical Examination - Internal Medicine, Vinmec International General Hospital Da Nang.
For more detailed information about Glaucoma package, please contact by phone: 02033 828 188 or book an appointment HERE

MORE:
Cataracts (glaucoma): Causes, Warning Symptoms Glaucoma Glaucoma (Central Head System): How to diagnose and treat? Glaucoma, glaucoma can be operated?