1. posterior chamber (filled with vitreous humor), 2. ora serrata, 3. cilliaire muscle, 4. suspensory ligament, 5. Schlemm canal, 6. ward, 7. anterior chamber (filled with aqueous humor), 8. cornea, 9. iris, 10. cortical lens, 11. nucleus of the lens, 12. cilliaire body, 13. conjunctiva, 14. oblique muscle below 15. muscle right below 16. muscle right median, 17. Retinal veins and arteries, 18. optic papilla or blind spot, 19. blade riddled, 20. Retinal central artery, 21. Central Retinal vein, 22. optic nerve, 23. vortiqueuse vein, 24. tissue, 25. macula, 26. fovea, 27. sclera, 28. choroid, 29. right upper muscle, 30. retina.
The term refers to all glaucoma eye diseases in which intra-ocular pressure (IOP) is too high and leads repercussions on the optic nerve.
"Glaucoma is a vague term if there involves a specific qualifier. Indeed, the types of glaucoma are many. The most common glaucoma is a chronic open-angle glaucoma.
It does not include the word of the glaucome ocular hypertension (usually mild) without repercussions on the optic nerve that are still monitoring because some may develop into glaucoma.
We now know that the level of hypertension may cause glaucoma is unique to each individual, making diagnosis difficult for his debut.La border is sometimes difficult to draw between consequence hypertonia simple and hypertonia with a risk of glaucome.Il there is a relationship and continuity but not systematically frequently between glaucoma and ocular hypertension who are in fact different stages of the same pathology.
Diagnostic criteria have evolved in recent years. All people with ocular hypertension does not develop glaucoma and some people with pressure seen by the old criteria as normal (ie between 10 and 21 mm Hg) will be affected by glaucoma.
The intra-ocular pressure (IOP) is based on the volume of aqueous humor in the anterior chamber of the eye. The aqueous humor is secreted by the ciliary body in space called posterior chamber, then passes through the pupil (between the iris and lens) in the anterior chamber (space between the cornea and the curtain irien). She then resolved in the corner irido-corneal through the filter trabecular trabeculum, then drained into the canal of Schlemm. It finally flows in the veins scleral to join the general venous circulation.
The intra-ocular pressure (IOP) usual adult is between 10 and 21 mm of mercury (Hg) (average 16). IOP is measured today with tonometers automated air-jet. Set PIO in a normal person needs to know the rigidity of the cornea which depends primarily on its thickness. Indeed, the measure is not directly in the aqueous humor but through the cornea. Also, it influences the measure. People with a thick cornea eye pressure measured higher than those with a thin cornea. Moreover, the eye pressure naturally rises with age.
In other words, the measurement of eye pressure is a parameter that needs to be interpreted according to the corneal thickness and age. This criterion alone does not allow to say that a person is carrying a disease glaucoma patients and it is free.
The mechanisms of ocular hypertension
The ocular hypertension is a symptom as is the fever for example. The eye pressure can be found high in many different eye conditions that will define all types of ocular hypertension or glaucoma.
The most common mechanisms are:
* Reduced by the elimination of obstruction-angle irido congenital corneal home by a residual embryonic membrane (membrane Barkan) glaucoma with congenital or acquired by the age of trabeculum sclerosis. The second case is the chronic open-angle glaucoma (angle said open because anatomically normal). This is the cause of ocular hypertension by far most common in practice.
* Blocked by the lens pupillary secondary aging. This increases the volume and can cause a blockage of the pupillary hole. The aqueous humor accumulates behind the iris and pushes it forward, resulting in some people predisposed (people whose angle iridocornen is already close, if you meet especially among farsighted) a complete closure of the angle. This is the mechanism of acute crises said by closing the angle. More rarely pupillary blocking is done by synechies irido-cristalliniennes complicate an acute uveitis earlier untreated. The crystalline glue on the edge irien and prevents the passage of aqueous humor.
* Increased secretion by cilia. It is traditional in previous acute uveites (we are talking about uveitis hypertensive rather than glaucoma). It is a rare cause.
The consequences of intraocular hypertension are mainly in fiber optics. These correspond to the extensions of ganglion cells of the retina that will leave the eye at the optic papilla to form the optic nerve. The ocular hypertension (or HTO) will cause an acceleration of the degeneration of these fibers. Hypertonia This will have consequences even faster and it is high time.
The impact of the HTO, especially if it is chronic, will also depend on the quality of microcirculation of the topic, the "vascular factors of chronic open-angle glaucoma. Thus, vascular risk factors of atherosclerosis (hypertension, diabetes mellitus, smoking, high cholesterol) will also correct when treating chronic glaucoma.
In practice, ocular hypertension is responsible for a degenerative optic neuropathy. A normal optic nerve contains over one million fibers at birth. Naturally, the number of fibers decreases over time at approximately 5000 fibers per year. The ocular hypertension will lead to an acceleration of this degeneration.
Another consequence of ocular hypertension, if most (more than 40 or 50 mmHg, as we observed in acute glaucoma) is a sideration of the acivities or destruction of corneal endothelial cells causing the 'emergence of a corneal edema described as a "fog epithelial".
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