Glaucoma is a disorder that manifests itself in frequent clinic visits, is produced by increased intraocular pressure and affecting more than 2% of the population of the world from between 40 and 50 years. It is not a disorder that is deve move left over because if untreated, leads to blindness.
The normal intraocular pressure is maintained by the continuous secretion of aqueous humor by the ciliary body, then offset by its absorption into the anterior chamber through seepage from the trabecular network of the iris to the periphery of Schlemm canal. Glaucoma in this balance is altered, usually by alterations in the filtration and resorption of aqueous humor (there are various pathological processes is an studied but an associated with genetic processes).
((Studies of molecular genetics have pointed the way to alternative methods for the examination of mass population with glaucoma. We have several techniques. Chromosomal abnormalities were found in the Rieger syndrome (chromosome 4q). It would be useful to the analysis of genes with higher probability if it is believed that the disease is caused by one of the hundred or more genes, such as autosomal dominant RP. has not been shown to be useful for the genetics of glaucoma.))
In the two clinical syndromes orientacion the chronic and acute glaucoma.
What is the difference between chronic and acute glaucoma?
Chronic glaucoma occurs when the increase in intraocular pressure is set and slowly progressive and, if untreated, produces a slow and progressive deterioration of visual acuity. Acute glaucoma is associated with a rapid increase in intraocular pressure, and cause intense pain and redness of the eye, with rapid deterioration of vision (which may be permanent if not treated with urgency). The consequential intraocular hypertension are the excavation of the optic papilla, which is achieved by means of scanning the bottom of the eye in the consultation clinic, and degeneration of retinal ganglion cells. Symptoms and signs that are produced are a progressive loss of peripheral vision, leading to blindness if untreated. In acute glaucoma destroys the endothelium, which leads to corneal edema and corneal painful blisters. In chronic glaucoma the processes are very different manifestation of the sclera can relax and form bumps called estafilomas.
The more or less without glaucoma is due to a lack of filtering the aqueous humor by the trabecular network
There are various processes of Pathological frequent source of glaucoma, which can classified as primary and secondary.
Primary glaucoma
Are two major changes in the aqueous humor drainage:
1. The gradual closure of the trabecular network, which normally communicates with the canal of Schlemm, is a disease whose incidence increases with age, mainly affects older than 40 to 50 years and is often familial (autosomal dominant decendencia possible). Since the drainage angle is normal, is called primary open-angle glaucoma.
2. As age progresses, patients have a congenitally narrow anterior chamber can develop a greater narrowing of the angle between iris and cornea, leading to a functional blockade of the aqueous humor drainage by raising the intraocular pressure in ending this disease. This happens especially when the pupil is dilated, as the iris is thickened over the contract. Therefore, acute attacks may be precipitated by prolonged darkness. Since the drainage angle is abnormal, is known as primary angle-closure glaucoma
Secondary glaucoma
As the name refers to is by diseases that obstruct the drainage of aqueous humor. For example, there may be adhesions between iris and cornea caused by uveitis or secondary vascular proliferation by retinal ischemia (secondary angle-closure glaucoma). It can also cause a blockage of the trabecular network of solid particles of the aqueous humor, especially degenerated lens material, pigment from melanocytic lesions and abundant macrophages in response to hemorrhage or inflammation (secondary open angle glaucoma, or subsequent to infection).
Congenital glaucoma
The term of congenital glaucoma is considered a number of diseases, the majority of hereditary origin, characterized by ocular anomalies exist in the source responsible for an increase in intraocular pressure (IOP).
The most common of congenital glaucoma is the primary congenital glaucoma (50%), but anyway, a unique disease. It comes in the first three years of life.
There is a defective development of the exit routes of aqueous humor. In the first weeks or months of life is to be presented and tearing the child is not able to keep their eyes open when there is light (photophobia). The cornea loses transparency and is whitish. Simultaneously, the eye, as a result of increased pressure inside it increases in size. Be especially careful with children who have their eyes much bigger than other children their own age, especially if it bothers them a lot of light.
sources
Spanish Association for Prevention of Glaucoma
State Institute of Ophthalmology
Mexican Society of Ophthalmology
Revista Mexicana de Oftalmología March-April 2009, Volume 83
Manual de Oftalmologia Author Peña
By: Arturo Moreno Perez
Posts Tagged ‘Aqueous Humor’
Glaucoma is a leading cause of irreversible blindness throughout the world
January 19th, 2010What Does the Eye Tell Us About Evolution
December 12th, 2009I previously cited the eye as an example of an organ that demonstrates irreducible complexity. It’s an old argument in the creation-evolution debate but has never been properly defeated. That is not to say materialists don’t give it a shot.
They will say it came about as the result of a “long and complex pathway.” We are supposed to never mind that nobody knows how “long” and nobody has ever attempted to detail the “complex pathway” in other than storybook fashion.
The evolutionary eye tale goes something like this: light sensitive pigment evolved to light sensitive cells, then to a primitive eyespot, to a deep recessed eyespot, to a pinhole lens eye and finally to the complex eye. The “proof” is that there are creatures alive today that have each of these things. But doesn’t that very fact contain the disproof that any of these sight organs evolved from one to the other? If “precursor” eye organs are fully functional for the creatures that have them, there is no need for them to evolve further.
Let’s get to the nitty gritty of what real proof should be. How did the first light sensitive pigment come into being? By what mechanism, what physical laws, what chemistry? How, by what mechanism (details please) did the complex assemblage required for light sensitive cells and fully functioning eyes, complete with lids, lacrimal (tear) apparatus, mucosal membranes, eye ball, cornea, aqueous humor, iris, lens, a complex array of focusing muscles, automatic neural control (we don’t have to think to focus or to adjust the iris for the amount of light), vitreous humor, retina (rods, cones, etc.), optic nerve and brain to translate the images, come into being?
Look at the simplified graphic here of the eye and some of the biochemistry associated with it. Nobody can imagine, much less describe in detail, how such an array of complexity could come into being by steps. Neither can they fathom a detailed mechanism for creating any single part.
None of this skepticism or questioning holds back evolution-to-the-death believers. When faced with the irreducible complexity argument one evolutionary apologist basically solved the problem by proclaiming that an eye is really not very perfect at all, and by implication not complex! If it is not complex, then reducing it to simple components is no problem.
Referring to the layered configuration of the retina and its connection to the neurons feeding signals to the brain, he remarked: “The world is simply not always so intelligently designed!… For optimal vision why would an intelligent designer have built an eye backwards and upside down?” (Why people believe, p XXI http://www.amazon.com/gp/product/0716733870/103-4950061-5008665?v=glance&n=283155) He is here referring to the layered configuration of the retina and its connection to the neurons feeding signals to the brain.
I hardly know what to say to a comment like that. But I will. The first thing that comes to mind is, let’s see you do better Mr. Smarty Pants. He won’t and he can’t. Nowhere in the anatomical or physiological literature is there even one article by any researcher or scientist describing this flawed design and a proposal as to how the eye’s “backwards and upside down” mistake should be fixed. Nowhere in the hundreds of thousands of medical articles on optometry and ophthalmology is there any mention that the eye is defective in this way. (I have only reviewed the medical literature for about the past 35 years but I’ll bet there is nowhere my upside down eyes haven’t looked either.)
Incredible. Humans with all of their smarts, science and technology (not to mention 20-20 eyesight) can’t even create one light sensitive pigment, but this one knows how to make a better complex eye! It’s like not being able to add 2 +2 but then cockily pronouncing how differential equations performed by a Nobel Prize laureate are “backwards and upside down.”
John Ciardi summed it up so well:
“Who could believe an ant in theory?
A giraffe in blueprint?
Ten thousand doctors of what’s possible
Could reason half the jungle out of being.” (7:27)
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By: Dr. Randy Wysong
