Research Paper On Glaucoma

Glaucoma is several eye conditions that can damage to your optic nerve. Increased pressure in the eye can cause glaucoma, which leads to vision loss or blindness (Healthline). There are five different types of glaucoma, which are open-angle (chronic) glaucoma, angle-closure (acute) glaucoma, congenital glaucoma, secondary glaucoma, and normal-tension glaucoma (Healthline). Open-angle (chronic) glaucoma is the most common type of glaucoma, and there are no signs or symptoms expect gradual vision loss (Healthline). People that over sixty years old are at risk for glaucoma, and African Americans risk starts at forty years old. There is no cure for glaucoma, but surgeries and medicine can help

The guidelines of the European Glaucoma Society (EGS) for the management of glaucoma due to corticosteroid treatment are; (1) discontinuation of corticosteroid therapy or switch to weaker steroid (2) administration of topical or systemic IOP lowering medications (3) laser trabeculoplasty and (4) glaucoma surgery in intractable cases. These recommendations are, however, not specific for intravitreal administration of

Left untreated it may cause blindness in one to two days. Phenylephrine is used as a decongestant that shrinks the blood vessels. It is not used for narrow angle glaucoma. is used to relieve eye redness, dryness, burning, and irritation caused by wind, sun, and other irritants. to

"Glaucoma is a condition that causes damage to your eye's optic nerve and gets worse over time". (WebMD) Glaucoma is interlinked with the pressure in the eye. No one knows the exact cause of the glaucoma. Doctors think the main cause of the glaucoma is the pressure in the eye. Some people with the normal eye pressure also suffer with glaucoma. There are different kinds of glaucoma such as open angle glaucoma, Angle closure glaucoma, Normal tension glaucoma, Congenital and infantile glaucoma, and secondary glaucoma’s. Beta–adrenergic blockers and prostaglandins are the most frequently used topical medications at present.

In a study done by Dustin Dees et. al. looking at the efficacy of prophylactic anti-glaucoma medications on canines with primary glaucoma studied a total of 88 patients. The study looked at the long term effects of the medications and if they prevented an increased intraocular pressure, and clinical signs of glaucoma in eyes that are at risk of developing glaucoma. Out of the 88 patients observed, medical failure was seen in all. Demecarium Bromide, a miotic, had the longest estimated time till medical failure at 330 days, followed by

When comparing the chemical ablation, TSCP, evisceration and the drainage shunts, all are considered good treatment options for glaucoma because they can maintain a low intraocular pressure long term. The chemical ablation and TSCP worked well for some patients, but some needed a second treatment for it to be successful. While the drainage shunt shows promise, data suggests that it is not as good as the other treatments due to the high risk of fibrin obstructing the shunt. That makes it a good short term glaucoma treatment, but it would eventually need to be removed and a second procedure would need to follow

Time to time there has been development in new drugs for glaucoma. With these new drugs comes new benefits and risks. Glaucoma being the second leading cause of blindness in the world (after cataract) (1) is expected to affect around 11 million people worldwide by 2020 (1). Most of the affected population are greater than 50 years of age, who are also expected to have other health issues. For a clinician, it becomes extremely important to understand the potential side effects of the medications before prescribing it to the patients. These adverse drug reactions can occur from the drug itself, the preservatives or the vehicle of the drug, and can be ocular or systemic. Unabsorbed topical ocular medication for glaucoma may drain out of the eye through naso-lacrimal duct and can be absorbed by conjunctiva, nasal mucosa, oropharynx, and GI mucosa (occasionally) to rise to sufficient levels in the blood to cause systemic side effect or interact with other drugs. It has been estimated that roughly 80% of an eye drop can pass through the nasal nasolacrimal duct and get absorbed into the nasal mucosa and its microvasculature. Considering that these eye drops are often used in either eyes twice or thrice a day, the systemic implications can be extremely dangerous. (8)(14)

The results have indicated that the dipeptide (glycine-valine and tyrosine-valine) monoester prodrugs of gancyclovir exhibited superior corneal absorption and bioavailability compared with unmodified gancyclovir 58. These amino acid (valine, tyrosine, and glycine) prodrugs of gancyclovir have also shown higher permeability values than unmodified gancyclovir, due to their interaction with oligopeptide transporter present in retina 59. A water soluble prodrug of cyclosporine A, UNIL088 was developed via an ester linkage which gets converted to parent drug by enzymatic or chemical hydrolysis of the terminal ester group 60. Recently, a leucyl-histidyl-hydrazide based dipeptide prodrugs of N-acetylcarnosine were investigated for safety and efficacy in cataract and diabetic ocular complications. A nine month clinical study revealed that the N-acetylcarnosine treatment resulted in improved visual acuity of patients with cataract61. Various prodrugs based on prostaglandins were widely investigated in clinical trials. Prostaglandin prodrugs like latanoprost, bimatoprost, and travoprost were clinically proven to reduce intraocular pressure. The prodrugs latanoprost and travoprost have an isopropyl ester group at carbon-1 position of the alpha chain which gets hydrolyzed by enzymes to their respective biologically active free acid

Intraocular pressure (IOP) is the result of a dynamic balance between aqueous humor formation and outflow. As a main parameter in the evaluation of patients at risk from glaucoma, it also provides the baseline pressure in ocular disease studies. While glaucoma is often associated with elevated IOP, glaucomatous changes in the retina and optic nerve sometimes occur at normal IOP; this is termed

Artificial tears- and other lubricating eye drops, preferably preservative free, should be used generously for comfort.

Redness of the eye. This is often accompanied by a ring of redness around the outside of the cornea or clear covering at the front of the eye (ciliary flush).

Glaucoma is an optic neuropathy that can cause visual dysfunction. The first line treatment for open angle glaucoma is prostaglandin analogs or beta-adrenergic antagonists. These agents decrease intraocular pressure. Lumigan, a prostaglandin analog that works by increasing the outflow of aqueous humor through the trabecular meshwork and uveoscleral routes.1 Cosopt is a combination product that contains dorzolamide and timolol. Its mechanism of action is by inhibiting carbonic anhydrase II which lowers bicarbonate ion formation. This leads to a decrease of sodium and fluid transport therefore decreasing aqueous humor secretion.2 The beta- blocker effect of timolol on intraocular pressure is unknown. These agents may also be used for ocular hypertension.

Latanoprost is prostanoid selective FP receptor agonist is believed for decrease the intraocular pressure by growing the flow of aqueous humor. Studies in man and animals suggest that the mechanism of action is increased uveoscleral flow. Elevated IOP represent major risk factor to glaucomatous field loss. The higher the level IOP, the greater likelihood of visual field loss and optic nerve damage.

As a conclusion, blood vessels may relax and open up which makes it easier for blood to flow through the vessels so in this event it can reduce the blood pressure. Renin inhibitors contributes to another medication to balance hypertension. The side effects to Renin inhibitors is dizziness, headache, diarrhea, and stuffy nose. As a result of direct renin inhibitors which help the regulation of blood pressure, blood vessels relax and widen, making it easier for blood to flow through the vessels, which also lowers blood pressure. Direct renin inhibitors, angiotensin-converting enzyme (ACE) inhibitors, and angiotensin II receptor blockers (ARBs) all help the same process that narrows blood vessels, but each type of medicine blocks a different part of the process. Calcium channel blockers is another medication treatment option. The side effects of this medication is lightheadedness, low blood pressure, slower heart rate, drowsiness, constipation, swelling of feet, ankles and legs, increased appetite, and gastroesophageal reflux disease (GERD). Calcium channel blockers dilate the blood vessels and this makes it easier for blood to flow through the vessels and balances blood

After ester hydrolase catalyzed hydrolysis of travoprost in the cornea, travoprost free acid has been found in the aqueous humor of the anterior cavity of the eye.1,2 The free acid compound binds with high selectivity and affinity (Km = 52 nM) to PGF2a G-protein coupled receptors that are predominantly localized in the longitudinal ciliary muscle as well as the iris sphincter of the eye.1,3 Although the exact mechanism of intraocular pressure