Glaucoma ppt.pptx
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National University of Sciences & Technology
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GLAUCO MA Dr Md Shamshir Alam, PhD Assistant Professor College of Pharmacy National University of Science & Technology Muscat Learning Objectives At the end of this lecture the students shall be able to: • Describe open angle and angle closure glaucoma. • Differentiate between types of glaucoma ba...
GLAUCO MA Dr Md Shamshir Alam, PhD Assistant Professor College of Pharmacy National University of Science & Technology Muscat Learning Objectives At the end of this lecture the students shall be able to: • Describe open angle and angle closure glaucoma. • Differentiate between types of glaucoma based on signs & symptoms. • Explain the pathophysiology and the risk factors of glaucoma. • Compare and contrast the clinical presentation of POAG and ACG. • Definiti GLAUCOMA-ona Greek word, meaning- Clouded or blue green hue. • GLAUCOMA is a group of eye diseases in which the optic nerves is damaged leading to irreversible loss of vision, in the most cases this damage is due to increase pressure within the eye. • GLAUCOMA caused by:- increased intraocular pressure / ocular hypertension (high pressure of fluids "aqueous humor" within the eye). • Normal intraocular pressures average from 12-21 mmHg. • IOP ˃ 21 mmHg- Glaucoma • Progressive optic neuropathy (death of retinal ganglion cells). • Liquid aqueous humor: produced by ciliary bodies posterior chamber pupil anterior chamber drained by trabecular meshwork. • In a healthy eye the rate of secretion is balanced with the rate of drainage. • In glaucoma, the drainage canal is partially or completely blocked, fluids build up in the eye chamber leading to increased pressure. I. Classification of glaucoma • Pretrabecular Primary glaucoma • Open angle • Angle closure • With pupillary block • Without pupillary block II. Secondary glaucoma • Open angle • Trabecular • Posttrabecular • Angle closure • Without pupillary block • With pupillary block I. Congenital glaucoma Etiolo gy • It is related to the consequences of elevated IOP. • A proper balance between the rate of aqueous production and rate of aqueous drainage is essential to maintain the IOP within normal limits. • When the rate of inflow is greater than rate of outflow, IOP can rise above the Risk factors for primary glaucoma Pathophysiol ogy • All types of glaucoma– progressive optic neuropathy due to death of retinal ganglion cells (RGCs) RGCs death is initiated block in transport of neurotrophins from brain to RGCs damaging cascade activation Apoptosis of RGCs RGCs death– loss of retinal fibers– optic neuropathy & visual field defects. Pathophysiol POAGogy PCAG 1. Trabecular meshwork becomes less efficient at draining aqueous humor. 2. Intraocular pressure (IOP) builds up. 3. Decreased retinal blood flow 4. Retinal ganglion cellular apoptosis 5. Activation of autoimmune reaction, release of excess nitric oxide and glutamate 6. Neurodegeneration and optic neuropathy 7. Cupping and increased cup- 1. 2. 3. 4. 5. 6. 7. 8. The iris is displaced forward Usually due to iris thickening caused by pupil dilation The angle is closed so aq humor cannot flow in to the trabecular meshwork Rapid buildup of aq humor in the anterior chamber Decreased retinal blood flow Retinal ganglion cellular apoptosis Activation of autoimmune reaction, release of excess nitric oxide and glutamate Neurodegeneration and optic neuropathy Cupping and increased cup-to- Clinical POAGmanifestation PACG Insidious Open-angle glaucoma is slowly progressive and is usually asymptomatic until the onset of substantial visual field loss. Central visual acuity is maintained, even in late stages. Gradual loss of peripheral vision (over months to years) Sudden Patients typically experience intermittent prodromal symptoms (e.g., blurred or hazy vision with halos around lights and occasionally, headache). Acute episodes produce symptoms associated with a cloudy, edematous cornea; ocular pain; nausea, vomiting, and abdominal pain; and diaphoresis. Recommended Frequency of Screening Age With risk factors No risk factors > 65 years 6 – 12 months 1 – 2 years 55-65 years 1 – 2 years 1 – 3 Years 40 – 54 years 1 – 3 years 2 – 4 Years <40 years 2 – 4 years 5 – 10 years Diagnostic evaluation • • • • History collection and Physical examination. The diagnosis of open-angle glaucoma is confirmed by the presence of characteristic optic disk changes and visual field loss, with or without increased IOP. Normal tension glaucoma refers to disk changes, visual field loss, and IOP of less than 21 mmHg. Ocular hypertension refers to IOP of more than 21 mmHg without disk changes or visual field loss. Diagnostic evaluation Procedure s Comments Visual field Checking for areas of vision test loss Gonioscopy Differentiates the type of glaucoma Tonometry Measuring intraocular test pressure Pachymetry Measuring corneal thickness Fundoscopic Measuring cup-to-disc ratio examination Corticosteroi Steroid provocative test is d used to evaluate genetic dinstillation predisposition of glaucoma.