Glaucoma 1 PDF

GLAUCOMA 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...

GLAUCOMA 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.  Definition GLAUCOMA- a 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 is the 2nd most causes of blindness after cataract.  Definition Glaucoma: The word comes from Greek, meaning "clouded" or "blue-green hue.“ It's a group of eye diseases that damage the optic nerve, often due to high pressure in the eye. This damage can lead to irreversible vision loss. Glaucoma is the second leading cause of blindness after cataracts  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). Causes of Glaucoma: Increased Intraocular Pressure (IOP): High pressure from the fluid (aqueous humor) in the eye. Normal IOP: Averages between 12-21 mmHg. Glaucoma Diagnosis: IOP greater than 21 mmHg. Optic Nerve Damage: Leads to progressive optic neuropathy, causing 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. Aqueous Humor: Production: Made by the ciliary bodies. Pathway: Flows from the posterior chamber → through the pupil → into the anterior chamber. Drainage: Exits via the trabecular meshwork. Healthy Eye: The production and drainage rates are balanced. In Glaucoma: The drainage canal is blocked (partially or completely), causing fluid buildup and increased eye pressure.  Classification of glaucoma I. Primary glaucoma Open angle Angle closure With pupillary block Without pupillary block II. Secondary glaucoma Open angle Pretrabecular Trabecular Posttrabecular Angle closure Without pupillary block With pupillary block III. Congenital glaucoma Types of Glaucoma: Primary Glaucoma: Open Angle: Common form; drainage angle is open but fluid drains slowly. Angle Closure: With Pupillary Block: The iris blocks the drainage angle due to pressure buildup. Without Pupillary Block: Other factors cause angle closure without iris blockage. Secondary Glaucoma: Open Angle: Pretrabecular: Issues before the trabecular meshwork. Trabecular: Direct problems in the trabecular meshwork. Posttrabecular: Issues after the trabecular meshwork. Angle Closure: With Pupillary Block: Similar to primary angle closure. Without Pupillary Block: Other causes lead to angle closure. Congenital Glaucoma: Present at birth, often due to developmental issues in the eye.  Etiology 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 normal limits. If IOP remains elevated, permanent vision loss occurs.  Etiology Consequences of Elevated IOP: Balance: Normal IOP relies on a proper balance between the production and drainage of aqueous humor. Increased Inflow: If the production rate exceeds the drainage rate, IOP rises above normal limits. Risks: Sustained elevated IOP can lead to permanent vision loss. Risk factors for primary glaucoma  Pathophysiology 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.  Pathophysiology Pathophysiology of Glaucoma: Progressive Optic Neuropathy: All types of glaucoma lead to damage of retinal ganglion cells (RGCs). RGC Death Initiation: Blockage of Neurotrophin Transport: Disruption in the transport of neurotrophins from the brain to RGCs. Damaging Cascade Activation: Triggers processes that harm RGCs. Apoptosis: RGCs undergo programmed cell death. Consequences: Loss of retinal fibers. Development of optic neuropathy and visual field defects. Pathophysiology Block in Neurotrophic Transport: There's a block in the transport of neurotrophins from the brain to RGCs. This disruption damages the communication between the brain and RGCs. Cascade ‫ تتالي‬Activation: A cascade of events is triggered due to the block in neurotrophic transport. Activation of Apoptosis: The cascade of events leads to the activation of apoptosis in RGCs. Apoptosis is a programmed cell death process. RGC Death: As a result of apoptosis, retinal ganglion cells undergo cell death. Loss of Retinal Fibers: The death of RGCs results in the loss of retinal fibers. Optic Neuropathy: The cumulative effect of RGC death ‫ تراكم‬and loss of retinal fibers leads to optic neuropathy. Visual Field Defects: Optic neuropathy contributes to visual field defects.  Pathophysiology POAG PCAG 1. Trabecular meshwork becomes 1. The iris is displaced forward Usually less efficient at draining aqueous due to iris thickening caused by pupil dilation humor. 2. The angle is closed so aq humor cannot 2. Intraocular pressure (IOP) builds flow in to the trabecular meshwork up. 3. Rapid buildup of aq humor in the 3. Decreased retinal blood flow anterior chamber 4. Retinal ganglion cellular apoptosis 4. Decreased retinal blood flow 5. Activation of autoimmune 5. Retinal ganglion cellular apoptosis reaction, release of excess nitric 6. Activation of autoimmune reaction, oxide and glutamate release of excess nitric oxide and 6. Neurodegeneration and optic glutamate 7. Neurodegeneration and optic neuropathy neuropathy 7. Cupping and increased cup-to-disc 8. Cupping and increased cup-to-disc ratio greater than 0.55 ratio greater than 0.55 8. Visual field loss 9. Visual field loss  Pathophysiology POAG PCAG Primary Closed-Angle Glaucoma (PCAG): Primary Open-Angle Glaucoma (POAG): Iris Displacement: The iris is pushed forward, Drainage Issue: Trabecular meshwork often due to thickening from pupil dilation. becomes less efficient at draining aqueous Angle Closure: The drainage angle is closed, humor. preventing aqueous humor from reaching the Increased IOP: As a result, intraocular trabecular meshwork. pressure builds up. Rapid Aqueous Humor Buildup: Fluid Decreased Blood Flow: Reduced blood flow accumulates in the anterior chamber. to the retina occurs. Decreased Blood Flow: Reduced blood flow to RGC Apoptosis: Retinal ganglion cells the retina occurs. undergo programmed cell death. RGC Apoptosis: Retinal ganglion cells undergo Autoimmune Reaction: Activation leads to programmed cell death. the release of excess nitric oxide and Autoimmune Reaction: Triggers the release of glutamate. excess nitric oxide and glutamate. Neurodegeneration: This results in optic Neurodegeneration: Results in optic neuropathy. neuropathy. Cupping: Increased cup-to-disc ratio, often Cupping: Increased cup-to-disc ratio, typically greater than 0.55. greater than 0.55. Visual Field Loss: Patients experience loss of Visual Field Loss: Patients experience loss of visual field. visual field.  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. In PACG IOP is generally markedly elevated (e.g., 40 to 90 mmHg) when symptoms are present  Diagnostic evaluation Diagnostic Evaluation: History and Physical Examination: Initial assessment involves collecting medical history and conducting a physical exam. Open-Angle Glaucoma: Diagnosis is confirmed by characteristic optic disk changes and visual field loss, with or without increased IOP. Normal Tension Glaucoma: Identified by optic disk changes and visual field loss, but IOP remains below 21 mmHg. Ocular Hypertension: Defined as IOP greater than 21 mmHg without any optic disk changes or visual field loss. Primary Angle-Closure Glaucoma (PACG): Typically presents with markedly elevated IOP (e.g., 40 to 90 mmHg) when symptoms are present.  Diagnostic evaluation Procedures Comments Visual field test Checking for areas of vision loss Gonioscopy Differentiates the type of glaucoma Tonometry test Measuring intraocular pressure Pachymetry Measuring corneal thickness Fundoscopic Measuring cup-to-disc ratio examination Corticosteroid Steroid provocative test is used to dinstillation evaluate genetic predisposition of glaucoma.