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Questions and Answers
What is considered the most important barrier in glaucoma?
What does a thin cornea indicate in relation to glaucoma risk?
Which factor relates to the overall ocular structural rigidity?
What role does glutamate play in relation to nerve fiber health?
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What risk factor is associated with primary open-angle glaucoma (POAG) prevalence?
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What occurs when excess glutamate damages nerve fibers?
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What is the role of the corneal hysteresis (CH)?
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How does delayed calcium deregulation occur in glaucoma?
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Which of the following is a proposed goal of pharmacological therapy for glaucoma?
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What does the term 'ischemic insult' refer to in the context of glaucoma?
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What primarily characterizes glaucoma?
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Which factor contributes to the resistance to trabecular aqueous outflow?
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What percentage of aqueous outflow occurs through uveoscleral pathways?
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Which mechanism is NOT a primary mechanism of glaucoma?
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What role does decreased ocular blood flow play in glaucoma?
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What happens to collagen in the trabecular meshwork with increased treatment from prostaglandin agonists?
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Which of the following is a factor contributing to increased IOP?
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What determines the pattern of visual field loss in glaucoma?
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Which statement is true regarding the pathophysiology of resistance to aqueous outflow?
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What is a result of increased episcleral venous pressure?
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Study Notes
Glaucoma Overview
- Glaucoma is an optic neuropathy characterized by optic nerve head atrophy and retinal ganglion cell death, leading to specific patterns of visual field loss.
- Initial damage is caused by multifactorial primary mechanisms of damage (PMOD).
Primary Mechanisms of Disease
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Elevated Intraocular Pressure (IOP)
- Major cause of glaucoma, influencing 80% of aqueous humor outflow through the trabecular meshwork (TM).
- Resistance often originates from the posterior ciliary body leading to decreased drainage through Schlemm's canal.
- Increased pressure in the episcleral veins impedes fluid circulation.
- Uveoscleral Outflow (USO): Accounts for 20% of outflow; increased collagen among ciliary muscle fibers can hinder fluid passage.
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Decreased Ocular Blood Flow (OBF)
- Insufficient blood flow leads to further deterioration of the optic nerve head (ONH).
Ocular Biomechanical Properties
- High IOP can exceed the resistance capabilities of ocular structures, primarily the cornea.
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Key Components:
- Corneal Hysteresis (CH): Reflects the eye's ability to absorb and dissipate pressure.
- Corneal Resistance Factor (CRF): Indicates overall structural rigidity of the eye.
- Central Corneal Thickness (CCT): Thinner corneas correlate with a higher risk of developing glaucoma.
Secondary Mechanisms of Damage
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Types of Damage:
- Mechanical damage and ischemic insult.
- Glutamate excitotoxicity disrupts neurotransmitter function and ion homeostasis in nerve fibers.
- Excess glutamate can lead to prolonged NMDA receptor activation, causing increased calcium (Ca²⁺) influx and potential toxic levels.
- Resulting conditions include delayed calcium deregulation, nitric oxide synthesis, neurotrophin deprivation, and apoptosis of nerve cells.
Glaucoma Risk Factors
- Elevated IOP.
- Suspicious changes in optic disc appearance.
- Family history of glaucoma.
- Increased susceptibility in specific populations; higher prevalence in Hispanics and blacks (Primary Open-Angle Glaucoma).
- Age increases risk.
- Conditions such as myopia, diabetes mellitus, systemic vascular diseases, and central retinal vein occlusion are associated with higher glaucoma risk.
Pharmacological Therapy Goals
- Aim to reduce mean intraocular pressure (IOP) to minimize risk of optic nerve damage and preserve vision.
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Description
This quiz delves into the multifaceted aspects of glaucoma, focusing on its characterization as an optic neuropathy. Participants will explore primary mechanisms of disease, including elevated intraocular pressure and its effects on retinal ganglion cells and visual field loss.
