Ocular Anti-Hypertensives (Glaucoma Drugs) PDF

Glaucoma: an optic neuropathy initially provoked by multifactorial primary mechanisms of damage (PMOD) characterized by optic nerve head atrophy and secondary induced programmed retinal ganglion cell death causing a characteristic pattern of VF loss Evidence-based supported Primary Mechanisms Of...

Glaucoma: an optic neuropathy initially provoked by multifactorial primary mechanisms of damage (PMOD) characterized by optic nerve head atrophy and secondary induced programmed retinal ganglion cell death causing a characteristic pattern of VF loss Evidence-based supported Primary Mechanisms Of Disease ○ Elevated IOP: Causes Resistance to trabecular aqueous outflow (TO)- collagenous structure 80% out of trabecular meshwork ○ Most posterior ciliary body and then scleral spur Pathophysiology of resistance to TO: ○ Increased herniation TM cytoskeleton ○ Decreased inflammatory signaling to Endothelial Cells Schlemm Canal ○ Increased episcleral VP Any fluid produced that is not blood, has to enter circulation; what only enters veins? Increased pressure in vein Resistance to uveoscleral aqueous outflow (USO) 20% outflow Pathophysiology of resistance to USO: ○ Animal study- longstanding treatment on cynomolgus monkeys w/ a prostaglandin agonists increased spaces b/w CM fibers Too much collagen b/w fibers -> water exiting interrupted -> fluid held back -> increased IOP ○ Decreased ocular blood flow: impacts deterioration of ONH due to GLC Vascular Concept of OBF Look at scribes notes ^ Factors Involved in DOBF What about ocular biomechanical properties? Barriers that limit eye size ○ Weak barrier: IOP too much for intraocular structures b/c can’t hold pressure properly Cornea most important barrier in glaucoma ○ Has resistance Basically ocular pressure might be too high for ocular structures Biomechanical concept Corneal hysteresis (CH): Viscoelasticity Corneal resistant factor (CRF): relates to the overall ocular structural rigidity Central corneal thickness (CCT): extrapolated measurement to imply corneal rigidity; viewed as a protective factor ○ Those who have thin corneas have a higher risk of glaucoma and low CH Factors involved in altered OBMP Properties Secondary mechanism of damage concept Mechanical damage/ischemic insult Glutamate excitotoxicity (diminish glutamate transporter function) ○ Glutamate is a neurotransmitter that maintains the health of nerve fiber layer and maintains homeostasis flow of ions into nerve fiver for maintenance of NMDA receptor NMDA receptor activation (excitement) ○ If you have excess glutamate (damages the nerve), receptor stays open and you can get excess (toxic levels) of Ca Increases Ca+ influx Delayed calcium deregulation Nitric oxide synthesis Neurotrophin depravation Apoptosis Glaucoma risk factors Elevated IOP Suspicious optic disc Family history Race (POAG- Hispanics and blacks) Increasing age Myopia Diabetes mellitus Systemic vascular disease Central retinal vein occlusion Goals for pharmacological medical therapy Reduction in mean IOP to