Age-related Macular Degeneration (1) Flashcards
AMD Risk Factors
Age > 55 years
Smoking (32% increase)
Hard drusen
small, round, well-defined spots located far away from one another on the retina (Not a concern)
Soft drusen
larger, not well-defined
Increased risk for AMD (specifically wet AMD)
Two Forms of AMD
Dry and Wet
Dry AMD
Less severe form
subretinal hard and soft drusen deposits, macular thinning, photoreceptor–retinal pigment epithelial (RPE) atrophy, and hyperpigmentation of the retina
Can evolve into wet macular degeneration
Wet AMD
More severe form
loss of central vision caused by choroidal neovascularization (abnormal growth of new blood vessels from the choroid into the macula and retina)
Causes a faster and more severe form of visual loss
Symptoms of AMD
Difficulty reading or driving
Visual distortion
Blurred images
Difficulty seeing in low light
Decreasing central vision
Colors may not appear as bright as they once were
VEGFs
Vascular endothelial growth factor - ligands
major factor responsible for angiogenesis, inducing blood vessel development, after injury and in tumors
VEGF inhibitors
Monoclonal antibody VEGF inhibitors
Nonmonoclonal antibody VEGF inhibitors
Monoclonal antibody VEGF inhibitors
bevacizumab (Avastin and Byooviz)
ranibizumab (Lucentis)
brolucizumab (Beovu)
faricimab (Vabysmo)
Nonmonoclonal antibody VEGF inhibitors
aflibercept (Eylea)
oligonucleotide pegaptanib (Macugen)
VEGF receptors (VEGFR)
receptor tyrosine kinases
Bevacizumab
Humanized monoclonal IgG1 antibody binds to VEGF
Prevents the interaction of VEGF with its receptors on the surface of endothelial cells
Administered by injection into the vitreous cavity of the eye
Ranibizumab
modified fragment of bevacizumab
Aflibercept
Acts as a trap for VEGFR ligands
AEs: hypertension and diarrhea
Contraindicated in active eye infection or active ocular inflammation