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Flashcards in eye and vision problems continued and eye drugs Deck (16):

What is retinal detachment?

separation of the neurosensory layer of the retina from the outermost pigmented epithelium, which normally shields the retina from excess light and provides structural supsport for the retina. this leads to degeneration of photoreceptors and vision loss.


What are some causes of retinal detachment? What patients are more at risk?

retinal breaks, diabetic draction, inflammatory effusions
breaks are more common in pts with high myopia


Clinical picture of retinal detachment?

often preceded by posterior vitreous detachment- patient will see flashes and floaters. This leads to eventual monocular vision loss like a "curtain drawn down. this is a surgical emergency


What is age-related macular degeneration?

degeneration of the macula (center of the retina). this causes distortion (metamorphosia) and eventual loss of centrla vision


What is dry age-related macular degeneration? Speed of degeneration? Findings? Treatment?

most common type this causes deposition of yellowish extracellular material in and beneath the Bruch membrane (innermost layer of choroid) and the retinal pigment epithelium. causes a gradual decrease in vision. prevent with mutivitamin and antioxidants


What is exudative macular degeneration? Speed of degeneration? Treatment?

rapid loss of vision d/t bleeding secondary to choroidal neovascularization. Treat with anti-VEGF or laser


Describe the MLF.

Key points: if lesioned, abducting eye gets nystagmus (overstimulated to try to get the CNIII to follow). Convergence is normal.
aka intranuclear ophthalmoplegia. (the INO refers to the paralyzed eye).
May be best to draw a picture, but wordy explanation exists below

allows for cross talk btw the CN VI and CN III nuclei. very myelinated, and lesions may be seen in patients with demylination disorders like MS. If lesioned, ipsilateral CNVI nucleus (controlling gaze to ippsilateral side) works, but contralateral CN III nucleus doesn't stimulate the medial rectus to fire.


What is the end goal of glaucoma drugs?

decrease intro-ocular pressure via decrease in aqueous humor (inhibit synthesis or secretion or increase drainage)


What are some classes of glaucoma drugs? (5)

alpha agonists, beta blockers, diuretics, chloinomimetics, prostaglandins


Epinephrine for glaucoma: mechanism, sides, contraindications

causes mydriasis. don't use in closed angle glaucoma
this will decr. aqueous humor synthesis via vasoconstriction


Brimonidine: MOA, sides

will decreased aqueous humor synthesis.
alpha 2 agonist
may cause blurry vision, ocular hyperemia, foreign body sensation, ocular allergic reactions, and ocular pruritis


What beta blockers are used to treat glaucoma? MOA, sides?

timolol, betaxolol, carteolol
decreased humor synthesis
no pupillary or vision changes


How is acetazolamide used to treat glaucoma? MOA, class, sides

decreases aqueous humor synthesis via inhibition of carbonic anhydrase
no pupillary or vision changes


What are direct cholinomimetics for glaucoma treatment? Side effects?

pilocarpine, carbachol.
these increase outflow of aqueous humor via contraction of the ciliary muscle and opening of trabecular meshwork.
cause miosis and cyclospasm (contraction of ciliary muscle). remember that the ciliary muscle does accomodation, not pupil size


What are indirect cholinomimetics for glaucoma treatment?

physostigmine, echothiophate. they also incr. outflow of aqueous humor via contraction of the ciliary muscle and opening of trabecular meshwork. sides are also miosis and cyclospasm


What prosgtaglandin can be used for glaucoma treatment? MOA? Sides?

latanoprost (PGF2a). increases outflow of aqueous humor. causes darkening of color of the eyes

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