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18 Cards in this Set
- Front
- Back
Where is the aqueous in the eye produced?
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Through a combination of active secretion, ultrafiltration, and diffusion, aqueous is produced by the epithelial cells of the inner nonpigmented layer of the ciliary processes (pars plicata region of the retina).
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How does the aqueous in the eye drain?
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The majority of aqueous outflow is through the trabecular meshwork (TM) and is referred to as the “conventional” pathway.
10-20% (and up to 50% in younger patients) is through the ciliary body face and is referred to as the “uveoscleral” or “alternative pathway”. |
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Why is intraocular penetration of systemically delivered medications so poor? What are notable exceptions?
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Intraocular penetration of systemically delivered medications is very poor because of the blood-retinal and blood-aqueous barriers. Fluoroquinolone antibiotics and oral carbonic anhydrase inhibitors are notable exceptions.
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Brimonidine
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Intraocular pressure lowering agent. Alpha agonist which activates alpha 2 receptors in the ciliary body inhibiting aqueous secretion. Local side effects include irritation, allergy, mydriasis. Systemic side effects include dry mouth, hypotension, lethargy.
Contraindications: MAO inhibitor use. Brimonidine (Alphagan) is not to be used in children younger than 2 years of age; it has been associated with apnea in children. |
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Timolol maleate
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Intraocular pressure lowering agent; beta blocker that blocks beta-receptors in the ciliary body reducing intraocular pressure by decreasing aqueous humor production. Local side effects include blurred vision, corneal anesthesia, and superficial punctate keratitis. Systemic side effects include bradycardia/heart block, bronchospasm, fatigue, depression, impotence, decreases sensitivity to hypoglycemic symptoms in insulin dependent
diabetics, worsening of myasthenia gravis. Contraindications: Asthma, severe COPD, bradycardia, heart block, congestive heart failure, myasthenia gravis |
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Dorzolamide hydrochloride
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Carbonic anhydrase inhibitor that decreases aqueous production in
ciliary body. When given parentally, CAIs will also dehydrate the vitreous. Local side effects with drops includes bitter taste. Systemic side effects include diuresis, fatigue, GI upset, Stevens-Johnson syndrome, and risk of aplastic anemia. |
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Acetazolamide
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Carbonic anhydrase inhibitor that decreases aqueous production in
ciliary body. When given parentally, CAIs will also dehydrate the vitreous. Systemic side effects include hypokalemia, acidosis, renal stones, paresthesias, nausea, cramps, diarrhea, malaise, lethargy, depression, impotence, unpleasant taste, aplastic anemia, Stevens-Johnson syndrome Contraindications: sulfa allergy, hypo -natremia/ -kalemia, recent renal stones, thiazide diuretics, digitalis use |
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Hyperosmolar Agents
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Dehydrates the vitreous and decreases intraocular fluid volume by osmotically drawing fluid into the intravascular space. The agents are given orally or intravenously.
These agents include mannitol, glycerin, and isosorbide. Contraindications: Congestive heart failure, diabetic ketoacidosis (glycerin), subdural or subarachnoid hemorrhage, pre-existing severe dehydration. |
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Pilocarpine
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Miotic; Direct cholinergic that stimulates muscarinic receptors.
Local side effects include brow ache, breakdown of blood/aqueous barrier, angle closure (increases pupillary block & causes the lens/iris diaphragm to move anteriorly), decreased night vision, variable myopia, retinal tear/detachment, and possibly anterior subcapsular cataracts. |
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Echothiophate iodide
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Miotic; indirect cholinergics that blocks acetylcholinesterase. Local side effects include retinal detachment, cataract, myopia, intense miosis, angle closure,
increase bleeding post surgery, punctal stenosis, increase formation of posterior synechiae in chronic uveitis. Systemic side effects include diarrhea, abdominal cramps, enuresis, and increases effect of Succinylcholine. Contraindications: succinylcholine administration, predisposition to retinal tear, anterior subcapsular cataract, ocular surgery, uveitis. |
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Latanoprost
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Mechanism of Action: Prostaglandin F2alpha analogues increase uveoscleral outflow by increasing extracellular matrix turnover in the ciliary body face.
Side Effects Local: increase in melanin pigmentation in iris, blurred vision, eyelid redness; cystoid macular edema and anterior uveitis have been reported. Systemic: systemic upper respiratory infection symptoms, backache, chest pain, and myalgia Contraindications: pregnancy, inflammatory conditions |
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Dipivefrin
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Mechanism of Action: In the ciliary body, the response is variable (beta stimulation increases aqueous
production, but alpha stimulation decreases aqueous production). In the trabecular meshwork, beta stimulation causes increased trabecular outflow and increased uveoscleral outflow. The overall effect is IOP lowering. Side Effects Local: Cystoid macular edema in aphakia (more likely with epinephrine than dipivefrin, mydriasis, rebound hyperemia, blurred vision, adenochrome deposits, and allergic blepharoconjunctivitis. Systemic: tachycardia/ectopy, hypertension, headache Contraindications: narrow angles, aphakia, pseudophakia, soft lenses, hypertension, and cardiac disease. |
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Tropicamide
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Parasympatholytic; block acetylcholine receptors in iris sphincter and ciliary body causing mydriasis and cycloplegia.
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Atropine
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Sympathomimetic agents stimulate the dilator muscle causing mydriasis.
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VEGF
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Vascular Endothelial Growth Factor (VEGF) is a homodimeric protein secreted by a variety of cells in response to hypoxia/ischemia and other signaling molecules. It induces vascular permeability and angiogenesis and has multiple isoforms. Angiogenesis plays an important role in the complications of many ocular diseases including macular degeneration, diabetic retinopathy, retinal vein occlusions, and neovascular glaucoma. Inhibitors of VEGF have transformed the way we treat ocular diseases associated with neovascularization. The effect of this is most notable with wet macular degeneration which previously had very few and not very effective treatment options.
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Macugen (Pegaptanib Na+)
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One of the first agents employed.
An aptamer, a pegylated modified oligonucleotide, which binds to extracellular VEGF 165 and inhibits its ability to bind VEGF receptors. Approved December 2004, 1st drug for this use was delivered in a series of intravitreal injections and was well tolerated and more efficacious than photodynamic therapy. |
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Lucentis (Ranibizumab)
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Recombinant monoclonal antibody fragment targeting VEGF-A and designed for intraocular use
Approved June 2006 for treatment of macular degeneration and trials demonstrated 95% of patients maintained vision and 35% improved over 2 years $$$$ and the frequency and duration of treatment is unkown. *Possible increased risk of thromboembolic events |
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Avastin (Bevacizumab)
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Side Effects
Local: blurred vision, pain, redness of the eye, sensitivity to light, increased intraocular pressure, cataract, and risk of infection, retinal detachment, or allergic reaction. Systemic: dizziness, headache, nausea, diarrhea, flu-like symptoms, burning with urination, thromboembolic events*, and possible anaphylaxis/anaphylactoid reaction. These agents are contraindicated in patients with hypersensitivity to any component and adverse events and possible side effects continue to be evaluated. |