1 / 43

Ocular Pharmacology

Ocular Pharmacology. Acute Eye Course Dr. Sonya Bennett May 2011 . Routes of Administration. Overview. delivery methods - eye drops, ointments, injections drug classifications case. Eye drops.

taro
Download Presentation

Ocular Pharmacology

An Image/Link below is provided (as is) to download presentation Download Policy: Content on the Website is provided to you AS IS for your information and personal use and may not be sold / licensed / shared on other websites without getting consent from its author. Content is provided to you AS IS for your information and personal use only. Download presentation by click this link. While downloading, if for some reason you are not able to download a presentation, the publisher may have deleted the file from their server. During download, if you can't get a presentation, the file might be deleted by the publisher.

E N D

Presentation Transcript

  1. Ocular Pharmacology • Acute Eye Course • Dr. Sonya Bennett • May 2011

  2. Routes of Administration

  3. Overview • delivery methods - eye drops, ointments, injections • drug classifications • case

  4. Eye drops • most ocular medications are delivered topically - maximizes anterior segment concentrations and minimizes systemic toxicity • drug gradient from tear reservoir to corneal and conjunctival epithelium forces passive absorption

  5. Eye drops • Factors affecting absorption: • drug concentration (limited by tonicity) and solubility (aqueous solution v’s suspension) • viscosity (increased residence time)

  6. Eye drops • lipid solubility: lipid rich epithelial cell membrane v’s water rich stroma • pH and ionic charge - most eye drops are weak bases existing in both charged and uncharged forms enhancing absorption

  7. Eye drops • Surfactants - preservatives used are surface-active agents that alter cell membranes in the cornea as well as bacteria, increasing drug permeability and preventing bacterial contamination

  8. Eye drops • Reflex tearing: ocular irritation and secondary tearing wash out of the drug reservoir in the tears and reduce contact time with cornea. This occurs when drops are not isotonic, have non-physiological pH or contain irritants

  9. Eye drops • Tissue binding: proteins in the tears and on the ocular surface may bind drug making the drug unavailable or creating a slow release reservoir. This may affect peak effect and duration of action as well as delayed local toxicity eg. ongoing toxic retinal effects of hydroxychloroquine even after discontinuation

  10. Eye ointments • increases contact time of drug with ocular surface • mixture of petrolatum and mineral oil • water-soluble drugs are insolvent in the ointment and are present as microcrystals. The surface microcrystals dissolve in the tears, the rest are trapped until the ointment melts

  11. Eye ointments • only drugs with high lipid solubility and some water solubility will get into both tears and corneal epithelium eg. chloramphenicol and tetracycline both achieve higher aqueous levels as ointment rather than drops

  12. Peri-ocular injections • subconjunctival, subTenon’s and retrobulbar • allow drugs to bypass the conjunctival/corneal epithelial barrier and reach therapeutic levels in the posterior segment • eg anaesthetic agents, steroids, botulinum toxin

  13. Intraocular injections • allow instant drug delivery at therapeutic concentrations to target site • intracameral eg. antibiotics, viscoelastics, miochol • intravitreal eg. triamcinolone, avastin

  14. Systemic • drug getting into eye from systemic circulation limited by tight junctions in vascular endothelium of retinal vessels, and non-pigmented epithelium of ciliary body • drugs with higher lipid solubility pass through blood-ocular barrier more readily

  15. Systemic • extent of drug bound to plasma proteins also effects access of drug into eye - only unbound form can pass blood-ocular barrier • bolus administration exceeds the capacity of a drug to bind to plasma proteins and so leads to higher intraocular drug levels than with slow IV drip

  16. Sustained release devices • devices available for steroid, gancyclovir delivery within vitreous cavity

  17. Classes of Drugs

  18. Cholinergics • Muscarinic • Nicotinic

  19. Adrenergic agents • direct acting eg.phenylephrine • indirect acting eg. brimonidine • agonists eg dipivefrin

  20. Beta-blockers • important to be aware of side effect profile before administering

  21. Carbonic anhydrase inhibitors • dorzolamide, brinzolamide, acetazolamide

  22. Osmotic agents • glycerol, mannitol

  23. NSAIDs • topical, oral

  24. Steroids • prevent or suppress local hyperthermia, vascular congestion, oedema, pain of inflammatory responses.... and late inflammatory responses such as capillary and fibroblast proliferation, collagen deposition and scarring

  25. Antivirals • acyclovir, gancyclovir, foscarnet

  26. Local anaesthetics • oxybuprocain, alacaine, tetracaine • lignocaine, bupivacaine

  27. so many..... • pick one drug per week and learn its indications, contraindications, actions, side effects

  28. Case AJ

  29. Presentation • 48 yr old man with five year history of low grade anterior uveitis OD • VA 6/5 • IOP 38mmHg on cosopt BD, brimonidine BD, pred forte QID

  30. Case AJ

  31. clear cornea • quiet anterior chamber • larger area of iris transillumination • open drainage angle, though surface appeared irregular • clear lens • disc 0.7, full HVF, healthy macula

  32. Questions • What other IOP lowering drops are safe to use? • Is the steroid having an effect on the IOP? • Should I give him Diamox tablets? • Can he be controlled medically? • the roller coaster ride starts.....

  33. Choice of IOP lowering agents • potential for exacerbation of uveitis (and CMO) with hypotensive lipids and brimonidine

  34. Choice of IOP lowering agents • Order of introduction of agents that I use: timolol, brinzolamide, brimonidine, latanoprost • speed of effect of drops important? • yes want fast response • hypotensive lipids can lower IOP sooner than initially thought (days not weeks)

  35. Choice of IOP lowering agents • theoretically using topical NSAIDs may reduce the effectivity of hypotensive lipids, though clinical evidence lacking

  36. Choice of IOP lowering agents • Diamox • long list of side effects, interaction with cyclopsorin and folic acid antagonists • in chronic uveitis, ciliary body aqueous production can be reduced, and so may be exquisitely sensitive to CAIs (oral or topical)

  37. Is it a Steroid Response? • not often evident as to if it is directly related to steroids or attributable to uveitis • more likely in younger patient • need to treat uveitis adequately or the IOP can elevate due to trabeculitis or increased aqueous viscosity • balancing act!

  38. Treating steroid response • reduce the steroid as much uveitis allows • choice of steroid: prednisone, dexamethasone, fluoromethalone

  39. Progress • reduced the pred forte quickly and added diamox • IOP reduced so came off diamox • several weeks later IOP bounced up again so latanoprost added • excellent response initially but after a couple of months IOP back up at 42mmHg

  40. Progress • Added diamox and increased pred forte • reduced pred forte but IOP didn’t lower enough to stop diamox..... • time for a trabeculectomy (after 5 months)

  41. Progress • Trab with MMC - IOP 12 mmHg • Phaco/PCIOl with IOL and Morcher implants to block iris defects • VA 6/6 IOP 14

  42. Thank you!

More Related