Pharm final 6

kelseyfmeyer's version from 2015-05-08 19:24


Question Answer
what are the anatomical entities that serve as a drug reservoir?(ie, where do drugs get 'stuck' in the eye?) cornea, lens, uveal pigment(melanin)
what is a biochemical characteristic of the eye, which when combined with the physical barriers, makes drug delivery to the eye difficult?outward ABC transporters
fluid in the ant chamber is? post chamber is?ant= aqueous humor. post= vitreous humor
what is the particular substance in the eye that some drugs will bind to?melanin
what is metabolism of drugs in the eye like?there is enzymatic biotransformation in the eye, esp with esterases (use of prodrugs for epinephrine and prostaglandine F2-alpha)
what kinda vd do eye drugs need?large
what is the main route of entry when drugs are topically administered?cornea
how can you change the elimination half-life of drugs in tears? (2 ways) (and what is the t1/2?)(3-6 min). (1) changes in tear production (2) changes in drainage and blinking rate
if drugs cross the conjunctiva and the sclera, how are they eliminated?eliminated mainly by choroidal circulation (pic on slide 9). (BVs between retina and sclera)
explain the three paths a drug can take to get from topical admin (tears) to SYSTEMIC circulation?(1) Tears--> CORNEA(main route)-->aqueous humor-->iris(lots of BVs)-->systemic (2) Tears-->conjunctiva-->sclera-->ciliary body(lots of BVs)-->systemic (3) nasolacrimal route (mucous membs with lots of BVs)--> systemic. (note: cornea and sclera can have the drug go back and form from sideways, same thing with iris and ciliary bodies)
what are the two diff types of liquid topical drugs? explain what they are(1) solutions (drugs dissolved in a solute) (2) suspensions (drugs as solid particles suspended in a solute-- NEED TO SHAKE THESE)
4 advantages to solutions/suspensions?(1) less effects on vision (most are see through, and can be blinked away if can't see) (2) less incidence of contact dermatitis (isnt staying in one place for super long- I think the 3-6min tear t1/2 plays into this) (3) less toxic to ocular structures (4) easier to apply
what are the 4 disadvantages to solutions/suspensions?(1) SHORT contact time (2) dilution effects (3) expense (4) inc systemic absorption
how much is a sufficient dose with solutions/suspensions, and how do you apply?allow drop to fall on eye one drop is enough
what are the 4 advantages of ointment?(1) longer contact time (2) not diluted (3) protects cornea from drying (4) less expensive
what are the 5 disadvantages of ointment?(1) difficult to dose precisely (2) inc ocular discharge (3) more difficult to admin (4) more contact dermatitis (5) may delay epithelial wound healing
how much is a sifficient dose with ointments?5mm ribon
which type of topical drug is less expensive? which one delays epithelial wound healing? which one has more systemic absorption?ointment less expensive, ointment delays healing, solutions/suspensions have more systemic absorption
5 things which determine absorption after topical admin?(1) time the drug stays in the cul-de-sac and precorneal tear film (2) elim by nasolacrimal drainage (3) drug binding to tear proteins (4) drug metabolism by tear and tissue proteins (5) diffusion across cornea and conjunctiva
what is/are ways a topically administered drug can get into systemic circulation? (not path, just the structure)nasal mucosal absorption (mentioned twice), iris, ciliary body
transcorneal distribution leads to the drug going where?cornea--> aqueous humor--> intraocular structures AND systemic circulation
how does subconjunctival therapy work? what must you do?medication is injected under the conjunctiva. Requires SEDATION and TOPICAL ANESTHETIC
what is the max volume to be injected in subconjunctival therapy? (sp diffs)dog 0.5ml. horse 1ml
what kinda drugs is subconjunctival therapy used for?abx n corticosteroids
what are the three main disadvantages of subconjuntival therapy?(1) limited # of injections (2) scar tissue formation (3) can't be removed once given
what is the benefit of intracameral therapy?you can achieve very high drug conc
what are the 4 big risks of intracameral therapy?hemorrhage, cataract, retinal detachment/degradation
*how do you tentatively diagnose a bacterial eye infection?corneal ulcer scrapings--> gram staining
*Which animals are usually infected by G+? G-?G+(staph/strep) usually dogs/cats/horses. G- usually rumis (ruminants are rated more negatively than the other animals)
*first choice antimicrobials for corneal ulcers and bacterial conjunctivitis (non-specific infections)? (2)(1) NPB-- this is bacitracin+neomycin+polymyxin B.(aka neopolybac) (neo and poly do G- and baci(penicilin equivalent) does both bc cell wall distruction) (2) NPG-- this is neomycin+polymyxin B+gramicidin (In short--- combine G- and G+ shit to cover your ass)
*what is the first choice abx for SMALL ANIMALS? note about this? side effects?chloramphenicol. NOTE: DOES NOT WORK ON PSEUDOMONAS. look out for HYPERSENSITIVITIES (first choice-- throw chloriene in their eyes! Excellent!)
*which abx will penetrate intact cornea?ciprofloxacin (Cipro, Cornea) (I will sip fluids through your cornea) (and so does chloramphenicol, bc that's first choice for small animals, and so it does both)
NEOMYCIN/POLYMYXIN/BACITRACIN (NEOPOLYBAC) (NPB) is used to tx what? what is its spectrum?Corneal ulcers, conjunctivitis, Broad Spectrum
TICARCILLIN/CLACULANATE/AMPICILLIN has what side effects?hypersensitivities
is chloramphenicol static or cidal?static (even though it's number one in small animals, that doesnt mean it's awesome at everything, like killing)
are fluoroquinolones (ciprofloxacin) static or cidal?cidal (flo will kill a bitch)
what does tobramycin tx best in the eye?pseudomonas (toby will kill pseudo-posers)
how should you tx keratomycosis?AGRESSIVE tx, surgical intervention usually required so drug can penetrate
polyenes--> amphotericin B--> penetration is like? use against what? spectrum?poor penetration, broad spectrum, more active against yeast (yeast on all my membranes, yo)
polyenes--> natamycin--> how is it administered? what does it work well against?topical suspension, more effective against fungi, less against yeast, good against Fusarium(type of fungi) (FUNA)
how do you admin azoles for eye (miconazole, clotrimazole, itraconazole)derm cream
what is the penetration of polyenes like? how much binding do polyenes have?highly tissue bound with poor penetration (they stick into the membrane and cause pores, which means they wont go inside, remember
what are the two polyenes used?amphotericin B and natamycin (many AMs for NAT)
Nucleoside analogues--> which drug? (spectrum? what two other things should we know about the drug?)FLUCYSTOSINE. broad spectrum, Synergistic w/ Amphotericin B, and resistance can develop (too much AMP will give you the FLU)
what are the three azoles used on the eye?MICONAZOLE, CLOTRIMAZOLE, ITRACONAZOLE (MY IT CLOTTED in my eye)
miconazole--> spectrum? how is it administered? how bioactive is it? does it bind to things? what is it used to tx?BROAD spectrum, administered via subconjunctival injection, 30% bioactive, highly tissue bound, and used to tx yeast and fungi (Mi overachiever antifungal doesnt wanna sit on the eye, it wants to GET IN THERE and treat both!)
how is clotrimizole administered? what is it used to tx?derm cream used on eye, tx aspergillus (a clot of asparagus)
combined with 1% DMSOitraconazole ( It raDM SO hard)
what tx aspergillus?clotrimiazole
which azole tx yeast?miconazole
what is the optimum tx for corneal ulcers?equal amounts of: natamycin - tobramycin - cefazolin (combination is more effective than individual tx) (one antifungal and two abx, tobra for pseudomonas) (got an ulcer? I bet you're NotTooCarefree)
what are the main reasons youd use use antivirals for the eye? who does this usually pertain to?herpes virus keratitis and keratoconjunctivitis. RARE in dogs. MORE COMMON but self-limiting in cats and horses
what are the three antivirals mentioned to be used on the eye?DEOXYURIDINE(eptheliotoxic - teratogenic), acyclovir(less toxic), IFN γ (interferon gamma)(inhibits viral protein synth)
what is the pathogenesis of a corneal ulcer? (what two things happen?)happens when there is an amplification of biochemical degradation of (1) stromal collagen (2) extracellular matrix glycosaminoglycans (what holds the cornea together)
what are the two main causative agents of a corneal ulcer?(1) host-derived proteinases (zinc metalloproteinases (MMPs), neutrophil serine proteinases) (2) exogenous microbial hydrolases
what are the two HOST proteinases which contribute to corneal ulcers?zinc metalloproteinases (MMPs), neutrophil serine proteinases
plasma alpha2-macroglobulin--> spectrum? works on what?(proteinase inhibitor), broad spectrum means it works on host AND microbial proteinases (alpha and macro= the big #1 does everything!)
why would you use a chelating agent to tx a corneal ulcer? what are the drugs?Chelation= a particular way that ions and molecules bind metal ions.. My guess is that this means you're binding up the proteinase and rendering it useless. what are the three chelating agents used to inhibit proteinases? EDTA, acetylcysteine, tetracyclines(doxy)
what is a systemic proteinase inhibitor used to tx corneal ulcers? how do you apply it? what can you combine it with?homologous(self) plasma or serum which is applied topically; combo with EDTA or acetylcystei
explain why we use heparin to tx corneal ulcersheparin has an indirect action impedes extravasation of leukocytes(which produce proteinases)
explain ilomastat (how does it work?)inhibits endogenous and Pseudomonas proteinases ( IL ma stat(fast) anti proteases, esp if theyre from pseudomonas)
polysulphated glycosaminoglycans--> used for what? how are they applied?5% solution in artificial tears. (remember that glycosaminoglycans are what the extracellular matrix of the eye is made of. if you have them polysulphated, not incorporatedback into eye matrix-- provide antiinflammatory action instead)
what are the 4 main choices in how to dec intraocular pressure in glaucoma?(1) decreasing the production of aqueous humor (2) inc outflow (3) do some neuroprotection: prevent damage by increased glutamate(NMDA receptor) signalling (pressure on optic n-->inc glutamatic signaling--> can lead to neurodegeneration) (4) decide if sx is needed
trabecular outflow is mediated by what drugs?muscarinic agonists (alex TRABEC eating MUSHROOMS)
uvealsclearal outflow is mediated by?prostaglandin agonists
aqueous humor inflow is mediated by?beta blockers, alpha2 agonists, CAIs
way to remember flow in eye stuffbeta is only antagonist, rest are agonists
what are the three topical prostaglandine analogs? what do they do?(uvealsclearal outflow) latanoprost; bimatoprost; travoprost (PROST= PROSTAGLANDIN). facilitates outflow through uveoscleral pathway (mechanism unknown-- works on Gq) (prostate has stuff flow OUT,and for U(uveo), Quick!) (outflow is prostate carps. awesome.)
what are the beta-adrenoceptor antagonists? What do they do?timolol; metipranolol, betaxolol (BETA BLOCKERS END IN LOL!!!) regulate aqueous humor production (B stoppin the pool from fillin up)-->beta2-receptor most prominent(wanna open shit up); non-selective drugs, used in clinic
why do we use carbonic anhydrase inhibitors to tx glaucoma?reduced formation of bicarb leads to a reduction in fluid transport (pumps not pumping to exchange fluid or sthing)
what are the local carbonic anhydrase ihibitors? what are the oral carbonic anhydrase inhibitors?LOCAL= dorsolamide and brinzolamide. ORAL= methazolamide, dichlorphenamide, acetazolamide (bicarb-lamide. except dichlor) (MAD oral skills. local is BadDay when you gotta put crap in your eye)
what is the topical miotic used? what does it do?pilocarpine, increase aqueous outflow via trabecular outflow. (muscarinic) (carp swimming on the outflow of the river, avoiding the TReachery) (alex TRABEC eating mushrooms and carp)
what are the two neuroprotection drugs used, and why are they used?used to prevent excitotoxicity of the optic nerve in glaucoma. (1) amlodipine; calcium channel blocker (2) memantine; NMDA channel blocker (both end in ine, calcified pines and sniffing NMDA off fork tines)
what are the 4 groups of antiinflammatories used on the eye?NSAIDs, antihistamines and mast-cell stabilizers, glucocorticoids, cyclosporin A (highly lipophilic immunosuppressant drug)
what is the absorption of NSAIDs like? how is it administered?rapid absorption, can be admin topically or subconjunctival injections-- can consider systemic tx
what are antihistamines/mast cell stabalizers used for?allergic conjunctivitis
how strong are glucocorticoids as antiinflmmatory agents? what side effects should you know? when should you not use?STRONG antiinflammatory effects, but they are IMMUNOSUPPRESSIVE And SHOULD NEVER BE USED ON DAMAGED CORNEA(impede healing i think)
cyclosporin A-- hydro or lipophilic? what side effect should you know? what is it used to tx?highly lipophilic. can be immunosuppressive. Is used to tx ERU- equine recurrent uveitis (trying to treat a recurrently dzed horse is a vicious CYCLE)
timolol acetate is a what used to tx what, with what effect on the eye?sympatholytic, used to tx glaucoma, causes constriction of the pupil (lol= beta blocker, so know it's adrenergic. Think that Tim is under a lot of pressure and so he is constricting inwards in sympathy)
para-sympatholytic drugs--> what pupillary response? what are the drugs? what is the dz this is used to tx?dilation (mydriasis). The drugs are atropine, tropicamide, scopolamine. Used to treat uveitis in the horse, and also used as a diagnostic agent (PS- atropine makes you all dewey eyed)
sympathomimetic drugs--> what pupillary response? what are the drugs? what is the dz this is used to tx?dilation (mydriasis). phenylephrine, epinephrine. Used to treat anterior uveitis
what are the topical local anesthetics?proparacaine and tetracaine (TP just stays on the eye surface)
what are the infiltrative local anesthetics?lidocaine and bupivacaine (LB infiltrates!)
what is a disinfectant that can be used on the eye?povidone iodine (iodine scrub on the eye)