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68 Cards in this Set
- Front
- Back
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in north america what is the general flow of glaucoma treatment using laser, surgery and medial treatment
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medical, laser, and then surgery
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aqueous is secreted by what cells
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the non pimented ciliary epithelium
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using CB, SC space, uveaoscleral outflow, and sclera describe the aqueous outflow
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uveoscleral outflow --> CB--> SC space --> sclera
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is glaucoma usually associated with an increase in aqueous production or a decrease in outflow.
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decrease in outflow
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what are the three theories of glaucoma damage? (three ways damage occurs)
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1. direct mechanical therory where pressure blocks axoplasmic flow
2. ischemic theory where pressure blocks circulation to nerve 3. apoptosis |
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three main ways of treatment for glaucoma
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reduce aq. production
increase outflow neuroprotection |
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name two types of drugs that reduce aq. production and give some examples of each
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adrenergic antagonists - Beta blockers
carbonic anhydrase inhibitors - dorzolamide, acetazolamide, methazolamide... |
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what happens when Beta 1 receptors are stimulated?
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tachycardia and increased cardiac output
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what occurs when beta 2 receptors are stimulated
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bronchial dilation
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what receptor is involved with negative feedback?
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alpha 2
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what is the only beta 1 selective beta blocker
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betaxolol
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what time of day do you not want to have a pt take a beta blocker
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at night
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betoptic s (betaxolol) is in what form
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suspention this is the only beta blocker in this form it is less stingy than others
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if a person has a history of asthma what beta blocker would you give them
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betaxolol b/c it is the only one that is beta 1 selective so it will not affect the lungs as much
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what is the typical dose for a beta blocker?
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BID, many docs will try qd first
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what is the mechanism of action fro a beta blocker
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decrease the aqeous production by blocking the beta receptors on the ciliary body
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what percentage do beta blockers drop the iop by usually
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22 to 33%
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what types of glaucomas are beta blocker used to treat, your choices are POAG, angle closure and secondary
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all of the above
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list the side effects of beta blockers from most common to least common. 5 of them
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CNS deprssion, ocular sting/burn, bradycardia, bronchospasm, and aggravate lipid levels/mask hypoglycemia.
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what is the beta blocker that is least likely to cause CNS depression and why
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carteolol b/c it doesnt cross the blood brain barrier.
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what must you do before you prescribe a pt a beta blocker
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ALWAYS CHECK BLOOD PRESSURE, PULSE, RESPIRATORY/BLOOD STATUS BEFORE AND DURING TREATMENT AND RECORD
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what are the contraindications for beta blockers
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bronchial obstruction/asthma
chronic obstructive pulmonary disease bradycardia/congestive heart failure uncontrolled diabetes/hyperlipidemia not in notes but mentioned in lecture was a pt that is already on systemic betablockers |
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drugs ending in -amide are in what class
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carbonic anhydrase inhibitors
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CAI's are used by themselves or rarely used by themselves for treatment of glaucoma
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rarely used by themselves in drop form unless the pt is already on systemic beta blockers
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what is the mechanism of action for CAI's? also do they decrease aqueous production or outflow
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they inhibit the carbonic anhydrase that is on the non pigmented ciliary epithelium there for decreasing aqueous production
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what percentage of reduction in IOP is seen with CAIs
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15 to 20%
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what is cosopt what % of reduction in IOP is seen when used
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combo drug that includes the CAI dorzolamide and timolol. 30 to 35%
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what CAI is in suspension form, what is its benefit
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brinzolamide (azopt) it has less sting than non suspension forms
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what are the two main systemic CAIs and what are they used for
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acetazolamide and methazolamide, they are primarily used for emergency situations and are not intended for long term use. note that acetazolamide is cheaper but requires q6hrs as opposed to BID
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a person diagnosed with pseudotumor cerebri would be given what drug to reduce CSF pressure? ...........................hint ........also used for altitude sickness
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systemic CAIs like acetazolamide (diamox)
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what type of ocular problems that a pt has would make you consider not giving them a CAI
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if they have a compromised cornea b/c CAIs cause superficial punctate keratitis, ocular allergies, sting and burn and the kicker is endothelial cell function
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what are the ocular side effects of a CAI
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superficial punctate keratitis, ocular allergies, sting and burn and the kicker is endothelial cell function
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what type of allergies do you need to ask about before giving a CAI
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sulfa alergies, this is a different form but caution is advised
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what are some of the systemic SE of CAIs
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loss of appetite, nausia/fatigue, tinnitus, parasthesias in extremities, and electrolyte distubances.
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what are the contraindications for CAIs
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sulfa alergy
sickle cell anemia or other blood dyscrasias corneal surgery or epithelial/endothelial disease |
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what drug is essencially epinephrin in a bottle
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dipivefrin, it really doesnt get converted into epinephrin until it is in tissues and contacts enzymes
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what was the first drop for glaucoma that acted by increasing the outflow and not seen much anymore but may be on boards
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dipivefrin (propine)
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dipivefrin (propine) is not commonly used as a gluacoma treatment any more and is contraindicated with aphakes and pseudophakes du to increased risk of what
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cystoid macular edema
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brimonodine, dipivefrin, and apraclonidine are all in what type of class of drugs? (ex. cholinergic agonist)
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adrenergic agonist
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alpha 2 agonists such as apraclonidine do what to the pupil
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dilate it
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what is the mechanism of action that apraclonidine is able to lower IOP
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it causes a decrease in aqueous production and increases uveoscleral outflow
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brimonidine, a glaucoma drug acts on what kind of receptors and lowers IOP by doing what
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is an alpha 2 agonist and works by decreasing production and increasing outflow.
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what percentage does brimonidine lower IOP
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25 to 30%
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which drug has a lower chance of causing tachyphylaxis, brimonidine or apraclonidine?
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brimonindine
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if a pt is alergic to apraclonidine what other adrenergic agonist could you try
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brimonidine
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what are some contraindications of apraclonidine
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concomitant use of MAO inhibitors
severe cardiovascular disease low blood pressure/bradycardia |
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what are the ocular se of apraclonidine
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eyelid retraction, mydriasis, conjuctival blanching, and 20 to 30% of people are allergic
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what are the contraindications for brimonidine
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concomitant use of MAOIs
severe cardio dz depresion cerebral or coronary insufficiency |
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combigan is a combo of what (only in canada)
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brimonodine and timolol
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what effect does a cholinergic agonist have on the pupil
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miotic
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what general class is pilocarpine in
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cholinergic agonist (parasympathometic)
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are concentrations of 4% of pilocarpine more effective in lowering IOP than the regular concentration of .25% to 10%
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no
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what forms does pilocarpine come in
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drops, gel and ocuserts
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what is the mechanism of action for pilocarpine
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it contracts the muscles in the ciliary body stretching the TM increasing the outflow and it also pulls the iris away from the angle to allow outflow
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what is an example of a person that you would not want to use pilocarpine on
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a person with pre existing retinal dz or high myopia, they have the increased risk of RD
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what type of glaucoma do you NOT want to use pilocarpine on
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inflammatory or vascular
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if you think that you have an adies tonic pupil what drug and conc. would you use
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pilocarpine the pupil is not reacting to light but is super sensitive to pilo so use .125% and if you get a reaction it is positive for adies
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pilocarpine and what class of drugs cancel each others IOP effectivness out
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prostaglandins
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in general what percentage of drop in IOP would you expect from a prostaglandin
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about 30%
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how does latanoprost (xalatan) work to lower the IOP? increase outflow or decrease production
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increases the out flow by loosening the intercellular spaces in the ciliary body. (same as latanoprost, and xalatan)
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what may be the single most effective glaucoma medication available
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bimatoprost (lumigan)
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are there systemic issues with latanoprost (xalatan)
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none
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what race is it thought that travaprost is more effective
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African Americans
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what is the mechanism of action that bimatoprost (lumigan) lowers IOP
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increases the out flow by loosening the intercellular spaces in the ciliary body (same as latanoprost, and xalatan)
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what is the mechanism of action that travaprost (travatan) lowers IOP
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increases the out flow by loosening the intercellular spaces in the ciliary body (same as latanoprost, and xalatan)
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what side effect is seen with the use of prostaglandins in aphakes/pseudophakes?
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CME
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what are some of the inflammatory SE that could occur with the use of prostaglandins for glaucoma
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HSV, uveitis and/or conjunctivitis
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what are some of the contra indications for prostaglandin use for IOP lowering
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Aphakia/pseudophakia, Hx of uveitis, YAG posterior capsulotomy, Hx of HSV, or if the pt has cosmetic concerns
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