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108 Cards in this Set
- Front
- Back
Mucous layer of the tears is ___ soluble.
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lipid and water
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What corneal layers are lipid soluble? Water soluble?
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Lipid = epith, endoth
Water = stroma |
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The ideal ocular drug should have what kind of lipid solubility, molecular size, ionization, and pH?
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high lipid solubility, small molecular size, low ionization, and as a weak base
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T/F - Muscarinic receptors are found in smooth muscle parasymp postganglionic synapses.
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True
Nicotinic = skeletal NMJ and in both symp and parasymp preganglionic synapses |
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T/F - Nicotinic receptors are found in both parasymp and symp preganglionic synapses
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True
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T/F - Postganglionic neurons are shorter in the sympathetic pathway.
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False - longer
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What ocular components have alpha adrenergic receptors? What are the actions?
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Iris dilator (A1) = dilation of pupil
CB (A2) = constriction of BVs thus reduce blood flow to CB This relates to A2 adrenergic agonists (e.g. Iopidine, Alphagan) for IOP control |
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What ocular components have beta adrenergic receptors? What are the actions?
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TM (B2) = relax TM, incr outflow
Ciliary muscle (B2) = relaxes NPCE (B1, B2) = incr aqueous formation Relates to B-blockers for IOP control |
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What blood vessel serves as the direct source of aqueous?
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MACI (Maj Arterial Circle of the Iris), which comes off LPCA
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The NPCE allows active secretion of what molecules in order to draw water from MACI?
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Bicarb (inhibited by CAIs) and Na cross the NPCE, then water follows (thus active formation of aqueous)
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MOA of cholinergic agonists with the eye? Example of a drug?
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stimulate longitudinal muscle of CB, which pulls on scleral spur and thus opens up TM pores - results in incr outflow, decr IOP
Main example = pilo! |
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Three main structures that get parasymp innervation in eye? Actions?
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sphincter muscle (miosis), ciliary muscle (incr accom), lacrimal gland (incr tears)
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What drug is used during an LPI?
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Pilo - to pull iris taut
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1% pilo is used in this diagnostic test...
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to DDx CN III palsy vs sphincter tear w/ fixed, dilated pupil or pharm block
CN III palsy will constrict, tear or pharm block won't |
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0.125% pilo is used in this diagnostic test. MOA?
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Dx adie's - normal pupil won't respond, but Adie's will result in miotic pupil
Ciliary ganglion has lesion, so sphincter is starved for ACh so even a little pilo will cause miosis |
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Pilo ADEs?
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Browaches, HAs, myopic shift (these apply only to pre-presbyopes since ciliary muscle still works)
Also decr vision in cataract pts (miosis exacerbates), *RDs, secondary ACG |
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T/F - Cataract is a CI to pilo.
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True - smaller pupil can worsen visual problems related to cataract esp if opacity in visual axis
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What drug is used for the Tensilon Test? What Dz is involved? MOA?
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Edrophonium - for Dx MG; stimulates muscle strength
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T/F - Echothiophate is an irreversible acetylcholinesterase
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True
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Neostigmine is used to Tx...
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MG
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What cholinergic agonist has a fast onset and short mydriatic duration?
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Tropicamide
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What is the most potent ocular cholinergic agonist?
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Atropine
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How does Atropine decrease AC rxn?
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constrict blood vessels (stabilizing blood-aqueous barrier) in the CB, which contributes to aqueous formation
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Physostigmine can be used as an antidote for ___ toxicity.
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Atropine
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Botox falls in what drug class? MOA?
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Cholinergic antagonist; inhibits release of ACh at neuromuscular jxn thus inhibit muscular contraction
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Norepinephrine acts on what receptors?
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A1, A2, B1 (NOT B2, thus minimal effect on aqueous production)
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T/F - All of the adrenergic receptors in the anterior segment have B2 receptors
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True
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What percent Phenylephrine is useful for DDx Horner's? How does it work?
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1% - this is not enough to dilate normal eyes, but will give full dilation for Horner's pts
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Why is Phenylephrine not useful as a cycloplegic?
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It is an Alpha-1 agonist (which is in iris dilator). No effect on Beta receptors thus no cycloplegia
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What adrenergic agonist is useful as a Tx for reducing ptosis?
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Phenylephrine - incr sympathetic innervation to Muller's muscle, which retracts lid
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Your pt fails to dilate with cocaine and dilates with Paredrine (Hydroxyamphetamine). You suspect...
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No dilation on cocaine = (+)Horner's
Dilation with Paredrine = preganglionic lesion so must R/O Pancoast's tumor at lung apex "Paredrine has a PreDilection to tumors" |
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Epinephrine acts on what receptors?
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All adrenergic receptors (both Alphas and Betas)
Compare vs Norepi - acts on all but B2 |
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Naphazoline class, MOA, use, ADEs
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aka Naphcon-A (which also has antihistamine); Adrenergic agonist; used to constrict conj BVs (decr redness)
ADEs = greater alpha vs beta effects so have potential to depress CNS; excessive use can also cause dilation since affects alpha (therefore iris dilator) |
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Tetrahydrazoline class, MOA, use, ADEs
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aka Visine; Adrenergic agonist; used to constrict conj BVs (decr redness)
ADEs = greater alpha vs beta effects so have potential to depress CNS; excessive use can also cause dilation since affects alpha (therefore iris dilator) |
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Apraclonidine class, MOA, use
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aka Iopidine; A2 adrenergic agonist; decr aqueous production AND incr uveoscleral outflow; used to control IOP spikes after ocular surgery and for acute angle closure attack, not effective for chronic glaucoma
*Apraclonidine for Acute |
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What glaucoma drug class has two IOP lowering actions in one? Name these actions.
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A2 adrenergic agonists ("onidines")- decr aqueous production and incr uveoscleral outflow
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Brimonidine class, MOA, use, ADEs
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aka Alphagan; A2 agonist; decr aqueous production AND incr uveoscleral outflow; used for long-term glaucoma Tx (compare vs Apraclonidine/Iopidine)
ADEs = follicular conjunctivitis, but Alphagan P has purite as the preservative which decr incidence of rxns |
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Epinephrine MOA in lowering IOP?
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No longer used to lower IOP, but MOA = incr outflow (B2) decr aqueous production (A2)
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Contraindications for Epi?
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1) Aphakes: incr risk of CME
2) Narrow angles: slight mydriasis can lead to angle closure 3) Cardiovasc dz and hyperthyroidism: B1 effects can cause HAs, tachycardia, hypertensive crisis 4) MAOIs: incr effect |
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Topical application of B-blockers can cause these ADEs...
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can be absorbed systemically, causing depression, impotence, bradycardia, bronchospasm
(hence block sympathetic) |
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T/F - There is little difference in effectiveness between 0.25% and 0.50% conc in B-blockers
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True
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What type of Beta receptors are predominant in the eye? Where are these receptors exactly?
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Beta-2 ("two eyes, two lungs" - this rule applies to Beta!)
In TM, Ciliary muscle, NPCE |
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Which beta blockers are cardioselective (both topical and systemic)?
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Atenolol, Betaxolol, Esmolol, Acebutol, Metoprolol
"A BEAM of B1 blockers" |
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What is the only topical cardioselective beta blocker?
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Betaxolol (Betoptic-S)
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Cosopt is made of...
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Timolol (B blocker) and Dorzolamide (CAI)
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Combigan is made of...
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Timolol (B blocker) and Brimonidine (A2 agonist)
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What is the difference between Alphagan and Betagan?
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Alphagan (Brimonidine) = A2 agonist
Betagan (Levobunolol)= B blocker |
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This drug intentionally induces ptosis. Why would you want to do this? MOA of this drug?
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Guanethidine; to Tx lid retraction in Grave's; causes ptosis by limiting NE through increasing release at synapse then enhance reuptake - thus decr symp response, also blocks receptors to Muller's muscle. Both contribute to ptosis
"Guanethidine Graves" |
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Dapiprazole class, MOA, use
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aka Rev-Eyes; A1 antagonist; induces miosis post-dilation
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CAI MOA?
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Acts in CB epith (nonpig and pigmented), prevents carbonic anhydrase from combining CO2 + H20 into Bicarb
Bicarb normally enters into posterior chamber and draws Na and water to follow, which incr IOP. In a nutshell: CAIs decr IOP by decr aqueous outflow |
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CAI should not be used w/ pts who have a ___ allergy.
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Sulfa
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Name the topical and oral CAIs.
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Topicals = Brinzolamide (Azopt) and Dorzolamide (Trusopt)
"BRIan and DORothy" Orals = Acetazolamide (Diamox) and Methazolamide (Neptazane) "Ace and Meth" - you can think Ace Frehley of KISS and Method Man (yeah I know but it works for me...) |
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ADEs of CAIs? How about Acetazolamide ADEs specifically?
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Metallic taste, tingling of hands, *metabolic acidosis, GI irritation
In acetazolamide = bone marrow suppression, aplastic anemia, myopic shifts |
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MOA of prostaglandins?
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Incr uveoscleral outflow
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ADEs of prostaglandins?
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iris heterochromia, incr pigmentation and growth of lashes, skin darkening around eyes
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MOA of topical ocular anesthetics
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block nerve conduction by stopping influx of Na ions into nerve cytoplasm; w/o Na entry, nerve cannot depolarize (thus won't send off signal)
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This drug is used along with local anesthetics to minimize systemic absorption
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epinephrine - BV constriction
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You're having trouble remembering which anesthetic is an ester, and which is an amide, and then you remember this mnemonic...
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Amides contain an "i" somewhere before the -aine.
Esters do not (with the exception of dimethocaine). |
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T/F - All topic anesthetics are amides.
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False - esters
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Which anesthetic class gets metabolized by the liver?
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Amides ("Lidocaine Longer Liver")
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Which anesthetic class is metabolized locally?
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Esters
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Cocaine causes vaso(dilation/constriction)
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constriction - thus enhances the effects of anesthesia on its own, without need for epinephrine
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Fluoress includes what anesthetic?
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Benoxinate
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Antihistamine MOA?
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Block cell receptors to histamine (H1 or H2)
DO NOT prevent histamine release from mast cells and basophils |
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Naphcon-A consists of...
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Naphazoline (vasoconstrictor) + Pheniramine Maleate (H1 antihistamine)
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Topical antihistamines are (H1/H2) blockers?
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H1
Recall that H2 is in the stomach |
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Mast Cell stabilizer MOA
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acts on exposed mast cells and inhibits degranulation upon re-exposure to antigen
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Mast Cell stabilizers are not effective for (acute/chronic) allergic Sx
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not effective for acute since mast cells already degranulated
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Cromolyn Sodium class, use
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Mast cell stabilizer, used for chronic allergic conjunctivitis, vernal conjunctivitis, atopic keratoconjunctivitis
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Alocril and Alomide are what class drug?
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Mast cell stabilizers
Also Alamast |
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Patanol consists of...
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H1 receptor blocker and mast cell stabilizer
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VKC is almost always associated with...
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atopy (asthma, eczema, seasonal allergic rhinitis)
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VKC vs AKC?
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VKC = kids, less involved w/ outer lid & periorbital skin, *Trantas Dots (limbal papillae), *cobblestone papillae), seasonal, stringy discharge
AKC = young adults, *scaly thickened swollen ITCHY lids, all year long |
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Corticosteroid MOA
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binds to receptors on target cells - steroid/receptor complex enters nucleus and makes new mRNA
Inhibits phospholipase A2, an enzyme that is in the arachidonic acid pathway; the latter pathway leads to inflammatory agents incl leukotrienes and prostaglandins |
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Corticosteroids (incr/decr) capillary permeability?
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decr
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Critical corticosteroid ADEs?
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Incr risk of secondary infections (HSV!), PSCs, glaucoma (incr IOP)
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NSAID MOA?
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Blocks COX, thus stop conversion of arachidonic acid into prostaglandins and thromboxanes
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Diclofenac Sodium class, use
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aka Voltaren; ocular NSAID; for post-op inflammation/prevent CME and Tx allergic conjunctivitis
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Ketorolac Tromethamine class, use
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aka Acular; ocular NSAID; for post-op inflammation/prevent CME and Tx allergic conjunctivitis
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Trifluridine MOA
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inhibits replication of viruses by producing faulty viral DNA
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Antimetabolites are used in ophthalmic practice mostly for ___. Name two.
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trabeculectomy; 5-fluorouracil, Mitomycin C
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Rose bengal stains...
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healthy epith cells that are not covered by mucous (does not enter epith defects like NaFl or Lissamine Green)
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Lissamine green stains...
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epith cells unprotected by mucous AND epith defects
vs Rose Bengal - does not stain epith defects |
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IV Fluoroscein Dye takes ___ secs for it to show up in choroidal and retinal vessels.
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10-20
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What drug class is the best to decr IOP? MOA?
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Hyperosmotic agents (draws gradient towards blood to decr outflow)
ex = Isosorbide, Glycerine |
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Isosorbide class, MOA, use, ADEs
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Hyperosmotic agent; huge molecular weight compounds that draw water back into blood vessels from posterior chamber thus decr IOP; for acute angle closure attack
ADEs = vomiting if not sipped Mixed with soft drink over crushed ice |
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Glycerine class, MOA, use, ADEs
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Hyperosmotic agent; huge molecular weight compounds that draw water back into blood vessels from posterior chamber thus decr IOP; for acute angle closure attack ADEs = vomiting if not sipped, NOT for DM b/c incr BG Mixed with soft drink over crushed ice |
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Which has more ocular contact time - methylcellulose or polyvinyl alcohol? Why?
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methylcellulose b/c more viscous
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Benzalkonium chloride MOA, use, ADEs
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aka BAK; ruptures bacterial cell memb; used as preservative
ADEs = epithelial toxicity with prolonged use |
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Viroptic uses this preservative...
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Thimerosal
hence prolonged use not recommended |
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Chlorhexidine use...
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preservative in Boston Simplicity and other RGP cleaners
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What causes whorl keratopathy? Although rare, this drug also causes this other ADE?
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Amiodarone; also causes optic neuritis
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T/F - Antianxiety agents tend to cause dry eyes
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True
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T/F - Antihistamines tend to cause dry eyes
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True
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Ritalin causes (miosis/mydriasis)?
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mydriasis
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Antihistamines cause (miosis/mydriasis)?
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mydriasis
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Amphetamines cause (miosis/mydriasis)?
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mydriasis
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Heroin causes (miosis/mydriasis)?
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miosis (opiate drug causes pinpoint pupils e.g Morphine, Codeine)
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Digitalis ocular ADEs...
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B/Y color defect, pain on eye movement
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Ethambutol toxicity to eye...
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optic neuritis
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Isoniazid toxicity to eye...
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optic neuritis
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Chloramphenicol toxicity to eye...
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optic neuritis
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Crystalline retinopathy is caused by toxicity from this drug...
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Tamoxifen
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These drugs cause RPE and outer retinal degeneration, pigment deposits throughout eye, and cataracts. What is this drug class?
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Phenothiazines (Chlorpromazine, Thioridazine)
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Canthaxanthin ocular toxicity?
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crystalline retinopathy, color blindness
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Oral contraceptive ocular toxicity?
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optic neuritis, papilledema, pseudotumor cerebri, dry eyes
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T/F - A drug with a aigher therapeutic index is safer
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True
TI = LD50 / ED50 |
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Therapeutic Index =
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LD50 / ED 50
Lethal Dose that kills 50% of experimented animals Effective Dose = does necessary to be effective in 50% of population |