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156 Cards in this Set
- Front
- Back
How much of a topical drug is lost via evaporation upon instillation? Where does the rest go?
|
25%
1) drainage into nasolacrimal apparatus 2) absorption into systemic circulation via conjunctival and lid vasculature 3) Penetration into cornea |
|
What is bioavailability?
Which types of molecules have the highest bioavailability? |
Percent of unchanged drug delivered to desired site.
Small, uncharged, lipid-soluble |
|
The higher the degree of ionization the more _______ soluble a drug. What determines the degree of ionization of a drug?
|
water.
The pH of a drug determines its degree of ionization. The non-ionized portion will penetrate the cornea while the ionized portion (water soluble) is left behind. |
|
Epithelium: ______ soluble
Stroma: _______ soluble Endothelium: ______ soluble |
lipid
water lipid Therefore most of the cornea is lipid soluble. |
|
Most ocular drugs are formulated as ________.
|
weak bases = more non-ionized portions of the drug reach the aqueous humor
|
|
Somatic neurons innervate?
Autonomic neurons innervate? |
Somatic: Skeletal muscles
Autonomic: Smooth muscle, cardiac muscle, glands. |
|
What are the effects of activating the sympathetic pathway?
|
DRY
Dilation Brochodilation fight or flight functions Overall decrease in secretions |
|
Organs that are innervated by the sympathetic system contain alpha and beta receptors. Where are these receptors located in the eye?
|
Iris dilator (alpha 1)
Trabecular meshwork (beta 2) Ciliary muscle (beta 2) Nonpigmented ciliary epithelium (beta 1 and beta 2) CB vasculature (alpha 2) |
|
What does sympathetic activation lead to at these ocular locations?
|
alpha 1 --> dilation of iris dilator
beta 2 --> relaxation of TM, relaxation of CM, increased outflow, opposes accommodation, increases aqueous formation at NPCE Beta 1 - increases aqueous formation at NPCE Alpha 2- constrict CB vasculature, reduces aqueous formation |
|
What are the effects of activating the parasympathetic pathway?
|
SLUD: salivation, lacrimation, urination and defecation
bronchoconstriction and miosis rest and digest functions |
|
The parasympathetic system acts on muscarinic and nicotinic receptors. What are the three main structures in the eye that receive parasympathetic innervation? What type of receptors are found there?
|
All muscarinic receptors
iris sphincter M3 Ciliary muscle M2, M3 Lacrimal gland M2, M3 |
|
What effect does parasympathetic activation have at these 3 locations in the eye?
|
Miosis (iris sphincter)
Accommodation (ciliary muscle) Tear production (lacrimal gland) |
|
What neurotransmitters are released at the site of action in the sympathetic system?
Parasympathetic system? |
sympathetic - epinephrine and norepinephrine
para - Ach |
|
Where are sympathetic cell bodies located?
Parasympathetic cell bodies? |
sympathetic - thoraco-lumbar regions of CNS
Para - Cranio-sacral regions of CNS |
|
List 2 direct cholinergic agonists.
|
Pilocarpine
Carbachol |
|
How do cholinergic agonists work to reduce IOP?
What other therapeutic uses to do cholinergic agonists have? |
Stimulate the longitudinal muscle of the ciliary body, which pulls posteriorly on the scleral spur and secondarily opens up the trabecular spaces.
This leads to increased outflow and decreased IOP. Treatment of glaucoma (formerly) and accommodative esotropia. |
|
How is pilocarpine useful in an angle closure attack?
|
The miotic action of the drug pulls the iris taut and allows the laser peripheral iridotomy (LPI) to be more effective
|
|
What is 1% pilocarpine used for?
|
In a patient with a fixed dilated pupil:
To differentiate a CN 3 palsy from a sphincter tear. CN 3 palsies will constrict with pilocarpine. |
|
What is 0.125% pilocarpine used for?
|
In the diagnosis of Adie's tonic pupil, which is an acute dilated pupil due to ciliary ganglion lesion.
The iris sphincter is supersensitized in Adies and will respond with miosis to a diluted form of pilocarpine. The sphincter muscle is starved of Ach. |
|
What are the main side effects of pilocarpine?
|
Headaches
Browaches Myopic shifts |
|
What are the other main side effects of pilocarpine?
|
Cataracts centrally, after longterm use
Retinal breaks which may lead to retinal detachments, uncommon |
|
What % IOP reduction does pilocarpine provide?
|
30%, but has short half life so need to administer 4x/day.
|
|
List 5 indirect cholinergic agonists (anticholinesterase inhibitors)
|
Neostigmine
Edrophonium Echothiophate Isofluorophate Pyridostigmine |
|
Which drug is used in the Tensilon test in the diagnosis of Myasthenia Gravis?
|
Edrophonium.
It has rapid onset (via injection) and short duration of action (10 mins). If ptosis improves, test is positive for myasthenia gravis. |
|
Which types of drugs worsen myasthenia gravis?
|
Beta blockers
|
|
What is neostigmine used for?
|
Follow-up test for myasthenia gravis (limb strength test)
and also for treatment of myasthenia gravis. |
|
Which two drugs are irreversible AchE inhibitors?
What are the clinical uses theoretically? |
Echothiophate and Isofluorophate
used for diagnosis and treatment of accommodative esotropia and rarely for glaucoma. |
|
What is pyridostigmine used for?
|
Tx of Myasthenia gravis.
|
|
What are cholinergic antagonists used for?
|
cycloplegic refractions,
pupillary dilation, management of uveitis by blocking Ach at muscarinic sites in the ciliary body and iris sphincter. |
|
List the 5 cholinergic antagonists.
Think "STopACH" |
Scopolamine
Tropicamide Atropine Cyclopentolate Homatropine |
|
List the cholinergic agonists from shortest to longest lasting mydriatic and cyloplegic effects.
|
Tropicamide (4 hours)
Cyclopentolate (24 hours) Homatropine (1-3 days) Scopolamine (up to 7 days) Atropine (7-12 days) |
|
Why is CNS toxicity more likely with scopolamine than atropine?
What are the adverse effects of scopolamine? |
Scopolamine penetrates blood brain barrier better than atropine.
Hallucinations, amnesia, unconsciousness, confusion, restlessness, incoherence, vomiting and urinary incontinence. Special caution recommended in Down's patients, small children, and the elderly. Just like atropine. |
|
Why is Tropicamide the standard drug used for dilation?
What are the side effects? |
Fastest onset and shortest duration of mydriatic effects. A much longer mydriatic than cycloplegic effect.
Maximum mydriatic effect occurs in 20-35 minutes. Max cycloplegic effect 20-45 minutes. Very safe agent, even in patients with cardiovascular disease. Never the answer to a side effect question. |
|
What's the difference between 1% and 0.5% tropicamide?
|
Similar mydriatic effects, but more cycloplegic effect.
|
|
Which drug is the most potent mydriatic and cyloplegic agent?
What is the onset till cycloplegic effects? |
Atropine
60-180 minutes for cycloplegia onset |
|
What are the symptoms of atropine toxicity?
|
Dry mouth (1st sign)
dry flushed skin rapid pulse disorientation fever (due to effects on hypothalamus) = sympathetic effects. |
|
What is the standard cycloplegic agent?
|
Cyclopentolate becasue it has the fastest onset and shortest duration of cycloplegic effects.
Cycloplegic effects are better than homatropine. They are similar to atropine but with faster onset and shorter duration. |
|
Which cholinergic antagonist is standard for treating anterior uveitis?
|
Homatropine. Useful in minimizing pain and for prevention of posterior synechiae. Also decreases anterior chamber reaction by constricting blood vessels (stabilizing blood aqueous barrier) in ciliary body. Only 10% as potent at atropine, weak cycloplegic action.
Cyclopentolate and atropine can also be used in treatment of uveitis. |
|
List 5 adrenergic agonists (sympathetic system!) that are used for dilation, conjunctival constriction, and management of minor allergic conditions.
|
Norepinephrine
Phenylephrine Hydroxyamphetamine Naphazoline Tetrahydrozoline |
|
Which adrenergic agonists are used for glaucoma therapy?
|
apraclonidine
brimonidine |
|
How is norepinephrine different from epinephrine?
|
NE does not act on beta 2 receptors, whereas epinephrine does.
NE has no effect on aqueous production. |
|
What is the mechanism of phenylephrine?
|
alpha 1 agonist. This allows it to cause dilation (radial muscle on iris) without cycloplegia.
|
|
What is phenylephrine 1% used for?
What is phenylephrine 2.5% used for? What is phenylephrine 10% used for? |
1% - Gives full dilation in patients with postganglionic Horner's because adrenergic receptors are supersensitized.
2.5% - dilation without cycloplegia, palpebral widening. Used in combination with tropicamide. Cannot provide a fixed dilated pupil alone. Also differentiates scleritis and episcleritis. Blanched conj vessels means episcleritis. 10% - break posterior synechiae |
|
How does phenylephrine cause palpebral widening?
|
Acts on Muller's muscle to retract upper eyelid.
|
|
Phenylephrine is contraindicated in patients taking what drugs?
Phenylephrine should be avoided in patients with what disease? |
Atropine
MAOis e.g. isoniazid, phenelzine, moclobemide, isocarboxazid TCAs e.g. amitriptaline, imipramine reserpine guanethidine methyl-dopa MAOi and TCAs can exacerbate the cardiovascular effects of phenylephrine causing hypertensive crisis. Graves' disease because of extreme blood pressure elevations. |
|
What is the mechanism of Hydroxyamphetamine?
|
Causes release of norepinephrine and possibly inhibits its re-uptake. Causes dilation and conjunctival blanching (similar to phenylephrine).
Little to no effect on accommodation, refractive state or IOP. |
|
When is hydroxyamphetamine used?
|
After cocaine or apraclonidne to determine lesion location in Horner's syndrome.
Post-ganglionic: no dilation Preglanglionic: dilation |
|
How does cocaine affect a Horner's pupil (miotic)?
How does apraclonidine affect a Horner's pupil (miotic)? |
Cocaine has no effect on Horner's pupil regardless of lesion location.
Cocaine will dilate a normal eye. Apraclonidine will dilate a Horner's pupil. Apraclonidine will have no effect on a normal eye. |
|
Anisocoria in Horner's syndrome is greater in the ___?
|
Dark
|
|
What are Naphazoline and Tetrhydrozoline used for? What is their mechanism of action?
What is Naphcon A? |
Topical ocular decongestants to constrict the conjunctival blood vessels.
Mechanism: greater alpha than beta effects. Have the potential to depress the CNS. Excessive tetrahydrozoline can cause dilation because of alpha effects on radial muscle. Naphcon A = naphazoline + pheniramine maleate (antihistamine H1 antagonist) |
|
What are the two mechanisms of action of Apraclonidine and Brimonidine?
|
Alpha 2 agonists. Brimonidine is 30x more alpha 2 selective than apraclonide. Apraclonidine also has week alpha 1 activity which is enough to cause dilation in Horner's pupil.
1) Decrease aqueous humor production 2) increase uveoscleral outflow |
|
What is apraclonidine used for?
What is the expected IOP reduction? |
To control IOP spikes following laser iridotomy, trabeculoplasty, posterior capsulotomy.
During acute angle closure - rapid potent decrease in IOP - 30-40% decrease. Onset within 1 hour, peak effect 3-5hrs. |
|
Why is apraclonidine no good for longterm glaucoma therapy?
|
Tachyphylaxis - within 8 days of continous treatment, efficacy is reduced. >1 year of use has high allergic response (approx 50%)
|
|
What are the two topical neuroprotective agents?
|
Brimonidine
Betaxolol |
|
Why was Alphagan P introduced?
|
The preservative in brimonidine caused follicular conjunctiviitis in 30% of patients.
Alphagan P uses purite as a preservative. |
|
How is brimonidine helpful in Lasik/PRK patients?
|
Causes miosis and can be used to reduce glare, haloes and other night vision symptoms. Repeated daily use is not recommended due to rebound mydriasis and tachyphylaxis.
|
|
What are the systemic side effects of Brimonidine and Apraclonidine?
What drugs are Brimonidine contraindicated with? |
Dry mouth
MAOIs - isoniazid, phenelzine, moclobemide, isocarboxazid |
|
Adrenergic antagonists:
What are the beta1 selective beta blockers? What is the only topical beta 1 selective blocker? |
A BEAM
Atenolol Betaxolol Esmolol Acebutolol Metoprolol Betaxolol is only topical beta 1 selective drug. |
|
List the non-selective beta blockers
|
Metipranolol
Timolol Carteolol Levobunolol (betagan) |
|
What systemic side effects can topical beta blockers cause?
What systemic diseases are contraindicated for topical beta blockers? |
Depression
Impotence Bradycardia Bronchoconstriction Asthma COPD Bradycardia CHF B1 selective (A BEAM) minimize lung side effects B2 selective minimize heart side effects. |
|
Which nonselective beta blocker is most effective at reducing IOP?
|
Timolol. 26% reduction in IOP.
Unilateral use commonly reduces IOP in contralateral eye. |
|
How do beta blockers decrease IOP?
|
Act primarily on Beta 2 receptors in the ciliary epithelium to decrease aqueous production.
|
|
Timolol should be used cautiously in patients with _______because the cholinergic effects of beta blockers can mask the clinical signs and symptoms of these conditions.
|
Diabetics
Hyperthyroidism |
|
Timolol can worsen the symptoms of _________.
|
Myasthenia gravis
|
|
What is long term drift and short term escape with regard to Timolol?
|
Long-term drift: IOP starts to gradually rise
Short term escape: IOP initially lowers but returns to normal within weeks after starting therapy. |
|
What drugs are in Cosopt?
|
0.5% Timolol
2% Dorzolamide (Trusopt) Dosed BID |
|
What drugs are in Combigan?
|
0.5% Timolol
0.2% Brimonidine (Alphagan) Dosed BID |
|
What are the advantages of Carteolol versus other topical beta blockers?
|
1) intrinsic sympathomimetic ISA (reduced potential for systemic effects)
2) Reduces nocturnal bradycardia (compared to timolol) 3) Less stinging than timolol 4) Modest reduction in cholesterol in pts with hypercholesteremia |
|
The beta 1 activity of Betaxolol
minimizes ____________. It worsens ______________. |
Minimizes risk of respiratory effects.
Worsens congestive heart failure. |
|
What is the mechanism of Dapiprazole?
|
Alpha 1 antagonist to induce miosis post dilation.
|
|
Which drug is useful for topical use in Graves' disease to induce ptosis/combat lid retraction?
|
Guanethidine- causes release of NEP and enhances its reuptake limiting amount of NEP in sympathetic system.
|
|
Which class of glaucoma drugs increase outflow via
TM pathway? Uveoscleral route? |
TM - Cholinergic agonists e.g.pilocarpine, carbachol, neostigmine etc.
Uveoscleral: Alpha 2 adrenergic agonists - apraclonidine and brimonidine Prostaglandins - Latanoprost, Bimatoprost, Travoprost |
|
Which classes of glaucoma drugs decrease aqueous production?
|
Beta blockers e.g. Timolol, Betagan, Carteolol, Betaxolol
Alpha-2 adrenergic agonists: apraclonidine and brimonidine Carbonic Anhydrase Inhibitors: Brinzolamide, Dorzolamide, Cosopt |
|
What are the topical carbonic anhydrase inhibitors?
What are the oral CAIs? |
topical: Brinzolamide, Dorzolamide (rarely a primary med, but effective in combination e.g. with timolol - Cosopt)
Orals: Acetazolamide, Methazolamide, Dichlorphenamide |
|
What are the side effects of CAIs?
|
Metallic taste
Stinging Tingling in hands and feet Metabolic acidosis Depression Diarrhea Acetazolamide (oral): Thrombocytopenia, agranulocytosis, aplastic anemia, myopic shifts |
|
Where does carbonic anhydrase act? What does it do?
|
Ciliary body epithelium (non-pigmented and pigmented)
catalyzes the joining of CO2 and H2O to yield bicarbonate. The entry of bicarbonate into the posterior chamber causes water and sodium Na2+ to follow, which increases IOP. |
|
Before prescribing carbonic anhydrase inbitors, make sure the patient does not have ______ allergies.
|
sulfa allergies
CAIs are sulfa based. |
|
Which glaucoma drugs provide the highest IOP lowering effect?
|
Prostaglandin analogs - 27-35%
Latanoprost 0.005%, Bimatoprost 0.03%, Travoprost 0.004%. |
|
What is the mechanism of prostaglandin analogs?
|
Act on FP/PGF2a receptors on the ciliary muscle which, via metalloproteinases, causes reduction of neighbouring collagen, decreasing resistance in uveoscleral meshwork for increased outflow.
CHEW UP THE COLLAGEN, ALLOW MORE AQUEOUS TO GET OUT VIA UVEOSCLERAL PATHWAY Also act on skin receptors, activating phospholipase C to alter hair follicles. |
|
What time of the day is best for prostaglandin dosing?
|
Bedtime dosing allows daytime peak effect (12 -24hrs after administration)
|
|
What are the contraindications for Prostaglandins?
|
Patients at risk for CME e.g. post-op cataract patients
Cases of active inflammation e.g. uveitis Patients with previous episodes of Herpes Simplex Keratitis |
|
What are the side effects of prostaglandins?
|
Iris heterochromia
Increased pigmentation and growth of eyelashes (length, thickness, number) Skin darkening around eyes Conjunctival hyperemia (worse with lumigan, least with xalatan) Pruritis with lumigan. |
|
Name 3 topical ocular anesthetics.
|
Tetracaine
Proparacaine Benoxinate |
|
What is the mechanism of local anesthetics?
|
Block nerve conduction and change membrane permeability by stopping the influx of Na ions into the nerve cytoplasm. Prevents depolarization of the neuron.
|
|
What 3 groups make up the structure of local anesthetics?
|
1. Aromatic residue (lipophilic)
2. Intermediate chain ( increases length, increases the potency) 3. Amino group (hydrophilic) |
|
Topical ocular anesthetics have an ______ linkage between their intermediate chain and amino group.
What properties does this result in? |
Ester linkage
Shorter duration of action Metabolized locally (not in the liver) |
|
What is an adverse effect of topical ocular anesthetics?
|
Corneal melting.
|
|
Fluoress is a combination of:
|
Fluorescein and benoxinate
|
|
Topical antihistamines block _________.
|
H1 receptors.
H2 antihistamines are of no benefit topically. |
|
Give an example of a topical antihistamine.
|
Emedastine
|
|
List four topical mast cell stabilizers.
|
1) Cromolyn Sodium
2) Lodoxamide 3) Pemirolast 4) Nedocromil |
|
What is the mechanism of topical mast cell stabilizers?
What ocular conditions are they used to treat? |
Stabilizes mast cell membranes, by preventing Ca2+ influx and mast cell degranulation.
Effects begin days to weeks after beginning therapy. Used for chronic allergic conjunctivitis, vernal conjunctivitis, atopic keratoconjunctivitis |
|
List 5 mast cell - antihistamine combinations.
|
1) Azelastine (Optivar)
2) Epinastine 3) Ketotifen (Zaditor) 4) Olopatadine 0.20% (pataday) and 0.10% (patanol) "EZ POP" |
|
Which hormone acts on the adrenal cortex causing it to release cortisol?
|
ACTH
|
|
What are the mechanisms/actions of corticosteroids?
|
Inhibits phospholipase A2 and thus the arachidonic acid pathway.
Anti-inflammatory Immunosuppressive Decreases inflammatory mediators Decreases capillary permeability Decreases fibroblast and collagen formation - this prevents healing. |
|
What are the three main ocular side effects of corticosteroids?
|
1) increased secondary infections
2) PSC cataracts 3) Glaucoma |
|
List 3 potent topical steroids.
|
1) Prednisolone Acetate 1%
2) Rimexolone 3) Dexamethasone 0.1% |
|
List 2 "soft" topical steroids.
|
Fluoromethalone (FML) 1%
Loteprednol (Lotemax) 0.5% Less likely to cause a spike in IOP. |
|
What percentage of the general population are high steroid responders?
What percentage of patients with POAG are steroid responders? |
5% of general population
90% of POAG |
|
Which ocular drugs are in suspension and need to be shaken prior to use?
|
Prednisolone Acetate
Azopt (topical CAI) Fluoromethalone (FML) |
|
What are topical NSAIDs used for?
|
To prevent and treat CME in post-op cataract patients.
Ketorolac tromethamine is used for seasonal allergic conjunctivitis. |
|
List four topical NSAIDs.
|
Bromfenac (Xibrom)
Flurbiprofen (Ocufen) Diclofenac sodium (Voltaren) Ketorolac tromethamine (Acular) |
|
What are the side effects of topical NSAIDs?
|
Burning and stinging upon instillation
Corneal melting with prolonged use SPK with Acular |
|
Trifluridine is the drug of choice for_______?
|
HSV keratitis, types 1 and 2
|
|
What is the mechanism of Trifluridine?
|
Inhibits viral DNA in virus infected and normal epithelial cells by inhibiting DNA polymerase.
|
|
Why should Trifluridine not be used on patients for more than 3 weeks?
|
Because it is preserved with Thimerosal which causes toxicity.
Zyrgan does not have Thimerosal. |
|
What does 5-FU do?
|
Inhibitor of fibroblast proliferation, which helps prevent scarring.
Mechanism: Pyrimidine analogue that inhibits DNA synthesis. |
|
Is Fluorescein water soluble or lipid soluble?
What does it stain? |
Water soluble. Quickly dissolved in aqueous portion of tears.
Epithelial defects. |
|
What does Rose Bengal stain?
|
Dead and devitalized cells and cells that have lost their mucous surface.
It does not enter epithelial defects like Fluorescein. Stains the edges of herpetic dendritic lesions and can cause toxicity to HSV type 1. |
|
Why is Lissamine Green preferred over Rose Bengal for dry eye evaluations?
|
Causes less discomfort and ocular irritation
|
|
What happens when fluorescein dye is exposed to visible spectrum light?
|
Emits longer wavelength light
|
|
How long does it take fluorescein dye to reach the retina after 5cc are injected into the brachial vein?
|
15-20 seconds
|
|
List 3 agents used for exudative ARMD.
|
Macugen anti-VEGF
Lucentis anti-VEGF Visudyne - not anti-VEGF, targets LDL lipoprotein receptors. Pts must avoid sunlight exposure for up to 5 days after treatments. |
|
What is Glycerine used for?
|
Lower fluid volume during an acute angle closure attack.
|
|
How does Glycerine work?
|
High molecular weight, water-soluble compound that is unable to cross the blood aqueous barrier.
This creates an osmotic gradient whereby the plasma in the ciliary stroma region is HYPERTONIC to the aqueous humor. This sucks water out, lowering IOP. |
|
Why is Glycerine not recommended in diabetics?
What should be used instead? |
It is rapidly absorbed and metabolized into carbohydrates, increasing blood sugar levels.
Isosorbide should be used instead. |
|
What is Muro128 used for?
|
Corneal edema.
|
|
What are the main components used in artificial tears?
|
Cellulose esters:
Carboxymethylcelllulose Hydroxymethylceullulose Polyvinyl alcohol (PVA) Methylcellulose increases the viscosity of solutions allowing more contact time on the cornea. PVA is less viscous. |
|
What is the mechanism of Restasis (cyclosporine 0.05%)?
|
Inhibits T-cell activation by stopping the production of IL-2.
|
|
What is a side effect of BAK?
|
Corneal toxicity --> SPK
However, it also increases drug penetration |
|
What is EDTA used for?
|
Chelating calcium in band keratopathy.
|
|
Which drugs cause whorl keratopathy?
|
"swirl your CHAI T"
Chloroquine Hydroxychloroquine Amiodarone Indomethacin Tamoxifen |
|
Which drug causes SPK?
|
Isotretinoin
BAK (preservative) |
|
Which drugs cause Endothelial/Descemet's pigmentation?
|
Anti-psychotics:
Chlorpromazine & thiuridazine |
|
What side effect is caused by gold salts?
|
Stromal gold deposits
|
|
Which class of drugs causes delayed healing?
|
Corticosteroids
e.g. Pred Acetate, FML, Dexamethasone |
|
What are some ocular side effects of Amiodarone?
|
1) whorl keratopathy --> glare, photophobia and coloured rings
2) anterior subcapsular lens deposits 3) NAION |
|
What is Fabry disease?
|
Lysosomal storage disease that causes cardiovascular death.
It may also lead to corneal verticillata/whorl keratopathy and spoke-like lens opacities. |
|
Which drugs cause anterior subcapsular effects?
e.g. stellate cataracts deposits vacuoles gold deposits |
chlorpromazine (stellate cataracts)
amiodarone (deposits) Miotics e.g. pilocarpine(vacuoles) Gold salts (gold deposits) |
|
Which class of drugs causes posterior subcapsular cataracts?
|
Corticosteroids
|
|
How does Isotretinoin affect the lids and conjunctiva?
|
Blepharoconjunctivitis
Dryness & SPK Lid edema |
|
How do NSAIDs affect the conj?
|
Subconjunctival hemorrhage
(also retinal hemorrhage) |
|
How do Sulfonamides e.g. sulfamethaxozole, acetazolamide, hydrochlorothiazide affect the conjunctiva and lids?
|
Stevens-Johnson syndrome
Lid edema Ocular findings are rare. |
|
How does tetracycline affect the conj?
|
Pigmented cysts on the conj.
|
|
How does Sildenafil affect the conjunctiva?
|
Subconjunctival hemorrhage
Conjunctival hyperemia/chronic red eye |
|
Which classes of drugs decrease tear secretion?
|
Anticholinergics e.g. atropine, scopolamine
Antihistamines (especially 1st generation e.g. Benadryl) Isotretinoin Beta blockers e.g. timolol, atenolol, propranolol Antidepressants: SSRIs (Fluoxetine) and TCAs Phenothiazines: chlorpromazine, thioridazine Hormone therapies e.g. oral contraceptives CNS stimulants: e.g. methylphenidate, dextroamphetamine Diuretics: e.g. hydrochlorothiazide |
|
Which classes of drugs cause dilation?
|
Anticholinergics
Antihistamines Phenothiazines CNS stimulants CNS depressants: Phenobarbital Anti-anxiety: diazepam |
|
Which classes of drugs cause miosis?
|
Opiates e.g. morphine, heroin, codeine
Anticholinesterases (indirect cholinergic agonists) neostigmine |
|
What is Pralidoxime (Protopam) used for?
|
Can be given intravenously to counteract toxicity due to anticholinesterase agents such as those found in toxic nerve gases and insecticides which can lead to miosis that lasts up to a month.
|
|
Which drugs can cause nystagmus?
|
anti-epileptics: Phenytoin
Phenobarbital Salicylates (NSAIDs) |
|
Which classes of drugs can cause diplopia?
|
Antidepressants
Anti-anxiety agents |
|
Which drug affects smooth pursuits?
|
Alcohol
|
|
Which drugs can cause oculogyric crisis?
|
Chlorpromazine
Thiuridazine Cetirizine |
|
Which drugs can cause uveitis?
|
Cidofovir
Mycobutin (Rifabutin) Sulfonamides |
|
Which drugs and diseases can cause blue sclera?
|
Corticosteroids e.g. prenisolone, hydrocortisone, triamcinolone, dexamethasone
Minocycline Can also be caused by osteogenesis imperfecta and Ehlers Danlos syndrome. |
|
What drugs can affect the optic nerve?
|
Digoxin
Ethambutol Isoniazid Methotrexate Sildenafil Sumatriptan Amiodarone Oral contraceptives |
|
What are the ocular side effects of Digoxin?
|
Retrobulbar optic neuritis
Blue/yellow colour defects Entopic phenomena e.g. snowy vision, flickering lights |
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How do Ethambutol, Chlorampheicol, Streptomycin and sulfonamides affect the optic nerve?
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Optic neuritis, typically retrobulbar and bilateral
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How do Isoniazid and Methotrexate affect the optic nerve?
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Optic neuritis (but unlikely)
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How do Sildenafil, Sumatriptan and Amiodarone affect the optic nerve?
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NAION
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What are some rare optic nerve effects of oral contraceptives?
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Optic neuritis
Papilledema Pseudotumor cerebri |
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Which drugs can cause retinal toxicity?
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Chloroquine (bull's eye maculopathy)
Epinephrine: CME Tamoxifen: White crystalline deposits in macula +/- macular edema Thioridazine: Pigmentary retinopathy Indomethacin: Retinal hemorrhage, pigmentary changes in macula Talc: Retinopathy - seen in arterioles Isotretinoin: colour vision loss, nyctalopia NSAIDs: retinal hemorrhages Oral contraceptives: Vasculopathy e.g. CRVO, CRAO, retinal hemorrhage |
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Which drugs can cause intracranial hypertension?
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Tetracyclines e.g. minocycline and doxycycline
Isotretinoin can cause pseudotumor cerebri. |
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Which systemic drugs can decrease IOP?
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systemic beta blockers
Digoxin alcohol cannabinoids |
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Which drug classes increase IOP?
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Corticosteroids
Anticholinergics: atropine, scopolamine 1st gen antihistamines: bropheniramine, diphenhydramine TCAs: amitriptyline, imipramine Antipsychotics: chlorpromazine, thioridazine |
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How do corticosteroids increase IOP?
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Decrease aqueous outflow via TM pathway.
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