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Ocular Pharmacology > KMK oc pharm > Flashcards

KMK oc pharm Flashcards

1
Q

What percentage of topical drug concentration is lost via evaporation?

A

around 25%

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2
Q

After evaporation what are the three places a topical drug could go in the eye?

A
  1. drainage into the nasolacrimal apparatus
  2. absorption into the systemic circulation by the conjunctival and lid vasculature
  3. penetration into the cornea
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3
Q

Which layers of the eye and tears are lipid vs. water soluble, (affecting bioavailability of topical drugs)?

A

lipid soluble: lipid and mucous layer of tears, epi and endothelium of cornea
water soluble: aqueous and mucous layer of tears, stroma of cornea

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4
Q

What drug solubility composition is best for maximizing bioavailability?

A

small, uncharged (non-ionized), lipid-soluble molecules

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5
Q

Ocular drugs are formulated most often as _______ because this allows more non-ionized portions of the drug and better bioavailability

A

formulated most often as weak bases

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6
Q

What regions of the CNS are sympathetic cell bodies located

A

thoraco-lumbar regions

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7
Q

What regions of the CNS are parasympathetic cell bodies located

A

cranio-sacral regions

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8
Q

Preganglionic neurons are longer in which autonomic pathway?

A

parasympathetic

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9
Q

Postganglionic neurons are longer in which autonomic pathway?

A

sympathetic

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10
Q

The sympathetic system acts on which receptors?

A

alpha and beta

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11
Q

The parasympathetic system acts on which receptors?

A

muscarinic

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12
Q

What are the major actions of the parasympathetic system?

A

“rest and digest”, bronchoconstriction, miosis, vasodilation, increase SLUD: salivation, lacrimation, urination, defecation

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13
Q

What are the major actions of the sympathetic system?

A

“fight or flight”, bronchodilation, mydriasis, vasoconstriction, decrease in secretions

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14
Q

What are the cholinergic receptors in the eye?

A

M3 in iris sphincter for miosis, M2/M3 in ciliary muscle for accommodation, and M2/M3 in lacrimal gland for tears production

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15
Q

What are the adrenergic receptors in the eye?

A

a1 in iris dilator, a2 in CB vasculature (reduces aqueous production), b2 in TM and ciliary muscle, and b2/b1 in NPCE (increases aqueous production)

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16
Q

What eye conditions/diseases are cholinergic agonists commonly used to treat?

A

glaucoma and accommodative esotropia

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17
Q

Why are cholinergic agonists used to treat accommodative esotropia?

A

Directly stimulating the cholinergic receptors on the ciliary muscle decreases the amount of CNS stimulation to the ciliary muscle resulting in reduced convergence (which depends on CNS stimulation)

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18
Q

What is the MOA of pilocarpine?

A

stimulates the longitudinal muscle of CB, which pulls posteriorly on the scleral spur and opens up the trabecular spaces for an increase in outflow and decrease in IOP

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19
Q

Clinical uses for pilocarpine:

A
  • utilized after angle closure attack and in preparation for LPI
  • 1% pilocarpine used to differentiate a CN3 palsy from a sphincter tear in a patient with a fixed dilated pupil (palsies will still constrict pupil)
  • 0.125% pilocarpine used in dx of Adie’s tonic pupil, supersensitized will respond with miosis even to the diluted drug
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20
Q

What are the main side effects of pilocarpine?

A

brow ache, headache (tension), myopic shifts, miosis, cataracts after long-term use, RRDs, secondary angle closure glaucoma (pupillary block)

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21
Q

What are indirect cholinergic agonists?

A

anticholinesterase agents (AchE inhibitors) act as indirect agonists by inhibiting acetylcholinesterase which normally breaks down ACh

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22
Q

Edrophonium (Enlon)

A

an AchE inhibitor, used in dx of myasthenia gravis (Tensilon test), if ptosis improves the test is positive

rapid onset (30-60s) and short duration (10min)

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23
Q

Neostigmine (Prostigmin)

A

an AchE inhibitor, treatment of myasthenia gravis, and for limb strength eval (Neostigmine test)

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24
Q

Echothiophate (Phospholine)

A

an AchE inhibitor, can be used for the dx or tx of accommodative esotropia, rarely for glaucoma

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25
Q

Pyridostigmine (Mestinon)

A

an AchE inhibitor, used for tx of myasthenia gravis

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26
Q

Which AchE inhibitors are irreversible and have more side effects?

A

Echothiophate and isofluorophate

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27
Q

Pralidoxime (Protopam)

A

IV drug used to reverse the effects of irreversible AchE inhibitors, usually in cases of pesticide poisoning

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28
Q

What is the MOA for cholinergic antagonists?

A

these drugs block ACh at muscarinic receptor sites in the ciliary body and iris (sphincter) resulting in dilation and cycloplegia

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29
Q

Which cholinergic antagonist has the fastest onset and shortest duration of mydriatic effects?

A

tropicamide, mydriasis onset of 20-30min and duration of 6 hours

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30
Q

Which cholinergic antagonist has the highest potential for severe side effects?

A

Scopolamine - hallucinations, amnesia, unconsciousness, confusion, incoherence, vomiting, urinary incontinence, etc.

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31
Q

Which cholinergic antagonist is commonly used for treating anterior uveitis?

A

Homatropine is the standard, but atropine and cyclopentolate can also be used

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32
Q

What are the symptoms of atropine toxicity?

A

dry mouth (usually 1st sign), dry flushed skin, rapid pulse, disorientation, fever

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33
Q

Which cholinergic antagonist has the fastest onset and shortest duration of cycloplegic effects?

A

Cyclopentolate, average cycloplegic onset of 45mins, (20-45min for mydriatic effect), routine for cycloplegic refractions in pts under 10yo especially

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34
Q

What are the three ways that homatropine helps in treating anterior uveitis?

A
  • dilates the pupil and decreases the likelihood of posterior synechiae formation
  • reduces pain by paralyzing ciliary and sphincter muscles
    • stabilizes the blood-aqueous barrier by constricting the iris and CB vasculature to limit passage of blood contents into the aqueous humor
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35
Q

How does botulina toxin (Botox) work?

A

somatic drug that blocks the release of ACh at the neuromuscular junction, which inhibits muscle contraction

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36
Q

Which receptors do epinephrine and norepinephrine act on?

A

Epinephrine acts on all four adrenergic receptors, a1/a2/b1/b2, and norepinephrine does not act on b2

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37
Q

What is the MOA of phenylephrine (Neo-Synephrine)?

A

a1 agonist, no effect on beta receptors, allows dilation without cycloplegia

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38
Q

Clinical uses of phenylephrine besides dilation:

A
  • palpebral widening (Mullers muscle)
  • blanches conj vessels to indicate episcleritis from scleritis
  • dx Horner’s syndrome
  • 10% phenyl for breaking posterior synechiae (*adverse CV effects!*)
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39
Q

Phenylephrine 10% is contraindicated in:

A

patients taking MAOIs, tricyclic antidepressants, atropine, patients with Graves disease and heart conditions

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40
Q

Naphazoline (Naphcon) and Tetrahydrozoline (Visine)

A

topical ocular decongestants to constrict conj blood vessels, greater alpha effects than beta, have the potential to depress the CNS

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41
Q

What common drop use can cause fixed dilated pupils if used excessively?

A

Visine, because of alpha effects on the radial muscle of the iris

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42
Q

What is the MOA for alpha2 agonists used for glaucoma treatment?

A

decreasing aqueous humor production by causing vasoconstriction of the CB vasculature and also increases uveoscleral outflow

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43
Q

Which alpha agonist glaucoma drop is highly selective a2 agonist with no a1 effects?

A

Brimonidine (Alphagan 0.20%), allows effective IOP lowering and long-term tx of glaucoma

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44
Q

Which glaucoma drops have shown neuroprotective properties?

A

Brimonidine and Betaxolol

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45
Q

What is the difference between Alphagan-P (0.10 or 0.15%) and Alphagan 0.20% besides concentration?

A

Alphagan-P has purite as the preservative which is believed to have decreased the incidence of allergic or toxic reactions to the drop that before was causing follicular conjunctivitis (30% of pts had to d/c bc of)

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46
Q

What is the recommended dosing for Alphagan when it is the only drop being used?

A

TID, relatively short duration of action

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47
Q

What is another use for brimonidine besides in glaucoma patients?

A

causes miosis, so can be used to reduce glare, halos, and other night vision symptoms for patients after LASIK, PRK, etc.

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48
Q

When is brimonidine contraindicated?

A

in patients taking MAOIs

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49
Q

What is the most common systemic side effect of brimonidine and apraclonidine?

A

dry mouth

50
Q

What receptors does Apraclonidine (Iopidine) act on?

A

primarily alpha2 agonist, with limited alpha1 activity

51
Q

What are the clinical uses for Apraclonidine (Iopidine)?

A
  • used to control IOP spikes before and after ocular surgeries such as LPIs, trabeculoplasties, and posterior capsulotomies
  • used for rapidly decreasing IOP in an acute angle closure attack
  • can be used in dx Horner’s syndrome (causes a Horners pupil to dilate from the weak alpha1 activity, but is not strong enough to dilate a normal healthy pupil)
52
Q

What % does apraclonidine reduce IOP and how long does it last?

A

30-40% IOP reduction onset <1hr (peak 3-5hrs), efficacy reduces after 8 days of using drop so is not useful for chronic treatments

53
Q

How can you diagnose Horner’s syndrome before pharmacological testing?

A

observe the miotic pupil when turning off lights, a delayed dilation (most apparent in first 5 seconds) will exist due to abnormal sympathetic innervation to the dilator muscle, and with a ptosis is dx of Horners

54
Q

How do you diagnose Horners pharmacologically?

A
  • cocaine 4% OU blocks reuptake of NE, healthy eyes dilate, but a pupil with lost sympathetic innervation will not dilate
  • Apraclonidine 2gtts 0.5% OU causes dilation of affected pupil due to supersensitivity (weak a1 activity is enough to cause dilation), healthy pupils will not be affected (or will have mild constriction from decreased NE release on a2)
55
Q

How do you determine the location of innervation loss in Horners syndrome pharmacologically?

A
  • hydroxyamphetamine 1% OU will increase NE release and block reuptake, if the damage is preganglionic, both pupils will dilate, if the damage is postganglionic the Horner pupil will not dilate (no NE terminals)
  • low concentration adrenaline (1:1000) or phenylephrine 1% - postganglionic Horner pupil will dilate due to supersensitivity
56
Q

What are the beta-blockers used for treating glaucoma?

A

Timolol, levobunolol, betaxolol, metipranolol, and carteolol

57
Q

What are the systemic side effects of beta-blocker drops?

A

CNS - disorientation, depression, fatigue

CV - bradycardia, arrhythmias, syncope

Pulmonary - dyspnea, wheezing, bronchospasm

GI - nausea, vomiting, diarrhea, pain

Reproductive - ED

58
Q

Topical beta-blockers are contraindicated when?

A

in patients with asthma, COPD, bradycardia, or CHF

caution with diabetics (masks hypoglycemic symptoms), hyperthyroidism (masks symptoms), and myasthenia gravis patients (symptoms of weakness can be exacerbated)

59
Q

What is the MOA of beta-blocker drops?

A

block beta-adrenergic receptors throughout the body, primarily b2 in the NPCE to decrease aqueous production

60
Q

Which beta-blocker is the only topical b1 selective drug and what is its advantage?

A

Betaxolol (Betoptic-S) is the only topical b1 selective drug, it is safer for patients with lung conditions (less lung side effects) and also possibly has neuroprotective qualities, however not as effective as Timolol for reducing IOP and may be worse for pts with CHF

61
Q

Which beta-blocker drop is the most effective at lowering IOP?

A

Timolol (Timoptic), around 25% reduction in IOP

62
Q

Crossover effect with beta-blockers

A

unilateral use of beta-blocker drop reduces the IOP in the contralateral eye as well

63
Q

What is the dosage for beta-blocker drops?

A

typically BID, but can be once daily if dosed in the morning (better daytime efficacy)

64
Q

What are the combination glaucoma drops with timolol?

A

Cosopt (0.5% timolol and 2% dorzolamide) and Combigan (0.5% timolol and 0.2% brimonidine) dosed q12hr

65
Q

What are some advantages of Carteolol (Ocupress) when compared to the other beta-blockers?

A

does not lower IOP as well, but has intrinsic sympathomimetic activity, significantly reduces nocturnal bradycardia, is more comfortable (less stinging) than timolol, some reduction in cholesterol in pts with hypercholesterolemia, overall less side effects

66
Q

Summary of glaucoma drug MOA

A

cholinergic agonists - increased corneoscleral outflow

alpha-adrenergic agonists - decreased production and increased uveoscleral outflow

beta-blockers - decreased production

carbonic anhydrase inhibitors - decreased production

prostaglandins - increased outflow via the uveoscleral route

Rho kinase inhibitors - decrease aq prod, increase corneal scleral outflow

67
Q

What is the MOA for carbonic anhydrase inhibitor drugs?

A

block carbonic anhydrase enzyme from catalyzing the formation of bicarbonate from CO2 and H2O, which is believed to increase aqueous production by increasing Cl- and Na+ flux into the posterior chamber. so CAIs block bicarbonate and decrease production of aqueous

68
Q

When are CAIs contraindicated?

A

severe COPD, pregnancy, sulfa allergies, caution in pts with liver or renal disease

69
Q

What are the side effects of oral CAIs?

A

most common: metallic taste, tingling in hands and feet, metabolic acidosis (compensatory hyperventilation not good in COPD pts)

most serious: thrombocytopenia, agranulocytosis, aplastic anemia (can be fatal!)

other adverse effects: malaise, fatigue, weight loss, anorexia, impotence, depression, diarrhea, and myopic shifts in refractive error

70
Q

Brinzolamide 1% (Azopt) and Dorzolamide 2% (Trusopt)

A

topical CAIs

71
Q

Acetazolamide (Diamox) Methazolamide (Neptazane)

A

oral CAIs

72
Q

Travatan Z

A

new formulation of Travoprost with Sofzia as the preservative instead of BAK

73
Q

What % of IOP lowering do prostaglandins provide?

A

27-35%, highest of the glaucoma drops

74
Q

Latanoprost (Xalatan 0.005%) Bimatoprost (Lumigan 0.03%) and Travoprost (Travatan 0.004%)

A

prostaglandin analogues

75
Q

What dosing is recommended for prostaglandins?

A

QHS, allows for better diurnal control than morning dose, has a daytime peak effect 12-24hrs after administration

76
Q

What is the MOA for prostaglandin analogues?

A

act on FP receptors (PGF2a receptors) on ciliary muscle, which causes reduction of neighbouring collagen (via metalloproteinases), decreasing resistance within the uveoscleral meshwork for increased outflow

77
Q

What are the contraindications for prostaglandin analogues?

A

pts who are at risk for CME (cataract sx post-op), cases of active inflammation (ex. uveitis), and pts with history of HSV keratitis

78
Q

What are the side effects of prostaglandin analogues?

A

iris heterochromia, increased pigmentation and growth of eyelashes, skin darkening around the eyes, MGD, orbital fat atrophies, conjunctival hyperemia (worse with Lumigan, least with Xalatan), pruritis also worse with Lumigan

79
Q

Summary of % IOP reductions of glaucoma drops

A

prostaglandins decrease 33%, beta-blockers decrease 25%, brimonidine and dorzolamide both decrease 18%

80
Q

What is the MOA of topical ocular anesthetics?

A

local anesthetics block nerve conduction and change membrane permeability by stopping the influx of Na+ ions into the nerve cytoplasm. without Na+ entry, the nerve can no longer be depolarized

81
Q

What are the differences between amide and ester anesthetics?

A

Amides have longer duration and are metabolized by the liver so less toxic - ex. lidocaine

Esters have shorter duration and are metabolized locally - all topical anesthetics are esters

82
Q

Main topical anesthetics we use in the eye

A

Proparacaine (Ophthaine/Alcaine) and Benoxinate

onset 10-20sec, duration 10-20min

83
Q

What is the MOA of antihistamines?

A

block Type I hypersensitivity reactions by blocking the cell receptors that histamine acts on (they don’t prevent histamine release from mast cells and basophils), results in minimizing redness, watering, itching symptoms of allergies

84
Q

Emedastine difumarate 0.05% (Emadine)

A

antihistamine, for mild-moderate cases of allergic conjunctivitis, binds to H1 to out-compete histamine, rapid response

1gtt QID, >3yo

85
Q

What is the MOA for mast cell stabilizers?

A

act on exposed mast cells and inhibits their degranulation upon re-exposure to the antigen, stabilizes mast cell membranes, preventing Ca2+ influx. Not effective for acute symptoms, used more for chronic allergic conjunctivitis, vernal conjunctivitis, and atopic keratoconjunctivitis

86
Q

Cromolyn sodium (Crolom), Lodoxamide (Alomide), Pemirolast (Alamast), Nedocromil (Alocril)

A

mast cell stabilizers

87
Q

mast cell and antihistamine combination drops

A

ketotifen fumarate 0.025% (Zaditor, Alaway, Zyrtec eye, Claratin eye, Refresh eye itch relief)

olopatadine hydrochloride 0.10% (Patanol) or 0.20% (Pataday)

bepotastine (Bepreve), epinastine (Elestat), azelastine (Optivar)

88
Q

What is the MOA of steroid drops?

A

inhibit phospholipase A2 (arachidonic acid pathway), decreases inflammatory mediators and decreases capillary permeability (significant decrease in immune system response), also decreases fibroblast and collagen formation so prevents healing

89
Q

What are the most clinically relevant side effects for ocular steroids?

A

increased risk of secondary infections (~HSV), PSC cataracts, and glaucoma (increase IOP from clogging TM with GAGs), delays healing

90
Q

“Soft” steroid drops

A

fluorometholone (FML) 0.1% and loteprednol (Lotemax) 0.5%

91
Q

Potent steroid drops

A

prednisolone 1% acetate, rimexolone (Vexol), difluprednate (Durezol), dexamethasone (Maxidex) 0.1%

92
Q

What is the MOA for NSAID drops?

A

NSAIDs block cyclooxygenase I and II, which decreases inflammation by inhibiting the conversion of arachidonic acid into prostaglandins and thromboxanes (platelets)

93
Q

Which NSAID drops are dosed QID?

A

Diclofenac sodium 0.1% (Voltaren) and ketorolac tromethamine 0.4% (Acular LS)

94
Q

How are Nepafenac (Nevanec) and Bromfenac (Xibrom) dosed?

A

BID

95
Q

Which NSAID drop is the only one approved for once a day dosage?

A

Bromday (bromfenac)

96
Q

Which NSAID is used prior to ocular surgery (1gtt q30min, starting 2 hours before sx)

A

flurbiprofen 0.03% (Ocufen)

97
Q

When are topical NSAIDs used clinically?

A

post-op cataract surgery patients, to decrease the risk of CME, recurrent corneal erosions, corneal abrasions, and allergic conjunctivitis, etc.

98
Q

Which is the only NSAID approved to the topical treatment of seasonal allergic conjunctivitis

A

ketorolac

99
Q

What are the ocular side effects for topical NSAIDs?

A

corneal toxicity, SPK, corneal melt (from repeated use of anesthetics and generic diclofenac), stinging on instillation

100
Q

fluorescein dye

A

effective evaluation of tear film quality and epithelial defects

101
Q

Rose Bengal

A

stains dead and devitalized cells, also can stain the edges of herpetic dendrite lesion

102
Q

Lissamine green

A

similar stain to Rose Bengal but less discomfort

103
Q

Methylene blue

A

similar to staining to Rose Bengal but also stains corneal nerves, used to outline blebs and for staining lacrimal sac before dacryocystorhinostomy

104
Q

Pegaptanib (Macugen)

A

IVT, antineoplastic agent that binds and inhibits VEGF

105
Q

Ranibizumab (Lucentis)

A

IVT, monoclonal antibody (fab portion) that targets VEGF

106
Q

VEGF promotes…

A

vascular permeability (macular edema) and new blood vessel formation (neo)

107
Q

Sodium chloride (Muro 128)

A

hypertonic solutions that is prescribed for reduction of corneal edema (Fuchs, RCE) as a drop 2 or 5% or in ointment

108
Q

Glycerine (Osmoglyn)

A
109
Q

Restasis (cyclosporin 0.05%)

A

inhibits T-cell activation by stopping the production of interleukin-2

110
Q

cellulose esters (carboxymethylcellulose and hydroxymethylcellulose) and polyvinyl alcohol (PVA)

A

substances used in artificial tears to enhance lubrication

111
Q

Benzalkonium chloride (BAK)

A

very common preservative in drops, well-known to cause corneal toxicity (SPK)

112
Q

Thimerosal

A

preservative used in Trifluridine (Viroptic), toxicity happens after 3 weeks+ , mercury component

113
Q

Ethylenediaminetetraacetic acid (EDTA)

A

chelating agent (binds and inactivates), most commonly sequesters calcium, tx for band keratopathy (in JIA, gout, hyperparathyroidism)

114
Q

purite/sodium perborate

A

oxidative preservatives found in Refresh Tears and GenTeal, favoured over chemical preservatives as they are effective but with less toxicity

115
Q

latanoprostene bunod (Vyzulta)

A

increases uveoscleral and corneal scleral pathways

116
Q

Rho kinase inhibitors

A

vasodilates and decreases episcleral venous pressure which increases corneal scleral pathway outflow and decreases IOP. SE: subconj hemes, caution w/blood thinners

also decreases aqueous production somehow

117
Q

Mast cell-antihistamine combo acronym

A

BEZPOP

Bepotastine (Bepreve)

Epinastine (Elestat)

(Zaditor) Ketotifen

(Patanol) olopatadine 0.10%

(Optivar) azelastine

(Pataday) olopatadine 0.20%

118
Q

Tobradex

A

tobramycin and dexamethasone

119
Q

Cosopt

A

timolol and dorzolamide, q12h

120
Q

Simbrinza

A

brinzolamide and brimonidine

121
Q

Combigan

A

timolol and brimonidine, q12h

Ocular Pharmacology (10 decks)

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