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Ocular Pharmacology > Midterm 1 > Flashcards

Midterm 1 Flashcards

1
Q

Diagnostic drug/agent

A

Chemical used to facilitate an examination and/or diagnosis

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2
Q

Therapeutic drug/agent

A

Chemical used to treat a disorder of the eye or vision

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3
Q

Medical conditions to consider when prescribing medications

A

Renal/hepatic disease, cardiovascular disease, respiratory disease, thyroid disease, DM, CNS conditions, affective/mental health disorders, pregnancy

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4
Q

Why do we ask patients about medications they are taking?

A

Concerned about drug-to-drug interactions (including OTC), drug allergies, and ocular side effects of those medications

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5
Q

Local adverse reactions from TOPICAL Medications

A

Cutaneous, conjunctiva, cornea, intraocular pressure, crystalline lens, retina, macula edema, bulbar follicles, corneal verticillata, PSC, etc.

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6
Q

Systemic adverse reactions from TOPICAL medications

A

Impact HR, respiration

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7
Q

Ocular adverse effects from SYSTEMIC medication

A

Dry eye, corneal verticillata, PSC, retinal toxicity, optic neuropathy, papilledema, accommodation issues

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8
Q

Special populations to consider

A

Pregnant/lactating patients, pediatric patients, geriatric patients

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9
Q

Pregnancy category A

A
  • adequate well-controlled studies have failed to demonstrate a risk to the fetus in the first trimester of pregnancy
  • very few drugs fall in this category
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10
Q

Pregnancy category B

A
  • animal reproductive studies have failed to demonstrate a risk to the fetus, and there are no adequate human studies
  • fair number of drugs in this category
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11
Q

Pregnancy category C

A

animal reproductive studies have shown an adverse effect on the fetus and there are no adequate human studies; potential benefits may warrant use of the drug in pregnant women despite potential risks

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12
Q

Pregnancy category D

A
  • there is positive evidence of human fetal risk based on adverse reaction data from investigational or marketing experience or studies
  • potential benefits may warrant use of the drug in pregnant women despite potential risks
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13
Q

Pregnancy category X

A
  • studies in animals or humans have demonstrated fetal abnormalities and/or there is positive evidence of human fetal risk
  • risks involved in the use of the drug in pregnant women clearly outweigh potential benefits
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14
Q

Geriatric patient considerations when prescribing

A
  • eyelid laxity may increase retention time and increase systemic absorption
  • arthritis/tremor may make instillation of topical meds more difficult
  • cognitive difficulties may lead to poor medication adherence
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15
Q

Pediatric dosing: Young’s Rule formula

A

Age (years) / (Age + 12) X Adult dose = pediatric dose

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16
Q

Pediatric dosing: Webster’s Rule

A
  • based on age and the fact that children are heavier now

- (age + 1) / (age + 7) X adult dose

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17
Q

Pediatric dosing: Clark’s rule***

A
  • based on weight, making it more accurate

- weight in pounds / 150 X adult dose

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18
Q

Properties of outer lipid layer of tear film

A

Readily washed away with irrigation and tearing; not very stable

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19
Q

Properties of middle aqueous layer

A
  • 95% of entire tear volume

- inherently unstable

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20
Q

Properties of inner basal layer (mucoid)

A
  • comprised of glycoproteins secreted by goblet cells

- very thin and hydrophilic

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21
Q

What properties must a drug contain to penetrate the cornea?

A

A balance of hydrophilic and lipophilic properties to go between both the epithelium and stroma

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22
Q

The epithelium can act as a depot/reservoir for ___ drugs

A

Lipophilic

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23
Q

The stroma can act as a depot/reservoir for ___ drugs

A

Hydrophilic

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24
Q

Properties of corneal epithelium

A
  • squamous layer with zonula occludens/tight junctions
  • resists penetration of hydrophilic drugs when intact
  • when eroded –> increased penetration of hydrophilic drugs
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25
Q

Properties of corneal stroma

A
  • 90% of corneal thickness

- collagen fibrils occupy space and increase the path of diffusion of molecules

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26
Q

Properties of corneal endothelium

A
  • monolayer of polygonal cells
  • non-regenerative
  • pumps its own weight in fluid from stroma to AC in 5 minutes
  • NOT a reservoir for drugs
  • contains tight junctions
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27
Q

Pigment granules in iris epithelium absorb ___ drugs

A

Lipophilic

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28
Q

Vascular endothelial cells in iris contain ___ junctions

A

Tight

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29
Q

When iris is inflamed, what happens to the blood-aqueous barrier?

A

It becomes compromised

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30
Q

Where are the tight junctions in the ciliary body?

A
  • between non-pigment epithelial cells
  • capillaries do not contain tight junctions
  • some systemic drugs pass through ciliary body vasculature and diffuse into the iris
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31
Q

Retina is developed from ____ in utero

A

Neural tube wall

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32
Q

RPE contains ___ junctions

A
  • tight

- prevent movement of drugs from blood to retina/vitreous

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33
Q

___ drugs can pass more easily into the retina via retinal capillaries

A

Lipophilic

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34
Q

What systemic drugs can cause toxicity of the optic nerve?

A
  • chloramphenicol
  • ethambutol
  • streptomycin
  • digitalis (retrobulbar optic neuritis)
  • Vitamin A (high concentrations can cause papilledema)
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35
Q

Properties of drug formulations that affect bioavailability

A
  • preservatives
  • vehicles
  • ointment
  • drug release systems
    • soft contact lens
    • collagen shield
    • punctal plugs
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36
Q

How do surfactants in preservatives damage ocular surface?

A
  • disrupt plasma membranes (dish soap on water)
  • BAK is toxic to corneal epithelium, enhances ocular penetration
  • Chlorhexidene doesn’t alter corneal epithelium as much as BAK, and isn’t used as often
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37
Q

How do mercurials in preservatives damage the ocular surface?

A

Thimerosal has a high rate of toxicity/poor tolerability, but not used often anymore

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38
Q

How do ionic buffering preservatives affect the ocular surface?

A
  • better tolerability but only available in a few medications
  • great for glaucoma due to long-term use of medications
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39
Q

What is a vehicle and what’s its purpose in drugs?

A
  • agents other than the active ingredient or preservative
  • provide proper tonicity, pH, buffering, viscosity
  • can be used to increase contact time, provide temporary lipid depot, moisturize/lubricate the cornea/ocular surface
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40
Q

Advantages of ophthalmic ointments

A
  • antibiotics are more stable in ointments than in solutions
  • 2X the contact time in a blinking eye
  • 4X the contact time in a closed (patched) eye
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41
Q

Disadvantages of ophthalmic ointments

A
  • blur
  • difficult to administer
  • more risk of trauma from tube
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42
Q

Advantages of ophthalmic solutions/suspensions

A
  • easier to use

- less impact on vision

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43
Q

Disadvantages of ophthalmic solutions/suspensions

A
  • shorter ocular contact time
  • imprecise/inconsistent delivery
  • contamination of bottle
  • suspensions MUST be shaken
  • clogged dropper tip with suspensions
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44
Q

Tan cap color

A

Anti-infectives

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45
Q

Pink cap color

A

Anti-inflammatories/steroids

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46
Q

Red cap color

A

Mydriatics and cycloplegics

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47
Q

Grey cap color

A

Non-steroidal anti-inflammatories

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48
Q

Green cap color

A

Miotics

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49
Q

Yellow cap color

A

Beta-blockers

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50
Q

Dark blue cap color

A

Beta-blocker combinations

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51
Q

Purple cap color

A

Adrenergic agonists

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52
Q

Orange cap color

A

Carbonic anhydrase inhibitors

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53
Q

Aqua blue cap color

A

Prostaglandin analogs

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54
Q

“SM” (sub-micron) technology

A
  • designed to adhere to the ocular surface and then penetrate key ocular tissues
  • been using for about 20 years
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55
Q

“Ncell” technology

A
  • enhances the ocular delivery of cyclosporine
  • supposed to get through cornea faster
  • micelles of hydrophobic core and hydrophilic shell
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56
Q

Microdose dispenser

A
  • new technology will be approved within the next year (2022)
  • 8 nanoliters of drug administered instead of 40 in a typical eyedropper
  • patient can sit upright for administration
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57
Q

Nano-dropper

A
  • replaces cap on commercially available eyedrop bottle
  • financial benefit to the patient
  • patient still has to tilt their head back
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58
Q

Intracameral injection

A
  • injection into anterior chamber
  • new glaucoma delivery system
  • pellet that eventually dissolves and delivers medication for 3 months
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59
Q

Intravitreal injections

A
  • antibacterial/fungal to treat endophthalmitis
  • corticosteroid to treat posterior uveitis
  • anti-VEGF therapy (Avastin, Lucentis, Eyelea) to treat wet AMD, proliferative diabetic retinopathy
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60
Q

Intravitreal implants

A
  • antiviral (ganciclovir - VITRISERT) - first intravitreal implant for HIV patients
  • corticosteroid (Retisert, Ozurdex, Yutiq)
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61
Q

Ozurdex (Dexamethasone)

A
  • fully bio-erodible
  • lasts approximately 6 months
  • FDA approved for DME, macular edema from retinal vein occlusion, and chronic non-infectious posterior uveitis
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62
Q

Retisert (fluocinolone acetonide)

A
  • intravitreal steroid implant
  • FDA approved for treatment of chronic non-infectious uveitis
  • lasts approximately 2.5-3 years
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63
Q

Yutiq (fluocinolone acetonide)

A
  • intravitreal steroid micro-insert
  • FDA approved for chronic non-infectious posterior uveitis
  • non-bio-erodible
  • insertion done in-office
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64
Q

Vitrisert

A
  • Gangiclovir (antiviral)

- used to treat infectious cytomegalovirus infection

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65
Q

What is included in the prescriber’s information in a prescription?

A

Name, address, phone, license # (NPI), DEA #

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66
Q

What all is included in the anatomy of a prescription?

A
  • prescriber’s information
  • date
  • patient data
  • superscription
  • inscription
  • subscription
  • signa or signatura
  • refill information
  • prescriber’s signature
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67
Q

What is included in the inscription?

A
  • name of drug
  • concentration/strength
  • formulation (gel, ointment, solution, etc.)
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68
Q

What is included in the subscription?

A
  • quantity of the drug the pharmacist should dispense
  • brief - number of tabs/capsules, weight of container, volume of bottle, etc.
  • usually preceded by the # sign
  • Ex: Dispense #5ml
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69
Q

What is included in the signatura?

A
  • instructions for use
  • how to use (take, instill, apply, etc.)
  • how much and how often to use
  • Ex: Instill 1 drop in each eye twice daily
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70
Q

a.c. stands for

A

before meals

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71
Q

p.c. stands for

A

after meals

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72
Q

h.s. stands for

A

at bedtime (also qhs)

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73
Q

ut. dict stands for

A

as directed

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74
Q

Definition of controlled substances

A

Substances that may produce physical, psychological dependence (or both)

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75
Q

Schedule I drugs

A
  • very high potential for abuse
  • no approved medical use; no research use; cannot be prescribed
  • Heroin, LSD
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76
Q

Schedule II drugs

A
  • high potential for abuse
  • strict limitations for medical use, must be electronically submitted, NO REFILLS allowed
  • opioids such as morphine, codeine (with certain concentrations), oxycodone, hydrocodone, amphetamines, and cocaine
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77
Q

Schedule III drugs

A
  • significant potential for abuse
  • often used for pain management; must be e-Rx; NO REFILLS
  • weaker opioids such as codeine, some amphetamine-like drugs
  • ODs can prescribe
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78
Q

Schedule IV drugs

A
  • less than III potential for abuse
  • medical use is accepted; up to 5 refills in 6 months
  • propoxyphene, diazepam, phenobarbital
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79
Q

Schedule V drugs

A
  • less than IV potential for abuse
  • often used for cough suppression or to treat diarrhea; up to 5 refills in 6 months
  • cough syrups with codeine; antidiarrheal diphenoxylate
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80
Q

Americans are ___X more likely to be hospitalized by a prescription rather than by a car accident

A

10

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81
Q

Sympathetic pre-synaptic fibers are ___ and post-synaptic fibers are ___

A

Short; long

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82
Q

Parasympathetic pre-synaptic fibers are ___ and post-synaptic fibers are ___

A

Long; short

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83
Q

The sympathetic NT on the effector organ is?

A

Norepinephrine

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84
Q

The parasympathetic NT on the effector organ is?

A

Acetylcholine

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85
Q

Cholinergic innervation to the eye is the same as

A

Parasympathetic

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86
Q

Where does cholinergic innervation to the eye originate?

A

In the Edinger-Westphal nucleus

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87
Q

What structure does cholinergic innervation to the eye travel with?

A

CN III

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88
Q

Where does cholinergic innervation to the eye synapse?

A

In the ciliary ganglion

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89
Q

Where does the post-synaptic cholinergic innervation to the eye travel?

A

To the iris sphincter muscle and ciliary body via short ciliary nerves (cause pupil constriction)

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90
Q

What happens to the lens when the ciliary body contracts?

A

It moves towards the cornea

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91
Q

How is the lacrimal gland innervated?

A

Parasympathetically via CN VII/sphenopalatine ganglion/CN V

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92
Q

What is the pupil size primarily determined by?

A

Iris sphincter muscle tone

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93
Q

Cholinergic stimulation to the eye causes what?

A

Miosis, contraction of the ciliary body, and decrease in IOP ( –> more AH outflow)

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94
Q

Cholinergic agents are also known as

A
  • miotics
  • cholinergic agonists
  • parasympathetic agonists
  • parasympathomimetics
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95
Q

What are the two types of miotics?

A
  • direct acting (which mimic Ach)

- indirect acting (which are AchE inhibitors)

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96
Q

What are some direct acting miotics?

A
  • pilocarpine
  • carbachol
  • civimeline (oral)
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97
Q

What is a reversible indirect acting miotic?

A

Edrophonium

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98
Q

What are the effects of miotics in the eye? (6)

A
  • pupillary constriction
  • spasm of accommodation
  • decreased IOP
  • narrowing/shallowing of the AC
  • increased thickness of crystalline lens
  • increased vascular permeability in iris blood vessels
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98
Q

What are systemic effects of miotics?

A
  • salivation
  • lacrimation
  • urination
  • defecation
  • GI upset
  • emesis
  • bronchoconstriction
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99
Q

What are some irreversible indirect acting miotics?

A
  • DFP

- echothiophate

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101
Q

What are the ophthalmic uses of miotics? (6)

A
  • diagnosis of some pupil abnormalities
  • glaucoma treatment
  • diagnosis of MG
  • treatment of phthiriasis palpebrum (pubic lice on lashes, rare to use this way)
  • treatment of dry eye in patients with aqueous deficiency
  • presbyopia treatment (Vuity)
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102
Q

How to know if anisocoria is physiologic or abnormal?

A

If the anisocoria (difference) is greater in the light than in the dark, it’s an abnormal cause of anisocoria

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103
Q

3 things to consider with abnormal anisocoria

A
  • damage to efferent CN III fibers –> EMERGENCY!
  • tonic pupil
  • pharmacologic blockade
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104
Q

General guidelines for pharmacologic anisocoria evaluation (how to administer drops, tests, procedures to avoid, etc.)

A
  • one drop of diagnostic agent in each eye; repeat after several minutes
  • no anesthetic or tonometry (can alter drug penetration)
  • if condition is bilateral, only instill in one eye (not common)
  • maintain same ambient illumination before and after instillation
  • eliminate accommodative stimulus and have patient look straight at distance
  • IR photography can be very helpful
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105
Q

What is tonic pupil (Adie’s pupil)?

A
  • pupil with parasympathetic denervation
  • typically unilateral
  • often associated with virus or trauma
  • women of 25-40 years of age, complain of photophobia
  • often resolves after 2 years
  • rare systemic association (zoster, giant cell arteritis, syphilis)
  • benign, and kind of unexplainable
  • constricts better to accommodative stimulus than to light
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106
Q

How to diagnose tonic pupil

A
  • 0.125% pilocarpine:
    • will not constrict a normal pupil (or very little)
    • significant constriction of tonic pupil due to the upregulation of receptors and the eye becoming super sensitive to parasympathetic stimulation
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107
Q

Describe CN III dilated pupil

A
  • considered a neurologic emergency (likely aneurysm of posterior communicating artery until proven otherwise!)
  • rare to find ONLY pupil involvement, usually oculomotor palsy (ptosis, motility, etc.)
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108
Q

Steps of pharmacologic testing of CN III dilated pupil

A
  • 0.125% pilocarpine to see if it’s tonic
  • if NO constriction then 0.5% - 1% pilocarpine
    • CN III - prompt constriction
    • pharmacologic blockade - NO constriction
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109
Q

What is likely happening in a CN III palsy that doesn’t involve the pupil?

A

Likely not an aneurysm pressing on the nerve, as the pupil fibers are on the outside, likely ischemia to the nerve

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110
Q

Approach to one dilated pupil (anisocoria)

A
  • evaluate lids and motility
  • check light response and near response - is there dissociation?
  • check for vermiform (wiggly)/sector paresis of iris sphincter at slit lamp (tonic)
  • pharmacologic testing:
    1) dilute pilocarpine (0.125%)
    2) normal strength pilocarpine (0.5 - 1%)
    3) if no constriction to either –> pharmacologic
  • *THERE WILL BE MORE THAN 1 QUESTION ON EXAM ON PUPIL PROBLEMS**
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111
Q

What is the mechanism of action of miotics in open angle glaucoma and what drugs are used to achieve this?

A
  • stimulate longitudinal muscle of the ciliary body
  • pull on scleral spur
  • opens spaces in trabecular meshwork
  • result in increased aqueous outflow through trabecular meshwork
  • drugs used: pilocarpine and rarely carbachol, which is much stronger
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112
Q

What is the conventional pathway of AH out of the anterior chamber?

A

60-80% of AH leaves through TM –> Schlemm’s canal –> episcleral veins

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113
Q

How is pilocarpine used in glaucoma therapy (concentrations, dosing, etc.)?

A
  • decreased effect in darkly pigmented irises due to pigment binding
  • available 0.5% - 10% solution, 4% gel
  • dosing QID (solution), nightly (gel)
  • not used frequently due to high incidence of local (in and around the eye) side effects and frequent dosing
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114
Q

Contraindications of pilocarpine (6)

A
  • young age due to accommodative spasm and brow ache
  • cataract (visual axis)
  • retinal disease (can negate effects of dilation drops that have to be used for annual eye exam)
  • uveitis (vascular permeability)
  • neovascular glaucoma (vascular permeability)
  • asthma
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115
Q

What is happening to the eye during pupillary block glaucoma?

A

In the mid-dilated position, the pupil pushes right up against the lens and AH can’t pass through –> iris bulges forward –> no access to the angle –> IOP goes up to 60-70 mmHg

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116
Q

How is pilocarpine used in treatment of pupillary block?

A
  • small concentrations of pilocarpine make the pupil smaller and move it off the lens
  • keep patient on pilocarpine until they are able to have iridotomy done
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117
Q

Additional side effects of irreversible AchE inhibitors

A
  • SLUDGE
  • iris cysts
  • anterior subcapsular cataracts
  • retinal detachment (a little bit stronger correlation)
  • acute angle closure glaucoma
  • uveitis
  • follicular conjunctivitis
  • decreased rate of hydrolysis of succinylcholine can lead to respiratory paralysis (used for anesthesia)
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118
Q

What is the drug of choice for the diagnosis of MG?

A

Edrophonium

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119
Q

What is myasthenia gravis?

A
  • disease that affects the neuromuscular junction
  • antibodies to acetylcholine receptors in the motor end plate of SKELETAL MUSCLE - effectively reduces the number of Ach receptors
  • characterized by muscle weakness and fatigue as the day goes on
  • ocular involvement in 90% of patients; only affects skeletal muscle (no effect on pupil or ciliary muscle)
  • ptosis, EOM involvement that is variable within minutes, hours, days or weeks
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120
Q

Diagnosis of myasthenia gravis includes

A
  • lid fatigue –> have patient stare in up gaze, preferably in the afternoon
  • lid twitch sign (cogan’s sign)
  • enhanced ptosis
  • variability in measuring tropia/phoria
  • tensilon/enlon test: positive test = diagnosis; negative test = may or may not have MG
  • Ach antibodies in 1/3 of patients
  • have to do tensilon test while patient is having symptoms
  • typically done in the hospital because it can be very risky
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121
Q

Treatment of phthiriasis palpebarum

A
  • typically done by removing nits, cutting lashes at the base and smothering with bland petrolatum
  • can use acetylcholinesterase but the SE limit usefulness (nobody really does this)
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122
Q

Miotics in dry eye treatment (drug name, dose, side effects, etc.)

A
  • Salagen (pilocarpine 5 mg) indicated for treatment of dry mouth due to radiotherapy of head/neck or Sjogren’s syndrome
    • off-label for dry eye
    • dose 5 mg orally TID-QID
    • side effects include LOTS of sweating and other expected cholinergic SE
  • Evoxac (civimeline) indicated for treatment of dry mouth from Sjogren’s
    • off-label for dry eye
    • dose 30 mg orally TID
    • side effects same as Salagen
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123
Q

Vuity is used to treat

A

Presbyopia

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124
Q

How does Vuity work?

A

Improves near vision by increasing the depth of focus by creating a small pupil

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125
Q

What are some side effects of Vuity that are seen in >5% of study patients?

A
  • headache due to accommodative spasm

- conjunctival hyperemia, likely from vascular permeability

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126
Q

What are some side effects of Vuity seen in 1-5% of study patients?

A
  • blurred vision (inducing myopia)
  • eye pain
  • eye irritation
  • impaired vision
  • lacrimation
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127
Q

How do anticholinergic (cycloplegic) agents work?

A
  • inhibit the actions of acetylcholine to cause mydriasis, cycloplegia, and potentially elevated IOP
  • affect autonomic effector sites
  • affect some smooth muscle sites
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128
Q

Cycloplegic agents are also known as

A
  • anti-muscarinics
  • cholinergic antagonists
  • anticholinergics
  • mydriatics (bad term)
  • cycloplegics
  • mydriatic-cycloplegics
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129
Q

What are some cholinergic antagonists?

A
  • atropine
  • homatropine
  • scopolamine
  • cyclopentolate
  • tropicamide
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130
Q

What is the most potent mydriatic and cycloplegic agent available?

A

Atropine

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131
Q

How long does mydriasis last after administering atropine?

A

Up to 10 days

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132
Q

How long does cycloplegia last after administering atropine?

A

Up to 12 days

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133
Q

How do dark irises affect the effects of atropine?

A

Pigment binding causes mydriasis and cycloplegia to have a delayed onset and longer duration of action

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134
Q

At what time is maximum mydriasis achieved when using atropine?

A

30-40 minutes unless it’s a very dark eye

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135
Q

At what time is maximum cycloplegia achieved when using atropine?

A
  • 60-180 minutes

- because of this, atropine isn’t very practical clinically for a refraction

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136
Q

Clinical uses of atropine

A
  • cycloplegic refraction if you want to find the most plus possible
  • treatment of anterior uveitis/hyphema
  • treatment of myopia
  • treatment of amblyopia
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137
Q

Under what special circumstances might you use atropine for cycloplegic refraction?

A
  • small children with active accommodation and suspected latent hyperopia or accommodative ET
  • would use nasolacrimal occlusion to reduce systemic SE
  • hand washing for parent instilling the drops
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138
Q

What can atropine be used to treat? (besides amblyopia and myopia, 3)

A
  • anterior uveitis or really any inflammation of the ciliary body - relieves pain associated with inflammation and ciliary body spasm
  • prevention of posterior synechiae
  • may decrease permeability of inflamed vessels
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139
Q

What is the mechanism of action of atropine when treating myopia?

A
  • CB is at rest and accommodation is relaxed

- use of very low dose showed significant effect in reducing myopia progression

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140
Q

How is atropine used to treat amblyopia?

A
  • alternative to patching
  • may be combined with overcorrection or undercorrection of the better eye (VA in amblyopic eye must be better than VA in non-amblyopic eye)
  • careful to not induce amblyopia in the other eye
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141
Q

Ocular side effects of atropine

A
  • allergic dermatitis
  • risk of angle closure, though this is remote/negligible if angles are open
  • increased IOP in open angles, but rare
  • ocular side effects may occur with systemic use
  • systemic side effects may occur with topical use
  • when using low concentrations, these risks are minimal
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142
Q

Systemic side effects of atropine

A
  • dose dependent
  • low: more likely to produce peripheral effects such as dry mouth, flushing of face, and inhibition of sweating
  • increasing dose: central (CNS) effects such as convulsions, cognitive impairment, delirium, and death but rare
  • use caution in lightly pigmented individuals, young children and down’s syndrome
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143
Q

How to treat overdose of atropine

A
  • supportive if peripheral effects and physostigmine if central effects
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144
Q

Contraindications to atropine

A
  • known hypersensitivity
  • POAG, but not absolute
  • caution in infants, small children and elderly
  • down’s syndrome
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145
Q

What is the potency of homatropine compared to atropine?

A

1/10 the potency of atropine

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146
Q

When is maximum mydriasis achieved with homatropine?

A

40 minutes

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147
Q

How long does mydriasis last with homatropine?

A

1-3 days

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148
Q

How long does cycloplegia last with homatropine?

A

Longer than cyclopentolate but not as strong as atropine or cyclopentolate

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149
Q

Clinical uses of homatropine

A
  • not typically used for cycloplegic refraction because less hyperopia is uncovered
  • primarily used to treat anterior uveitis
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150
Q

Contraindications of homatropine

A
  • known hypersensitivity
  • POAG, but not absolute
  • caution in infants, small children and elderly
  • down’s syndrome
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151
Q

When does maximum mydriasis occur with scopolamine?

A

20 minutes

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152
Q

How long does mydriasis last with scopolamine?

A

2-8 days

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153
Q

When does maximum cycloplegia occur with scopolamine?

A

40 minutes

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154
Q

Clinical uses for scopolamine

A
  • not first choice for cycloplegic refraction or treatment of anterior uveitis (but still effective for anterior uveitis)
  • more CNS effects because it crosses the BBB
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155
Q

Side effects of scopolamine

A
  • similar to atropine
  • slightly higher CNS toxicity:
  • restlessness
  • confusion
  • incoherence
  • violence
  • drowsiness
  • vomiting
  • urinary incontinence
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156
Q

Contraindications of scopolamine

A

same as atropine

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157
Q

Can mydriasis and cycloplegia result from hand to eye contact and from systemic absorption from transdermal scopolamine?

A

Yes

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158
Q

When does maximum mydriasis occur with cyclopentolate?

A
  • white patients: 20-30 minutes

- black patients: 30-60 minutes

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159
Q

When does maximum cycloplegia occur with cyclopentolate?

A
  • 30-60 minutes

- as early as 10 minutes in light color eyes

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160
Q

How long does cycloplegia last with cyclopentolate?

A
  • about 24 hours

- ALWAYS TELL THE PATIENT THIS

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161
Q

Clinical uses of cyclopentolate

A
  • DO1C for cycloplegic refraction
  • treatment of anterior uveitis
    • mild cases
    • people sensitive to atropine
    • more frequent doses needed than atropine (tid to qid)
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162
Q

Ocular side effects of cyclopentolate

A
  • stinging
  • allergic reaction (rare)
  • toxic keratitis with prolonged use
  • IOP increase in POAG (less common than atropine)
  • precipitation of angle closure in susceptible patients
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163
Q

Systemic side effects of cyclopentolate

A
  • similar to atropine (more CNS)
  • drowsiness, but also agitated
  • restlessness
  • memory loss
  • visual hallucinations
  • grand mal seizures reported but rare
  • MORE common in children, and with 2%
164
Q

Contraindications to cyclopentolate

A

> 0.5% solution may be contraindicated in patient profile similar to atropine contraindications

165
Q

When does maximum mydriasis occur with tropicamide?

A

25-30 minutes

166
Q

How long does mydriasis last with tropicamide?

A

6 hours, longer in dark irises

167
Q

Is the mydriatic effect of tropicamide dose-related?

A

No

168
Q

When does maximum cycloplegia occur with tropicamide?

A

30 minutes

169
Q

Is the cycloplegic effect of tropicamide dose-related?

A

Yes

170
Q

What cycloplegic drop has the greatest mydriasis effect at 30 minutes?

A

Tropicamide

171
Q

Clinical uses of tropicamide

A
  • ophthalmoscopy: less dependent of iris pigment; most commonly used with a sympathomimetic
  • cycloplegic refraction in school-aged children without suspected high hyperopia or suspected latent/accommodative ET (“damp” refraction)
172
Q

Side effects of tropicamide

A
  • stinging

- increased IOP in POAG

173
Q

Contraindications of tropicamide

A

Narrow anterior chamber angles

174
Q

Effects of adrenergic stimulation to the eye

A
  • pupillary dilation
  • widening of the palpebral fissure (Mueller’s muscle)
  • vasoconstriction
  • decreased IOP, but we’re unsure why
  • inhibition of accommodation (very small amount)
175
Q

What are some examples of topical adrenergic agonists?

A
  • phenylephrine
  • hydroxyamphetamine
  • cocaine (diagnostic of Horner’s)
  • apraclonidine (glaucoma)
  • brimonidine (glaucoma)
176
Q

Pharmacology of phenylephrine

A
  • direct-acting
  • analogy of epinephrine
  • acts primarily on alpha-1 receptors
  • may cause minimal release of NE at terminals
177
Q

Phenylephrine stimulates (3 things) and may cause what?

A
  • iris dilator muscle
  • conjunctival arteriole smooth muscle (blanches blood vessels)
  • Mueller’s muscle of the upper eyelid
  • may cause decreased IOP
178
Q

What are the common clinical uses of phenylephrine?

A
  • pupillary dilation

- breaking posterior synechiae

179
Q

When is maximum mydriasis achieved with phenylephrine?

A

45-60 minutes

180
Q

How much does phenylephrine affect accommodation?

A

very minimally (2D)

181
Q

What concentration of phenylephrine do we use for DFE?

A

2.5%

182
Q

What concentration of phenylephrine do we use for breaking posterior synechiae?

A

10%

183
Q

Ocular side effects of phenylephrine

A
  • transient pain, lacrimation, keratitis
  • allergic dermatitis/conjunctivitis if used routinely
  • release of pigment granules from iris
  • rebound congestion with chronic use
184
Q

Systemic side effects of phenylephrine (potential concern for DFE)

A
  • possibly systemic hypertension, but not really conclusive

- can punctal occlude if you’re concerned

185
Q

Patient populations likely to experience increased BP response to 10% phenylephrine

A
  • neonates
  • “insulin-dependent” DM
  • idiopathic orthostatic hypotension
186
Q

Other reported systemic side effects to 10% phenylephrine (6)

A
  • occipital HA
  • subarachnoid hemorrhage
  • ventricular arrhythmia
  • ruptured aneurysm
  • tachycardia/reflex bradycardia
  • blanching of skin
187
Q

What medications can exacerbate systemic side effects of phenylephrine?

A
  • atropine
  • TCAs
  • MAOIs
  • guanethidine, reserpine, methyldopa
188
Q

What is Horner’s syndrome?

A

sympathetic paralysis or denervation

189
Q

Signs of Horner’s syndrome

A
  • lid ptosis
  • miosis
  • anhidrosis of the face in some cases
190
Q

Why does congenital Horner’s syndrome result in one blue eye?

A

Need sympathetic stimulation for the development of iris pigment

191
Q

Pharmacology of cocaine

A
  • indirect-acting sympathetic agonist

- binds to receptors on sympathetic nerve endings and prevents re-uptake of NE

192
Q

How is cocaine used to diagnose Horner’s syndrome?

A
  • in a normally functioning system, effect is enhanced sympathetic activity
  • with complete sympathetic disruption, cocaine will not have the expected effect (patient has Horner’s)
193
Q

Effects of cocaine (systemic and local)

A
  • local anesthetic
  • mydriasis
  • increased heart rate
  • vasoconstriction
  • CNS stimulation
194
Q

Clinical uses of cocaine

A
  • diagnosis of Horner’s syndrome

- debridement of corneal epithelium

195
Q

Side effects of cocaine

A
  • CNS stimulation
  • Death from respiratory failure
  • rapid absorption from mucous membranes
  • corneal damage with topical use
196
Q

Contraindications of cocaine

A
  • cardiac disease

- hyperthyroidism

197
Q

Hydroxyamphetamine drug type

A

Indirect mydriatic

198
Q

Pharmacology of hydroxyamphetamine

A
  • similar structure to NE
  • indirect-acting adrenergic agonist
  • causes release of endogenous NE
  • if post-ganglionic neuron damaged (post-ganglionic Horner’s), then no NE is released; no dilating effect
  • little/no effect on accommodation
199
Q

Clinical uses of hydroxyamphetamine

A
  • mydriasis
  • max at 45-60 minutes and lasts about 6 hours
  • differentiation of pre- and post-ganglionic Horner’s syndrome
200
Q

What happens in central/pre-ganglionic Horner’s after administration of hydroxyamphetamine?

A

Post-ganglionic fibers should have normal amounts of NE: DILATION would result

201
Q

What happens in post-ganglionic Horner’s after administration of hydroxyamphetamine?

A

No/little NE in post-ganglionic fibers: NO DILATION with hydroxyamphetamine

202
Q

Side effects of hydroxyamphetamine

A
  • little ocular irritation
  • can cause elevated blood pressure
  • may be safer to use for mydriasis in patients with phenylephrine CI
203
Q

Apraclonidine (Iopidine) drug type

A

Direct-acting alpha-agonist (strong alpha-2, weak alpha-1)

204
Q

Apraclonidine pharmacology

A
  • causes decrease in IOP

- little effect on pupil size in normal eye

205
Q

What happens if you instill apraclonidine in a normal eye?

A

No/minimal dilation

206
Q

What happens if you instill apraclonidine in a Horner’s eye?

A

The pupil dilates (reversal of anisocoria)

207
Q

Clinical uses of apraclonidine (Iopidine)

A
  • prevents IOP spike following anterior laser procedures

- DIAGNOSIS of Horner’s (in lieu of cocaine test)

208
Q

Primary use of Brimonidine

A
  • management of glaucoma (not effective for Horner’s due to more alpha-2 selectivity and negligible alpha-1 activity)
209
Q

What are mydriolytics?

A

Alpha-adrenergic blocking agents used to reverse mydriasis (safer than miotics)

210
Q

Dapiprazole pharmacology

A
  • mydriolytic
  • alpha-adrenergic antagonist
  • produces miosis
  • reduces IOP
  • no shallowing of the AC
  • may be useful in angle closure
  • may partially increase AA caused by tropicamide
  • slower effect in dark irises
  • minimal systemic absorption
211
Q

Clinical uses of dapiprazole

A
  • reversal of pupillary dilation (phenylephrine)
  • partial reversal of pupillary dilation (tropicamide)
  • LITTLE EFFECT ON CYCLOPLEGIA
  • angle closure glaucoma??
212
Q

Dapiprazole side effects

A
  • burning
  • conjunctival hyperemia, chemosis
  • punctate keratitis; edema
  • ptosis
  • brow ache
  • no effect on blood pressure or pulse rate
213
Q

Contraindications of dapiprazole

A
  • anterior uveitis

- hypersensitivity

214
Q

What bacteria are we most concerned about in contact lens wearers?

A

Pseudomonas

215
Q

What are the most common bacteria that cause ocular infections?

A

Staphylococci and Streptococci (Gram +)

216
Q

What are other bacteria that cause ocular infections that are not Gram (+) cocci?

A
  • Gram (-): Neisseria gonorrhea, Haemophilus influenzae, E. coli, Serratia marcescens, Proteus, Pseudomonas aeruginosa
  • chlamydia
  • treponema pallidum (spirochete)
217
Q

If you can’t determine cause of a red eye, what should you do?

A

Have patient RTC in 1-2 days to re-evaluate. The red eye will eventually declare itself

218
Q

Adverse consequences of antibiotic use

A
  • allergic reactions
  • superinfection - another organism is allowed to overgrow (yeast)
  • resistance
219
Q

What are methods for minimizing potential for resistance?

A
  • use narrowest spectrum agent possible for given infection
  • use proper dose
  • use shortest effective duration of therapy, but finish course
  • DO NOT TAPER
220
Q

Drugs that affect cell wall synthesis

A
  • penicillins
  • cephalosporins
  • vancomycin
  • bacitracin
221
Q

Which of the drugs that affect cell wall are available in an ophthalmic ointment?

A

Bacitracin

222
Q

Commonalities between beta-lactams

A
  • all can cause hypersensitivity reactions
  • all share a common basic MOA (bind to PBPs)
  • all lack activity against atypical organisms (mycoplasma, chlamydia, ricketts, etc.)
  • all LACK activity against MRSA
223
Q

What are penicillins?

A
  • beta-lactam ring connected to a side chain
  • beta-lactam ring must be intact for activity
  • divided into four categories
224
Q

MOA of penicillins

A
  • inhibits synthesis of cell wall by inhibiting cross-linking of polysaccharide chains of peptidoglycan
  • works on actively dividing cells (once it’s formed, there’s no effect)
  • osmotic pressure causes lysis of the cell
225
Q

What are the four basic categories of penicillins?

A
  • natural penicillins
  • antistaphylococcal penicillins
  • aminopenicillins
  • anti-pseudomonal penicillins
226
Q

What are the natural penicillins and what is their spectrum of activity?

A
  • penicillin G - IM only
  • penicillin V - oral
  • Staph became resistant quickly so now has a very narrow spectrum
  • good: treponema pallidum (DOC), most strep
  • moderate: strep pneumoniae
  • poor: almost everything else (staph)
227
Q

What are antistaphylococcal penicillins?

A
  • methicillin - defines class
  • oxacillin
  • cloxacillin
  • dicloxacillin
  • nafcillin
228
Q

What is the spectrum of activity of antistaphylococcal penicillins?

A
  • good: MSSA, streptococci
  • poor: Gram (-) rods, MRSA
  • TOC: Vancomycin (in flux because now we have VRSA!)
229
Q

What is an ocular indication for oral antistaphylococcal penicillins?

A
  • internal hordeolum (MSSA): oral cloxacillin or dicloxacillin
  • preseptal cellulitis (MSSA): dicloxacillin 250mg qid
  • orbital cellulitis: IV nafcillin
230
Q

What patient history would make you suspect MRSA?

A
  • patient works in a hospital/nursing home
  • patient lives in a correctional facility or college dorm
  • MRSA can also be out in the community
231
Q

What are some aminopenicillins and what is their route of administration?

A
  • amoxicillin (oral)

- ampicillin (IV)

232
Q

What is the spectrum of activity of aminopenicillins and what diseases are they used to treat?

A
  • good: streptococci, enterococci
  • moderate: H. influenzae, E. coli
  • poor: staph
  • URI (strep throat), otitis media
233
Q

What are beta-lactamase inhibitors used for?

A
  • can counteract beta-lactamases and extend spectrum of aminopenicillins and antipseudomonal penicillins
  • beta-lactamase inhibitors have little antimicrobial activity by themselves
234
Q

What are some examples of beta-lactamase inhibitors?

A
  • clavulanate
  • sulbactam
  • tazobactam (only added to antipseudomonal pcn)
235
Q

What is Augmentin a combination of?

A
  • amoxicillin

- clavulanic acid

236
Q

What is Unasyn a combination of and what is its route of administration?

A
  • ampicillin
  • sulbactam
  • administered IV
237
Q

Sensitivity of beta-lactamase inhibitors

A
  • good: MSSA, strep, E. coli

- poor: MRSA

238
Q

Ocular indications for Augmentin

A
  • preseptal cellulitis
  • dacryocystitis
  • pediatric haemophilus
239
Q

Is Augmentin safe in pregnancy?

A

Yes

240
Q

Typical adult dose of Augmentin

A
  • 500 mg BID or 250 mg TID

- more severe: 875mg BID or 500mg TID

241
Q

What are some examples of antipseudomonal penicillins?

A
  • piperacillin
  • carbenicillin
  • mezlocillin
  • ticarcillin
242
Q

What is the spectrum of activity of antipseudomonal penicillins?

A
  • good: P. aeruginosa, strep, enterococci
  • moderate: haemophilus
  • poor: staph, anaerobes
243
Q

What are the side effects of penicillins?

A
  • hypersensitivity
  • alteration of normal flora (super-infection)
  • failure of oral contraceptives (although not clear which oral antibiotics cause this)
244
Q

Contraindications to penicillins

A
  • known hypersensitivity to any penicillin

- cross-sensitivity with cephalosporins

245
Q

Are there any topical ophthalmic preparations of cephalosporins?

A

No

246
Q

What is the preferred oral 1st generation cephalosporin?

A

Cephalexin (Keflex)

247
Q

What is the preferred oral 2nd generation cephalosporin?

A

Cefaclor (Ceclor)

248
Q

What is the preferred oral 3rd generation cephalosporin?

A

Cefixime (Suprax)

249
Q

What are common 1st generation cephalosporins we need to know for this exam?

A
  • Cefazolin (important in cornea, must be compounded)

- Cephalexin (500 mg BID)

250
Q

What is the spectrum of activity of first generation cephalosporins?

A
  • Good: MSSA, streptococci

- Poor: MRSA, pseudomonas

251
Q

Ocular indication of Cefazolin?

A

DOC for bacterial corneal ulcers when using a traditional “broad-spectrum” approach

252
Q

Ocular indications of cephalexin?

A

dacryocystitis, preseptal cellulitis if MSSA

253
Q

What are common 2nd generation cephalosporins we need to know for this exam?

A
  • cefaclor (Ceclor)

- cefuroxime (Ceftin)

254
Q

What is the spectrum of activity of 2nd generation cephalosporins?

A
  • more effective against gram (-) than first generation
  • particularly good against Haemophilus & Neisseria
  • “HENPEK”
  • good: Haemophilus, Enterobacter, Neisseria, Proteus, E. coli, Klebsiella
  • moderate: strep, staph
  • poor: MRSA, pseudomonas
255
Q

Ocular indications of oral cefaclor?

A

dacryocystitis, preseptal cellulitis (MSSA, haemophilus)

256
Q

Ocular indications of parenteral cefuroxime?

A

severe dacryocystitis, preseptal cellulitis in a child

257
Q

What are some 3rd generation cephalosporins we need to know for this exam?

A
  • ceftazidime
  • ceftriaxone
  • cefixime (Suprax - oral)
258
Q

What is the spectrum of activity of third generation cephalosporins?

A
  • increasing gram (-) coverage
  • decreasing gram (+) coverage
  • good: strep, pseudomonas (ceftazidime)
  • moderate: MSSA
  • poor: MRSA, pseudomonas (except ceftazidime)
259
Q

Ocular indications of third generation cephalosporins?

A

IV ceftriaxone for orbital cellulitis (in combo)

260
Q

Side effects of cephalosporins?

A
  • rash
  • fever
  • bronchospasm
  • rare anaphylaxis
  • uncommon cross hypersensitivity with penicillins
  • alteration of normal flora
  • vitamin K deficiency
  • reversible renal impairment
261
Q

Contraindications to cephalosporins

A
  • known hypersensitivity
  • hemophilia (due to vitamin K issues)
  • anaphylaxis to penicillin, but would be ok to Rx if had delayed hypersensitivity to PCN
262
Q

MOA of bacitracin?

A

inhibits the polysaccharide chain formation in cell wall synthesis

263
Q

Spectrum of activity of bacitracin?

A

Gram (+), plus Neisseria

264
Q

What is the formulation of bacitracin?

A

only available in an ointment because it’s not soluble

265
Q

What ocular conditions is bacitracin used to treat?

A

staph blepharitis - in combo with Polymyxin B (Polysporin) or Polymyxin B/Neomycin (Neosporin)

266
Q

Side effects of bacitracin?

A
  • hypersensitivity (dermatitis) is rare

- considered non-toxic and is well-tolerated when used topically

267
Q

MOA of vancomycin

A
  • inhibits synthesis of cell wall precursors

- inhibits RNA synthesis

268
Q

What is the spectrum of activity of vancomycin?

A
  • Gram (+) cocci (MRSA), Neisseria, Clostridium, Corynebacterium
269
Q

Is there an ophthalmic preparation of vancomycin?

A

No

270
Q

What are some systemic indications to use vancomycin?

A
  • TOC for C. diff infections
  • TOC for MRSA and penicillin-resistant S. pneumoniae (IN FLUX)
  • only used when REALLY necessary
271
Q

What are some ocular indications for vancomycin?

A
  • bacterial endophthalmitis (intravitreal)

- resistant blepharitis, keratitis

272
Q

Side effects of vancomycin

A
  • permanent deafness
  • fatal uremia
  • red man syndrome
273
Q

MOA of polymyxin B

A
  • detergents interact with the phospholipids of the cell’s membranes
  • doesn’t need actively dividing cells to work
274
Q

Spectrum of activity of polymyxin B

A

Mostly Gram (-)

275
Q

Clinical uses of Polymyxin B

A

used topically in combination for conjunctival and lid infections (minor things)

276
Q

Combinations of polymyxin B (3)

A
  • polymyxin B and bacitracin (Polysporin) has good Gram (-) and (+) coverage
  • polymyxin B and trimethoprim (Polytrim) is broad-spectrum and well-tolerated; inexpensive; good for bacterial blepharitis or prophylaxis from corneal erosion
  • polymyxin B and bacitracin and neomycin (Neosporin) is not prescribed often due to hypersensitivities to neomycin
277
Q

Side effects of systemic polymyxin B

A

neurotoxicity and nephrotoxicity

278
Q

Side effects of topical Polymyxin B

A

mild and infrequent

279
Q

Classes of drugs that affect protein synthesis (6)

A
  • aminoglycosides
  • tetracyclines
  • macrolides
  • linezolid
  • chloramphenicol
  • clindamycin
280
Q

Aminoglycoside drugs

A
  • neomycin
  • gentamicin
  • tobramycin
  • amikacin
281
Q

Spectrum of aminoglycosides

A
  • good: Gram (-) including some pseudomonas
  • moderate: IN COMBO with beta-lactam: staph (including MRSA)
  • poor: Gram (+) if used alone
282
Q

How do bacteria become resistant to aminoglycosides?

A
  • alteration of bacterial ribosomes (binding site)
  • decreased antibiotic uptake
  • enzymatic inactivation of the drug (most common)
283
Q

What are the routes of administration of aminoglycosides?

A

IM, IV or topical due to poor absorption from the gut

284
Q

Neomycin’s spectrum of activity?

A

broad spectrum (different from other aminoglycosides)

285
Q

Ocular indications of neomycin

A

topical surface disease (in combo or alone)

286
Q

Ocular uses of gentamicin

A
  • conjunctivitis
  • blepharitis
  • keratitis
  • endophthalmitis
287
Q

What is something to be aware of when prescribing gentamicin?

A

Can cause corneal toxicity - sloughing of epithelium with frequent dosing and prolonged use

288
Q

Between gentamicin and tobramycin, which has better activity against pseudomonas?

A

Tobramycin

289
Q

Ocular uses of tobramycin

A
  • bacterial keratitis - fortified gentamicin or tobramycin with fortified cefazolin
  • endophthalmitis - fortified gent/tobr with piperacillin/ticarcillin
290
Q

Which of the aminoglycosides is preferred for endophthalmitis?

A

Amikacin (with vancomycin)

291
Q

Systemic side effects of aminoglycosides?

A
  • auditory and vestibular toxicity

- nephrotoxicity

292
Q

Systemic side effects of gentamicin?

A
  • pseudotumor cerebri
  • auditory and vestibular toxicity
  • nephrotoxicity
293
Q

Side effects of topical gentamicin

A

corneal/conjunctival toxicity

294
Q

Side effects of intravitreal aminoglycosides (except amikacin)

A

macular infarction

295
Q

Spectrum of activity of tetracyclines

A
  • good: atypicals, rickettsia, spirochetes
  • moderate: staph (including MRSA), strep
  • poor: most gram (-) rods
296
Q

When are tetracyclines the DOC?

A
  • “oddball” infections: RMSF, lyme disease, chlamydia
297
Q

Ocular indications of tetracyclines?

A
  • infections (Adult inclusion conjunctivitis, AIC): doxycycline 100mg BID X 1-3 weeks
  • soft tissue infection (ild)
  • non-infectious conditions (acne rosacea, meibomianitis): therapy is long term, sub-antimicrobial dosing
298
Q

Side effects of tetracyclines

A
  • photosensitivity
  • GI disturbance
  • depressed bone growth in fetus/tooth discoloration
  • pseudotumor cerebri (rare)
  • vestibulotoxicity with minocycline
299
Q

contraindications to tetracycylines

A
  • hypersensitivity
  • pregnant or lactating women
  • children under 8 years old (8-13 controversial)
300
Q

Prescribing warning with tetracyclines

A
  • decreased absorption with dairy products, antacids containing calcium, magnesium, aluminum and sodium bicarbonate (baking soda)
  • decreased absorption with food (tetracycline)
  • esophagitis (doxycycline), so important to be upright for at least 30 minutes after taking and drink a glass of water
301
Q

Short-acting tetracyclines and sig for treating trachoma?

A
  • tetracycline

- trachoma: 250 qid X 14 days

302
Q

Examples of long-acting tetracyclines and their sigs

A
  • doxycycline
  • minocycline
  • AIC: 100mg BID x 7 days
303
Q

Spectrum of activity of macrolides

A
  • mostly gram (+)

- some gram (-)

304
Q

What type of infections can macrolides be used to treat? And what can they substitute for?

A
  • chlamydial infections, neisseria, treponema (good substitute for tetracyclines)
305
Q

How do bacteria become resistant to macrolides?

A

alteration of the ribosome structure - Gram (+)

306
Q

What are some drugs that are macrolides? And their available ROAs?

A
  • erythromycin: topical ophthalmic and oral
  • clarithromycin: oral only
  • azithromycin: topical ophthalmic and oral
307
Q

How is erythromycin administered?

A
  • parenterally, orally and topically

- gastric acid inactivates erythromycin base, so lots of formulations to stabilize and promote absorption

308
Q

Ocular uses of erythromycin

A
  • can be used orally for chlamydia in infants, children, pregnant women (250mg qid X 21 days for adult)
  • can be used topically in staph lid disease
309
Q

When is clarithromycin contraindicated?

A

pregnancy

310
Q

What is the signatura for azithromycin when treating chlamydia?

A

take 2 tablets by mouth at the same time (1 g dose)

311
Q

How is azithromycin ophth sol administered topically?

A
  • days 1 and 2: 1 drop twice daily

- days 3-7: 1 drop once daily

312
Q

How can ODs use azithromycin off-label?

A

long-term therapy to treat meibomianitis and is applied to the lids

313
Q

Side effects of macrolides

A
  • GI disturbance
  • cholestatic hepatitis (erythromycin estolate in adults)
  • palpitations, HA, dizziness (azithromycin)
314
Q

Spectrum of linezolid

A
  • good: MSSA, MRSA, strep
  • moderate: some atypicals
  • poor: gram (-), anaerobes
315
Q

Why isn’t linezolid used very often?

A

it’s reserved for severe hospital-acquired MRSA, so it’s advised to only be used if you have to use it

316
Q

Is there an ophthalmic preparation of linezolid?

A

No

317
Q

Side effects of linezolid

A
  • can cause bone marrow suppression, mostly after 2+ weeks

- serotonin syndrome

318
Q

adverse effects of linezolid

A
  • potentially fatal
  • confusion/agitation/tremor
  • nausea/vomiting/diarrhea
  • dilated pupils
  • increased temperature/shivering/sweating
  • very high fever/seizure/unconsciousness
319
Q

spectrum of activity of clindamycin

A
  • good: many gram (+) anaerobes
  • moderate: s. aureus (including some MRSA), strep, chlamydia, toxoplasma gondii
  • poor: c. diff
320
Q

Is there an ophthalmic preparation for clindamycin?

A

No

321
Q

Ocular indication for clindamycin

A

toxoplasmosis (may be effective against encysted form)

322
Q

side effects of clindamycin

A
  • pseudomembranous colitis (chloisteroides, c. dif), which can be very dangerous in older patients
  • hypersensitivity (dermatitis)
  • but generally well-tolerated
323
Q

Drug classes that affect intermediary metabolism

A
  • sulfonamides
  • pyrimethamine
  • trimethoprim
324
Q

spectrum of sulfonamides

A
  • broad spectrum
  • gram (+), gram (-), chlamydia, plasmodia, toxoplasma
  • but there is tons of staph resistance
325
Q

how bacteria become resistant to sulfonamides

A
  • overproduction of PABA
  • decreased enzyme affinity for drug
  • decreased cell permeability to drug
  • inactivation of drug
326
Q

what chemicals can negate the effects of sulfonamides?

A
  • anesthetics contain PABA and can reverse the sulfonamide-induced inhibition of folic acid synthesis
  • pus, blood in environment can decrease the bacterial requirement for folic acid
327
Q

clinical uses of oral sulfonamides

A
  • active toxoplasmosis infection in combination with pyrimethamine
  • pneumocystis infections
328
Q

clinical uses of topical sulfonamides

A
  • primarily in combination with steroid for blepharitis

- ALMOST never used topically in ophthalmic care today

329
Q

side effects of sulfonamides

A
  • mild: GI, skin reactions, transient myopia
  • severe: SJS, blood dyscrasias
  • topical: hyperemia, contact dermatitis, local photosensitivity
330
Q

what drugs have synergistic activity with sulfonamides?

A

pyrimethamine and trimethoprim (work further down in the pathway)

331
Q

clinical uses of oral pyrimethamine

A

toxoplasmosis (with sulfadiazine)

332
Q

clinical uses of trimethoprim and sulfamethoxazole

A

UTI, MRSA cellulitis

333
Q

clinical uses of trimethoprim and polymyxin B

A

ophthalmic drops good for bacterial blepharitis

334
Q

spectrum of TMP/SMX (Bactrim, Septra)

A
  • good: staph (some MRSA), haemophilus, pneumocystis jirovecii
  • moderate: s. pneumoniae
  • poor: pseudomonas, s. pyogenes
335
Q

clinical uses of TMP/SMX

A
  • uncomplicated UTI, pneumocystis pneumonia
  • good choice for MRSA
  • has a “double strength” available
336
Q

side effects of pyrimethamine

A
  • wbc and platelet suppression

- folate deficiency

337
Q

trimethoprim/sulfamethoxazole systemic side effects (3)

A
  • skin reaction
  • significant interaction with warfarin
  • hematologic problems IF patient is folate deficient
338
Q

is Bactrim a sulfonamide?

A

Yes

339
Q

side effects of polytrim

A
  • transient burning, stinging
  • hypersensitivity - lid edema, rash
  • NO CROSS-SENSITIVITY between sulfa and trimethoprim
340
Q

contraindications of pyrimethamine and trimethoprim

A
  • folate deficiency

- pus is NOT a contraindication to Polytrim use

341
Q

Drugs that affect DNA synthesis

A
  • metronidazole
  • rifamycins (Rifampin)
  • quinolones (more pertinent to ODs)
342
Q

spectrum of quinolones

A

good broad spectrum coverage

343
Q

bacteria that have developed resistance to quinolones

A
  • some pseudomonas resistance (2nd generation)

- some staph resistance (2nd generation)

344
Q

topical ophthalmic fluoroquinolone drug names

A
  • ciprofloxacin (Ciloxan) - ointment and drops (1st gen)
  • ofloxacin (Ocuflox) (1st gen)
  • levofloxacin (2nd gen)
  • moxifloxacin (Vigamox, Moxeza) (3rd gen)
  • gatifloxacin (Zymaxid 0.5%) (3rd gen)
  • besifloxacin (Besivance); 3rd gen; no generic available; never used as oral/systemic nor in livestock and feed
345
Q

Why are fluoroquinolones not really used by ODs?

A

Huge black box warnings that keep getting longer

346
Q

Oral fluoroquinolones that we need to know

A
  • levofloxacin
  • ciprofloxacin
  • moxifloxacin
  • ofloxacin
  • gemifloxacin
347
Q

Fluoroquinolone black box warnings

A
  • increased risk of tendinitis/tendon rupture
  • risk or worsening symptoms of MG
  • potential irreversible peripheral neuropathy, CNS effects
348
Q

Benefits of fluoroquinolones in eye care

A
  • greater efficacy and broader spectrum of activity than bacitracin, erythromycin, gentamicin and tobramycin
  • typically less toxic than aminoglycosides
349
Q

Clinical uses of FQs (in OD practice)

A
  • most are FDA approved for conjunctivitis
  • ciprofloxacin and ofloxacin are FDA approved to treat keratitis
  • moxi, gati, besi are used more often for keratitis off-label (newer)
350
Q

Side effects of topical FQs

A
  • local burning
  • bitter taste
  • white precipitate at base of keratitis (cipro)
  • conjunctival hyperemia
351
Q

FQ Contraindications with oral use

A
  • known hypersensitivity
  • erosion of cartilage in weight-bearing joints in immature animals
  • tendon rupture
  • inhibits metabolism of theophylline
352
Q

Are FQs indicated if you suspect MRSA in a bacterial keratitis?

A

Not unless it’s combined with trimethoprim

353
Q

What is the Sanford Guide to Antimicrobial Therapy for bacterial keratitis with no comorbidities?

A
  • Moxif 1 gtt/h X first 48 h then decrease

- alternative: cipro, levo or gati drops

354
Q

What is the Sanford Guide to Antimicrobial Therapy for bacterial keratitis for contact lens wearers?

A
  • cipro or levo q1-2h X 24-72h

- alternative: gent or tobra 0.3% hourly X 24h

355
Q

What is the Sanford Guide to Antimicrobial Therapy for bacterial keratitis for dry cornea, diabetes, immunosuppression?

A
  • cipro hourly

- alternative: vanc + ceftazidime (each 50mg/mL) topical

356
Q

What is the only topical ophthalmic anti-fungal preparation available in the US?

A
  • natamycin (Nystatin)
357
Q

What is the Sanford Guide for fungal keratitis?

A
  • Natamycin 5% drops 1 gtt q1-2h for several days, then reduce
  • alternative: amphotericin B 0.15% drops 1 gtt q1-2h for several days
358
Q

Why are there fewer effective antiviral medications?

A

they have to interfere with viral replication without harming the host, which is difficult because the viruses use our own cellular apparatus

359
Q

What are the five herpesviruses that cause ocular infection?

A
  • herpes simplex 1
  • herpes simplex 2
  • varicella zoster (VZV)
  • cytomegalovirus (CMV); usually problematic in AIDS patients
  • Epstein-Barr virus (EBV) aka mono
360
Q

Are there any approved antivirals for adenoviruses (most common infection in the eye)?

A

No

361
Q

What symptoms occur in the primary infection of HSV?

A
  • subclinical, flu-like symptoms
  • small vesicles around eyes
  • may have follicular conjunctivitis and/or corneal involvement
362
Q

What symptoms occur in the recurrent disease of HSV?

A
  • corneal involvement (1%)

- oral involvement is the most common

363
Q

What are triggers for recurrence of HSV?

A
  • stress
  • sunlight
  • age
  • illness (fever)
  • injuries, etc
364
Q

What are the three types of HSV keratitis?

A
  • epithelial keratitis (dendrites)
  • stromal keratitis (edema, anterior chamber rxn)
  • endothelial keratitis
365
Q

What is the leading cause of corneal blindness in the US?

A

stromal HSV keratitis

366
Q

Current topical anti-herpes medications

A
  • Trifluridine (Viroptic)

- Ganciclovir (Zirgan)

367
Q

MOA of trifluridine

A

inhibits thymidine synthetase and DNA synthesis in virus-infected and normal cells

368
Q

What preservative does use trifluridine use?

A

thimerosal and some patients don’t do well with it

369
Q

Clinical use of viroptic and instructions for use

A
  • treatment of HSV epithelial keratitis
  • 1% gtt q2h (max 9x/d) until re-epithelialized, then q6h for 3-7 days
  • treat no longer than 21 days
  • superior to IDU and Vidarabine for treatment of geographic and dendritic ulcers
370
Q

Side effects of viroptic

A
  • burning/irritation
  • punctate keratopathy
  • corneal edema
  • dry eye
  • conjunctival hyperemia
371
Q

MOA of ganciclovir

A
  • competitively inhibits DNA polymerase

- incorporates into DNA primer strand (terminates strand)

372
Q

clinical indications of ganciclovir ophthalmic gel (Zirgan)

A
  • acute epithelial HSK (as effective as topical acyclovir)
373
Q

Sig of ganciclovir

A
  • 1 gtt 5X/day until re-epithelialization, then 3X/day for additional 7 days
374
Q

Ganciclovir adverse events

A
  • blurred vision (gel)
  • ocular irritation
  • punctate keratitis
  • conjunctival hyperemia
375
Q

Possible alternative use of Zirgan (ganciclovir)

A

adenovirus conjunctivitis (off-label)

376
Q

Treatment options for HSK

A
  • trifluridine (Viroptic) - refrigeration required prior to opening; 9x/d dosing; potential for more toxicity (works on all cells); thimerosol preservative; available generic ($70)
  • ganciclovir (Zirgan) - minimal toxicity (works only in infected cells); 5x/d dosing; no refrigeration; BAK preserved; no generic available ($400)
377
Q

what is acyclovir?

A

synthetic purine analog to guanine

378
Q

Is there a topical acyclovir in the US?

A

no

379
Q

MOA of acyclovir

A
  • phosphorylated by herpes-specific thymidine kinase
  • acyclovir triphosphate inhibits herpes-specific DNA polymerase (selectively toxic)
  • very little resistance in immuno-competent patients
380
Q

Available ROA of acyclovir

A

oral and IV

381
Q

clinical uses of TOPICAL acyclovir

A
  • treatment of HSK in Europe and Canada
382
Q

Side effects of TOPICAL acyclovir

A
  • punctate keratitis

- burning/stinging

383
Q

clinical uses of ORAL acyclovir

A
  • has been shown to be as effective as topical acyclovir in EPITHELIAL HSK (which is as effective as IDU, vidarabine, or trifluridine)
384
Q

sig of oral acyclovir

A

400mg PO 5x/d

385
Q

does use of long-term oral acyclovir prophylactically reduce recurrence in immunocompetent patients?

A

Yes, but patients may want periodic renal function tests

386
Q

What is the sig for using oral acyclovir to treat herpes zoster?

A

800mg orally 5x/d for 7-14d

387
Q

Is oral therapy required to treat VZV?

A

Yes

388
Q

How soon after symptoms of VZV does treatment have to begin to prevent severe complications? And what are the severe complications?

A
  • 72 hours
  • decreases ocular inflammation
  • reduces post-herpetic neuralgia
389
Q

Side effects of oral acyclovir

A
  • nausea, vomiting, diarrhea
  • headache
  • rash
390
Q

contraindications to acyclovir

A
  • known hypersensitivity
  • renal insufficiency - MONITOR
  • lactose intolerance (generics)
391
Q

what is the sig for acyclovir when suppressing HSV in select patients?

A

400mg BID, indefinitely

392
Q

sig for valacyclovir (Valtrex) to treat epithelial HSK and zoster

A 
epithelial HSK:
   - active: 500mg BID-TID
   - prophylaxis: 500mg QD
and zoster:
   - 1g TID x 7-10 days, maybe 14 days in some cases
393
Q

sig for famciclovir (Famvir) to treat epithelial HSK and zoster

A

HSK:

  • 250 mg TID X 7-10 days
    zoster:
  • 500mg TID X 7-10 days
394
Q

Which drug is the DOC for HSK & VZV in elderly patients?

A

Famciclovir because acyclovir and valacyclovir have an increased risk of CNS adverse reactions in these patients?

395
Q

What is the DOC for HSK & ZVZ in neonates?

A

acyclovir

396
Q

What is the DOC for treating HSK & VZV in 2-18 year olds?

A

acyclovir or valacyclovir

397
Q

What drugs are used for initial presentation of HSV conjunctivitis and their sig?

A
  • Trifluridine (Viroptic) gtts q2h (up to 9x/d), or

- ganciclovir 5x/d

398
Q

Are steroids contraindicated in corneal epithelial disease?

A

YES (WILL BE ON TEST)

399
Q

When would oral antivirals be preferred over topicals?

A
  • patient physically unable to use drops
  • contact lens wearers?
  • pediatric patients’ refractory to topical antiviral (not responding)
  • patients that require length treatment antiviral agents
  • patients with pre-existing ocular surface diseases, who may be more susceptible to toxicity
  • prophylactic treatment after ocular surgery
400
Q

When would topical antivirals be preferred?

A
  • patients with renal impairment
  • elderly patients (>64 yrs) with renal impairment or when renal function is unknown at the time of drug administration
  • pregnant patients
  • nursing mothers
401
Q

What is the standard therapy of STROMAL HSK?

A
  • aim is to decrease inflammation/scarring
  • if very mild, off-axis: topical cycloplegic/tears only
  • not mild: topical trifluridine qid (or ganciclovir) AND
    • topical steroid
  • very slow taper needed, otherwise inflammation returns
  • can d/c topical antiviral when steroid is once daily
402
Q

How to treat stromal edema HSV with epithelial ulceration?

A
  • Prednisolone 1% gtt twice daily PLUS
  • acyclovir 800mg 3-5 times daily for 7-10 days OR
  • valacyclovir 1g 3 times daily for 7-10 days OR
  • famciclovir 500mg twice daily for 7-10 days
403
Q

How to treat endothelial keratitis? (will see crazy inflammation, KP, cells & flare in AC with active virus)

A
  • prednisolone 1% gtt 6-8 times daily PLUS
  • acyclovir 400mg 3-5 times daily OR
  • valacyclovir 500mg twice daily OR
  • famciclovir 250mg twice daily
404
Q

What are topical corticosteroid options for HSV?

A
  • fluorometholone 0.1% ophthalmic suspension
  • rimexolone 1% ophth susp
  • prednisolone sodium phosphate 1% ophth sol
  • prednisolone acetate 1% ophth susp
  • difluprednate 0.05% ophth emulsion
405
Q

potential indications for prophylaxis of recurrent HSV keratitis?

A
  • multiple recurrences of any type of HSV keratitis (especially stromal)
  • recurrent inflammation with scar/vascularization near visual axis
  • more than one episode of HSV keratitis with ulceration
  • post-keratoplasty performed for HSV-related scarring/astigmatism
  • postop in patients with a history of HSV ocular disease undergoing any type of ocular surgery
  • in patients with a history of ocular HSV during immunosuppressive treatment
406
Q

what is the mainstay of therapy for HZV (shingles)?

A

oral antivirals

Ocular Pharmacology (4 decks)

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