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Ocular Pharmacology > Midterm 2 > Flashcards

Midterm 2 Flashcards

1
Q

Biochemical properties of sodium fluorescein stain

A
  • emits energy green wavelength when it comes down from its high energy state
  • synthetic organic compound available as a dark orange water-soluble dye
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2
Q

When is sodium fluorescein stain used?

A
  • diagnostic agent in eyecare
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3
Q

Factors that affect fluorescence of NaFl

A
  • concentration (>2% will not glow)
  • pH of solution (increased fluorescence with increased pH)
  • intensity and wavelength of absorbed light
  • maximum intensity obtained by use of cobalt blue filter over high intensity white light
  • Wratten filter between blue light and our eyes maximizes the view of stained areas
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4
Q

Does sodium fluorescein stain tissue?

A

No, it’s water soluble so it colors tears. Only stains tissues if overlying tissue is damaged (corneal ulcer)

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5
Q

What is the molecular weight of regular sodium fluorescein stain?

A

367.27, which is smaller than pores in hydrogel lenses

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6
Q

What is the molecular weight of high molecular weight fluorescein?

A

710, which may be used with SCL

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7
Q

What is the mechanism by which sodium fluorescein stains the cornea?

A
  • normal corneal epithelium is impermeable to tears and polar compounds like fluorescein
  • corneal epithelial defects allow the tears (stained with fluorescein) to access deeper layers, and eventually can diffuse through hydrophilic stroma and into the AC
  • epithelial defects “stain” bright green
  • fluorescein will not stain devitalized (sick) cells
  • can produce pseudo-flare, Fischer Schweitzer mosaic, when you put pressure on the closed lid to give the pattern
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8
Q

Composition of fluorescein sodium

A

2%; 1, 2, 15 ml

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9
Q

Composition of Fluress, which we don’t typically use if really assessing corneal health

A

0.25% with 0.4% benoxinate Hcl boric acid povidine 1% chlorobutonal; 5mL

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10
Q

Composition of fluorocaine

A

0.25% with 0.5% proparacaine Hcl with thimerosal

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11
Q

Composition of Proparacaine Fluorescein (B&L)

A

0.25% with 0.5% proparacaine Hcl

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12
Q

Composition of Ful-Glo strips

A

0.6 mg sterile

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13
Q

Composition of Fluor-I strip

A

9mg with buffers; 0.5% chlorobutonal polysorbate

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14
Q

Composition of Fluor-I-strip-A.T.

A

1 mg with buffers; 0.5% chlorobutonal polysorbate

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15
Q

Composition of Fluorets strips

A

1 mg

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16
Q

Composition of Fluoresoft strips

A

0.35% in 0.5 mL pipettes

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17
Q

Is sodium fluorescein at a greater risk of contamination than majority of other eye drops?

A

Yes, but not the case with combo anesthetic fluorescein

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18
Q

Why is sodium fluorescein at serious risk of contamination?

A

It’s typically used in situations in which tissue is damaged

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19
Q

What is the most dangerous and common contaminant in sodium fluorescein?

A

Pseudomonas aeruginosa

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20
Q

What is the best preservative for NaFl?

A

Thimerosol

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21
Q

What is the safest form of using sodium fluorescein?

A

sterile, single-dose units of solution OR sterile fluorescein-impregnated paper strips

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22
Q

Clinical uses of topical fluoresceine dye (5)

A
  • assessment of ocular surface integrity: detect defects in corneal epithelium
  • fitting/assessment of rigid contact lenses
  • applanation tonometry
  • Seidel’s test (detection of globe perforation)
  • testing the lacrimal system (tear film integrity, nasolacrimal system function)
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23
Q

Does fluorescein penetrate an intact corneal epithelium?

A

No

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24
Q

How does fluorescein staining take place with a break in the corneal epithelium?

A
  • penetration of fluorescein in adjoining bowman’s and stromal layer
  • dye makes contact with an alkaline interstitial fluid (stroma has higher pH)
  • fluid turns bright green owing to its pH indicator properties and depending to extent of lesion
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25
Q

What other two purposes does fluorescein stain serve in optometry?

A

rigid contact lens assessment/fitting and Goldmann tonometry

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26
Q

What is Seidel’s test/sign?

A

the aqueous coming out of a penetrating corneal laceration that appears dark in an overall green system

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27
Q

Can you use fluorescein for corneal and conjunctiva staining?

A

Yes

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28
Q

definition of epiphora

A

overflow of tears onto face

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29
Q

Where can tear drainage problems/obstructions occur?

A
  • puncta
  • canaliculus
  • nasolacrimal duct
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30
Q

How to perform and grade Jones Test 1

A
  • instill fluorescein; swab inside nose
  • positive = presence of dye (no obstruction)
  • negative = no presence of dye (partial or absolute obstruction OR poor tear pump)
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31
Q

How to perform and grade Jones Test 2

A
  • done after negative Jones 1 test
  • use syringe to flush residual fluorescein from lacrimal sac
  • positive = dye recovered (partial obstruction aka functional obstruction)
  • negative = no dye recovered (complete obstruction)
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32
Q

What is fluorescein angiography and why do we use it?

A
  • invasive procedure in which sodium fluorescein is injected IV followed by serial fundus photography
  • used to document retinal blood flow and integrity of blood vessels
  • diagnostic tool in choroidal and retinal disease
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33
Q

Adverse reactions to FA

A
  • nausea
  • emesis
  • urticaria
  • syncope
  • extravasation of dye
  • anaphylaxis (1 in 300,000)
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34
Q

Procedure of FA

A
  • take red-free pictures
  • replace red-free filter with barrier filter
  • inject fluorescein dye as a bolus
  • start timer
  • insert exciter filter
  • begin shooting at first sign of choroidal flush
  • shoot every 1-2 seconds during transition
  • late photos as needed
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35
Q

Normal FA time frame

A
  • choroidal phase (8-12 sec)
  • retinal circulation - arterial, capillary, venous, recirculation phases
  • elimination phase
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36
Q

What do you see during choroidal phase of FA?

A

“choroidal flush” with choroid beginning to fill - patchy dark retinal vessels

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37
Q

What do you see during retinal arterial phase (10-13 sec)?

A

fluorescein begins to fill the arteries, veins appear dark

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38
Q

What do you see during retinal capillary phase (12-15 sec)?

A
  • arterioles are filled and beginning to see veins fill - bright sides and then fill
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39
Q

What do you see during retinal venous phase (13-17 sec)?

A

sometimes it’s hard to tell because veins have slightly more brightness than arteries, but all blood vessels appear white

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40
Q

What do you see during retinal recirculation phase?

A

overall glow starts to diminish

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41
Q

What do you see during elimination phase of FA?

A

all sodium fluorescein out of retinal vessels but will see NaFl if blood vessels are broken

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42
Q

What is the yellow pigment that limits the amount of blue light that enters the macula?

A

Xanthophyll

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43
Q

What could cause pre-injection fluorescence? (Why we take pictures before injection)

A

optic disc drusen fluoresce with filter

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44
Q

What are some pathological reasons we would see hyper-fluorescence in FA?

A
  • abnormal vessels from diabetes, choroidal neovascularization, and squiggly vessels from RVO
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45
Q

What are some reasons we would see hypofluorescence?

A
  • blocking defect - there’s fluorescein there, but we can’t see it
  • filling defect - blood vessels have issues with blood flowing through
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46
Q

Strategies for interpretation of FA

A
  • look for pre-injection fluorescence to ensure no auto-/pseudo-fluorescence
  • determine areas of hypo- and hyper- fluorescence
  • if hypo-, is it due to blocking or delayed/absent filling?
  • if hyper-, is it transmission defect, abnormal vessel, or leakage?
  • match findings to specific disease process
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47
Q

Properties of rose bengal stain

A
  • red/rose colored derivative of fluorescein but DOES NOT FLUORESCE
  • water soluble red powder
  • will stain cell membrane of dead (devitalized) cells - different from fluorescein
  • TRUE histological stain that binds to selective cellular components
  • also stains mucous and corneal filaments
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48
Q

Should you use anesthetic when using rose bengal?

A

Yes it stings and irritates the cornea

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49
Q

Indications to stain with rose bengal (3)

A
  • toxic keratitis
  • dry eye - classic conjunctiva and cornea staining
  • herpes simplex dendritic keratitis
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50
Q

Properties of lissamine green stain

A
  • vital stain very similar to rose bengal
  • much more comfortable on instillation
  • similar uses to rose bengal
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51
Q

When is trypan blue stain used?

A
  • testing the health of endothelium in corneal grafts

- used to stain the anterior lens capsule in certain cataract surgery cases

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52
Q

What is Indocyanine green stain and what can it be used for?

A
  • water soluble tricarbocyanine dye
  • rapidly and completely bound to plasma proteins after IV injection
  • fluoresces in the infrared spectrum
  • in eye care, can be used in fundus angiography
  • can be used in retinal surgeries to identify the inner limiting membrane
    contraindication: Iodine allergy
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53
Q

Is inflammation good in the cornea?

A

Not really, it can cause opacities with scarring

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54
Q

What does inflammation do in the body?

A
  • destroys invading pathogen
  • removes dead tissue
  • replaces damaged tissue with scar tissue (fibrosis)
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55
Q

What do steroids do in eye care?

A
  • control inflammation of anterior and posterior segments of the eye
  • help prevent sequelae of inflammation on ocular structure
  • typically used in ACUTE conditions
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56
Q

Pharmacology of corticosteroids: (how they affect the immune system)

A

Affect almost every aspect of the immune response

  • inhibit neutrophil migration
  • inhibit MQ access to inflammation site
  • interfere with lymphocyte activity
  • reduce number of T- and B- lymphocytes
  • block histamine synthesis
  • stabilize mast cells
  • block arachidonic acid release
  • influence tissue repair (decrease cap proliferation and decrease collagen deposition)
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57
Q

Indications for steroids in eye care

A

severe infections ONCE THE INFECTION HAS BEGUN TO RESOLVE and under carefully controlled situation

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58
Q

Can we use steroids in adenovirus eye disease?

A

Yes, it may prolong the infection, but the patient feels better

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59
Q

Can we use steroids in HSK epithelial disease?

A

NOOOOO!!!!!!!!

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60
Q

Can we use steroids in HSK stromal/disciform disease?

A

Yes, but with concurrent antiviral and they must be tapered VERY slowly

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61
Q

Can we use steroids with HZV?

A

Yes

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62
Q

Can we use steroids while treating bacterial eye disease?

A

Yes, staph organisms can produce secondary inflammation with exotoxins that can cause marginal ulcers and phlyctenules; must also address the underlying problem (can use combo gtts)

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63
Q

Can we use steroids to treat bacterial corneal ulcers?

A
  • it depends
  • for those with VA of CF or worse and those with central ulcers, adding a steroid to the Ab regimen showed a statistically significant improvement in prognosis
  • otherwise may not be necessary
  • no safety concerns
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64
Q

Can we use steroids in acanthamoeba and fungal keratitis?

A

NOOO!!!

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65
Q

What is the hallmark sign of acanthamoeba?

A

ring infiltrate

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66
Q

How to treat dermatologic manifestation of allergies around the eyes?

A
  • triamcinolone 0.1% cream
  • tell the patient to keep out of their eyes
  • long-term steroid creams can thin the skin so be cognizant
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67
Q

What do corticosteroids do in uveitis treatment? (3)

A
  • reduce inflammation
  • help relieve pain (with cycloplegics)
  • help prevent posterior synechiae
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68
Q

What type of steroid would we use to treat episcleritis (mild, moderate, heavy)?

A

Mild

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69
Q

What type of steroid would we use to treat scleritis?

A
  • doesn’t respond well to steroids

- NSAID may be better

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70
Q

What other “-itis” conditions can we treat with steroids?

A
  • pingueculitis

- inflamed pterygium

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71
Q

How are steroids used in post-op care for cataract surgery?

A
  • decreases risk of post-op cystoid macular degeneration (NSAIDs may be better)
  • reduces inflammation and pain
  • decreases corneal edema
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72
Q

How are steroids used in post-op care for refractive corneal surgery?

A
  • reduces myopic regression and corneal haze (PRK)
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73
Q

ocular side effects of topical steroid therapy

A
  • cataract
  • ocular hypertension/glaucoma
  • infection
  • delayed corneal epithelial healing
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74
Q

Do posterior subcapsular cataracts occur more frequently with systemic or topical steroid use?

A

Systemic

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75
Q

Why are posterior subcapsular cataracts so visually debilitating?

A

they are near the nodal point and on the visual axis

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76
Q

How long does an adult have to be on a steroid before a PSC appears?

A

at least 1 year

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77
Q

Does steroid-induced glaucoma occur more frequently with topical or systemic steroid use?

A

Topical, but also common with nasally administered steroid

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78
Q

When does increased IOP occur after using a steroid?

A

usually occurs within 2-8 weeks of initiation of therapy

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79
Q

Is increased IOP secondary to steroid use reversible with drug cessation?

A

Yes, typically

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80
Q

Armaly and Becker study found what regarding steroid-induced glaucoma?

A
  • steroid response is likely genetically determined

- different steroids are more/less likely to cause elevated IOP

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81
Q

What steroid drops are more likely to cause elevated IOP?

A
  • dexamethasone
  • difluprednate
  • prednisolone
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82
Q

What steroid drops are less likely to cause elevated IOP?

A
  • loteprednol
  • rimexolone
  • fluorometholone
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83
Q

What is the mechanism that causes decreased IOP in uveitis?

A

ciliary body shuts down so less aqueous is produced

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84
Q

What is the mechanism that causes increased IOP in uveitis?

A
  • trabeculitis (resistance to outflow)
  • cellular debris clogs the TM
  • posterior or anterior synechiae
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85
Q

Clinical pearls for prescribing steroids

A
  • NEVER prescribe a steroid without measuring IOP first
  • ALWAYS measure IOP on follow-up for patients on steroid
  • NEVER allow refills of steroids unless IOP is routinely checked
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86
Q

Do patients with glaucoma tend to be steroid responders?

A

Yes

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87
Q

What are complications of steroid use with infection? (4)

A
  • they lower patient resistance to infection
  • masks symptoms of disease
  • prolongs course of HSV
  • enhances ocular susceptibility to fungal infection
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88
Q

Principles of corticosteroid therapy

A
  • the type/location of inflammation determine the route of administration
  • dosage must be appropriate, reviewed, and modified during therapy according to the response
  • LONG TERM, HIGH DOSE therapy should be tapered rather than discontinued abruptly to avoid rebound inflammation
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89
Q

What ophthalmic preparations of steroids are best when corneal epithelium is intact?

A

acetate and alcohol

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90
Q

What ophthalmic preparation of a steroid is better to use if the corneal epithelium is damaged?

A

Phosphate

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91
Q

In general, which preparation(s) is/are better for topical corticosteroids?

A

acetates and alcohols

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92
Q

What are the topical ophthalmic corticosteroid agents?

A
  • prednisolone
  • dexamethasone
  • difluprednate
  • fluorometholone
  • loteprednol etabonate
  • rimexolone
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93
Q

What is the gold standard topical steroid?

A
  • Prednisolone acetate 1% (PredForte)

- have to shake because it’s a suspension - tell the patient to shake 100X

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94
Q

Properties of dexamethasone (3)

A
  • not well-metabolized once in AC
  • very good anti-inflammatory properties - very strong steroid
  • HIGHER INCIDENCE OF ELEVATED IOP compared to prednisolone acetate
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95
Q

What combo drops include dexamethasone?

A
  • Maxitrol (polymyxin B, neomycin) - ointment AND solution AND generic; Dr. Marrelli doesn’t like because patient can have high IOP and contact dermatitis with neomycin
  • Tobradex (tobramycin) - ointment (brand) AND solution (brand/generic) - is the #1 Ab/steroid combo drop, these become problematic when considering tapering
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96
Q

Properties of difluprednate (5)

A
  • newest ophthalmic steroid
  • VERY POTENT ketone steroid (more likely to increase IOP than ester steroid), formulated in emulsion
  • HIGHER INCIDENCE OF IOP ELEVATION than prednisolone acetate
  • Durezol 0.5% emulsion
  • can be dosed less often than prednisolone acetate 1%
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97
Q

Properties of fluorometholone (FML) (3)

A
  • structurally unrelated to prednisolone or dexamethasone
  • available as alcohol 0.1% suspension or ointment, 0.25% suspension (FML Forte), acetate 0.1% suspension (Flarex)
  • generally considered a “weaker” steroid; reasonable for external inflammation (lids, conj, episcleral, etc.)
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98
Q

Properties of loteprednol etabonate (4)

A
  • ester-based
  • site-specific steroid aka “soft” steroid = rapid metabolism
  • originally considered to be equivalent in anti-inflammatory properties to prednisolone acetate, now thought to be somewhat less effective but still good efficacy
  • SIGNIFICANTLY REDUCED POTENTIAL to cause elevated IOP than prednisolone acetate 1%
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99
Q

Brand names and formulations for Loteprednol Etabonate (6)

A
  • Lotemax 0.5% ointment, and generic suspension
  • Lotemax 0.5% gel drops (brand only)
  • Lotemax SM 0.38% gel drops (brand only)
  • Inveltys 1% suspension (brand only)
  • Alrex 0.2% suspension for allergies
  • Zylet 0.5% combination with tobramycin
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100
Q

What is Lotemax FDA approved for and dosing?

A

TID dosing for post-surgical inflammation

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101
Q

What is Inveltys used for and its dosing?

A

BID dosing for post-op inflammation

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102
Q

Is Rimexolone (Vexol 1%) still available?

A

No

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103
Q

List the topical steroids from highest chance of increasing IOP to lowest chance of increasing IOP

A

Dexamethasone, difluprednate, prednisolone, loteprednol, fluorometholone

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104
Q

What is the mechanism that causes decreased IOP in uveitis?

A

ciliary body shuts down, which leads to less aqueous being produced

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105
Q

What are the mechanisms that cause an increased IOP in uveitis?

A
  • trabeculitis, leading to resistance to outflow
  • cellular debris clogging trabecular meshwork
  • posterior or anterior synechiae
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106
Q

What are some of the golden rules to keep in mind when prescribing a steroid? (3)

A
  • NEVER prescribe a steroid without measuring IOP first
  • ALWAYS measure IOP on follow-up for patients on steroid
  • NEVER allow refills of steroids, unless IOP is routinely checked
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107
Q

What should you do if patient has elevated IOP that is intolerable?

A

Add IOP-lowering therapy

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108
Q

How do steroids affect infections? (4)

A
  • masks symptoms of disease
  • prolongs the course of HSV
  • enhances ocular susceptibility to fungal infection
  • may reduce scarring in the cornea
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109
Q

When should a steroid be tapered?

A

When it’s been used at high doses long-term

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110
Q

Which steroid bases have better penetration if the corneal epithelium is intact?

A

Alcohols and acetates

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111
Q

Which steroid bases have better penetration if the corneal epithelium is compromised?

A

phosphates

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112
Q

Which bases of steroids have better efficacy?

A

Acetates and alcohols

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113
Q

What formulations are phosphate-based steroids?

A

Solutions

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114
Q

What formulations are acetate-based steroids?

A

Suspensions

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115
Q

What formulations are alcohol-based steroids?

A

Either suspensions or solutions

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116
Q

Which steroid probably has the most flexibility according to Dr. Marrelli?

A

Prednisolone (she loves this drug)

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117
Q

What are some characteristics of prednisolone? (2)

A
  • synthetic analog of hydrocortisone

- available in acetate (suspension) and phosphate (solution) formulations

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118
Q

What are the formulations of prednisolone that we can prescribe? (3)

A
  • prednisolone acetate 1% suspension (PredForte): brand is better than generic because it has smaller, more uniform, particle size
  • prednisolone acetate 0.125% suspension (PredMild): no generic available
  • prednisolone phosphate 1% solution: generic only, but not used very often
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119
Q

What are some characteristics of dexamethasone? (3)

A
  • not well-metabolized once it enters the anterior chamber
  • very good anti-inflammatory properties - very strong steroid
  • HIGHER INCIDENCE OF ELEVATED IOP compared to prednisolone acetate
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120
Q

What are some formulations that we can prescribe of dexamethasone? (3)

A
  • dexamethasone 0.1% alcohol suspension (Maxidex): available as a generic
  • Maxitrol (with polymyxin B and neomycin): ointment and solution, brand and generic (Dr. Marrelli doesn’t like high chance of IOP increase with chance of contact dermatitis with Neo)
  • Tobradex (with tobramycin): ointment (brand) and solution (brand/generic)
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121
Q

What are some characteristics of difluprednate? (4)

A
  • newest ophthalmic steroid
  • VERY potent ketone steroid, formulated in emulsion, so no shaking required
  • HIGHER INCIDENCE OF IOP ELEVATION than prednisolone acetate
  • can be dosed less often than prednisolone acetate 1% by about half
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122
Q

What is the formulation we can prescribe of difluprednate?

A

Durezol 0.5% emulsion

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123
Q

What are some characteristics of fluorometholone? (2)

A
  • structurally unrelated to prednisolone or dexamethasone

- generally considered a “weaker’ steroid; reasonable for external inflammation (lids, conj, episcleral, etc.)

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124
Q

What formulations of fluorometholone can we prescribe? (3)

A
  • FML 0.1% alcohol (FML and generic, suspension or oinment)
  • FML 0.25% suspension (FML Forte): clinically not more anti-inflammatory effect, just more potential to raise IOP
  • FML 0.1% acetate suspension (Flarex): has better corneal penetration to reach AC
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125
Q

What are some characteristics of loteprednol etabonate? (3)

A
  • ester-based steroid
  • “site-specific” steroid aka “soft” steroid = rapid metabolism
  • originally considered to be equivalent in anti-inflammatory properties to prednisolone acetate, now thought to be somewhat less effective (but still good)
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126
Q

What formulations of Loteprednol etabonate can we prescribe? (6)

A
  • Lotemax 0.5% ointment, and generic suspension
  • Lotemax 0.5% gel drops (brand only)
  • Lotemax SM 0.38% gel drops (brand only): TID dosing for post-op inflammation
  • Inveltys 1% suspension (brand only): BID dosing for post-op inflammation; nanoparticles with mucus-penetrating attributes for enhanced penetration through mucus barriers
  • Alrex 0.2% suspension: allergies
  • Zylet (0.5% loteprednol with tobramycin)
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127
Q

Reminder to go through the slides to find

A

Her list of steroid drugs that will probably be used on a prescription writing question

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128
Q

What side effect is most common with topical steroids?

A

increased IOP

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129
Q

What ocular side effect is more common with systemic steroids?

A

cataracts

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130
Q

What are some examples of local steroid injections? (3)

A
  • periocular injections for chronic uveitis, cystoid macular edema
  • intralesional injection of chalazion
  • intravitreal injections and implants for macular edema, posterior noninfectious uveitis
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131
Q

What are some side effects of systemic steroid therapy? (8)

A
  • adrenal insufficiency (Addison’s)
  • cushings syndrome
  • peptic ulcer disease
  • osteoporosis
  • systemic hypertension
  • diabetes/hyperglycemia
  • infection (opportunistic pathogens)
  • psychiatric changes: can be pretty severe, insomnia
132
Q

Symptoms of Cushing’s disease (5)

A
  • weight gain (especially in the trunk)
  • HTN
  • “moon face”
  • hyperglycemia
  • a fat pad on the back
133
Q

Symptoms of Addison’s disease (5)

A
  • weight loss
  • low blood pressure
  • hypoglycemia
  • fatigue
  • skin hyperpigmentation
134
Q

What are the benefits to alternate day therapy for steroid use?

A

avoids adrenal suppression and steroid dependence (Addisons)

135
Q

Oral steroids are safe for SHORT term use IF (4)

A
  • NO GI disease (peptic ulcer disease: NO!)
  • no psychiatric illness
  • no hypertension
  • no diabetes
136
Q

What are some characteristics of oral methylprednisolone? (4)

A
  • high potency
  • convenient: automatically tapers over 6 days of therapy
  • inexpensive
  • relatively safe
137
Q

What are some precautions when taking oral methylprednisolone?

A
  • take with food or milk to avoid GI upset

- avoid in diabetes, gastric ulcer patients, hypertension, psychiatric patients

138
Q

When and why would we use systemic steroids?

A
  • severe inflammation of posterior segment, orbit, and optic nerve: scleritis, uveitis, inflammatory orbital pseudotumor, GCA (can cause CRAO), optic neuritis, thyroid eye disease
  • severe dermatologic manifestations: periocular insect bite, acute allergic blepharodermatoconjunctivitis
  • Bell’s palsy: CN VII pass through canal in temporal bone, where inflammation produces a compressed neuropathy
139
Q

Differentials of Bell’s palsy (4)

A
  • infectious (lyme, HZV)
  • autoimmune (Guillain-Barre, sarcoidosis)
  • tumor
  • stroke
140
Q

How to diagnose Bell’s palsy

A
  • often preceded by postauricular pain, dysgeusia, and hyperacusis
  • acute onset that progresses to complete facial hemispheres within 72 hours (slower progression than stroke)
  • involves whole half of face, stroke involves lower quadrant often
141
Q

How to treat Bell’s palsy

A
  • oral prednisone 50-60mg/day for 10 days, followed by taper for 5 days (taper by 10mg/day)
  • oral antivirals, not sure if really effective
  • PROTECT ocular surface with lubricants, patch, tape, etc. while waiting for recovery
142
Q

What do mast cells release when they degranulate? (8)

A
  • histamine
  • tryptase
  • prostaglandin D2
  • leukotrienes
  • eosinophilic chemotactic factors
  • platelet-activating factors
  • proteases
  • cytokines
143
Q

Type I (humoral) hypersensitivity

A
  • allergen activates B-lymphocyte; IgE binds to mast cells and basophils (sensitization)
  • cell membrane now more permeable to calcium ions; calcium influx triggers phospholipase A2 in mast cells
  • mast cell degranulates
144
Q

What are the components of allergic response? (6)

A
  • itching - hallmark
  • tearing
  • mucus production
  • conjunctival vasodilation
  • increased vascular permeability
  • papillary hypertrophy
145
Q

Type 1 Reaction (SAC, PAC)

A
  • occurs minutes to hours after exposure with immediate phase (5-30 min) and late phase (4-6 hours, lasts 2 days)
  • histamine release: benign - rhinitis/itching/sneezing/tearing or life-threatening - anaphylaxis
146
Q

Type 4 (delayed, cell-mediated) reaction

A
  • delayed onset of 12-72 hours after exposure mediated by activated T-cells
  • cytokines, IL, and interferon activate macrophages - cytotoxic, phagocytic, and lytic
147
Q

What is the primary chemical mediator in SAC/PAC?

A

histamine

148
Q

What is the most common form of ocular allergy?

A

seasonal allergic conjunctivitis

149
Q

SAC is often associated with

A

rhinitis and itchy throat

150
Q

Is there permanent tissue damage with histamine release in SAC?

A

No

151
Q

Signs of SAC

A
  • lid swelling (ptosis)
  • conjunctival hyperemia
  • conjunctival chemosis
  • papillary reaction
  • diagnosis is usually clinical
152
Q

VKC

A
  • a combo of Type 1 and Type 4 hypersensitivities
  • in addition to histamine, mediated by eosinophils (permanent tissue changes)
  • rare in patients <3 or >25 yo
  • males : females, 2:1
  • last 4-10 years, then resolves
  • more common in Mediterranean, central Africa, South America areas
  • associated with atopy history in 15-60%
153
Q

What are the 3 types of VKC?

A
  • limbal
  • tarsal (similar to GPC presentation)
  • mixed
154
Q

Is VKC usually bilateral and is it seasonal

A
  • usually bilateral

- most cases are seasonal or with seasonal exacerbations

155
Q

Symptoms of VKC (7)

A
  • itching
  • tearing
  • mucus production - lots of strands
  • photophobia
  • burning
  • blepharospasm
  • blurred vision (corneal molding)
156
Q

signs of VKC (7)

A
  • papillary reaction (inc GPC)
  • conjunctival hyperemia/edema
  • limbal gelatinous nodules
  • Trantas dots at the limbus
  • mucus discharge
  • conjunctival fibrosis
  • cornea: SPK, pannus, filaments, shield ulcer, keratoconus
157
Q

AKC (5)

A
  • combo response of Types 1 and 4 hypersensitivities
  • most severe form of ocular allergy
  • develops in up to 25% patients with allergic dermatitis
  • often have history of food allergies, hayfever, hives (atopy)
  • begins late teens/early 20s
158
Q

AKC symptoms

A
  • itching
  • tearing
  • watery discharge
  • burning
  • photophobia
  • blurred vision
159
Q

AKC signs (8)

A
  • tylosis
  • eyelid edema - permanent
  • derm signs (scaly, wrinkled skin)
  • Dennie-Morgan folds
  • upper lid ptosis
  • fissures @ lateral canthus
  • Hertoghe’s sign
  • marginal blepharitis
160
Q

Dennie- Morgan lines

A

the premature wrinkles under the eyes that patients with atopy get from their allergies

161
Q

Hertoghe’s sign

A

outer 1/3 of eyebrows are thin/gone

162
Q

Corneal signs of AKC

A
  • SPK, PEE
  • microcystic edema
  • corneal ulcer
  • pannus/neo extending to central cornea
  • keratoconus in 15-20% of AKC patients
163
Q

Lens signs of AKC

A
  • anterior subcapsular cataract

- posterior subcapsular cataract

164
Q

etiology of GPC

A
  • EW of contact lenses beyond FDA approval
  • exposed sutures
  • prosthesis
  • glaucoma surgery bleb
  • scleral buckle
165
Q

GPC symptoms

A
  • itching
  • FB sensation
  • lots and lots of mucus production
  • CL intolerance
166
Q

non-pharmacological recommendations for allergies

A
  • keep hands away from eyes, so not to disturb/burst open mast cells to release more histamine
  • keep windows closed in peak season
  • shampoo hair before bed
  • undress in room other than bedroom
  • use bed/mattress covers/frequent cleaning of bed and carpets for mites and dander
  • run AC if mold is a problem
  • high performance AC filters?
  • artificial tears to wash away antigen and histamine/mediators
  • saline rinse
  • cold compresses
  • avoid allergen
167
Q

Order of stepped approach for topical therapy for allergies

A
  • decongestants
  • antihistamines
  • mast cell stabilizers
  • NSAIDs
  • corticosteroids
  • immune therapy
168
Q

Order of stepped approach for oral therapy for allergies

A
  • antihistamines (may cause dry eyes)

- corticosteroids

169
Q

Characteristics of decongestants “vasoconstrictors” (8)

A
  • adrenergic agonists
  • available with or without an antihistamine
  • available OTC, inexpensive
  • typically only slightly effective
  • palliative only (doesn’t improve the allergic response)
  • tachyphylaxis - loses effect very quickly, so having to use more frequently
  • rebound hyperemia/inflammation
  • dosed BID - QID
170
Q

Available topical decongestants (4)

A
  • phenylephrine
  • naphazoline
  • oxymetazoline
  • tetrahydrazoline
171
Q

Side effects of topical decongestants (6)

A
  • stinging
  • pupillary dilation (primarily phenyl): not good for pts that are predisposed to angle closure
  • epithelial erosion
  • rebound congestion
  • follicular conjunctivitis
  • can affect cardiovascular system (sympathetic agonists)
172
Q

Contraindications of decongestants

A
  • narrow angles

- uncontrolled cardiovascular disease

173
Q

What is Upneeq?

A
  • oxymetazoline that has an affinity for Mueller’s muscle

- used to treat acquired ptosis

174
Q

Use of topical antihistamines (4)

A
  • decrease itching, decrease capillary dilation and permeability, decrease mucus production
  • may or may not decrease other symptoms (burning, pain)
  • can be very effective in acute reaction (unlike mast cell stabilizer)
  • not fast-acting enough to be useful in anaphylaxis
175
Q

First generation topical antihistamines

A
  • pheniramine maleate (Naphcon-A, Visine-A, Opcon-A)
  • antazoline phosphate (Vasocon-A)
  • both available only in combo with naphazoline; are OTC
  • dosed QID
176
Q

Second generation topical antihistamine and its characteristics

A
  • emedastine (Emadine 0.05% sol): significant decrease in itching and redness in 10 minutes, duration of 4-6 hours, dosed QID
  • selective H1-blockers, may also inhibit release of histamine and other mediators from mast cells
  • cost $130-150
177
Q

mast cell-stabilizing antihistamines (dual action) (6)

A
  • olopatadine (Patanol 0.1%, Pataday 0.2%, Pazeo 0.7%)
  • ketotifen (Zaditor 0.025%, Alaway, Claritin, Zyrtec)
  • azelastine (Optivar 0.05% sol, generic)
  • epinastine HCL (Elestat, and generic)
  • bepotastine (Bepreve)
  • alcaftadine (Lastacaft)
178
Q

Dosing of Patanol 0.1%

A
  • bid dosing, now called “Pataday Twice Daily Relief” (OTC)
179
Q

Dosing of Pataday 0.2%

A
  • once daily dosing
  • for severe symptoms, may need 2nd dose
  • now called “Pataday Once Daily Relief” (OTC)
180
Q

Dosing of Pazeo 0.7%

A
  • once daily dosing
  • RX ONLY
  • 4 mL = $200-300
181
Q

Characteristics of Ketotifen (Zaditor 0.025%, Alaway, Claritin, Zyrtec) (6)

A
  • definite mast cell stabilization
  • may decrease chemotaxis and action of eosinophils
  • rapid onset
  • BID dosing
  • OTC
  • cost ~ $10-15
182
Q

characteristics of azelastine (4)

A
  • very rapid relief
  • generic ~ $15
  • terrible taste in mouth
  • dosed bid
183
Q

Characteristics of epinastine hcl (Eleastat, and generic) (3)

A
  • dosed bid
  • $250 brand, $30 generic
  • less drying
184
Q

Characteristics of bepotastine (Bepreve) (2)

A
  • dosed bid

- $250

185
Q

Characteristics of alcaftadine (Lastacaft)

A
  • dosed ONCE daily

- $250

186
Q

Characteristics of Cetirizine (Zerviate) (6)

A
  • new topical antihistamine
  • same medication as in Zyrtec oral antihistamine
  • H1 antagonist
  • used bid (approx 8 hrs apart)
  • PRESCRIPTION ONLY
  • 30 single-use vials $200
187
Q

side effects of topical antihistamines

A

burning and stinging

188
Q

contraindications of topical antihistamines

A
  • possible to produce some mydriasis, so contraindicated in narrow angle patients (however very low risk)
189
Q

characteristics of mast cell stabilizers (7)

A
  • stabilize the mast cell from degranulation
  • may have other mechanisms
  • do not have an effect on histamine already released**
  • lag time of 1-3 weeks (not so with newer ones)
  • frequent dosing (qid+, except for newer ones)
  • typically well-tolerated
  • variable efficacy
190
Q

mast cell stabilizer drugs

A
  • cromolyn sodium (Crolom, Opticrom)
  • lodoxamid (Alomide)
  • nedocromil (Alocril)**
191
Q

dosing/cost of cromolyn sodium (Crolom, Opticrom)

A
  • qid

- only generics now $10

192
Q

lodoxamide (Alomide) cost, potency and dosing

A
  • $175
  • 2500X more potent!
  • qid
193
Q

nedocromil (Alocril)** cost, dosing, characteristics

A
  • $225
  • bid
  • multicellular action
  • quick decrease in symptoms
  • yellow color
194
Q

use/indications for NSAIDs

A
  • block prostaglandin synthesis
  • may have slight anesthetic effect
  • may decrease symptoms associated with inflammation
  • may rise “itch threshold”
195
Q

uses of corticosteroids in regards to allergies

A
  • typically reserved for severe cases (VKC, AKC, GPC)
  • may be of benefit in conjunction with other agents
  • loteprednol etabonate 0.2% (Alrex) is the only topical corticosteroid with FDA approval for ocular allergy; others may be used off-label
  • NOT ok for extended dosing
196
Q

Cyclosporine characteristics (4)

A
  • Cequa, Restasis
  • T-cell modulator that may have some value in allergies
  • primarily in AKC, VKC
  • NO FDA indication for allergic eye disease
197
Q

things to consider with oral antihistamines (3)

A
  • topical therapy is safer and more effective in most cases of ocular allergy
  • may be appropriate when other signs and symptoms are present (lid swelling, itchy throat, runny nose)
  • may actually exacerbate ocular symptoms (especially the more sedating ones)
198
Q

first generation antihistamines (2)

A
  • CNS depression/stimulation

- anticholinergic effects

199
Q

second generation antihistamines (2)

A
  • less dry mouth/blurred vision

- longer elimination time (less frequent dosing)

200
Q

clinical uses of systemic antihistamines

A
  • nasal and conjunctival itching, sneezing, coughing
  • rhinitis
  • eyelid edema
  • urticaria
201
Q

benefit of using topical antihistamine for ocular allergies

A

more direct and rapid effect on ocular surface

202
Q

side effects of oral antihistamines (9)

A
  • sedation
  • dizziness
  • tinnitus
  • blurred vision
  • anxiety
  • insomnia
  • tremor
  • dry mouth
  • GI upset
203
Q

First generation oral antihistamines in order from least to most sedating

A
  • chlorpheniramine
  • clemastine
  • diphenhydramine, promethazine
204
Q

fexofenadine (Allegra) OTC dosing for children aged 12 and over

A

180 mg qd

205
Q

fexofenadine (Allegra) OTC dosing for children aged 2-11

A
  • 30 mg bid
  • 30 mg rapid dissolve tab and regular tabs for aged 6-11;
  • 30 mg/5mL oral suspension for 2-11 years
206
Q

fexofenadine (Allegra) dosing for 6 months - under 2 years

A
  • 15 mg bid

- unsure if this is OTC

207
Q

Allegra-D

A

fexofenadine with pseudoephedrine

208
Q

Cetirizine (Zyrtec) dosing for adults and children 6 years and older

A
  • 10 mg/day
209
Q

Cetirizine (Zyrtec) dosing for children aged 2-5

A
  • 2.5 mg/day

- MAXIMUM 5 mg/day (single or divided)

210
Q

Cetirizine (Zyrtec) dosing for children 6 months - under 2 years

A
  • 2.5 mg/day

- MAXIMUM 5 mg/day DIVIDED

211
Q

Available forms of Cetirizine (Zyrtec)

A
  • 5 mg, 10 mg tablets
  • 5 mg, 10 mg chewable tablets
  • 1 mg/mL oral syrup
212
Q

What is the minimum age Zyrtec-D should be given?

A

12 years

213
Q

What is the dosing for Desloratadine (Clarinex) for adults and children 12 years and older?

A

5 mg QD

214
Q

Desloratadine (Clarinex) dosing for children 6-11 years

A
  • 2.5 mg per day
215
Q

Desloratadine (Clarinex) dosing for children 12 months to 5 years

A

1.25 mg per day

216
Q

Desloratadine (Clarinex) dosing 6-11 months

A

1 mg per day

217
Q

Available forms of Desloratadine (Clarinex)

A
  • 5 mg tabs
  • 5 mg, 2.5 mg redi-tabs (oral dissolving)
  • syrup 2.5mg/5mL
  • Clarinex-D: with pseudoephedrine
218
Q

Loratadine (Claritin) minimum age to take

A

2 years

219
Q

Available forms of Loratadine (Claritin)

A
  • 10 mg tabs
  • 10 mg liquigels
  • syrup 5mg/5mL
  • adult and children red-tabs - 10 mg once daily or 5 mg twice daily
  • children chewable tabs 5 mg once daily
  • claritin-D: with pseudoephedrine
220
Q

Side effects of oral antihistamines

A
  • sedation (worse with alcohol)
  • palpitations
  • drying of secretions
  • GI disturbance
  • dry eye
  • mydriasis
  • decreased accommodation
221
Q

Contraindications of oral antihistamines

A
  • 1st and 3rd trimester pregnancy
  • nursing mother
  • strong anticholinergic H-1 blockers: peptic ulcer disease, prostate hypertrophy, bladder obstruction, narrow angles
222
Q

Different types of pain

A
  • acute
  • chronic
  • neuropathic: from diseases of the nerves or injury to nerves
  • syndrome pain
223
Q

Most ocular pain is ____

A

Acute

224
Q

physiological effects of pain

A
  • tachycardia
  • systemic hypertension
  • tachypnea
  • exacerbation of pre-existing cardiovascular disease
225
Q

psychological effects of pain

A
  • poor sleep patterns
  • anxiety/depression
  • uncooperativeness
226
Q

What do neurons release upon pain?

A

Substance P

227
Q

What does substance P stimulate?

A

mast cells and blood vessels

228
Q

What is the ascending pathway of pain?

A
  • nociceptors on afferent nerve endings send AP to dorsal horn of SC
  • alpha-delta fibers: sharp localized pain (somatic pain); activated by chemical, thermal or mechanical stimuli (most eye pain)
  • C-fibers: dull, diffuse, aching pain (visceral pain); stimulated by bradykinin and prostaglandins
  • alpha-delta and C-fibers release substances in dorsal horn of SC that activate secondary neurons (from ascending spinothalamic pathway) –> thalamus –> third order neuron to somatosensory cortex
229
Q

Descending pathway of pain

A
  • starts in midbrain/medulla –> dorsal horn

- release NE, 5-HT, and endogenous opioid NTs; inhibit ascending pathway activity

230
Q

Reminder to look at slides

A

For the pain pathway picture

231
Q

Three categories of analgesics

A
  • opioid
  • non-opioid
  • analgesics used to treat specific pain syndromes
232
Q

opioid terminology (3)

A
  • narcotic: term that refers to opioids; a drug that produces a stuporous, sleeplike state (may or may not relieve pain)
  • opiates: refers to drugs specifically isolated from poppy (morphine and codein)
  • opioids: compounds of any type that interact with opioid receptors (3 types of receptors)
233
Q

non-opioid analgesic characteristics (3)

A
  • work on nociceptor pain (peripheral part of pain response)
  • includes NSAIDs which have analgesic, antipyretic, and anti-inflammatory properties
  • also includes acetaminophen (no anti-inflammatory properties)
234
Q

analgesics used to treat specific pain syndromes

A

treat neuropathic pain, migraine, gout, etc.

235
Q

peripheral agents: NSAIDs properties (3)

A
  • act on peripheral pain receptors and prevent sensitization/discharge of nociceptors
  • do not produce tolerance/dependence
  • good for mild to moderate pain
236
Q

what is the mechanism of acetaminophen?

A
  • not really known but similar to NSAIDs but may only work in the CNS
237
Q

characteristics of central agents/opioids

A

interact with specific receptors in the CNS - interrupt pain message and its emotional response

238
Q

peripherally acting agents characteristics (2)

A
  • prevent sensitization and discharge of nociceptors
  • NSAIDs (including aspirin) block the formation of inflammatory and pain mediation (prostaglandins) at the cyclooxygenase pathway
    NSAID shave analgesic, anti-inflammatory and anti-pyretic properties
239
Q

reminder to look at the slides for

A

the inflammatory cascade and where NSAIDs work

240
Q

What do both COX enzymes produce?

A

prostaglandins that contribute to pain, fever and inflammation

241
Q

What does COX-1 enzyme produce and what type of enzyme is it?

A
  • prostaglandins that activate platelets and that protect the stomach and intestinal lining
  • constitutive enzyme
242
Q

What does COX-2 enzyme produce and what type of enzyme is it?

A
  • responsible for production of prostanoid mediators of inflammation (prostaglandins, prostacyclins, thromboxane)
  • inducible enzyme
243
Q

salicylate characteristics (3)

A
  • non-specific cyclooxygenase blocker
  • clot prevention vs analgesic vs anti-inflammatory doses
  • acetylated vs non-acetylated
244
Q

Why was non-acetylated salicylic acid developed?

A

to reduce GI upset and GI bleeding

245
Q

ASA (aspirin) characteristics (5)

A
  • irreversibly block platelets (75 mg qd)
  • best for use as an anti-coagulant
  • none are safe in potential “bleeders”
  • adult dose is 325-650 mg every 4 hours (not more than 4 g/d) for pain/inflammation
  • take with food, full glass of water
246
Q

non-selective NSAIDs other than ASA characteristics (5)

A
  • less bleeding potential
  • less GI upset
  • greater efficacy compared to ASA
  • all have same efficacy in comparable doses
  • all have similar side effects
247
Q

comparable doses of non-selective NSAIDs

A
  • diclofenac 50mg qid
  • ibuprofen 800mg qid
  • naproxen sodium 220mg bid-tid
  • ketoprofen 300mg/day
248
Q

comparable doses of cox-2 inhibitors

A
  • celecoxib/celebrex 200mg bid
249
Q

NSAID side effects/adverse effects

A
  • inhibit platelets (only ASA is irreversible)
  • GI upset
  • GI bleeding/ulcer/perforation
  • increased risk of serious cardiovascular thrombotic events (heart attack/stroke) - FDA increased warnings in 2015
250
Q

Use NSAIDs with caution in patients with which pre-existing conditions? (7)

A
  • asthmatics/nasal polyps: aspirin-induced respiratory disease or aspirin-induced asthma
  • hypersensitivity (allergic to whole class)
  • diabetics: risk of increased protein binding in Type 2 and risk of renal insufficiency
  • children with fever, chicken pox, flu-like symptoms: NO ASA
  • avoid in pregnant/nursing mother
  • avoid in patients with GI problems
  • avoid in bleeding disorders, vitamin K deficiency, anticoagulant therapy
251
Q

max dosing for ibuprofen

A

800mg qid (3200mg/day)

252
Q

ophthalmic NSAIDs

A
  • ketorolac tromethamine
  • nepafenac
  • diclofenac
  • bromfenac
  • flurbiprofen
253
Q

ketorolac tromethamine uses

A
  • 0.5% (Acular, generic): itching associated with SAC: 1 gtt qid,
    post-op pain and inflammation: begin 24 hours pre-op, continue x 2 weeks
  • 0.4% (Acular LS, generic): up to 4x daily for post-refractive surgery pain
254
Q

nepafenac uses

A
  • post-op inflammation and pain but both forms are expensive
  • 0.1% (Nevanac): tid following cataract surgery
  • 0.3% (Ilevro): once daily dosing
255
Q

diclofenac uses

A
  • pain and inflammation after surgery
  • 0.1% (Voltaren, generic)
  • cataract and refractive surgery - qid dosing
  • report of rare corneal decompensation - mostly with generic formulation issue
256
Q

bromfenac uses

A
  • pain and inflammation after cataract surgery
  • once daily dosing
  • 0.07% (Prolensa)
  • 0.09% (generic)
257
Q

flurbiprofen uses

A
  • older, potentialy less effective
  • 0.03% (generic)
  • used by surgery DURING surgery (provides miosis)
258
Q

notes about topical NSAIDs (3)

A
  • any use other than post-cataract or refractive surgery pain and inflammation is OFF-LABEL (other than ketorolac for allergies)
  • can help with ocular pain from other causes
  • some are used for post-cataract surgery CME
259
Q

ways to manage corneal pain (5)

A
  • lubricants
  • bandage CL
  • pressure patch
  • cycloplegia
  • topical NSAIDs (OFF-LABEL)
260
Q

what conditions is cycloplegia useful for?

A
  • corneal abrasion
  • corneal FB
  • infectious keratitis
  • anterior uveitis
261
Q

what other analgesic besides NSAIDs?

A
  • acetaminophen = APAP (Tylenol)
  • unknown central mechanism
  • antipyretic - works on hypothalamus - good for aches/fever
  • NO ANTI-INFLAMMATORY EFFECT - not good for swelling
  • NO INHIBITION OF PLATELETS
262
Q

acetaminophen is the DOC for?

A
  • children
  • viral-induced fever
  • pregnancy
  • nursing mothers
  • patients with GI disorders
  • patients with bleeding/clotting disorders
  • overall safer drug and can be given after surgery
263
Q

acetaminophen max dosing

A
  • now recommend 3200mg/d but can use 4g/d for short periods of time
264
Q

acetaminophen dosing

A
  • regular strength: 325 mg tab or cap: 1-2 pills every 4-6 hours, not to exceed 10 tabs in 24 hours
  • extra strength: 500 mg tab or cap: 1-2 pills every 4-6 hours not to exceed 6 pills in 24 hours
265
Q

pediatric availability of APAP

A
  • oral suspension 160mg/5mL
  • chewable tablet 160mg tab (choking hazard until 3-4 years old)
  • dissolvable powder 160mg/powder pack
266
Q

acetaminophen and the liver

A
  • APAP is associated with liver failure in alcoholics/people who consume >3 drinks/day bc of how it’s metabolized
  • liver failure = decreased drug metabolism = overdose
  • major pathway: majority of drug is metabolized to produce non-toxic metabolite
  • minor pathway: small amount of drug produces highly reactive intermediate that conjugates with glutathione and is inactivated
  • at TOXIC APAP levels, the minor pathway can’t keep up (liver’s glutathione is limited), causing an increase in the reactive intermediate which is hepatotoxic
267
Q

centrally acting agents characteristics (4)

A
  • react with opioid receptors in the CNS
  • interrupt the ascending pain message AND the emotional response
  • opioids (morphine, oxycodone, codeine) MOA poorly understood
  • endorphins - naturally manufactured by the brain, they may block peripheral transmitters or hyperpolarize neurons (opioids mimic endorphins)
268
Q

MU opioid receptors

A
  • classic morphine receptor and most common endogenous opioid receptor
  • located in brain and spinal cord
  • stimulated by endogenous endorphins
  • drug ligands: morphine, methadone, fentanyl
  • effects decline as tolerance develops
269
Q

binding of mu receptors produces

A
  • analgesia
  • sedation
  • decreased BP
  • itching (not allergy)
  • nausea/GI upset/constipation
  • euphoria (potential for abuse)
  • decreased respiration
270
Q

kappa opioid receptors

A
  • stimulation relieves pain
  • stimulation produces nausea, sweating
  • endogenous transmitters are dynorphins
  • located in the periphery by pain neurons
  • NOT associated with euphoria response
271
Q

delta opioid receptors

A
  • stimulated by endogenous enkephalins
  • produces “ischemic preconditioning” - effect they have on tissue after stroke to reduce its effect
  • stimulation induces protective increase in blood flow to tissues surrounding an ischemic area
  • may have cardioprotective effect
272
Q

opiate analgesics

A
  • block central pain receptors, reduce perception of pain
  • inhibits descending pain pathways
  • allergic to one opiate, allergic to all**
  • schedule II (high abuse potential) to V (low)
273
Q

narcotics

A
  • morphine
  • codeine
  • heroin
  • fentanyl
  • methadone
  • hydrocodone
  • thebaine
  • oxycodone
  • meperidine
  • tramadol
274
Q

side effects of opiates

A
  • respiration: sleep apnea/COPD
  • urinary tract: enlarged prostate
  • GI tract: slows motility/constipation warning
  • interaction with other anticholinergics (dry/drowsy)
275
Q

withdrawal reactions

A
  • pain/irritability
  • hyperventilation
  • dysphoria and depression
  • restlessness and insomnia
  • fearfulness and hostility
  • increased blood pressure
  • nausea/vomiting/diarrhea
  • pupillary dilation
  • hyperthermia
  • lacrimation/runny nose
  • chills/goosebumps
276
Q

Tylenol 1, 2, 3, 4 combination

A
  • codeine with APAP
277
Q

Vicodin combination

A
  • hydrocodone and APAP
278
Q

Percodan combination

A

oxycodone and ASA

279
Q

Percocet combination

A

oxycodone and APAP

280
Q

ultracet combination

A

tramadol and APAP

281
Q

how much codeine is in tylenol 4?

A

60 mg

282
Q

how much codeine is in tylenol 3?

A

30 mg

283
Q

how much codeine is in tylenol 2?

A

15 mg

284
Q

how much codeine is in tylenol 1?

A

7.5 mg

285
Q

how many days’ worth of scheduled drugs can we prescribe as ODs?

A

three (which is plenty for eye pain)

286
Q

what combination of tylenol and ibuprofen can give the equivalent pain relief as opioids without the unwanted side effects?

A

500-1000mg Tylenol + 400-600mg ibuprofen taken simultaneously

287
Q

herpes zoster post-herpetic neuralgia

A
  • pain that lasts 3 months or longer after shingles rash has cleared
  • burning, stabbing, deep, aching pain
  • sensitive to touch
  • itching and numbness
  • a leading cause of suicide in older patients
288
Q

who’s at risk of getting PHN?

A
  • older than 50
  • severe rash and pain (worse case)
  • other chronic conditions (diabetes)
  • face/torso location of rash
  • delayed antiviral therapy
289
Q

how to manage post-herpetic neuralgia?

A
  • prevent: recognize HZ and prescribe oral antivirals ASAP
  • treat:
  • oral antivirals during acute phase
  • Zostrix cream to area 3-4 times per day (capsaisin)
  • low dose tricyclic antidepressants (amitriptyline 25mg/d)
  • gabapentin (Neurontin) - huge dose range
  • 5HT agonists (“triptan” drugs)
  • involve the PCP for treatments
290
Q

local anesthetics definition

A

drugs which produce reversible (transient) loss of sensory perception without producing loss of consciousness

291
Q

characteristics of local anesthetics

A
  • used in diagnostic and therapeutic procedures to numb a small part of the body
  • prevent the generation and conduction of a nerve impulse
292
Q

how do local anesthetics work?

A
  • unionized form penetrates the cell membrane
  • inside of neuron is slightly more acidic so anesthetic becomes ionized and has a high affinity for sodium channel - prevents influx of sodium into cell
293
Q

chemical structure of local anesthetics (3 main parts)

A
  • lipophilic group: aromatic structure (usually benzene) - as lipophilicity increases, potency, duration of action and toxicity increases
  • intermediate linkage group: either ester ( -CO) or amide ( -HNC) - determines properties such as metabolism: ester is unstabilized compared to amide
  • hydrophilic group: usually a tertiary amine/proton acceptor
294
Q

esters vs amides

A

esters - unstable, quickly hydrolyzed by pseudocholinesterases
amides - stable, metabolized by the liver and last longer

295
Q

between esters and amides, which are more likely to produce allergic reactions?

A

esters, but allergies to anesthetics are not very common

296
Q

examples of ester local anesthetics

A
  • cocaine
  • tetracaine
  • proparacaine
  • benoxinate
297
Q

examples of amide local anesthetics

A
  • bupivacaine**
  • lidocaine**
  • ropivacaine
  • etidocaine
  • mepivacaine
298
Q

general concepts of local anesthetics

A
  • affect every nerve, not just pain: autonomic, pain, temperature, touch, proprioception, motor fibers (although need lots to paralyze)
  • preferentially affect: smaller nerves, myelinated nerves, nerves that fire frequently
299
Q

factors that affect POTENCY of local anesthetics

A
  • hydrophobicity
  • hydrogen ion balance
  • vasoconstrictor/dilator properties
  • fiber size, type, myelination
  • frequency of nerve firing
  • pH (acidic environment antagonizes the block)
300
Q

duration of action of LA

A
  • anesthetics have some inherent vasodilation activity which can impact potency/doa
  • vasoconstrictors may be added to INJECTABLE local anesthetics to prolong time in tissue (typically epinephrine 1:100,000 concentration)
  • vasoconstrictors decrease potential for systemic toxicity but may cause local tissue hypoxia
  • protein binding can increase duration of action
301
Q

examples of short-acting LAs

A
  • procaine

- chloroprocaine

302
Q

examples of intermediate acting LAs

A
  • lidocaine
  • mepivicaine
  • prilocaine
303
Q

examples of long acting LAs

A
  • tetracaine
  • bupivacaine
  • etidocaine
  • ropivacaine
  • lovebupivacaine
304
Q

side effects of TOPICAL anesthetics

A
  • severe SE are extremely uncommon
  • minor toxic or allergic events involving eyelids, conjunctiva, cornea
  • toxicity: desquamation of epithelial cells of cornea (more common in elderly, can decrease vision temporarily)
  • systemic reactions are even more rare
  • max 7 drops/eye tetracaine; 14 drops/eye proparacaine
305
Q

prolonged topical anesthetic syndrome

A
  • occurs after 6 days to 6 weeks of use
  • severe corneal lesions with decreased epithelium
  • after just a few days: loss of epithelium, delayed/retarded healing of epithelial defect
    treat: d/c anesthesia, cycloplegia, antibiotic, bandage CL, systemic analgesic
306
Q

reminder to

A

read articles on teams regarding prolonged topical anesthetic use

307
Q

allergies to local anesthetics

A
  • true allergy to amides is EXTREMELY rare; need to know what type of anesthetic and situation
  • true allergy to esters is uncommon, except common dermatitis hypersensitivity to benzocaine
308
Q

acute toxicity to local anesthetics

A
  • typical order: CNS, cardiovascular, respiratory
309
Q

CNS acute toxicity to local anesthetics

A
  • stimulation followed by depression
  • paresthesia, tinnitus, dizziness, lightheadedness
  • anxiety –> disorientation –> loss of consciousness –> seizure –> respiratory arrest
310
Q

cardiovascular acute toxicity to local anesthetics

A
  • early: hypertension, tachycardia, arrhythmia

- late: hypotension, bradycardia, absent pulse (all are negative inotropes)

311
Q

psychomotor acute toxicity of local anesthetics

A

anxiety-related, NOT drug-related

312
Q

characteristics of topical anesthetics in OD practice

A
  • allow us to perform diagnostic and minor surgical procedures in office while keeping patient comfortable
  • drugs applied to conjunctiva/cornea
  • most topical anesthetics are similar in their onset/doa
  • do not provide anesthesia to skin surface (cannot use in eyelid lesion removal)
  • vary in ability to provide anesthesia to conjunctiva/limbus, but ALL do well on the cornea**
313
Q

topical anesthetics that are derivatives of PABA

A
  • tetracaine 0.5%

- benoxinate 0.4%

314
Q

forms of proparacaine

A
  • 0.5% solution
  • 0.5% with fluorescein sodium (Fluoracaine and Flucaine)
  • a little more tolerable than tetracaine
315
Q

forms of lidocaine

A
  • 3.5% gel (Akten) - AMIDE

- rarely used because it’s inconvenient and rough on cornea

316
Q

characteristics of proparacaine

A
  • low incidence of hypersensitivity
  • more comfortable than tetracaine, so generally considered DOC
  • however, has less conjunctival anesthesia than tetracaine
317
Q

characteristics of tetracaine

A
  • similar to proparacaine but has more stinging and more impact on corneal epithelium
  • some cross-reaction hypersensitivity with proparacaine
318
Q

characteristics of Benoxinate 0.4% topical anesthetic

A
  • stinging level between tetracaine and proparacaine
319
Q

characteristics of lidocaine 3.5% gel (AMIDE)

A
  • much better anesthesia for deeper conjunctiva
  • occasional use in optometry
  • no cross-sensitivity with other topicals (esters)
  • efficacious on vascular tissue
  • no local metabolism = long lasting
320
Q

side effects of topical anesthetics

A
  • conjunctival hyperemia
  • tearing
  • eyelid heaviness
  • increased corneal epithelial permeability
  • corneal epithelial desquamation
  • blink reflex diminished
  • delay contact lens use for 30-60 minutes post-use
321
Q

uses of topical anesthetics in optometry

A
  • tonometry
  • gonioscopy
  • culturing of ocular tissues
  • forced ductions (lidocaine)
  • pachymetry
  • lacrimal dilation and irrigation
  • pre-drug instillation
  • superficial foreign body removal
  • minor surgery of conjunctiva
  • prior to injected anesthesia
322
Q

optometric uses of injectable anesthetics

A
  • eyelid lesion removal
  • chalazion incision and drainage
  • repair of eyelid laceration
323
Q

different methods of injectable anesthetics

A
  • local infiltrative - provide excellent anesthesia to anterior lamellae, but distort tissue, used with epi
  • regional nerve block - excellent anesthesia without tissue distortion, no epi, must know anatomy extremely well*
324
Q

injectable local anesthetics

A
  • lidocaine 0.5 to 2% with or without epi: onset 4-6 minutes, lasts 40 min - 1 hour
  • bupivacaine 0.5% usually without epi: onset 5-10 minutes, lasts 4-12 hours, often combined with lidocaine
325
Q

pre-injection evaluation

A
  • age (has to be cooperative if child)
  • systemic health
  • medications
  • allergies (RARE to have amide anesthetic allergy)
  • level of anxiety (may need to administer diazepam if patient has a driver)
326
Q

procedure of injecting anesthetics

A
  • informed consent prior to injection
  • clean area to be injected with disinfectant
  • mark skin if needed
  • jaeger plate if desired
  • 25-27 gauge needle in tuberculin syringe
  • bevel up and skin pulled taut, very shallow angle to inject, withdraw plunger to ensure no IV penetration
  • inject 0.2 to 0.6 cc while withdrawing syringe
  • SLOW and steady injection to decrease pain
  • WATCH for diffuse rather than linear infiltration
  • 2-3 injection sites may be needed
  • pressure/massage to disperse bolus, restore anatomy and decrease hematoma risk
  • after 5 minutes: pinch to skin to see if anesthetized

Ocular Pharmacology (4 decks)

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