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Ocular Pharmacology > Final Exam New Material > Flashcards

Final Exam New Material Flashcards

1
Q

What are some quality of life concerns of dry eye disease?

A
  • similar to those undergoing dialysis or enduring disabling hip fractures
  • Sjogren’s patients have an increased risk of anxiety and depression
  • potential for severe economic loss through decreased worker productivity
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2
Q

What are the two types of dry eye and what percentage of dry eye sufferers are attributed to each?

A
  • aqueous deficient dry eye (ADDE) accounts for 14% of dry eye sufferers by itself
  • evaporative dry eye (EDE) accounts for 50% by itself, and 86% are at least partially EDE sufferers
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3
Q

What is aqueous deficient dry eye?

A

an overall decrease in lacrimal gland secretion due to several factors such as low androgens, aging, autoimmune disease, etc.

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4
Q

What is evaporative dry eye?

A

high evaporation of tears due to several underlying causes such as anterior blepharitis, MGD, ocular rosacea, poor blinking, etc.

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5
Q

Complaints of dry eye sufferers (9)

A
  • burning, stinging, dry, sticky lid, gritty
  • short wear time with lens
  • transient blur
  • painful A&R, difficult lens removal
  • increase blinking
  • photophobia
  • epiphoria
  • ocular fatigue/discomfort
  • injection
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6
Q

Contributing factors that lead to dry eye (10)

A
  • old age
  • female gender (pregnancy, labor, etc.)
  • environment (running AC, fans)
  • poor diet
  • anterior segment disease (allergies)
  • medications
  • systemic disease (RA)
  • refractive surgery
  • smoking
  • caffeine
  • alcohol
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7
Q

Topical medications that may induce or worsen DED? (12)

A
  • adrenergic agonists
  • anti-allergics
  • anti-virals
  • beta-blockers
  • carbonic anhydrase inhibitors
  • cholinergic agonists
  • decongestants
  • miotics
  • mydriatics/cycloplegics
  • prostaglandins
  • topical and local anesthetics
  • topical ocular NSAIDs
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8
Q

the pathogenesis (inflammatory pathway) of dry eye

A

1) increased tear osmolarity –> stress signaling pathways in epithelium and resident immune cells
2) dendritic cell maturation and migration to draining lymph nodes
3) priming of autoreactive CD4-postiive T-cells that home to ocular surface, involving ICAM-1 binding to LFA-1
4) activation of T-cell mediators: IFN-gamma causes goblet cell loss and epithelial apoptosis; IL-17 causes corneal epitheliopathy
5) inflammatory mediators (IL-1, IL-6, IFN-gamma) that decrease the threshold of corneal nociceptors, making them more sensitive to innocuous environmental stimuli –> discomfort

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9
Q

properties of NaFl staining

A
  • water-soluble dissolved in aqueous

- adheres to dead epithelial cells (breaks or loss)

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10
Q

properties of rose bengal staining (4)

A
  • has mild anti-viral effect
  • stains dead and devitalized cells
  • stains cells that have lost their mucus surface
  • stings
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11
Q

properties of lissamine green staining (3)

A
  • stains dead and degenerated cells
  • does not stain healthy cells
  • stains mucous-free areas
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12
Q

management of mild aqueous deficiency

A
  • AT support

- environmental modifications

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13
Q

management of moderate aqueous deficiency (4)

A
  • frequent ATs or gels with increased contact time
  • topical anti-inflammatories/secretagogues
  • punctum occlusion
  • nasal stimulator
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14
Q

management of severe aqueous deficiency (7)

A
  • ATs or gels
  • topical anti-inflammatories/secretagogues
  • punctal occlusion
  • nasal stimulator
  • autologous serum
  • amniotic membrane
  • scleral lens
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15
Q

options for artificial tears (3 types)

A
  • electrolytes
  • ointments
  • gels
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16
Q

what do electrolyte ATs do? (3)

A
  • treat ocular surface damage secondary to DES
  • potassium and bicarbonate are critical to maintaining K thickness, increase goblet cell density, increase corneal glycogen content, decrease tear osmolarity, decrease tear staining on conj
  • Bion Tears and Thera-Tears restore the epithelial barrier function and maintain the mucin layer on the conj
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17
Q

What do ointment ATs do? (4)

A
  • high viscosity solutions provide long relief
  • good for kids (less tear wash-out)
  • bedtime use
  • mineral oil and petrolatum combinations
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18
Q

What do gel ATs do? (3)

A
  • high molecular weight cross-linked polymers
  • good retention with less blur
  • methylcellulose and PVA to increase contact time
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19
Q

BAK (preservative) properties (3)

A
  • not great, found in tons of ATs
  • used for mild dry eye
  • well documented toxicity (increases drug penetration)
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20
Q

EDTA (preservative) properties

A
  • augments preservatives in other formulations
  • CA2 chelator - binds and inactivates
  • may not work for moderate to severe dry eye
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21
Q

Thimerosal (preservative) properties

A
  • sensitivity to mercury component - toxicity (used in Viroptic)
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22
Q

Polyquad (preservative) properties

A
  • less toxic
  • usually in Alcon products
  • molecule is 4X bigger, so doesn’t penetrate a lot of things
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23
Q

single dose of BAK can ____ affect TBUT _________________

A
  • adversely

- by as much as 4 seconds in 3 hours

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24
Q

What are the “vanishing preservatives” and what are their properties?

A
  • Sodium chlorite (Purite) degrades to chloride and water in UV
  • Sodium perborate degrades to water and oxygen when touches the tear film
  • BUT may not work in severe dry eye when there’s not enough tear film
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25
Q

FreshKote properties (3)

A
  • has high oncotic pressure to decrease corneal epithelial edema
  • can be used in Fuch’s
  • another option to Muro 128
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26
Q

components and properties of Systane Ultra (8)

A
  • ions: K
  • polyethylene glycol 400
  • propylene glycol
  • boric acid
  • hydroxypropyl guar
  • sorbitol
  • preserved with polyquad
  • Rx for aqueous deficiency
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27
Q

actions of steroids to treat dry eye

A
  • anti-inflammatory and immunosuppressive
  • inhibits phospholipase A2 in the arachidonic acid pathway
  • decreases inflammatory mediators and decreases capillary permeability - causes decreased immune response
  • decreases fibroblast and collagen formation - prevents healing
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28
Q

properties of cyclosporine A 0.05% (Restasis) updated bottle design (4)

A
  • no preservatives
  • lasts for a month
  • great for patients on the go, while other patients like the vials
  • $656 without insurance
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29
Q

MOA of Restasis

A
  • prevents T-cell activation (calcineurin inhibitor)
  • activated T-cells produce inflammatory cytokines that result in recruitment of more T-cells and more cytokine production
  • tissue damage in lacrimal glands and ocular surface occur
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30
Q

How long does it take Restasis to work?

A
  • 2-3 months because it works late in the pathway

- the drop also burns so a lot of patients will discontinue use before it starts working

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31
Q

Is Restasis used for EDE or ADDE?

A

Probably ADDE

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32
Q

Dosing of Restasis

A

bid but can be used more

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33
Q

Klarity-C properties/components

A
  • 0.1% cyclosporine/chondroitin sulfate
  • lower cost compared to Restasis
  • not FDA-approved
  • also preservative free a little sketchy?
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34
Q

Cequa components/properties

A
  • 0.09% cyclosporine (highest FDA approved concentration)
  • NCELL - nano micelles (22 nanometers in size)
  • hydrophilic shell that transports hydrophobic core of drug to achieve better penetration
  • claims 3X greater corneal delivery and 1.6X greater conjunctival delivery
  • works faster, vehicle is more comfortable
  • works in 2-6 weeks
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35
Q

Cequa studies results (4 key components)

A
  • Schirmer’s: improved >10 mm from baseline in 16.8% of patients vs 8.6% and 9.2% with vehicle
  • 65% central corneas completely clear in 3 months
  • significant improvement in conjunctival staining (earliest sign)
  • takeaways: less than 1% blurred vision, no taste alteration, 85% said no installation discomfort
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36
Q

Lifitegrast (Xiidra) MOA

A
  • binds to integrin LFA-1 and blocks its interaction with ICAM-1 to prevent T-cell activation/migration (before cyclosporine A in pathway)
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37
Q

How long does it take Xiidra to work?

A

about 2 weeks according to the OPUS study

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38
Q

Lifitegrast properties (price, PF?, dosing, SEs)

A
  • similar cost to Restasis (expensive)
  • non-preserved vials
  • bid dosing
  • side effects include burning/irritation, dysgeusia (bad taste), and blurring
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39
Q

OC-01 varenicline (Tyrvana) study results (2)

A
  • 47% of those with 1.2mg/ml dose had 11.2 mm improvement on Schirmer’s
  • 44% of those with 0.6mg/ml dose had 11.0 mm improvement on Schirmer’s
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40
Q

OC-01 (Tyrvaya) drug type, MOA, aka, and dosing

A
  • selective nicotinic acetylcholine receptor agonist
  • aka Chantix
  • bind to receptors on a branch of the trigeminal nerve, which then sends signals to the eye to produce its own tears
  • dosing: spray Tyrvaya once in each nostril twice a day, may cause nasal/throat irritation
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41
Q

how to manage severe aqueous deficiency (7)

A
  • moisture chamber goggles
  • punctum occlusion/cautery
  • topical acetylcysteine
  • therapeutic CLs (sclerals)
  • amniotic membrane
  • autologous serum tears
  • tarsorrhaphy
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42
Q

amniotic membrane properties (4)

A
  • have healing and growth factors
  • very expensive
  • variable duration, so must have a plan
  • must be secured by a soft contact lens
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43
Q

Properties of autologous serum (5)

A
  • biochemical similarities between an individual’s serum and tears
  • contains essential components for healing not found in OTC gtts
  • PF and low allergy risk
  • store in fridge/freezer
  • potentially useful for patients with RCE, autoimmune conditions, neuropathic cornea with central sensitization
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44
Q

Dosing of autologous serum (4)

A
  • 3 mL bottles: 1-4 drops delivered 1-4 times a day
  • professional strength - refrigerated (expires 90 days after opening)
  • LITE - can be stored at room temp
  • most patients require 3-4 bottles to start
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45
Q

How do nasal stimulators work for tear production?

A
  • the trigeminal nerve is responsible for innervating the lacrimal function unit, specifically ophthalmic division VI
  • innervates the lacrimal gland, meibomian glands and goblet cells
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46
Q

How to use nasal stimulators (3)

A
  • TrueTear provides a temporary increase in tear production during neurostimulation to improve dry eye symptoms
  • daily disposable tips
  • 5 levels of intensity - 1 minute cycle shut off, no longer than 30 minutes/day
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47
Q

contraindications to nasal stimulation (3)

A
  • pacemaker
  • nose bleeds
  • nose rings
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48
Q

Risk factors for neurotrophic keratitis (7)

A
  • herpes eye infections
  • conditions such as diabetes and MS
  • chronic use of topical treatments (preserved glc meds)
  • chronic contact lens wear
  • chronic inflammation from dry eye
  • surgical procedures involving the eye or brain
  • injury to the eye such as chemical burns
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49
Q

properties of oxervate (4)

A
  • first FDA-approved treatment for people with neurotrophic keratitis
  • MOA: cenegermin, a recombinant form of human nerve growth factor, is structurally identical to the NGF that is naturally produced by our eyes
  • NGF is thought to foster healing of the cells on the corneal surface, help promote tear secretion and help improve the function of the nerves in the cornea
  • studies have shown that this helps corneal epithelial cells and corneal nerves survive
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50
Q

clinical findings of Oxervate

A
  • after 8 weeks of treatment, 6 times daily 72% healing, vehicle response rate of 33.3%
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51
Q

properties of Lumify (5 - drug name, who it’s used on, study outcomes, strength and price)

A
  • Alphagan
  • good for patients that are always red
  • studied 4 times a day use with no claimed SE, IOP changes, nor rebound congestion
  • 0.025% stregnth
  • retails $12-20
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52
Q

Upneeq properties (3)

A
  • oxymetazoline hydrochloride oph sol 0.1%
  • FDA approved drop for acquired ptosis
  • MOA: alpha adrenoreceptor agonist targeting a subset of receptors in Mueller’s muscle of the eyelid
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53
Q

Indications, dosing and contraindications for Upneeq

A
  • acquired blepharoptosis in adults
  • dose 1 drop in ptotic eye(s) once daily
  • no contraindications
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54
Q

How to manage mild evaporative dry eye

A
  • warm compresses bid for 4-6 weeks
  • lid hygiene
  • AT support for lipid deficiency - Systane Balance, Refresh Endura, FreshKote
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55
Q

How to manage moderate evaporative dry eye (additive)

A
  • topical anti-inflammatories/antibiotics/testosterone
  • in-office heat/expression
  • microblepharoexfoliation
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56
Q

How to manage severe evaporative dry eye (additive)

A
  • scleral lenses
  • autologous serum
  • amniotic membrane
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57
Q

Pharmacological management of moderate EDE (additive)

A
  • Anterior: Erythromycin ung X 3 months
  • Posterior: Azasite qhs or bid X 1 month or Tobradex/Lotemax/Zylet qid 4-6 weeks until inflammation resolves
  • oral Omega-3s
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58
Q

Pharmacological management of severe EDE

A
  • systemic minocycline/doxycycline
  • 50mg bid X 1 month
  • 20 mg qd X 1-2 months
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59
Q

Patient education of Omega-3s

A
  • 4-8 weeks for symptomatic relief
  • long term use to maintain results
  • potential for stomach upset so divide into 2 or 3 doses/day
  • take with fatty food for best absorption
  • risk of increased bleeding/bruising
  • inform all doctors
  • caution in liver disease, diabetics, low blood pressure
60
Q

What can Systane Balance be prescribed for?

A

EDE

61
Q

traditional ocular rosacea management

A
  • doxycycline load dose of 100 mg bid X 1-2 weeks, then 40 mg daily
62
Q

Less traditional options of ocular rosacea

A
  • minocycline 100mg daily, SE: potential risks of drug-induced lupus, skin hyperpigmentation, and DRESS syndrome
  • IPL
  • LLLT (low-laser light therapy)
  • radiofrequency
63
Q

What is the conventional pathway of aqueous outflow?

A

Trabecular pathway (65-85%)

64
Q

What is the minor pathway of aqueous outflow?

A

uveoscleral outflow (about 20%)

65
Q

IOP is determined mathematically by what?

A

(AH production)/(AH outflow) + episcleral venous pressure

66
Q

Which classes of drugs decrease the TM outflow resistance?

A
  • latanoprostene bunod

- netarsudil

67
Q

Which class of drugs open the angle by mechanical tension (still working on the TM)?

A

miotics

68
Q

Which classes of drugs suppress aqueous production?

A
  • beta blockers
  • carbonic anhydrase inhibitors
  • alpha-adrenergic agonists
  • netarsudil (minimal)
69
Q

Which classes of drugs increase the uveoscleral outflow?

A
  • prostaglandins

- alpha-adrenergic agonists (minimal)

70
Q

Which class of drug lowers the episcleral venous pressure?

A

netarsudil, but that’s not its primarily action

71
Q

beta-blocker MOA

A

decrease aqueous production

72
Q

What is the IOP response to beta-blockers?

A
  • 25-30% decrease with non-selective BBs

- beta-1 is les efficacious

73
Q

systemic side effects of beta-blockers

A
  • cardiovascular: bradycardia, arrhythmia and mild hypotension
  • pulmonary: bronchospasm, asthma, dyspnea
  • neurological: depression, headache, insomnia, sexual dysfunction
  • other: mask symptoms of hypoglycemia, change in lipid profile
74
Q

ocular side effects of beta blockers

A
  • SPK
  • dry eye
  • local allergy, but uncommon as they’re usually well-tolerated locally
75
Q

contraindications to beta-blockers

A
  • asthma
  • COPD
  • bradycardia
  • cardia failure
76
Q

In Texas, what must ODs ensure before prescribing beta-blockers?

A

The patient has to have seen their physician in the last six months

77
Q

available forms of timolol maleate (4)

A
  • Timoptic and Timoptic PF
  • Timoptic XE (gel-forming solution or gfs)
  • Istalol (with potassium sorbate)
  • generic timolol maleate (and gfs)
78
Q

what are the non-selective beta-blockers used to treat glaucoma?

A
  • timolol maleate
  • timolol hemihydrate (Betimol)
  • levobunlol (Betagan and generic)
  • metipranolol (generic)
  • carteolol (generic)
79
Q

What is the beta-1 selective beta-blocker and what are some of its available brands/characteristics?

A
  • betaxolol: generic 0.5% bid dosing & Betoptic-S (suspension) 0.25% once a day
  • much less potent IOP-lowering effect
  • may be used in patients with pulmonary disease (with caution)
80
Q

Other considerations with beta-blockers (dosing, systemic use, vials, etc.)

A
  • once a day vs twice a day dosing (but only work when we’re producing AH - in the AM)
  • concurrent use with systemic beta-blockers
  • baseline vitals important
  • monocular trial, which isn’t really used anymore
81
Q

prostaglandin analogues MOA

A

increase uveoscleral outflow

82
Q

prostaglandin analogue IOP response

A
  • 25-36% + reduction in IOP
  • most efficacious of glaucoma meds
  • more reduction in super high IOP
83
Q

Local side effects of PGA

A
  • hyperemia - very common
  • iris color change
  • eyelash changes
  • cystoid macular edema after cat sx (exacerbations vs cause?)
  • exacerbation of ocular inflammation (???)
  • prostaglandin-induced orbitopathy
84
Q

What drug works best for patients with a history of uveitis?

A
  • bimatoprost is effective at lowering IOP in patients with uveitic glaucoma in whom the uveitis is controlled on immunomodulatory therapy, and it doesn’t increase the rate of flares or uveitis in these patients
85
Q

What is prostaglandin-related orbitopathy?

A
  • deepening of the upper eyelid sulcus
  • aka “sunken eye”
  • more difficult to detect in bilateral therapy
  • may be reversible with discontinuation of therapy - partially or fully
86
Q

contraindications to PGAs

A
  • pseudophakic cystoid macular edema (CME)
  • light colored/mixed colored irises (relative CI)
  • uveitic/inflammatory glaucoma (but probably ok)
87
Q

What are the four available PGA drugs?

A
  • latanoprost 0.005%
  • travaprost
  • bimatoprost
  • tafluprost
88
Q

What are the available forms of latanoprost 0.005%?

A
  • generic
  • Xalatan
  • Xelpros: micelle micro-emulsion, preserved with potassium sorbate instead of BAK
89
Q

What are some characteristics of travaprost (Travatan-Z)?

A
  • no BAK preservative (preserved with ionic bufered SofZia)

- generic, which is BAK preserved, not called Travatan-Z

90
Q

What are some characteristics of bimatoprost (Lumigan 0.01%)?

A
  • has 4X the amount of BAK

- generic is 0.03% which is more irritating, so must be specific when prescribing

91
Q

tafluprost (Zioptan) characteristics

A
  • unpreserved, single unit dose packaging
92
Q

other PGA considerations (how it’s used in glc treatment, dosing, cost, etc.)

A
  • additive to other glaucoma meds
  • dosed once daily - usually at night due to hyperemia
  • monocular use should be avoided given the side effects
  • cost (now several are available in generic)
  • not effective in children
93
Q

latanoprostene bunod (Vyzulta) characteristics

A
  • latanoprostene = latanoprost, which increases uveoscleral outflow
  • bunod donates NO, which exerts its effect in the TM, activates cGMP signaling pathway, resulting in trabecular relaxation and increased conventional outflow (secondary action)
  • mechanisms would be expected to be additive
94
Q

how does the efficacy of latanoprostene bunod compare to timolol in the APOLLO study?

A
  • lowered IOP about 0.5-2.5 mmHg more than timolol
95
Q

how does the efficacy of latanoprostene bunod compare to latanoprost in the VOYAGER study?

A
  • lowered IOP by 1-1.5mmHg more than latanoprost, which may be worth it in some patients
96
Q

non-selective adrenergic agonists MOA

A
  • increase aqueous outflow
97
Q

What is the response of adrenergic agonists?

A
  • moderate and not additive with non-selective beta-blockers
  • really of historical significance only, not used anymore, just know the pharmacology of it because not a glaucoma drug anymore
98
Q

systemic side effects of adrenergic agonists/epinephrine compounds

A
  • headache
  • palpitations
  • tachycardia
  • hypertensive crisis
99
Q

local side effects of epinephrine compounds/adrenergic agonists

A
  • irritation
  • allergy
  • adenochrome deposition
  • pupil dilation
  • CME (epinephrine)
100
Q

contraindications of adrenergic agonists

A
  • narrow angles
  • aphakia (epinephrine)
  • CV disease
101
Q

alpha-adrenergic agonists MOA

A
  • decrease aqueous production (primarily) AND increase uveoscleral outflow (minimal)
102
Q

IOP response in alpha-adrenergic agonists

A

20-25% reduction

103
Q

systemic side effects of alpha-adrenergic agonists for glaucoma

A
  • fatigue
  • dry mouth
  • hypotension
  • dizziness (in petite ladies)
104
Q

local side effects of alpha-adrenergic agonists for glaucoma

A
  • allergy (follicular conjunctivitis)
  • mydriasis (minimal with apraclonidine)
  • miosis (minimal with brimonidine)
  • mild lid retraction
105
Q

contraindications for alpha-adrenergic agonists for glaucoma

A
  • MAOIs
  • children < 6 YO due to CNS depression
  • women that are nursing
106
Q

available alpha-adrenergic drugs for glaucoma

A
  • apraclonidine
  • brimonidine (more alpha-2 selective)
  • brimonidine/timolol fixed combination (Combigan)
  • brimonidine/brinzolamide fixed combination (Simbrinza)
107
Q

Available drugs and concentrations of apraclonidine

A
  • 0.5% for more chronic use, but loses efficacy over time

- 1% for pre- and post-laser use to prevent IOP spike (main use)

108
Q

Available drugs and concentrations of brimonidine

A
  • brimonidine 0.2% generic (BAK)
  • “pseudo-generic” brimonidine 0.15% preserved with Polyquad (not Purite)
  • Alphagan-P 0.1% (non-BAK, preserved with Purite)
109
Q

characteristics of Combigan

A
  • brimonidine 0.2% with 0.5% timolol maleate

- dosed bid

110
Q

characteristics of Simbrinza

A
  • brimonidine and brinzolamide fixed combination

- brinzolamide is a carbonic anhydrase inhibitor (CAI)

111
Q

Iopidine vs. alphagan considerations

A
  • iopdine really only used to prevent post-laser IOP spike, not for chronic care
  • alphagan can be used for more chronic care
112
Q

other considerations for alpha-adrenergic agonists (first line, dosing, etc.)

A
  • possible first line drug
  • tid vs bid dosing (bid when combined with other drugs)
  • neuroprotection?: the idea of protecting the ONH without affecting IOP; Brimonidine isn’t definitively neuroprotective
113
Q

CAI MOA

A

decrease aqueous production

114
Q

IOP response of oral CAI

A

very good, IOP will drop fast but patients don’t tolerate very well

115
Q

IOP response of topical CAI

A
  • variable, not 1st line therapy
116
Q

systemic side effects of oral CAIs

A
  • paresthesia (pins and needles in phalanges with chronic use)
  • metallic taste and taste aversion
  • GI upset
  • metabolic acidosis
  • hypokalemia
  • renal calculi (acetazolamide)
  • transient myopia (choroidal/ciliary body effusion with forward movement of lens/iris diaphragm) –> close AC angle
117
Q

local side effects of topical CAI

A
  • local irritation (especially with dorzolamide)
  • SPK
  • corneal edema/decompensation
118
Q

Contraindications to oral CAIs

A
  • liver disease
  • COPD
  • kidney stones (acetazolamide)
  • pregnancy
  • sulfa allergy (???) - controversial, weigh risk:benefit
119
Q

Is it safe to administer a topical CAI in patients who report a history of sulfa allergy?

A

Yes if benefits outweigh the risks

120
Q

available oral CAI drugs for glaucoma

A
  • acetazolamide (Diamox)

- methazolamide (Neptazane)

121
Q

available topical CAI drugs for glaucoma

A
  • dorzolamide (Trusopt)
  • brinzolamide (Zaopt)
  • dorzolamide/timolol maleate (Cosopt)
  • brinzolamide/brimonidine (Simbrinza)
122
Q

available forms and dosages of acetazolamide (Diamox)

A
  • 250 mg tablets (1 tab po qid)

- 500 mg sustained released capsules (Sequels) 1 cap po bid

123
Q

available forms of topical dorzolamide

A
  • Trusopt

- generic

124
Q

available forms and dosages of topical brinzolamide

A
  • Azopt - has better pH –> less stinging
  • generic
  • tid
125
Q

available forms and dosages of dorzolamide with timolol maleate

A
  • Cosopt
  • Cosopt PF
  • generic
126
Q

available forms and dosages of brinzolamide/brimonidine

A
  • Simbrinza

- indicated tid but we use bid

127
Q

other considerations for CAIs (dosing, side effects, etc.)

A
  • tid vs bid dosing (topical)
  • warn patients of bitter taste
  • stinging is worse in dorzolamide than brinzolamide
128
Q

MOA of rho-kinase inhibitors

A
  • increases TM outflow (primary)
  • reduces episcleral venous pressure (secondary)
  • reduces aqueous production (via NE transporter inhibition) (minimal)
129
Q

Rho-kinase inhibitor drug

A

netarsudil

130
Q

available forms and dosages of netarsudil

A
  • Rhopressa (netarsudil): qd dosing, 5-7 mmHg drop in IOP

- Rocklatan (netarsudil + latanoprost): only fixed dose combo with pga and only fixed dose combo dosed once daily**

131
Q

side effects of netarsudil

A
  • significant hyperemia
  • small conjunctival hemorrhages
  • corneal verticillata
  • all go away after discontinuation and none require discontinuation
132
Q

MOA of miotics (cholinergic agonists)

A
  • open angle glaucoma: increase TM outflow (mechanical tension on scleral spur)
  • pupillary block angle closure: cause pupillary miosis and relieve pupillary block
133
Q

Describe the IOP response to miotics

A

good to very good

134
Q

Are miotics used for long term management of glaucoma?

A

Rarely due to the high incidence of ocular side effects and frequent dosing requirements

135
Q

local side effects of miotics

A
  • miosis
  • brow-ache
  • accommodative spasm/pseudomyopia
  • retinal break?
136
Q

systemic side effects of topical miotics

A
  • few

- bronchiole constriction so avoid in asthmatic patients

137
Q

Contraindications to topical miotics for glaucoma

A
  • PSC
  • young patient
  • neovascular or uveitic glaucoma
  • retinal detachment
  • high myopia
  • asthma
138
Q

Available miotic drug for glaucoma treatment

A
  • pilocarpine
139
Q

Available forms of pilocarpine and dosing

A
  • solution (1%, 2%, 4%) - used qid for chronic therapy; 1% used for in-office angle closure
  • gel 4% (nightly dose; not currently available)
140
Q

other considerations for using miotics to treat glaucoma

A
  • frequent dosing
  • cost
  • secondary glaucomas: effective in pigmentary, ineffective in angle recession
  • acute angle closure with pupillary block has a different MOA: pulls iris off of anterior lens and breaks pupillary block
141
Q

MOA of hyper-osmotics used to treat glaucoma

A
  • dehydrate and shrink the vitreous
142
Q

response of hyper-osmotics to treat glaucoma

A
  • very good in acute primary angle closure with pupillary block
143
Q

side effects of hyper-osmotics

A
  • nausea/vomiting
  • hyperglycemia/glycosurea (glycerin only)
  • really, really sweet, so patient has to be prepared
144
Q

contraindications of hyper-osmotics

A

diabetes (glycerin only)

145
Q

available hyper-osmotic drugs

A
  • mannitol (IV) - hospital only
  • glycerin (contraindicated in diabetics and currently not available in the US)
  • isosorbide (currently not available in the US)
146
Q

Other considerations for using hyper-osmotics to treat glaucoma

A
  • isosorbide vs glycerin
  • nausea prevention
  • concomitant use with oral CAI

Ocular Pharmacology (4 decks)

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