Download Primary open-angle glaucoma

evidence in patient care
The articles in this series are independently researched and compiled by PSA commissioned authors and peer reviewed.
Primary open-angle glaucoma
Continuing Professional Development
By Dr Luke Bereznicki
Case study
Mabel, a regular customer, asks for
advice about the different medications
used in the treatment of glaucoma.
She was diagnosed with glaucoma
several years ago and currently
uses Xalacom eye drops. Recently,
her friend has been diagnosed with
glaucoma but has been prescribed
Tenopt eye drops instead. Mabel
is concerned that her friend may
not have been prescribed the best
medication to treat her glaucoma.
Pathophysiology of
glaucoma
Primary (or chronic) open-angle
glaucoma is a common cause of legal
blindness and visual impairment.
Due to its insidious nature it has been
Learning objectives
After reading this article you should
be able to:
Vol. 30 – February #02
• Define primary open-angle
glaucoma.
• Discuss the role of
pharmacological treatments.
• Discuss techniques which
optimise the effectiveness of
pharmacological treatments.
Competency standards (2010)
addressed:
3.1.2, 3.1.3, 3.2.2, 4.2.2
Accreditation number:
CAP110202e
Dr Luke Bereznicki is Senior Lecturer in
Pharmacy Practice at the Tasmanian School
of Pharmacy.
140
referred to as the ‘sneak-thief of
sight’. The prevalence of open-angle
glaucoma increases exponentially
with age and in people aged over
50 years it is approximately 3%.1
It is estimated that about half
of all cases remain undiagnosed
because the disease progression is
slow, painless and visual acuity is
only affected late in the disease.2
Therefore, targeted screening is
required to identify affected patients.
Prevention or slowing of visual
loss is possible with a range of
management options, which include
medical, surgical and laser therapies.
This article will briefly review the
pharmacological management of
primary open‑angle glaucoma.
Glaucoma describes a group of
eye diseases in which there is
progressive damage to the optic nerve
characterised by specific structural
abnormalities of the optic nerve
head and associated patterns of
visual field loss.3 Elevated intraocular
pressure (IOP) is not included in this
definition as glaucoma may occur with
or without a rise in IOP (the normal
range is 10–21 mmHg). Glaucoma
is classified according to variations
in the anterior segment of the eye,
which may result in elevated IOP. The
anterior segment of the eye features a
circulatory system that nourishes the
lens and the cornea, which lack their
own blood supply. Aqueous humour is
produced by the ciliary body, circulates
through the anterior chamber of the
eye and drains via the trabecular
meshwork in the angle formed by the
iris and the cornea (the iridocorneal
angle) and the uveoscleral pathway via
the interstitial spaces between the iris
root and ciliary muscle.4 Imbalances
in the outflow of aqueous humour
may result in elevated IOP leading
to optic nerve damage. As the optic
nerve is not capable of regenerating,
deterioration of the optic nerve leads
to permanent visual field loss.4
Glaucoma is classified based on
the appearance of the iridocorneal
angle; there are open-angle, closedangle and developmental categories,
of which there are primary and
secondary types. Primary open-angle
glaucoma is the predominant form
in Western countries and represents
approximately 90–95% of all reported
cases of glaucomas.5,6 It may occur
with or without an elevation in
IOP; and in the case that IOP is not
elevated, it is referred to as normaltension glaucoma (NTG).7 In the
Baltimore Eye Survey, more than half
of patients with newly diagnosed
glaucoma had a normal IOP on a
single tonometry assessment.8 People
with NTG may account for a third to a
half of open-angle glaucoma cases.8,9
Conversely some people have raised
IOP but do not have glaucoma – this
is referred to as ocular hypertension.
Closed angle glaucoma may be acute
or chronic. Acute primary-angle
closure causes a painful, unilateral
red eye with markedly elevated
IOP.10 Chronic closed-angle glaucoma
may also occur in some populations
(e.g. Chinese and South-East
Asian people).1
Clinical presentation
The main clinical features of primary
open-angle glaucoma are an open
iridocorneal angle and cupping
of the optic-nerve head (or optic
disc). Cupping of the optic disc is
an important sign in diagnosis and
management of patients with openangle glaucoma. The patterns of
visual field changes that occur in
glaucoma relate to the extent and
location of optic nerve cupping.11
Submit your answers online at www.psa.org.au and receive automatic feedback
Table 1. Risk factors for glaucoma available from patient history.
Modified from the NHMRC guidelines for the screening,
prognosis, diagnosis, management and prevention of glaucoma.3
Risk factors for developing Strength of
glaucoma
evidence*
Risk of developing
glaucoma
Quantitative risk
increase
(when compared with
patients without these
risk factors)
IOP > 21 mmHg
A–B
Extremely high
12x or more
A–B
High
3x or more
A–B
Moderate
1.5x or more
Smoking*
C
Low
Similar risk to baseline
Steroid use*
C
Unknown
Migraine †
D
Increased risk stated with
no statistics provided
Age over 80 years
Age over 50 years
Family history
Specific ethnic origin
Diabetes
Myopia
Rural location
Eye injury†
High blood pressure
IOP = intraocular pressure
*Refers to the National Health and Medical Research Council (NHMRC) levels of evidence and grades for
recommendations. An evidence grade of A and B is based on evidence from systematic reviews and randomised
controlled trials, an evidence grade of C is based on evidence from controlled cohort studies and an evidence grade of
D is based on evidence from observational studies.
Risk factors and screening
Continuing Professional Development
Primary open-angle glaucoma is
frequently missed as a diagnosis
due to its lack of symptoms when
compared with acute primary angle
closure, which often presents with
ocular pain, redness, blurred vision
and nausea and vomiting. Progression
of open-angle glaucoma is usually
slow, painless and irreversible; visual
acuity is affected late in the disease
and symptoms of peripheral vision
loss with mobility difficulties do not
occur until the disease has progressed
significantly.10 In the Melbourne Visual
Impairment Project, nearly half of
the patients that were diagnosed
with glaucoma during the survey had
seen an eye-care practitioner in the
preceding 12 months and had not
been diagnosed with glaucoma.12
The authors concluded that raised
IOP should not be relied on as the
only triggering factor for initiating
glaucoma investigations. Glaucoma
may be diagnosed at a normal IOP if
there is characteristic optic disc and/
or visual field damage.10 People who
have glaucoma are at a higher risk
of motor vehicle accidents than
people without and are more likely to
become dependent on others for daily
activities. This may lead to a reduction
in quality of life.13,14
Early diagnosis with appropriate
management is the best way to
prevent, or at least slow, visual
loss associated with primary openangle glaucoma. Evidence strongly
supports a screening approach that
targets individuals at high risk of
developing glaucoma, rather than
the general population.3 Targeted
screening may be more cost-effective
in populations such as older adults,
people of African descent and those
with a family history of glaucoma.3
There is currently no consensus
on the optimal test or group of
tests for glaucoma screening, but a
combination of optic disc assessment,
visual field assessment, IOP and angle
assessment are suggested.3
Vol. 30 – February #02
The most important risk factors for
primary open-angle glaucoma are
older age, African origin, elevated
IOP and family history of openangle glaucoma.3 Other risk factors
include myopia, diabetes, smoking,
steroid use, migraine, eye injury and
high blood pressure (see Table 1). In
patients who have an elevated IOP
141
evidence in patient care
The articles in this series are independently researched and compiled by PSA commissioned authors and peer reviewed.
relative corneal thinness is another
major risk factor.15 Regular eye
checks and screening for glaucoma
is recommended in those who
have a moderate or greater risk for
developing glaucoma.3 Groups of
patients who should be screened for
glaucoma include people over the
age of 50 years (40 years in those of
African descent), first-degree relatives
of people with glaucoma and those
with other risk factors (e.g. myopia,
high blood pressure, diabetes).3
Continuing Professional Development
Management
There are an effective range of options
to manage glaucoma including topical
medications, laser trabeculoplasty
or surgery (e.g. trabeculectomy).
The aim of treatment is to slow or
halt disease progression so that any
visual loss has the least impact of the
patient’s quality of life.3 The reduction
of IOP is the cornerstone of all current
treatment options as it is the only
modifiable risk factor. Topical ocular
hypotensive medication is effective
in delaying or preventing the onset of
open-angle glaucoma in patients with
elevated IOP.16 Trials also demonstrate
that lowering IOP decreases glaucoma
progression17,18 so adequate control of
IOP in primary open-angle glaucoma is
the aim of treatment. There is general
consensus that medications should
be the first choice for most patients
with primary open-angle glaucoma.3
However, laser therapy may be used
as the first choice agent in some
patients who are at risk of visual loss
within their lifetime.3
Vol. 30 – February #02
Pharmacological management
Medication is generally the first
management choice by prescribers
for patients with open-angle
glaucoma. Medications reduce IOP
by reducing aqueous outflow and/
or formation. Table 2 shows the
five main classes of medication
used to manage glaucoma. Factors
that influence the initial choice of
medication include, IOP-lowering
potency, additive effects, interactions
with concomitant medications and
disease states, adverse effects
and ease of administration.3
Table 3 shows a summary of the
adverse effects associated with
glaucoma medications.
Using a target IOP is currently the
best way to measure the short‑term
142
Table 2. Medications available in Australia for the management
of chronic open-angle glaucoma. Modified from the
NHMRC guidelines for the screening, prognosis, diagnosis,
management and prevention of glaucoma.3
Preparations by
class
Mechanism
of action
Efficacy
Dosage
frequency
Washout
period
Order of
treatment
choices
Prostaglandin
analogues
Increase
aqueous
outflow
25–30%
Once daily
4–6 weeks
First
Decrease
aqueous
production
20–25%
Once to twice
daily
2–5 weeks
First
As for
individual
components
25–30%
Twice daily
As for
individual
components
Second
Bimatoprost 0.03% eye
drops (Lumigan)
Latanoprost 0.005% eye
drops (Xalatan)
Travoprost 0.004% eye
drops (Travatan)
Beta-blockers
Non-selective
Timolol 0.25%, 0.5%,
0.1% eye drops (Tenopt,
Timoptol, Nyogel)
b1-receptor selective
Betaxolol 0.25%, 0.5% eye
drops (Betoptic)
Proprietary-fixed
combinations
Brimonidine 0.2%/
timolol 0.5% eye drops
(Combigan)
Dorzolomide 2%/timolol
0.5% eye drops (Cosopt)
Bimatoprost 0.03%/timolol
0.5% eye drops (Ganfort)
Once daily
Latanoprost 0.005%/
timolol 0.5% eye drops
(Xalacom)
Travoprost 0.004%/timolol
0.5% eye drops (DuoTrav)
Alpha-2 agonists
Brimonidine 0.2% eye
drops (Alphagen)
Apraclonidine 0.5% eye
drops (Iopidine)
Carbonic anhydrase
inhibitors
Topical
Increase
aqueous
outflow and
decrease
aqueous
production
20–25%
Two to three
times daily
1–3 weeks
Second
Decrease
aqueous
production
15–20%
Two to three
times daily
1 week
Second
25–30%
Two to four
times daily
3 days
Third
20–25%
Three to four
times daily
3 days
Third
Brinzolamide 1% eye drops
(Azopt, BrinzoQuin)
Dorzolamide 2% eye drops
(Trusopt)
Systemic
Acetazolamide 250 mg
tablets (Diamox)
Cholinergics
Pilocarpine 1%, 2% eye
drops (P.V. Carpine,
Isopto Carpine Pilopt,
Minims Pilocarpine
Nitrate)
Carbachol 1.5%,
3% eye drops
(Isopto Carbachol,
Miostat)
Increase
aqueous
outflow
evidence in patient care
The articles in this series are independently researched and compiled by PSA commissioned authors and peer reviewed.
Table 3. A summary of adverse effects associated with
medications used to lower IOP. Modified from the NHMRC
guidelines for the screening, prognosis, diagnosis,
management and prevention of glaucoma.3
Class
Adverse
effects
Prostaglandin
analogues
Bradyarrhythmias/
hypotension
BetaAlpha-2
blockers agonists
Carbonic
anhydrase
inhibitors
Systemic Topical Cholinergics
√
Continuing Professional Development
Tachycardia/
hypertension
√
Depression
√
Masking of
hypoglycaemia
√
Bronchospasm
rare
√
√
√
Elevated serum
lipids
√
Falls in elderly
√
Anaphylaxis
√
Altered taste
√
Dizziness
√
Paraesthesia
√
Impotence
Other minor
systemic
√
√
√
√*
Drowsiness/
fatigue
Dry mouth
Minor ocular
symptoms
√
Major ocular
symptoms
√
√**
√
√
√
√
√
√
√
√
√
√
√
√
Subsequent treatment
* Headaches, pruritis, urticaria
** Hearing dysfunction, gastrointestinal disturbance, reduced libido
Vol. 30 – February #02
NB: While the same cautions apply to non-selective and relatively selective beta-blockers, there is a wider margin of
safety for the latter (betaxolol)
effectiveness of the chosen
medication regimen. There is no
fixed target for IOP – the target
IOP is a theoretical value that will
minimise the progression of optic
nerve damage and visual field loss.
The target IOP typically is set as a
30–50% reduction in pre-treatment
IOP.3 Target IOPs are not static and
may need to be modified based
on the response to treatment. As
glaucoma progression may still occur
in patients with apparently stable IOP,
continuing evaluation of the optic disc
and visual field is more important
than monitoring of the IOP in the
longer term.
Treatment usually begins with topical
eye drops as they have a localised
144
treatments for glaucoma. Over the
past decade, prostaglandin analogues
have gradually superseded older
medications for the initial treatment
of primary open-angle glaucoma.20
Prostaglandin analogues are highly
effective with a lower risk of systemic
adverse effects when compared
with beta-blockers, although they
are more expensive.21 Beta-blockers
should generally be avoided in
patients with reactive airways disease
(although as betaxolol is selective
for beta1 receptors it can be used
with care)22 or cardiac conduction
defects as systemic absorption may
lead to significant adverse effects.
Prostaglandin analogues have a
lower risk of systemic adverse
effects, but may increase eyelash
growth, and result in iris and eyelash
pigmentation changes.23 If topical
prostaglandin analogues or betablocker therapies cannot be tolerated
or are contraindicated, either an
alpha-2-adrenergic agonist or
carbonic anhydrase inhibitor should
be considered.3 It is recommended
that treatment begin in one eye only
(the worst eye), using the other eye
as a control to test for effectiveness.3
Response to lowering the IOP should
be checked within 2–6 weeks, as this
is considered a reasonable time-frame
for the medication to reach full effect
before treatment is extended to the
other eye.
effect and a lower incidence of
adverse effects. In some situations,
such as an inability to instill eye drops,
oral acetazolamide may be used.3
Oral acetazolamide is poorly tolerated
by up to 50% of patients, which
significantly limits its use. Systemic
beta-blockers are not as effective
at reducing IOP as topical betablockers and their use in combination
with topical beta-blockers is not
recommended.3,19
Initial treatment
The initial choice of medication should
be based on effectiveness, safety
and convenience. Prostaglandin
analogues and beta-blocker eye
drops are the preferred first-line
Depending on the response to the
initial topical medication, the patient
may require either a change in
medication or an additional topical
agent. A change to therapy is justified
if there is an inadequate response
despite optimal patient adherence
to the initial agent.3 Switching to an
alternative agent within a class or an
alternative class is recommended if
the initial response is poor. Increasing
the dose of the initial agent is not
recommended as it will not lower
the IOP further and may expose the
patient to a higher risk of adverse
effects. In this case, a wash out
period should be followed by another
trial in one eye. It is worth noting
that prostaglandin analogues are
structurally different to each other and
patient response to agents within the
class may differ.22
If an adequate response (a response,
but not to the target level) has been
achieved with the initial medication,
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Optimising adherence and
persistence
Current therapy relies heavily
on patient cooperation in selfadministration. So it is not surprising,
given the asymptomatic nature of
open-angle glaucoma, that adherence
and persistence is often reported to
be poor. Adherence rates to glaucoma
medications of 24% to 59% have
been reported in the literature.26–30 To
maximise adherence it is important
to simplify the medication regimen
wherever possible. The lowest dose
of the most effective medication
should be used to reach the target
IOP and prevent progression of visual
field defects.3 Once daily dosing
has been shown to improve patient
satisfaction and adherence, and is
often possible when only one or two
topical medications are required.31
Patient education and informed
participation in treatment decisions
also improves adherence.32
Pharmacists can assist patients
with glaucoma to optimise their
adherence by:
• encouraging patient adherence
and persistence with using their
glaucoma medications
• educating patients about the risks
and prognosis of their disease
• providing a medication profile; it is
important to include the name of
their glaucoma medications, the
time of day to administer them, the
number of drops and information
on how to identify the medications
(e.g. colour of bottle cap)
• ensuring that all medications have
clear labels and patients know how
to use them
• providing information to patients
about their disease to improve their
understanding, such as publications
from Glaucoma Australia
• providing contact details for
consumer groups that provide
support and education.3
Instillation of topical
medications
Patients need to understand how to
instill drops effectively and efficiently.
The preferred method for eye drop
self-instillation included holding
the head horizontal with tear duct
occlusion and eyelid closure for
2–3 minutes (DOUBLE DOT: Digital
Occlusion of Tear Duct and Don’t
Open Technique). Systemic absorption
can be reduced by up to 70% using
this technique.3,33 If two or more
drops are being instilled then there
should be an interval of at least five
minutes between drops. Videos and
printed material are available from
the Glaucoma Australia website for
patients and there are also devices
available that can aid with instillation
of eye drops if patients require them.
Further information can be found at:
www.glaucoma.org.au/eyedrops.htm
Advice for Mabel
Primary open-angle glaucoma is an
irreversible optic neuropathy that is a
leading cause of blindness. Medications
are generally the first management
choice and a range of considerations
influence the choice of initial treatment.
The pharmacist should advise Mabel
that there are many different treatment
options available for glaucoma and
that treatment for each patient is
individualised. Combination products are
often used when one medication alone
is not sufficient to meet the target IOP.
Pharmacists can encourage patients
who have a greater risk of developing
glaucoma to see their eye-care
professional for screening and advice.
Topical medications have an important
role in the management of primary
open angle glaucoma. Pharmacists
play a central role in helping patients to
achieve the true benefits of treatment
providing education on glaucoma
medications; encouraging adherence;
and identifying and assisting patients
who are experiencing adverse effects
from their medication or having difficulty
instilling their eye drops.
145
Vol. 30 – February #02
If more than two topical medications
are required to lower the IOP then
other options, such as laser therapy
or surgery, should be considered as
alternatives to additional medications.3
If patients are not candidates for laser
therapy or surgery then systemic
therapy is another option at this stage.
The purpose of laser therapy and
surgery is to make a selective lesion
in one or more structures of the eye
to reduce the IOP. Currently Australian
guidelines recommend the use of
argon laser trabeculoplasty in older
patients with open-angle glaucoma
who are at risk of visual loss within
their lifetime, particularly when they
have difficulty administering eye
drops, are unresponsive to medication
alone or are poor candidates for
incisional surgery.3 Patients who
have undergone laser therapy require
continual monitoring due to the
diminishing treatment benefit over
time. Surgical interventions are at
least as effective as medication for
reducing IOP in open-angle glaucoma
and are currently recommended when
target IOP is not being achieved with
two or more medications, adherence
is problematic, and when laser therapy
has failed or is not likely to succeed.3
Continuing Professional Development
an additional medication is normally
added. There is currently no
consensus on the optimal combination
of topical medications to manage
primary open-angle glaucoma. No
specific combination of medications
has been identified as optimal in
terms of visual field preservation
or optic nerve head health.3 The
bulk of the literature focuses on
combinations of a beta-blocker with
either a prostaglandin analogue or
carbonic anhydrase inhibitor.24 There
are a number of fixed combination
products available that combine
timolol with a prostaglandin analogue,
carbonic anhydrase inhibitor or alpha2-adrenergic agonist. One advantage
of the prostaglandin analogue/
timolol combinations are that they
can be administered once daily to
optimise adherence. Medications
from the same class should not
be combined and if combination
products are used, it is important
that existing medications are not
duplicated (e.g. timolol or betaxolol
drops should not be used with any of
the fixed-dose combination products
currently available). Combinations
of prostaglandin analogues may
result in a paradoxical increase in
IOP and should be avoided.22 The
combination of topical and systemic
beta-blocker occurs quite commonly in
Australian practice, one study finding
that approximately 20% of patients
supplied topical beta-blockers were
also supplied systemic beta-blockers.25
This combination should be avoided
because research shows that patients
using both topical and systemic betablockers have significantly smaller
decreases in IOP compared to those
using a topical beta-blocker alone.
They also have significantly greater
variations in systolic and diastolic
blood pressure and a notably greater
decrease in heart rate.19
evidence in patient care
The articles in this series are independently researched and compiled by PSA commissioned authors and peer reviewed.
Continuing Professional Development
References
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with glaucoma worldwide in 2010 and 2020. Br J
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3. National Health and Medical Research Council.
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DC, Taylor HR. Detection of undiagnosed glaucoma
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20,000 eyes and its relationship to driving performance.
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GA, Ritch R, Sherwood M, Meng K, Mangione CM.
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Parrish RK, 2nd, Wilson MR, Kass MA. The Ocular
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16. Kass MA, Heuer DK, Higginbotham EJ, Johnson CA,
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hypotensive medication delays or prevents the onset
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2002;120:701–13; discussion 829–730.
17. Heijl A, Leske MC, Bengtsson B, Hyman L, Hussein
M. Reduction of intraocular pressure and glaucoma
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18. Leske MC, Heijl A, Hussein M, Bengtsson B, Hyman L,
Komaroff E. Factors for glaucoma progression and the
effect of treatment: the early manifest glaucoma trial.
Arch Ophthalmol. 2003;121:48–56.
19. Schuman JS. Effects of systemic beta-blocker therapy
on the efficacy and safety of topical brimonidine
and timolol. Brimonidine Study Groups 1 and 2.
Ophthalmology. 2000; 107:1171–7.
20. Charles J, Britt H, Fahridin S. Glaucoma. Aust Fam
Physician. 2009;38:763.
21. Hedman K, Alm A. A pooled-data analysis of three
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latanoprost and timolol. Eur J Ophthalmol. 2000;10:
95–104.
22. Australian Medicines Handbook Pty Ltd. Australian
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Handbook; 2010.
Questions 1. The prevalence of open-angle
glaucoma in people aged over
50 years is approximately?
a) 1%.
b) 2%.
c) 3%.
d) 5%.
Vol. 30 – February #02
2. Which one of the following
characteristics is not included
in the definition of primary
open-angle glaucoma?
a) Progressive damage to the optic
nerve.
b) Elevated intraocular pressure.
c) Patterns of visual loss.
d) Structural abnormalities of the
optic nerve head.
146
23. Alm A, Widengard I. Latanoprost: experience of 2-year
treatment in Scandinavia. Acta Ophthalmol Scand.
2000;78:71–6.
24. Webers CA, Beckers HJ, Nuijts RM, Schouten JS.
Pharmacological management of primary open-angle
glaucoma: second-line options and beyond. Drugs
Aging. 2008;25:729–59.
25. Goldberg I, Adena MA. Co-prescribing of topical and
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A score of 4 out of 5 attracts 1 CPD credit.
3. Which one of the following
medications is not regarded
as a first-line treatment in the
management of primary open
angle glaucoma?
a) Latanoprost.
b) Brimonidine.
c) Bimatoprost.
d) Timolol.
4. Which one of the following
statements concerning
pharmacological treatment of
primary open angle glaucoma
is incorrect?
a) There is no fixed target for
intraocular pressure (IOP)
monitoring.
b) Systemic beta-blockers are as
effective at reducing IOP as topical
beta-blockers.
c) Prostaglandin analogues have a
lower risk of systemic adverse
effects compared to beta-blockers.
d) Combinations of prostaglandin
analogues may result in a
paradoxical increase in IOP and
should be avoided.
5. Which one of the following
medication classes is
associated with major ocular
adverse effects?
a) Prostaglandin analogues.
b) Beta-blockers.
c) Carbonic anhydrase inhibitors.
d) Cholinergics.