DIS - Glaucoma Medications I - Week 5 Flashcards

1
Q

Must glaucoma patients whose treatment is initiated by an optometrist be referred to an ophthalmologist? Explain.

A

Yes, within 4 months of initiating treatment, for chronic glaucoma to consider surgical options

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2
Q

List the four types of aqueous suppressants. Note which isnt yet available in Australia.

A

Adrenergic alpha agonist
Adrenergic beta blocker
Carbonic anhydrase inhibitor
Rho-kinase inhibitor (NA)

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3
Q

List two types of outflow modulators for the uveoscleral route.

A

Prostaglandin Analogues (PGAs)
Adrenergic alpha agonists

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4
Q

List three types of outflow modulators for the trabecular meshwork. Note which isnt yet available in Australia.

A

Muscarinic
Rho-kinase inhibitor (NA)
Nitric oxide (NA)

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5
Q

List two alpha agonist aqueous suppressant drugs and concentrations used.

A

Iopidine (0.5%)
Brimonidine (0.15%, 0.2%)

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6
Q

List two rho-kinase inhibitor aqueous suppressant drugs and concentrations used.

A

Rhopressa (0.02%)
Netarsudil (0.02%)

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7
Q

List three beta blocker aqueous suppressant drugs and concentrations used.

A

Betaxolol (0.25%, 0.5%)
Timolol (0.25%, 0.5%)
Nyogel (0.1%)

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8
Q

List three carbonic anhydrase inhibitor aqueous suppressant drugs and concentrations used.

A

Brinzolamide (1%)
Dorzolamide (2%)
Diamox (azetazomalide 250mg PO)

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9
Q

List five prostaglandin analogue uveoscleral outflow modulator drugs and concentrations used.

A

Latanoprost (0.005%)
Tafluprost (0.0015%)
Travoprost (0.004%)
Bimatoprost (0.03%)
Latanoprostene bunod (0.024%)

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10
Q

List an alpha agonist uveoscleral outflow modulator drug and the concentration used.

A

Brimonidine (0.15%, 0.2%)

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11
Q

List a muscarinic trabecular meshwork outflow modulator drug and the concentration used.

A

Pilocarpine (1%, 2%, 4%)

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12
Q

List two rho-kinase inhibitor trabecular meshwork outflow modulator drugs and concentrations used.

A

Rhopressa (0.02%)
Netarsudil (0.02%)

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13
Q

List a nitric oxide trabecular meshwork outflow modulator drug and the concentrations used.

A

Latanoprostene bunod (0.024%)

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14
Q

What enzyme sustains ionic flux within the ciliary body and how does water diffuse passively?

A

Carbonic anhydrase
Water diffuses via aquaporins

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15
Q

What does the inhibition of carbonic anhydrase do to aqueous production and how (3)?

A

Decreases aqueous production
By blocking carbonic anhydrase, you block the conversion of CO2 and H2O into HCO3- and H+
This prevents the exchange of these two molecules with Cl- and Na+ into the cell and out into the posterior chamber (these ions stay put), disrupting ionic flux

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16
Q

Where are alpha and beta receptors located (3)?

A

Ciliary epithelium
Veins of schlemms canal
Veins of the ciliary body

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17
Q

Describe how a beta-blocker reduces aqueous production by explaining what a beta agonist does (5).

A

Stimulates a g-protein cascade resulting in an increase to adenyl cyclase, increasing levels of cAMP
This activates a kinase which increases aqueous production
A beta-blocker would stop this from happening

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18
Q

Describe how an alpha-agonist results in a decrease in aqueous production. Note whether this is a1 or a2. Describe where receptors of the other alpha are found and two things an agonist results in.

A

An a2 agonist stimulates a g-protein cascade (different to a beta g-protein cascade) resulting in an inhibition of adenyl cyclase, decreasing levels of cAMP
This inactivates a kinase which results in decreased aqueous production
Veins have a1 receptors, agonists reult in increased TM outflow and uveoscleral outflow

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19
Q

Compare the onset and duration of the effects of beta blockers and alpha agonists (both a1 and a2) on aqueous production.

A

Alpha a2 and beta blockers have a slow onset and are long lasting
Alpha a1 agonists have a fast onset, short duration

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20
Q

Are diamox tablets (oral) available for optomtrists? Explain (2).

A

No, do it via a GP or pharmacist

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21
Q

Can diamox tablets and drops be used concurrently?

A

No, avoid concurrent use

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22
Q

What percentage rise in IOP is seen if you swap from oral diamox to topical?

A

25%

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23
Q

What percentage drop in IOP is seen with oral diamox? What about topical use?

A

Oral - up to 50%
Topical - up to 20%

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24
Q

What is oral diamox often taken with? How long does IOP take to decrease with this combo? what about if diamox is injected?

A

500mg KCl
120 mins for IOP decrease if oral
15 mins if injected

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25
List two contraindications for diamox. Explain why if applicable (3). Also mention a certain diuretic in this context.
Allergy if sensitive to sulpha drugs Kidney disease - risk for acidosis and potassium depletion - especially if with thiazide diuretic (+500mg K po)
26
What are the systemic effects of carbonic anhydrase inhibitor drops? Explain why.
Few to no systemic effects because they bind to red blood cells
27
How often are carbonic anhydrase inhibitor drops taken? What is the half life and what is this due to?
bid Half life ~4h due to corneal reservoir
28
Do carbonic anhydrase inhibitor drops decrease IOP more, the same, or less than most other drugs?
Less
29
How do carbonic anhydrase inhibitor drops affect IOP diurnal fluctuation? Is this good or bad?
Reduces it - a good thing
30
Do carbonic anhydrase inhibitor drops have a good or poor vascular and nocturnal profile?
Good
31
Are the effects of carbonic anhydrase inhibitor drops fast or slow?
Fast (1h)
32
With what other IOP lowering drug are carbonic anhydrase inhibitor drops a good adjunct (and how many drops per day).?
Prostaglandins -carbonic anhydrase inhibitor drops bid for adjunct therapy
33
List two primary therapies for which carbonic anhydrase inhibitor drops are used (and how many drops per day).
For large diurnal IOP fluctuation (tid) For patients with low tension glaucoma (tid) -to promote vasobenefits
34
Are there any allergic responses to carbonic anhydrase inhibitor drops?
No
35
In which case should carbonic anhydrase inhibitor drops be avoided? Explain why.
Avoid in corneal grafts -cornea needs carbonic anhydrase to pump
36
What kind of formulary are brinzolamide (Azopt) generally made, are different drugs in this class similar, and what kind of release does this formulary have?
All have similar formularies Azopt - buffered suspension - shake before use Suspensions give slower release
37
Does Azopt sting more or less on instillation? Compare the IOP reduction it has to dorzolamide (Trusopt).
Less stinging Same IOP effect as Trusopt
38
How should Azopt be stored?
Upside down as its a suspension
39
Is Azopt ok for use in pregnancy and lactation?
Yesd
40
What advice is given to patients who need to use Azopt (3)?
Shake before use Store upside down May feel discomfort for a while, if vision blurs avoid driving and operating machinery
41
Do beta blockers have a small or large effect on IOP?
Large
42
Do beta blockers have many side effects/contraindications or few?
Many
43
Can the effects of a beta blocker wear off?
Yes
44
Are beta blockers effective at night?
No
45
Using IOP and blood pressure, describe how beta blockers are not helpful in low tension glaucoma, especially at night.
Beta blockers do not work at night Blood pressure decrease coupled with high IOP means decreased perfusion pressure - must avoid in low tension glaucoma
46
Describe why beta blockers do not work at night.
They are aqueous suppressants. Aqueous flow decreases at night on its own, these drugs cant decrease it any further
47
What happens to ~50% of beta blocker patients after 1-2 years?
Tachyphylaxis
48
List 5 ocular side effects of beta blockers.
Blurred vision Corneal hypoaesthesia SPK Macular oedema Conjunctivitis
49
List four side effects beta blockers can have on the lungs (1), heart (2), and endocrine system (1).
Bronchospasm Bradycardia Reduced blood pressure Increased HDLs
50
What effect do beta blockers have on myasthenia gravis?
Worsens it
51
What effect do beta blockers have on hyperthyroidism and diabetes?
Masks their signs
52
What effect do beta blockers have on libido and sleep disorders? Explain why if applicable and what it can lead to.
Decreases libido Increases sleep disorders -depresses melatonin (can lead to depression)
53
What ocular condition is a contraindication for beta blockers?
Low tension glaucoma
54
When prescribing beta blockers, for what 5 conditions should a patient be worked up for by their GP?
Bradycardia Athsma Myasthenia gravis Diabetes Depression
55
Is there an additive effect of topical + systemic beta blocker? Should it be used in this manner with caution? Explain (1).
There is an additive effect Use with caution and monitor for bradycardia Effect most on blood pressure and pulse
56
Must a patients Gp be informed in long term beta blocker therapy?
Yes
57
Do oral beta blockers have an effect on IOP?
Yes, 1mmHg
58
Is timolol (nyogel) a selective or non-selective beta blocker?
Non-selective
59
How is timolol best used?
As an adjunct with an alpha agonist or PGA for night time benefit
60
Is betaxolol a selective or non-selective beta blocker?
Selective b1 blocker
61
What is the safest beta blocker for asthmatics?
Betaxolol
62
Does betaxolol have more, the same, or less effects on cardiac/blood pressure as timolol?
The same
63
Does betaxolol have more, the same, or less effects on IOP as timolol?
Less
64
What does recent evidence suggest of the effect non-selective beta blockers have on blood vessels and why is this significant?
Suggests they (timolol) can cause vasoconstriction, offsetting IOP benefit
65
In what disease is betaxolol contraindicated?
Cardiac disease
66
Where are a1 receptors found, and what is the mechanism of action for alpha 1 agonists?
Found on the veins They increase the uveoscleral outflow and increase TM outflow (major)
67
Explain how alpha agonists have a neuroprotective effect.
Increased blood flow to the optic nerve
68
What effect can alpha agonists have in kids? what about adults (2)?
Kids - can make them drowsy Adults - systemic hypotension and lethargy in some
69
List three contraindications for alpha agonists.
Tricyclic antidepressants MAO inhibitors Severe cardiovascular disease
70
Is there an IOP effect at night with a1 agonists? What about blood flow?
No IOP effect at night But increased blood flow
71
Is the effect of a1 immediate?
Yes
72
What drug is recommended for use in glaucoma and what kind of drug is it (including selectivity). Why does it have short term applications? Explain why IOP control wears off (and after how long).
Apraclonidine -a1 selective agonist Short term application due to tachyphylaxis Its a1 selectivity means IOP control wears off in 30% of people after 3-4 months
73
List three ocular effects apraclonidine can have.
Mydriasis Lid retraction Conjunctival vasoconstriction
74
What selectivity does brimonidine have? Does it cause tachyphylaxis? How quickly does it act and what kind of IOP response does it elicit?
Selective a2 agonist Doesnt cause tachyphylaxis Fast response (<2h) Moderate IOP response (4-5mmHg)
75
Is brimonidine good for short or long term application?
Long term
76
Is brimonidine good to use for low tension glaucoma or should it be avoided?
Good for low tension glaucoma
77
What line drug is brimonidine considered?
Acceptable as 2nd line drug
78
How many drops per day is brimonidine used? What gives better compliance? How should it be used if as an adjunct?
tid for max effect bid gives better compliance bid as an adjunct
79
Does brimonidine have neuroprotective effects like some other alpha agonists?
Yes
80
What is combigan and why is it used?
IOP benefits of timolol and blood flow benefits of alphagan (brimonidine) as well as night time alpha benefits (IOP not reduced)
81
Compare IOP control and night time effect in beta blocker vs alpha agonists. Describe an advantage of alpha agonist over beta blockers. Are a combination of the two good or avoided?
Beta blocker - good IOP control excpet at night Alpha agonist - good IOP control except at night -good pOBF effect Combination of the two is good overall
82
Describe the direct (3) and indirect (3) pathways of how muscarinic drugs act on aqueous flow.
Direct -M3 receptors on ciliary body activates muscles -cells pull on the scleral spur -decreases IOP Indirect -muscarinic receptors on trabecular cells activate actin fibres -trabecular pores close -IOP increases
83
Do cholinergic agonists activate muscarinic/nicotinic receptors?
Yes
84
What kind of agonist is pilocarpine (2)?
Muscarinic and nicotinic
85
Does pilocarpine have a fast or slow onset? How long does the response last?
Fast onset (1h) and short lasting response
86
How many drops for pilocarpine per day? What effect does having brown eyes have and why? What should be done in these cases?
tid Reduced effect in brown eyes due to non-specific pigment binding (use 2%)
87
What is the major applicaiton of pilocarpine and why (2)? Is it used for modern glaucoma? Explain.
Low doese (0.016%) useful in PDS/PDG where miosis and reduced iris movement is desired Not used much for glaucoma due to adverse effects
88
List 5 contraindications for pilocarpine.
History of peripheral retinal detachment High myopia Central media opacity Young patients Uveitis
89
Why does cholinergic toxicity happen mostly due to?
Systemic absoprtion Reduce with digital occlusion and closed eyes
90
Does latanoprost have a quick or delayed onset? what is done with dosing as a result?
Delayed - dose at night
91
What happens to IOP early with latanoprost? What about with chronic application? What is this mainly due to?
IOP spike early on Chronic application - no spike -mainly MMP3 related
92
Describe the dual action of latanoprost (2 each). Note which is the main effect.
Inhibition of MMPs (main effect) -reduces IOP -small initially, large effect chronically Inhibition of TNFα -decreased inflammatory response, increased venous outflow -increased endothelial vacuoles/veins -fast IOP effect
93
Do PGAs tend to be very individual dependent in terms of response or do most poeple respond the same way?
Very individual dependent
94
Are PGAs safe?
Yesd
95
What are 5 ocular side effects of PGAs?
Iris darkening Skin discolouration Reduced adipocyte activity (sunken eyes) Thicker lashes Promotes ocular inflammation
96
What can PGAs predispose you to?
Recurrent HSV keratitis
97
List two contraindications for PGAs.
Pregnancy Ocular inflammatory disease
98
What is the safest PGA for glaucoma PGF2a activation?
Latanoprost (xalatan)
99
Does xalatan have an increased or decreased response in low tension glaucoma compared to other glaucomas?
Reduced
100
What is the major benefit of xalatan compared to other PGAs?
Additive to all other drugs, including pilocarpine
101
List three side effects of xalatan.
Iris darkening Lash growth Loss of orbital fat (sunken eyes)
102
List two reasons why xalatan can cause red eye. Note which is short term and long term.
Short term (up to 30 days) - due to altered outflow in veins Long term - due to MMP3 related cell swelling
103
What benefit does travoprost (travatan) have over latanoprost (xalatan)? List a consequence of this.
Better receptor binding -more adverse effects
104
Which PGA causes greater eyelash growth and can cause significantly more conjunctival hyperaemia?
Bimatoprost (lumigan)
105
How does the IOP reduction of latanoprost compare after 1 month and what is typically done?
It has poor IOP reduction after 1 month - switching to bimatoprosy may control IOP
106
Which of the gluacoma eyedrops should be avoided for 2 months after eye surgery and why? What can its effect be blocked by?
Avoid PGs for 2 months after eye surgery -increased PGs in the eye after surgery promotes cystoid macular oedema PG effect can be blocked with NSAID treatment Can cotreat with NSAID to suppress inflammation