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OD3 (S1&2) > DIS - Glaucoma Medications I - Week 5 > Flashcards

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
Q

List two contraindications for diamox. Explain why if applicable (3). Also mention a certain diuretic in this context.

A

Allergy if sensitive to sulpha drugs
Kidney disease - risk for acidosis and potassium depletion - especially if with thiazide diuretic (+500mg K po)

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26
Q

What are the systemic effects of carbonic anhydrase inhibitor drops? Explain why.

A

Few to no systemic effects because they bind to red blood cells

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27
Q

How often are carbonic anhydrase inhibitor drops taken? What is the half life and what is this due to?

A

bid
Half life ~4h due to corneal reservoir

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28
Q

Do carbonic anhydrase inhibitor drops decrease IOP more, the same, or less than most other drugs?

A

Less

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29
Q

How do carbonic anhydrase inhibitor drops affect IOP diurnal fluctuation? Is this good or bad?

A

Reduces it - a good thing

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30
Q

Do carbonic anhydrase inhibitor drops have a good or poor vascular and nocturnal profile?

A

Good

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31
Q

Are the effects of carbonic anhydrase inhibitor drops fast or slow?

A

Fast (1h)

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32
Q

With what other IOP lowering drug are carbonic anhydrase inhibitor drops a good adjunct (and how many drops per day).?

A

Prostaglandins
-carbonic anhydrase inhibitor drops bid for adjunct therapy

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33
Q

List two primary therapies for which carbonic anhydrase inhibitor drops are used (and how many drops per day).

A

For large diurnal IOP fluctuation (tid)
For patients with low tension glaucoma (tid)
-to promote vasobenefits

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34
Q

Are there any allergic responses to carbonic anhydrase inhibitor drops?

A

No

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35
Q

In which case should carbonic anhydrase inhibitor drops be avoided? Explain why.

A

Avoid in corneal grafts
-cornea needs carbonic anhydrase to pump

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36
Q

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?

A

All have similar formularies
Azopt - buffered suspension - shake before use
Suspensions give slower release

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37
Q

Does Azopt sting more or less on instillation? Compare the IOP reduction it has to dorzolamide (Trusopt).

A

Less stinging
Same IOP effect as Trusopt

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38
Q

How should Azopt be stored?

A

Upside down as its a suspension

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39
Q

Is Azopt ok for use in pregnancy and lactation?

A

Yesd

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40
Q

What advice is given to patients who need to use Azopt (3)?

A

Shake before use
Store upside down
May feel discomfort for a while, if vision blurs avoid driving and operating machinery

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41
Q

Do beta blockers have a small or large effect on IOP?

A

Large

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42
Q

Do beta blockers have many side effects/contraindications or few?

A

Many

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43
Q

Can the effects of a beta blocker wear off?

A

Yes

44
Q

Are beta blockers effective at night?

A

No

45
Q

Using IOP and blood pressure, describe how beta blockers are not helpful in low tension glaucoma, especially at night.

A

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
Q

Describe why beta blockers do not work at night.

A

They are aqueous suppressants. Aqueous flow decreases at night on its own, these drugs cant decrease it any further

47
Q

What happens to ~50% of beta blocker patients after 1-2 years?

A

Tachyphylaxis

48
Q

List 5 ocular side effects of beta blockers.

A

Blurred vision
Corneal hypoaesthesia
SPK
Macular oedema
Conjunctivitis

49
Q

List four side effects beta blockers can have on the lungs (1), heart (2), and endocrine system (1).

A

Bronchospasm
Bradycardia
Reduced blood pressure
Increased HDLs

50
Q

What effect do beta blockers have on myasthenia gravis?

A

Worsens it

51
Q

What effect do beta blockers have on hyperthyroidism and diabetes?

A

Masks their signs

52
Q

What effect do beta blockers have on libido and sleep disorders? Explain why if applicable and what it can lead to.

A

Decreases libido
Increases sleep disorders
-depresses melatonin (can lead to depression)

53
Q

What ocular condition is a contraindication for beta blockers?

A

Low tension glaucoma

54
Q

When prescribing beta blockers, for what 5 conditions should a patient be worked up for by their GP?

A

Bradycardia
Athsma
Myasthenia gravis
Diabetes
Depression

55
Q

Is there an additive effect of topical + systemic beta blocker? Should it be used in this manner with caution? Explain (1).

A

There is an additive effect
Use with caution and monitor for bradycardia
Effect most on blood pressure and pulse

56
Q

Must a patients Gp be informed in long term beta blocker therapy?

A

Yes

57
Q

Do oral beta blockers have an effect on IOP?

A

Yes, 1mmHg

58
Q

Is timolol (nyogel) a selective or non-selective beta blocker?

A

Non-selective

59
Q

How is timolol best used?

A

As an adjunct with an alpha agonist or PGA for night time benefit

60
Q

Is betaxolol a selective or non-selective beta blocker?

A

Selective b1 blocker

61
Q

What is the safest beta blocker for asthmatics?

A

Betaxolol

62
Q

Does betaxolol have more, the same, or less effects on cardiac/blood pressure as timolol?

A

The same

63
Q

Does betaxolol have more, the same, or less effects on IOP as timolol?

A

Less

64
Q

What does recent evidence suggest of the effect non-selective beta blockers have on blood vessels and why is this significant?

A

Suggests they (timolol) can cause vasoconstriction, offsetting IOP benefit

65
Q

In what disease is betaxolol contraindicated?

A

Cardiac disease

66
Q

Where are a1 receptors found, and what is the mechanism of action for alpha 1 agonists?

A

Found on the veins
They increase the uveoscleral outflow and increase TM outflow (major)

67
Q

Explain how alpha agonists have a neuroprotective effect.

A

Increased blood flow to the optic nerve

68
Q

What effect can alpha agonists have in kids? what about adults (2)?

A

Kids - can make them drowsy
Adults - systemic hypotension and lethargy in some

69
Q

List three contraindications for alpha agonists.

A

Tricyclic antidepressants
MAO inhibitors
Severe cardiovascular disease

70
Q

Is there an IOP effect at night with a1 agonists? What about blood flow?

A

No IOP effect at night
But increased blood flow

71
Q

Is the effect of a1 immediate?

A

Yes

72
Q

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).

A

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
Q

List three ocular effects apraclonidine can have.

A

Mydriasis
Lid retraction
Conjunctival vasoconstriction

74
Q

What selectivity does brimonidine have? Does it cause tachyphylaxis? How quickly does it act and what kind of IOP response does it elicit?

A

Selective a2 agonist
Doesnt cause tachyphylaxis
Fast response (<2h)
Moderate IOP response (4-5mmHg)

75
Q

Is brimonidine good for short or long term application?

A

Long term

76
Q

Is brimonidine good to use for low tension glaucoma or should it be avoided?

A

Good for low tension glaucoma

77
Q

What line drug is brimonidine considered?

A

Acceptable as 2nd line drug

78
Q

How many drops per day is brimonidine used? What gives better compliance? How should it be used if as an adjunct?

A

tid for max effect
bid gives better compliance
bid as an adjunct

79
Q

Does brimonidine have neuroprotective effects like some other alpha agonists?

A

Yes

80
Q

What is combigan and why is it used?

A

IOP benefits of timolol and blood flow benefits of alphagan (brimonidine) as well as night time alpha benefits (IOP not reduced)

81
Q

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?

A

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
Q

Describe the direct (3) and indirect (3) pathways of how muscarinic drugs act on aqueous flow.

A

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
Q

Do cholinergic agonists activate muscarinic/nicotinic receptors?

A

Yes

84
Q

What kind of agonist is pilocarpine (2)?

A

Muscarinic and nicotinic

85
Q

Does pilocarpine have a fast or slow onset? How long does the response last?

A

Fast onset (1h) and short lasting response

86
Q

How many drops for pilocarpine per day? What effect does having brown eyes have and why? What should be done in these cases?

A

tid
Reduced effect in brown eyes due to non-specific pigment binding (use 2%)

87
Q

What is the major applicaiton of pilocarpine and why (2)? Is it used for modern glaucoma? Explain.

A

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
Q

List 5 contraindications for pilocarpine.

A

History of peripheral retinal detachment
High myopia
Central media opacity
Young patients
Uveitis

89
Q

Why does cholinergic toxicity happen mostly due to?

A

Systemic absoprtion
Reduce with digital occlusion and closed eyes

90
Q

Does latanoprost have a quick or delayed onset? what is done with dosing as a result?

A

Delayed - dose at night

91
Q

What happens to IOP early with latanoprost? What about with chronic application? What is this mainly due to?

A

IOP spike early on
Chronic application - no spike
-mainly MMP3 related

92
Q

Describe the dual action of latanoprost (2 each). Note which is the main effect.

A

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
Q

Do PGAs tend to be very individual dependent in terms of response or do most poeple respond the same way?

A

Very individual dependent

94
Q

Are PGAs safe?

A

Yesd

95
Q

What are 5 ocular side effects of PGAs?

A

Iris darkening
Skin discolouration
Reduced adipocyte activity (sunken eyes)
Thicker lashes
Promotes ocular inflammation

96
Q

What can PGAs predispose you to?

A

Recurrent HSV keratitis

97
Q

List two contraindications for PGAs.

A

Pregnancy
Ocular inflammatory disease

98
Q

What is the safest PGA for glaucoma PGF2a activation?

A

Latanoprost (xalatan)

99
Q

Does xalatan have an increased or decreased response in low tension glaucoma compared to other glaucomas?

A

Reduced

100
Q

What is the major benefit of xalatan compared to other PGAs?

A

Additive to all other drugs, including pilocarpine

101
Q

List three side effects of xalatan.

A

Iris darkening
Lash growth
Loss of orbital fat (sunken eyes)

102
Q

List two reasons why xalatan can cause red eye. Note which is short term and long term.

A

Short term (up to 30 days) - due to altered outflow in veins
Long term - due to MMP3 related cell swelling

103
Q

What benefit does travoprost (travatan) have over latanoprost (xalatan)? List a consequence of this.

A

Better receptor binding
-more adverse effects

104
Q

Which PGA causes greater eyelash growth and can cause significantly more conjunctival hyperaemia?

A

Bimatoprost (lumigan)

105
Q

How does the IOP reduction of latanoprost compare after 1 month and what is typically done?

A

It has poor IOP reduction after 1 month - switching to bimatoprosy may control IOP

106
Q

Which of the gluacoma eyedrops should be avoided for 2 months after eye surgery and why? What can its effect be blocked by?

A

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

OD3 (S1&2) (114 decks)

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