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Endocrine > Glaucoma > Flashcards

Glaucoma Flashcards

1
Q

What is glaucoma?

A

Progressive deterioration of the optic nerve head and retinal nerve fiber layer.

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2
Q

What are the characteristics of primary open angle glaucoma?

A
  • Increased resistance to aqueous humor drainage due to trabecular network dysfunction = increased IOP.
  • Increased IOP is only partially a factor, other factors are not totally understood (autoimmune, ischemic changes, etc.).
  • Vision loss takes several years (variable)
  • Usually treated with topical mediations (eye drops)
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3
Q

What are the characteristics of primary angle closure glaucoma?

A
  • Drainage pathway is obstructed by the forward bowing of the iris (physical blockage of the trabecular meshwork).
  • Vision loss over course of days = emergency situation!!
  • Requires surgery to treat.
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4
Q

What are the risk factors for open angle glaucoma?

A

Elevated IOP >21 mmHg
Older age
Family history
Diabetes (T2DM)
Low blood pressure
Hypothyroidism
Obstructive sleep apnea
Steroid use
Cardiovascular disease
Thin central cornea
Myopia (nearsightedness)

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5
Q

What are the risk factors for closed angle glaucoma?

A

Asian heritage
Alaskan heritage
Hyperopia (farsightedness)
Medications

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6
Q

What drugs can cause medication-induced open angle glaucoma?

A

Glucocorticoids
Atropine
Succinylcholine

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7
Q

What drugs can cause medication-induced closed angle glaucoma?

A

Antidepressants
Anticholinergics
Adrenergics
Sulfonamides
Diuretics
Topiramate

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8
Q

How may some of the symptoms present in open angle glaucoma?

A

Symptoms are slow to present, and are often asymptomatic until vision loss.
* Blind spots over time
* Loss of contrast sensitivity
* Affects both eyes

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9
Q

True/false: Increased IOP is indicative of glaucoma.

A

False. IOP can be increased or normal in glaucoma. You can have increased IOP without glaucoma (ocular hypertension).

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10
Q

How may some of the symptoms present in closed angle glaucoma?

A
  • Blurred/hazy vision, halos, ocular pain
  • HA
  • N/V, abdominal pain
  • Diaphoresis (extreme sweating)
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11
Q

What objective finding is found in PACG?

A

Acute hyperemic conjunctiva

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12
Q

What are the potential symptoms of acute hyperemic conjunctiva?

A
  • Redness
  • Increased blood flow
  • Cloudy cornea
  • Shallow anterior chamber
  • Hyperemic optic disc
  • Marked elevation in IOP (40-90 mmHg) in acute ACG
  • Disk changes and vision loss in chronic ACG, IOP can be normal or elevated
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13
Q

What is the main goal for treatment of POAG?

A

Preservation of visual function through reduction in IOP.

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14
Q

What general IOP mmHg is desired?

A

<21 mmHg

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15
Q

Some patients may need a lower mmHg target. Why? What is this target?

A
  • Greater levels of glaucoma damage, advanced disease, or continued damage at a higher IOP goal.
  • <10 mmHg
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16
Q

What percentage of IOP reduction is desired?

A

20-30%

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17
Q

When is a greater percentage reduction of IOP desired? What is the percentage?

A
  • Patients with higher baseline IOP.
  • 40-50%
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18
Q

Reduction goals should be balanced with what?

A

Treatment-related toxicity/symptoms and QOL

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19
Q

What two classes are considered first line for POAG?

A

Prostaglandin analogs and beta blockers

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20
Q

If the two first line classes are contraindicated, what can be used instead?

A

Brimonidine (alpha 2 agonist) or topical CAI

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21
Q

What should be done if there is an inadequate response at 2-4 weeks?

A
  • Ensure adherence
  • Discuss nasolacrimal occlusion, eye closure (techniques for administration)
  • Partial response = consider increased frequency or concentration or add second agent
  • No response = switch to alternative
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22
Q

What should be done if there is intolerance to a first line agent?

A
  • Reduce concentration if can
  • Switch formulation, switch to alternative agent in same class, or switch alternative first line agent
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23
Q

What should be done if there is an inadequate response to monotherapy?

A
  • Ensure adherence
  • No response = alternative first line topical agent
  • Partial response = add second or third first line agent or topical CAI (may need up to 2-4 agents!)
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24
Q

What should be done if there is an inadequate response to multiple first/second line agents or topical combination therapy?

A
  • Ensure adherence
  • Consider direct-acting cholinergic agent (4th line)
  • Consider oral carbonic anhydrase inhibitor in place of topical CAI (short term use)
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25
Q

What is the name of the laser surgical treatment option for POAG?

A

Selective laser trabeculoplasty (SLT)

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26
Q

How should treatment be initiated?

A

Monotherapy
* Can start in one eye if concerns for drug tolerability or efficacy

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27
Q

When should IOP be checked after treatment initiation?

A

4-6 weeks

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28
Q

Once IOP reaches target level, how frequently should it be monitored?

A

Every 3-4 months
* Can go longer if prolonged control without disease progression

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29
Q

When should IOP be monitored more frequently?

A
  • Target IOP not achieved
  • Disease progression is noted
  • Any change in drug therapy
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30
Q

When should visual fields and disk changes be monitored?

A

Every 6-12 months

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31
Q

What is tachyphylaxis and why is it a concern?

A

Progressive decrease in response after repeated administration.
* Initial IOP response does not predict long term control (may wane over time)

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32
Q

What is the main goal for treatment of acute angle-closure crisis?

A

Rapid IOP reduction to preserve vision

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33
Q

What is the definitive treatment for AACC?

A

Laser or surgical iridotomy (may use drug therapy to rapidly decrease IOP beforehand)

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34
Q

What are the drug options for AACC?

A
  • Miotics (pilocarbine)
  • Secretory inhibitors (BBs, alpha-2 agonists, topical/systemic CAIs, or prostaglandin)
  • Osmotic agents (most rapid decrease in IOP, oral glycerin, IV mannitol)
  • Topical steroid (reduced ocular inflammation)
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35
Q

What is the MOA of prostaglandin analogs?

A

Increase uveoscleral and trabecular outflow of aqueous humor.

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36
Q

What line of therapy are PGF2a analogs?

A

First line

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37
Q

What is the dosing of PGF2a analogs?

A

Once daily at bedtime; 24 hour IOP control

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38
Q

How does IOP reduction of PGF2a analogs compare to beta blockers?

A

Superior

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39
Q

How is the tolerability and cost of PGF2a analogs?

A

Good tolerability (less systemic effects), low cost

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40
Q

What is brand name of latanoprost?

A

Xalatan

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41
Q

What is the brand name of bimatoprost?

A

Lumigan, Latisse

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42
Q

What is a common side effect of PGF2a analogs?

A
  • Altered iris pigmentation - usually seen in people with brown eyes, not reversible, no harm
  • Hypertrichosis (excessive growth/thickening) of eyelashes - reverses when discontinued, no harm
  • Loss of periorbital fat - sunken eye, no harm
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43
Q

What are some of the rarer side effects of PGF2a analogs?

A
  • Punctate corneal erosions
  • Conjunctival hyperemia
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44
Q

True/false: PGF2a analogs can be used in combination with other antiglaucoma agents.

A

True - effective as both a monotherapy and adjunct

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45
Q

What is the contraindication for PGF2a analogs?

A

Avoid in patients with herpes simplex keratitis

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46
Q

What is the brand name of latanoprostene bunod?

A

Vyzulta

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47
Q

What is Vyzulta approved for?

A

OAG and OHT

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48
Q

What is the MOA of Vyzulta?

A

Dual MOA! Latanoprost prodrug and metabolized to a nitric-oxide moiety.

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49
Q

How does the IOP reduction of Vyzulta compare to latanoprost alone?

A

Greater reduction

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50
Q

What is durysta?

A

Bimatoprost implant

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51
Q

What is the dosage of durysta?

A

10 mcg dissolvable impant

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52
Q

How long does durysta reduce IOP?

A

About 15 weeks

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53
Q

How is durysta administered?

A

Via intracameral injection into anterior chamber

54
Q

What is durysta approved for?

A

OAG and OHT; one administration in each eye for the life of the patient

55
Q

How is the efficacy of durysta?

A

Noninferior to timolol at baseline, week 16, and week 32 (controlled at one year for most patients)

56
Q

What are the ADRs of durysta?

A
  • Corneal endothelial cell loss
  • Iritis
57
Q

What is the mechanism of action of beta blockers?

A

Reduced production of aqueous humor by ciliary body.

58
Q

What line of therapy are beta blockers?

A

Commonly used first line

59
Q

How much do beta blockers reduce IOP?

A

20-30%

60
Q

What is the dosing of beta blockers?

A

BID

61
Q

How well do beta blockers work on nocturnal IOP?

A

Minimally effective

62
Q

True/false: Beta blockers have significant local ocular ADRs.

A

False - minimal

63
Q

True/false: Beta blockers can be used as both monotherapy or in combination.

A

True - can combine with topical CAI, prostaglandin analogs, or brimonidine

64
Q

Which beta blocker is B1 selective?

A

Betaxolol

65
Q

Which beta blocker is non-selective and has sympathomimetic activity?

A

Carteolol

66
Q

Which beta blockers are nonselective?

A

Levobunolol, metipranolol, timolol

67
Q

Which beta blocker may provide a little less IOP lowering than the others?

A

Betaxolol

68
Q

What is significant about the timolol gel solution?

A

Provides similar IOP lowering with once daily dosing

69
Q

How frequently does tachyphylaxis occur with beta blockers?

A

20-25% of patients

70
Q

Should beta blockers for glaucoma be used alongside systemic beta blockers?

A

It should be avoided if possible. Mean IOP reduction may also be less in patients who are also receiving systemic.

71
Q

What are some common side effects of beta blockers?

A
  • Stinging on application
  • Dry eyes, blurred vision
  • Corneal anesthesia
  • Blepharitis (eyelid inflammation)
72
Q

What are some rarer side effects of beta blockers?

A
  • Conjunctivitis
  • Uveitis
  • Keratitis
73
Q

What should be done if having local intolerance to beta blockers?

A

Consider switching agent or formulation

74
Q

What are some systemic ADRs of beta blockers?

A
  • Bradycardia
  • Hypotension
  • Negative inotropic effects
  • Bronchospasm (nonselectives)
  • CNS effects
75
Q

Are systemic ADRs more or less common with B1 selective beta blockers?

A

Less

76
Q

What can be occluded to reduce risk of systemic ADRs?

A

Nasolacrimal pathway

77
Q

Use beta blockers with caution in what disease states?

A
  • Pulmonary diseases
  • Sinus bradycardia
  • Second or third degree heart block
  • CHF
  • Atherosclerosis
  • Diabetes
  • Myasthenia gravis
  • Patients receiving oral beta blocker
78
Q

What is the MOA of alpha-2 agonists?

A

Decrease rate of aqueous humor production, some increase in uveoscleral outflow

79
Q

What is the brand name of brimonidine?

A

Alphagan P

80
Q

How frequently is brimonidine administered?

A

Every 8-12 hours

81
Q

What administration method can be used with brimonidine to improve efficacy and extend dosing interval to 12 hours?

A

Eyelid closure

82
Q

How is brimonidine’s effect on nocturnal IOP?

A

Minimal - can be improved when combined with prostaglandins, BB, or CAIs

83
Q

How much does brimonidine reduce IOP?

A

18-27% at peak (2-5 hours) and 10% at 8-12 hours

84
Q

What is the potential benefit of using brimonidine purite as opposed to Alphagan-P?

A
  • Lower concentration, so can potentially be used in patient with brimonidine allergy
  • Less toxic preservative
85
Q

What are the symptoms of an allergy to brimonidine?

A
  • Lid edema
  • Eye discomfort
  • Foreign object sensation
  • Itching
  • Hyperemia (excess of blood in vessels)
86
Q

What should be done in the case of a brimonidine allergy?

A

Discontinuation

87
Q

What are some systemic ADRs of brimonidine?

A
  • Significant dizziness, fatigue, somnolence
  • Dry mouth
  • Slight decrease in BP/HR
88
Q

Brimonidine should be used in caution with which disease states?

A
  • Cardiovascular disease
  • Cerebrovascular disease
  • Diabetes
  • Renal compromise
  • Antihypertensives/CV meds
  • MAOIs/TCAs
89
Q

What is the contraindication for brimonidine?

A

Contraindicated in infants

90
Q

What is the MOA of CAIs?

A

Decrease ciliary body aqueous humor secretion.

91
Q

How often are CAIs given?

A

2-3 times a day - eyelid closure should optimize response

92
Q

What line of therapy are CAIs?

A

Second line monotherapy or adjunct therapy

93
Q

What is brinzolamide’s brand name?

A

Azopt

94
Q

What is dorzolamide’s brand name?

A

Trusopt

95
Q

What are some ADRs of CAIs?

A
  • Transient burning
  • Transient stinging (more dorzolamide)
  • Ocular discomfort
  • Transient blurred vision (more brinzolamide)
  • Tearing
96
Q

What are some rarer ADRs of CAIs?

A
  • Conjunctivitis
  • Lid reactions
  • Photophobia
  • Superficial punctate keratitis (10-15% of patients)
97
Q

How common are systemic ADRs in CAIs?

A

Rare

98
Q

What is the efficacy of CAIs?

A

Reduce IOP by 15-26%

99
Q

When should systemic CAIs be used?

A
  • Reserved for use in patients failing to respond to or tolerate maximum topical therapy
  • Sometimes used short term in patients with very high IOP or pre-surgery
100
Q

True/false: systemic CAIs can be used in combination with topical CAIs.

A

False

101
Q

How frequent are systemic CAIs given?

A

2-3 times per day

102
Q

What is the efficacy of systemic CAIs?

A
  • Reduce aqueous humor inflow by 40-60%
  • Reduce IOP by 25-40%
103
Q

What is acetazolamide’s brand name?

A

Diamox

104
Q

What is the other systemic CAI?

A

Methazolamide

105
Q

What line of therapy are systemic CAIs?

A

Third line - used short term

106
Q

What are some frequent intolerable ADRs of systemic CAIs?

A
  • Malaise, fatigue, anorexia, nausea, weight loss, altered taste, depression, decreased libido
  • Renal calculi, increased uric acid, blood dyscrasias (aplastic anemia), myopia
  • 30-60% of patients can tolerate oral CAIs for prolonged periods
107
Q

Systemic CAIs should be used with caution in which disease states?

A
  • Sulfa allergy
  • Sickle cell disease
  • Pulmonary disorders
  • Renal calculi
  • Electrolyte imbalance (hypokalemia)
  • Hepatic disease
  • Renal disease
  • DM
  • Addisons disease
  • Salicylate use (toxicity)
108
Q

What is the MOA of rho kinase inhbitors?

A

Increases trabecular meshwork outflow

109
Q

When is Rhopressa given?

A

Once daily in the evening

110
Q

How is Rhopressa’s efficacy with nocturnal IOP?

A

Reduces both daytime and nocturnal IOP

111
Q

Can Rhopressa be used in combinations?

A

Yes. Combination with latanoprost = Rocklatan

112
Q

What are some ocular ADRs of Rhopressa?

A
  • Conjunctival hyperemia
  • Conjunctival hemorrhage
  • Corneal verticillata
113
Q

What is the MOA of cholinergic agonists?

A

Increase aqueous humor outflow through pulling open the trabecular meshwork by ciliary muscle contraction

114
Q

Are cholinergic agonists commonly used?

A

No. Minimal use due to ocular ADRs and frequent dosing.

115
Q

What is the dosing for pilocarpine?

A

BID to QID

116
Q

What percentage does pilocarpine reduce IOP?

A

20-30%

117
Q

How does carbachol compare to pilocarpine?

A
  • Longer half life
  • Can be used if allergy/inadequate response to pilocarpine
  • Limited use because of more frequent/severe ADRs compared to pilocarpine
118
Q

How can pilocarpine response be improved?

A

Eyelid closure

119
Q

What can be done if have inadequate IOP reduction with pilocarpine?

A

Increase frequency or concentration

120
Q

What is different about patients with darker eyes when receiving pilocarpine?

A

May require higher concentration

121
Q

What are some ocular ADRs of pilocarpine?

A
  • Miosis (worsens vision in patients with cataracts)
  • Accommodative spasm
  • Frontal headache, brow ache, periorbital pain
  • Eyelid twitching
  • Conjunctival irritation
  • Retinal tears/detachment
  • Allergic reactions
  • Precipitation of closed angle glaucoma
122
Q

What are some systemic ADRs of pilocarpine?

A
  • Diaphoresis
  • N/V/D
  • Cramping
  • Urinary frequency
  • Bronchospasm
  • Heart block
123
Q

What drug class is echothiophate?

A

Cholinesterase inibitor

124
Q

Is echothiophate long acting or short acting?

A

Long. Relatively irreversible

125
Q

When should echothiophate be used?

A

Reserved for patients who do not tolerate or respond to any other therapy

126
Q

Echothiophate is cataractogenic. What does this mean?

A

Use only in patients without lenses or artificial lenses

127
Q

What are some risks of echothiophate?

A
  • Serious ocular and systemic toxic side effects
  • Severe fibrinous iritis
  • Synechiae
  • Iris cysts
  • Conjunctival thickening
  • Occlusion of nasolacrimal ducts
  • Muscle paralysis
128
Q

Echothiophate should be used with caution in which disease states?

A
  • Asthma
  • Retinal detachments, narrow angles
  • Bradycardia, hypotension, heart failure
  • Epilepsy, Parkinsonism
129
Q

What are the proper steps for eye drop administration?

A
  1. Wash & dry hands
  2. Shake bottle if a suspension
  3. Pull down outer portion of eyelid to form a pocket
  4. Brace bottle hand against cheek or nose with head held upward
  5. Look up and place single drop in eye
  6. Close lids for 5 minutes after instillation. Do not rub
130
Q

How long should you wait between instillations if 2 drugs are to be administered?

A

At least 5 minutes - 10 minutes is better

131
Q

How is nasolacrimal occlusion done?

A
  1. Press gently in corner of the eye by the nose while administering drops
  2. Hold for 2 minutes after instillation of the drop

Endocrine (4 decks)

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