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Glaucoma Flashcards

1
Q

What is glaucoma

A

Eye disease characterized by intraocular hypertension or increased pressure within the eye

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2
Q

At what intraocular pressure can a glaucoma be confirmed

A

> 22 mmHg

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3
Q

Why can glaucoma cause blindness or vision loss

A

Increased pressure in the eye can lead to damage of the optic nerve

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4
Q

Clear front of the eye that transmits and focuses light onto the eye

A

Cornea

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5
Q

Colored part of the eyes with muscles to constrict or relax the eye to regulate the size of the pupil

A

Iris

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6
Q

Size determines or regulates how much light enters the eye

A

Pupil

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7
Q

Transparent flexible tissue that help focus light and images on the retina

A

Lens

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8
Q

Senses light and create electrical impulse and sends them to the optic nerve

A

Retina

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9
Q

The chamber between the cornea and iris

A

Anterior chamber

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10
Q

Chamber between Iris and lens

A

Posterior chamber

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11
Q

Btw the Lens and retina carrying Virteous humor

A

Virteous Chamber

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12
Q

What chambers carry the aqueous humor

A

Anterior and posterior chamber

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13
Q

Clean water fluid produced by the ciliary body and brings nutrient to the eyes and maintains intraocular pressure

A

Aqueous humor

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14
Q

What is the roadway travel of aqueous humor

A

Starts from the posterior chamber to the anterior chamber through the pupil, across the iris and trabecular meshwork into the collecting duct (canal of schlemms) to the episcleral vein

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15
Q

What happens when aqueous humor enters the episcleral vein

A

It is absorbed into the bloodstream

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16
Q

What causes the intraocular pressure that leads to glaucoma

A

Interruption in flow of aqueous humor as a result of a blockage

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17
Q

Once blindness or damage to the optic nerve occurs is there treatment

A

No

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18
Q

What is the goal of glaucoma therapy

A

Prevent further damage to the optic nerve

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19
Q

What are the risk factors of glaucoma

A

Older adults

Family history of glaucoma

African Americans

Systemic or topical corticosteroid use

Patients with high intraocular pressure

Diabetes

Myopia

Genetic mutations

Thinner central corneal thickness

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20
Q

What is primary open angle glaucoma

A

Blockade in the trabecular meshwork causing increased resistance to aqueous humor drainage through the trabecular meshwork

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21
Q

What is primary closed angle glaucoma

A

Increase in the lens size that it presses against the cornea leading to obstruction of drainage pathways by the Iris

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22
Q

What are the diagnostic test

A

Visual field testing

Ocular tonometry

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23
Q

Open angle glaucoma symptoms

A

Asymptomatic until substantial vision loss occurs

Reduce IOP by 20-30% to reduce risk of optic nerve damage

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24
Q

True/False: in open angle glaucoma Intra ocular pressure can be normal or elevated ( > 21 mmHg)

A

True

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25
In open angle glaucoma what is considered mild IOP
Optic disk abnormalities with normal visual field
26
In open angle glaucoma what is considered moderate IOP
Optic disk changes with visual field abnormalities in one hemifield
27
In open angle glaucoma what is considered severe IOP
Optic disk changes with visual field abnormalities in both hemifield
28
Open angle glaucoma signs
Disk changes and visual field loss
29
Closed angle glaucoma symptoms
Asymptomatic Prodromal symptoms Acute episodes
30
Prodromal symptoms of closed angle glaucoma
Blurred vision Halos around light Occasional headache
31
Acute episodes of closed open Glaucoma
Cloudy Edematous corneas Ocular pain Discomfort Nausea and vomiting Abdominal pain Diaphoresis
32
What are the signs of closed angle glaucoma
Acute Hyperemia Conjuctiva Cloudy cornea Shallow anterior Chamber Occasional edematous and hyperemic optic disk
33
True/False: Closed angle glaucoma IOP is generally markedly elevated (40-90mmHg)
True
34
Which drugs induce open angle Glaucoma
Corticosteroids Ophthalmic anticholinergics Succinylcholine Vasodilator Cimetidine
35
Drugs that induce closed angle glaucoma
Anticholinergics BZ Topiramate Antihistamine Tetracycline Pratropium Phenothiazine SSRIs Venlafaxine Sympathomimetics
36
How are ways in which IOP is decreased
Decrease aqueous humor production Increase aqueous humor outflow Both ways
37
Drugs to decrease aqueous humor production
Beta-blockers Carbonic hydrase inhibitors
38
Drugs to increase aqueous humor outflow
Prostaglandin analogs Cholinergic analogs Rho kinase inhibitors
39
Drugs of both ways
Alpha 2 adrenergic agonist
40
Beta blockers cap color
Yellow
41
Beta blocker MOA
Decrease production of aqueous humor by the ciliary body
43
Non-selective beta blockers
Timolol Levobunolol Metipranolol Carteolol
44
Selective beta blocker
Betaxolol
45
Reduce IOP by 20-30%
Beta blockers
46
Frequency of beta blocker administration
BID
47
Systemic ADR of beta blockers
Decreased heart rate Decreased blood pressure Bronchospasm
48
Local adp of beta blockers
Ocular irritation and dry eyes
49
Carbonic anhydrase inhibitors cap color
Orange
50
Topical CAI
Dorzolamide Brinzolamide
51
CAI MOA
Inhibit aqueous humor production by blocking active secretion of sodium and bicarbonate ions from the ciliary body
52
Systemic CAI is typically reserved for?
Acute treatment
53
Reduce CAI by 15-26%
CAI
54
CAI Frequency of Dosing
BID or TID
55
CAI local ADR
Burning or stinging Dry eyes Ocular discomfort Transient blurred vision Tearing
56
CAI Systemic ADR
Malaise Fatigue Nausea Weight loss Altered taste Renal stones
57
What color are prostaglandin analog color
Blue
58
Drugs of prostaglandin analogs
Bimatoprost Lantanoprost Tafluprost Travoprost Lantanoprostene bound
59
Prostaglandin analog MOA
Increases uveoscleral outflow and trabecular outflow of aqueous humor Produces collagen changes in the matrix of the cilliary body and trabecular meshwork
60
Lantoprostene bunod
Latanoprost prodrug metabolized to nitric oxide donating moiety
61
Reduce IOP by 25-35%
Prostaglandin Analogs
62
Frequency of prostaglandin analog dosing
Once daily One drop at night
63
Local ADR of prostaglandin analogs
Lengthening and darkening of eyelashes Brown discoloration of eyes (irreversible) Macular edema
64
Systemic ADR of prostaglandin analogs
Minimal but may occasionally cause headache
65
Cholinergic agent cap color
Green
66
Drugs of cholinengic cholinergic agents
Pilocarpine Carbachol
67
Cholinergic agent MOA
Physical pulling of trabecular meshwork open thereby increasing outflow
68
IOP reduction by 20-30%
Cholinerigic agents
69
Cholinergic dosing frequency agents
TID or QID
70
Local ADR of cholinergic agents
Mitosis: decreasing vision and night vision IM patients with central cataracts Ocular discomforts
71
Systemic ADR of cholinergic agents
Frontal headache Brow ache Eyelid twitching
72
Rho kinase inhibitor
Netarsudil
73
Netarsudil MOA
Increases trabecular meshwork outflow
74
Decrease IOP by 15-22%
Netarsudil
75
Frequency of Netarsudil dosing
Once daily
76
Local ADR of Netarsudil
Conjunctival hyperemia and hemorrhage Corneal verticillate
77
Systemic ADR of Netarsudil
Rare
78
How can we increase outflow and decrease production
Alpha 2 adrenergic agonist
79
Drugs of alpha 2 adrenergic
Bromonidine Apraclonidine
80
Reduce IOP by 18-27%
Alpha 2 adrenergic agonist
81
Frequency of Dosing of alpha 2 adrenergic agonist
BID or TID
82
Local ADR of alpha 2 agonist
Allergic reactions Dry eyes Ocular discomfort
83
Systemic ADR of alpha 2 agonist
Dizziness Fatigue Dry mouth Reduction in blood pressure and pulse (postural hypotension)
84
Who should alpha 2 be dosed cautiously
Patient with insufficient coronary and cerebral function Hepatic and renal dysfunction
85
Timolol combination drop
Dorzolamide Brimonidine Prostaglandins
86
Brimonidine combo.
Brinzolamide
87
Netarsudil combo
Lantanoprost
88
First line therapy
Prostaglandin analogue Beta blocker
89
Alternate first line
Brominidine
90
If there is contraindication to first line therapies what should be used
Topical CAI
91
How long till patient is reassessed
2-4 weeks
92
If patient is intolerant fo therapies what should be done
Reduce dose/concentration first Or Change formulation Or Switch to Class alternative or alternative combination
93
If inadequate response what should be done
Ensure compliance Instruct on nasolacrimal occlusion Increase concentration or dose frequency Switch to alternative first line therapies
94
If partial response with first line agents what should be done
Add second or third first line agent or topical CAI
95
If there is inadequate response to first line and second line what should be done
Consider adding direct-acting cholinergic agent as fourth line and consider replacing with cholinestrase inhibitor Consider adding oral CAI over topical CAI Multiple topical therapies plus oral carbonic anhydrase inhibitor
96
When all pharmanologic therapy have failed that is left to do
Surgery or laser procedure
97
Surgery for open angle glaucoma
Trabeculoplasty
98
Surgery for closed angle glaucoma
Iridofomy
99
What is acute angle closure crisis (AACC)
Medical emergency: sudden closure of angle between the iris and trabecular meshwork lending to rapid increase of IOP
100
Symptoms of AACC
Rapid onset of blurred vision Red eye Pain Headache Nausea and vomiting
101
Goals of therapy for AACC
Rapidly Reduce IOP Avoid surgical or laser iridectomy
102
AAC treatment options
One or more anti-glaucoma agent: Miotics-pilocarpine Secretory inhibitors: beta blockers, alpha I agonist, topical/systemic CAI or Prostaglandins Give osmotic agents like oral glycerin 1-2 g/kg or IV mannitol 1-2 g/kg Quickly withdraw water from the eyes using osmotic gradient between the blood and eye
103
When all pharmacologic therapies for AACC fail what should be done.
Peripheral iridectomy
104
What should patients know prior to Administration
Do not administer more than one drop per dose When 2 or more drugs administered, meds should be separated by at least 5 minutes (10 minutes preferred) Remove contacts prior to administration
105
Systemic CAI
Acetazolamide Dichlorphenamide Methazolamide

Pharmacotherapy (12 decks)

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