Glaucoma Flashcards

(78 cards)

1
Q

What are the strong risk factors of glaucoma?

A
High intraocular pressure
Aging (>40y)
Family history (primary history)
Race (blacks)
Severe myopia
Optic disc appearance
Cup:disk ratio >0.5
Corneal thickness >0.5 mm
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2
Q

What does the literature set the upper limit of intraocular pressure as?
What is the general rule if there is glucomatous damage, no matter what the pressure is?

A

21 mmHg

General rule - lower the pressure

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3
Q

What is the clinical presentation of primary open angle glaucoma (POAG)?
Unilateral or bilateral?

A

Usually asymptomatic (until substantial visual field loss occurs).
Chronic progressive if not treated.
Subtle decrease in colour and contrast sensitivity.
Bilateral.

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4
Q

What is the clinical presentation of closed angle glaucoma (CAG)?
(symptomatic and non-symptomatic signs)

A
Symptomatic acute episodes:
-eye pain
-edematous cloudy cornea
-N/V
-abdominal pain
-unresponsive iris
Non-symptomatic:
-halos around lights (from edematous cornea)
-headache
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5
Q

What is the primary defect of OAG?

A

Usually decreased drainage of aqueous humor leading to increased pressure

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6
Q

What causes CAG?

A

Ballooning of the iris (floppy) blocks drainage of aqueous humor (blockage of trabecular meshwork)

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7
Q

Which of the glaucomas is an emergency situation?

A

Closed angle glaucoma

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8
Q

What is aqueous humor produced by?

Where is it filtered?

A

Ciliary non-pigmented epithelial cells.

Filtered and secreted into posterior chamber.

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9
Q

Where is the aqueous humor drained?

A

Trabecular meshwork and canal of schlemm (80%)

Uveoscleral (20%)

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10
Q

What does constant inflow and resistance to outflow result in?

A

Intraocular pressure

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11
Q

What are 2 ways to control intraocular pressure?

A

Decrease AH production

Increase drainage

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12
Q

What can you target to decrease AH production?

A

Receptors on the ciliary body (alpha and beta)

Carbonic anhydrase

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13
Q

3 Ways to increase AH drainage

A

Trabecular meshwork & canal of schlemm
Uveoscleral outflow
Surgical intervention

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14
Q

The 2 iris muscles and their receptors and what they cause the pupil to do

A

Circular muscle: cholinergic receptor, miosis

Radial muscle: alpha adrenergic receptor, mydriasis

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15
Q

What receptors are on the trabecular meshwork?

A

Receptors for epinephrine, dopamine, prostanoids, biogenic amines

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16
Q

What type of drug is Pilocarpine?

A

Parasympathomimetic (mitotic)

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17
Q

How does Pilocarpine work?

A

Increases AH outflow by reducing resistance to outflow through trabecular meshwork & canal of Schlemm - therby reducing IOP (by 20-30%)

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18
Q

What are the topical SE of Pilocarpine?

A

Miosis - decreased night vision and visual field.
Ciliary muscle contraction - causes accommodative spasm, frontal headache, brow ache, eyelid twitching, conjunctival irritation (decreases in 2-5 weeks)
Retinal tear or detatchment

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19
Q

What are systemic SE of Pilocarpine?

At what concentration are they seen?

A
NVD
Cramping
Urinary frequency
Bronchospasm
Heart block
GI, salivation
(think parasympathetic stuff)
Seen in concentrations 6-8%
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20
Q

What are the sympathomimetic (adrenergic) drugs for glaucoma?

A
Dipivefrin
Epinephrine (no longer marketed)
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21
Q

How do sympathomimetic drugs work?

What is up with depivefrine?

A

Adrenalin-mediated -
act on alpha and beta receptors in ciliary body
Increased outflow through trabecular meshwork and uvescleral route. (but may actually increase AH production)
Depivefrine is a prodrug (better tolerated)

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22
Q

What are topical SE of sympathomimetics (dipivefrin)?

A
Tearing and burning
Brow ache
Conjunctival hyperemia
Blepharoconjunctivitis
Stenosis of NLO
Blurred vision
Adrenochrome deposits (with prolonged use)
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23
Q

What are systemic SE of sympathomimetics (dipivefrin)?

A

Increased BP & HR
Arrhythmias, anxiety, persperation, headache, tremor (think adrenaline)
– use in caution with CV disease, cerebrovascular disease, hyperthyroid, DM
CI in closed angle

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24
Q

What are the two alpha-2 receptor agonists?

Which is more common?

A

Aproclonidine

Brimonidine (more common)

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25
When is aproclonidine used? | How does it work?
Used post eye surgery. | Decreases peak IOP by decreasing AH production
26
How does brimonidine work? | Why is it better?
Decreases AH production AND increases outflow (uveoscleral) | Less SE than aproclonidine
27
Topical SE of alpha-2 receptor agonists (aproclonidine, brimonidine)
``` Allergic type reactions: Itching Eye discomfort Lid edema Foreign object sensation Hyperemia ```
28
Systemic SE of alpha-2 receptor agonists (aproclonidine, brimonidine)
``` Dry mouth Dizziness, fatigue Decreased BP Somnolence (caution with CV disease, renal compromise, cerebrovacular disease, or on other antihypertensives) ```
29
List the 4 beta blockers used for glaucoma
Timolol (main) Levodunolol Betaxolol Cartealol
30
What drug is first line therapy because it does not cause miosis or mydriasis?
Beta blockers
31
What conditions are beta blockers useful for?
Both closed and open angle glaucoma
32
How do beta blockers decrease IOP? | By what percentage?
By blocking beta receptors in ciliary epithelial cells, thereby decreasing aqueous humor production Reduce IOP by 20-30% (same as Pilocarpine)
33
What conditions are beta blockers contraindicated in?
``` Heart failure Asthma COPD Diabetes Heart block Sinus bradycardia ```
34
Long term use of beta blockers can result in ______ in 20-25% of patients
Tachyphylaxis
35
What technique can you use to reduce beta blocker SE?
NLO technique
36
Topical SE of beta blockers
``` Stinging Dry eyes Blurred vision Blepharitis Rare: conjunctivitis, uveitis, keratitis ```
37
Systemic SE of beta blockers
``` Dec. HR/BP Negative inotropy Conduction defects Increased lipids Bronchospasm Block T2DM symptoms ```
38
What can beta blockers be used in combo with? | What shouldn't be used with them?
Can be used with carbonic anhydrase inhibitors, parasympathomimetics, prostaglandins, alpha2 agonists Don't use with epinephrine or dipivefrin
39
What are the two topical carbonic anhydrase inhibitors?
Dorzolamide | Brinzolamide
40
How do CAIs work to reduce IOP? | By what percentage is it reduced?
Inhibit carbonic anhydrase II, thereby decreasing ciliary epithelial cell production of AH Reduced ny 15-26%
41
What is the dosing schedule for topical CAIs?
Q8-12h
42
Topical SE of CAIs?
Burning/stinging on application Transient blurred vision Tearing Rare: photophobia, lid reaction, conjunctivitis
43
Systemic SE of topical CAIs?
Rare: sulfa allergy
44
What are the oral forms of CAIs?
Acetazolamide | Methazolamide
45
By what percentage do oral CAIs reduce IOP?
25-40%
46
Systemic SE of oral CAIs?
``` Acidosis Malaise Fatigue Anorexia Nausea Depression Decreased libido Renal calculi Increased uric acid Diuresis Blood dyscrasias ```
47
In what patients should CAIs be used with caution?
``` Sulfa allergy Sickle cell disease Respiratory acidosis Pulmonary disorders Electrolyte imbalance Hepatic & renal disease ```
48
What can you combine oral CAIs with?
Beta blockers Parasympathomimetics Prostaglandins
49
What situations are oral CAIs useful for?
Emergencies (not for chronic use)
50
List the prostaglandin analogues
``` Latanoprost Bimatoprost Travoprost Tafluprost Unoprostone ```
51
How do prostaglandin analogues reduce IOP? | By what percentage?
Increase uveoscleral outflow of AH (20% is drained by this route) Dec IOP by 25-35%
52
What is the dosing regimen of prostaglandin analogues?
Usually once daily HS
53
Topical SE of prostaglandin analogues
Iris pigment alteration (mixed colour becomes brown) Increased eyelash pigment, length, thickness Conjunctival hyperemia Punctae corneal erosions Uveitis Caution with eye inflammation
54
Systemic SE of prostaglandin analogues
``` Skin reactions URTI/cold/flu Chest pain GI disturbances Muscle/joint pain ```
55
Can you combine prostaglandins with other glaucoma agents?
You can combine with all other agents
56
What does pilocarpipne cause in the ciliary muscle?
Ciliary muscle contraction, decreases AH outflow
57
What does atropine cause in the ciliary muscle?
Ciliary muscle relaxation, increased outflow
58
Name the two hyperosmotic solutions for glaucoma
Isosorbide (oral) | Mannitol (IV)
59
When are hyperosmotic solutions used?
Emergency management of angle closure | May be used to decrease pressure pre-op
60
When should you use hyperosmotic solutions?
Severe dehydration Pulmonary edema CHF
61
What are the only 2 classes that affect the pupil? | How do they affect it?
Parasympathomimetics - miosis | Sympathomimetics (epinephrine/depivefrine) - mydriasis
62
List the classes of agents that increase AH outflow
Parasympathomimetics Sympathomimetics (epi + alpha-2 agonists) Prostaglandin analogues
63
List the agents that decrease AH production
Alpha-2 agonists Beta blockers CAIs
64
What is the first line in treatment of glaucoma?
Beta blocker - gold standard
65
What do you move to if beta blockers are contraindicated or ineffective? (2nd line)
Monotherapy with either: PG analogue Local CAIs Alpha-2 agonist
66
If monotherapy with PG analogue, CAI, or alpha-2 agonist is inneffective, what do?
Combo therapy: - Beta blocker + (PG or CAI or Miotic) - PG + (CAI or alpha-2 agonist)
67
When are parasympathetics used?
Third line due to side effects | May use as miotic with PG or beta blocker
68
What is the objective in the treatment of POAG?
Lower IOP 20-30% from baseline | decrease more if at higher risk
69
List the principles of treating glaucoma
1. Start in one eye - if tolerated treat both 2. If not tolerated, switch (sometimes same drug class, different formulation) 3. Once target IOP is reached, monitor IOP every 2-4 months. 4. Measure visual field and optic disc once yearly (unless unstable/worsening) 5. Ensure adherence to treatment and tolerance 6. Separate meds by 5-10 min if using more than one agent.
70
In closed angle glaucoma acute attacks, what therapy is contraindicated? When can you use it?
Pilocarpine CI in papillary block (may worsen) | Can use after lowering IOP with other agents first
71
In CAG acute attacks, what agent is only used short-term?
Hyperosmotic agents
72
What 4 agents can be used in acute attacks of CAG?
Beta blockers Alpha-2 agonists Prostaglandins CAIs
73
At what pressure might the iris be eschemic and unresponsive to miotics (pilocarpine)?
>60 mmHg
74
What are mydriatic agents used for?
Eye examination
75
What are cycloplegic agents used for?
Accurate refractions and relief from ciliary spasm during inflammation
76
Name two parasympathoplegic drugs
Atropine (7-10d) | Tropicamide (1-6h)
77
What do both parasympathoplegic drugs produce? | When are they contraindicated?
Produce both mydriasis and cycloplegia. | Contraindicated in glaucoma
78
What is phenylephrine? | When is it used with caution?
A sympathomimetic mydriatic agent with little/no cycloplegia. Used with caution in glaucoma, heart disease, HTN