1. Changes in optice nerve head (optic disk)

2. Asymptomatic, irreversible loss of visual senstivity and visual field

3. Elevated IOP

1. Made in ciliary body

2. Secreted in posterior chamber

3. Pressured into anterior chamber

4. Exits eye to venous circulation

1. Trabecular Meshwork to Schlemm's canal

(Main = 80-85% of the aqueous humor)

2. Ciliary body and suprachoroidal space (aka uvesocleral outflow)

1. Beta Antagonist

2. Alpha Antagonist

3. Dopamine Antagonist

4. Alpha2 Agonist

5. Carbonic Anhydrase inhibitors

1. ACH agonist

2. PG F2α Analogue

3. Beta Agonist

4. α2 Agonist

The equilibrium between the inflow (production) and the outflow (removal) of the aqueous humor.

~ 15.5 mmHg

It is the pressure required to flatten cornea with stream of air (applanation)

(aka the pressure needed to overcome the eye curvature)

15.5 +/- 2.2 mmHg

(range is 10-21 mmHg)

True

(Decreasing IOP by 1mmHg will drop glaucoma risk by 10%)

1. Optic nerve degeneration

2. Disk changes

3. Visual field loss (central visual acuity maintained)

It may be normal

(normal tension)

False; it is bilateral

Occurs in both eyes

Slow

Usually over the age of 50

Headache

Malaise

Nausea/Vomitting

To rapidly decrease there IOP to:

1. Preserve vision

2. Avoid emergent surgery

When there IOP is >22 mgHg but there is no disk change or apparent visual field loss.

The risk of Glaucoma depends on additional RF

There are many:

Rx

Systemic disease

Trauma

Surgery

Ocular Inflammatory disease

1. Evaluation the optic disk (Opthalmoscopy)

2. Assessment of visual fields (perimetry)
3. Measurement of the IOP

1. Optic Disk changes such as cupping of the disk

2. Asymmetry

3. Degeneration of retinal nerve fibers

1. Scotomas (blind spots)

2. Altered color vision

3. Reduced peripheral acuity

4. Central acuity that is lost in late stages

False; CAG is symptomatic early

POAG is a slow progressive chronic disease so is asymptomatic until significant disease progression.

1. Increased IOP

2. Increased susceptibility of optic nerve to ischemia/hypoxia

3. Decreased blood flow to retina

4. Glutamatergic excitotoxicity

5. Autoimmune rxns

6. Oxidative stress

1. Apoptosis of retinal ganglion cells

2. Axonal degeneration

3. Peripheral vision loss, scotomas, decrease in color and contrast sensitivity

4. Permanent vision loss

1. Age > 65 yro

2. Family Hx of Glaucoma

3. African American

4. IOP > 30 mmHg

5. Thin central corneal thickness (CCT < 555μm)

6. Myopia 

1. Systemic Vascular Disease

2. DM

3. Cup to Disk ratio > 0.5

1. Older age

2. Female

3. Hyperopia

4. Asian or Eskimo

5. Shallow anterior chamber

6. Family Hx of CAG

Hyperopia = Farsided

Myopia = Nearsided

1. Anti-ACH (especially eye products)

2. TCAs (have anti-Ach effects)

3. CS (all forms)

4. Sympathomimetics

5. Sulfa based drugs

1. Document status of optic nerve

2. Halt optic disk changes and prevent progressive vision loss

3. Lower IOP by at least 20%

4. Minimize ADE of Rx therapy

5. Educate and enage patient in disease managment

There is no goal number but we optimally want a 30-50% reduction from there baseline.

Optimally would like to have IOP < 15-18 mmHg

1. Start with 1 topical agent in 1 eye ("monocular trial")

2. Assess efficacy after 4-6 weeks

3a. If no response or intolerance = change to alternative Rx

3b. If partial response = add a 2nd Rx

4. Monitor: IOP, optic disk changes, visual field, ADRs and compliance

A Prostaglandin Analog PGF₂α

or a

Beta-Blocker

1. Increase Uveoscleral (major) outflow = thought to relax the ciliary muscle

2. Increase trabecular outflow (minor)

1. Latanoprost (Xalatan)

2. Travapost (Travatan)

1. Darkening of the irirs in patients w/ colored irises (15-30%)

2. Increase eyelash growth

3. Local:  Diplopia, conjunctival hypermia, foreign body sensation, ocular irritation, punctate corneal keratopathy, cystoid macular edema, uveitis

1. 20-30% decrease in IOP w/ fewer local ocular side effects (vs miotics and sympathomimetics)

2. May maintain lower pressure

Nonselective = Timolol, Levobunolol, Metipranolol

B1 Selective = Betaxolol

1. Bradycardia

2. Decrease in CO and B.P

3. Conduction effects

4. Bronchospasm

5. Masking Hypoglycemia

6. CNS effects

1. Stinging

2. Dry eyes

3. Corneal Anesthesia

4. Blurred vision

5. Blepharitis

rare:

6. Conjuctivitis

7. Uveitis

8. Keratitis

1. DM

2. Myasthenia Gravis

3. CHF

4. Those taking a PO B-Blocker

5. Sinus bradycardia

6. Pulmonary disease

7. 2 or 3rd AVB

1. Post surgery

2. As adjunctive therapy

1. Increase uveoscleral outflow (only true for Brimonidine)

2. Decrease aq. humor production

Local: hypersensitivity (eye discomfort, lid edema, hyperemia)

Systemic: Dizziness, sleepy, fatigue, dry mouth

False; they decrease IOP by 18-27% at peak (2-5 hrs) and only by 10% at 8-12 hrs.

(needs to be given frequently)

PNS agents

(Cholingeric Agents)

1. Pilocarpine

2. Carbachol

Irritation

Tearing

Miosis (decrease in night vision)

1. Headache

2. Browache

3. N/V/D

4. Decrease in HR

5. Decrease in BP

1. Pre-op

2. Pulmonary disease

3. Myopia

4. Cataracts

5. CAG

1. Decrease in BP and HR

2. Arrhythmias

3. Tremors

4. Anxiety

5. Sweating

6. Headache

1. B-blocker

2. CAI

3. Alpha 2

1. PG Analog

2. Cholinergic

3. CAI

1. PG Analog

2. CAI

3. B1 selective

1. B-blocker

2. PG Analog

Xalcom = Timolol + Latanoprost

Duotrav = Timolol + Travoprost

1. IOP every ~ 4 wks initially then every 3-4 months once they reach target IOP

2. Inspection of Optic disk and visual fields every 12 months

3. ADEs

4. Compliance

Same drug = wait 1-2 mins between drops

Different Rx = wait 5-10 minutes between them