High Yield Glaucoma for Step 1 and 2
Title: High Yield Glaucoma for Step 1 and 2
Author: Abigail Jebaraj, MSIV
Medical Student Education Outline > III. Additional Resources > New line “2. High Yield Glaucoma Review for Steps 1 and 2”
- Glaucoma: optic nerve damage that can result in vision loss, often associated with an increased intraocular pressure
- Key point: glaucoma is not elevated intraocular pressure (IOP), rather it is an optic neuropathy with multiple risk factors. The only modifiable risk factor in treating the disease is lowering IOP.
- Pain and Glaucoma: elevated IOP is only painful when there is a rapid rise or change in IOP. Slow, gradual IOP rises are not painful, but still vision threatening—sometimes a slow rise in IOP is even more dangerous because there are no symptoms until late in the disease process –irreversible, peripheral vision loss.
- Glaucoma is thought to occur due to an imbalance of the flow of fluid in and out of the anterior chamber of the eye. This pressure may be associated with increased pressure against the retina, causing optic disc atrophy with characteristic cupping.
- Anterior chamber: space between the cornea to the iris
- Posterior chamber: space between the iris to the lens
- Vitreous chamber: space behind the lens, filled with vitreous humor
- Aqueous humor: watery fluid within the anterior and posterior chambers to provide nourishment to tissue and maintain intraocular pressure
- Ciliary Body: produces aqueous humor
- Trabecular meshwork (TM): tissue that drains the aqueous humor from the anterior chamber to Schlemm’s canal
- Schlemm’s canal: returns aqueous humor to the blood via anterior ciliary veins
- Flow of aqueous humor: ciliary body à posterior chamber à through pupil à anterior chamber à through trabecular meshwork à canal of Schlemm à anterior ciliary veins à blood
Cupping: measurement of optic nerve cup diameter to optic disc diameter ratio to assess thickness of optic nerve head. More cupping (ratio greater than 0.5) = higher risk
- Open vs. Closed Angle Glaucoma:
- Angle of the anterior chamber: angle at which the cornea and iris meet that fluid passes to enter the trabecular meshwork.
- Open Angle Glaucoma: large angle between the iris and cornea, meaning fluid can still access the TM but is obstructed within the TM and slow drainage causes elevated pressures.
- Chronic, painless process of progressive, non-reversible, vision loss that begins peripherally and centralizes over time
- More common in the US than closed angle glaucoma
- Primary: unknown cause
- Secondary: cellular material blocking trabecular meshwork, such as blood in the case of a hyphema or white blood cells in a hypopyon.
- Closed angle: small angle between the iris and cornea, preventing the drainage of fluid and resulting in an increase in pressure
- Primary: anatomic tendency to block the angle
- Secondary: known secondary cause, such as hypoxic process (i.e. diabetes) inducing neovascularization of iris, blocking the angle
- Acute: sudden rise in IOP which is very painful, blurriness and haloing of lights, eye redness, headaches and nausea. Ophthalmologic emergency to lower IOP before irreversible optic nerve damage occurs.
- Firm eye, fixed dilated pupil, corneal clouding, conjunctival injection
- Chronic: optic nerve damage over time due to closed angle and resultant slow rise of pressure, which is painless
- Beware of atropine or epinephrine with closed angle
- Not curable, but medications and other interventions can slow the progression of disease
- Medications for glaucoma work by affecting different components of inflow and outflow of aqueous humor
- Laser procedures and surgical implants can also be used to treat glaucoma by augmenting outflow or decreasing production of aqueous humor.
|Drug Class||Examples||Mechanism of Action||Side effects|
|Beta adrenergic receptor antagonists||Timolol, betaxolol, carteolol||Decrease production of aqueous humor||Irritation, dry eye, blurry vision potential exacerbation of bradycardia, asthma exacerbation, or hypotension|
|Carbonic anhydrase inhibitors||Acetazolamide||Decrease production of aqueous humor||Dry eye, blurry vision if oral, dizziness, lightheadedness, dry mouth, drowsiness, allergic reaction with sulfa drug allergy|
|Prostaglandin analogues||Bimatoprost and latanoprost||Increase outflow of aqueous humor||Irritation, darkening of the iris, hypertrichosis (increased eyelash growth)|
|Cholinomimetics||Pilocarpine and carbachol (Direct)
Physostigmine and echothiophate (Indirect)
|Increase outflow of aqueous humor||Blurry vision, headache, miosis (constriction of pupil), and cyclospasm (contraction of ciliary muscle)|
|Alpha adrenergic agonists||Epinephrine and brimonidine||Decrease production and increase outflow of aqueous humor||Irritation, allergy, pruritis, dry eye, blurry vision, mydriasis (dilation of pupil)|
Tae L, Bhushan V, Sochat M, Chavda Y, Zureick A. First Aid for the USMLE Step 1 2018, 28th Edition. New York: McGraw-Hill Medical, 2017. Pages 520 and 535.
Weinreb RN, Aung T, Medeiros FA. The Pathophysiology and Treatment of Glaucoma: A Review. JAMA. 2014;311(18):1901-1911. doi:10.1001/jama.2014.3192
Boyd K. Glaucoma. American Academy of Ophthalmology. Eye Health A-Z. Available at: https://www.aao.org/eye-health/diseases/what-is-glaucoma. Accessed: September 25, 2018.
Root T. Introduction to Glaucoma. OphthoBook. Available at: https://timroot.com/glaucoma/ Accessed September 25, 2018.
National Eye Institute. Facts About Glaucoma. Available at: https://nei.nih.gov/health/glaucoma/glaucoma_facts. Accessed: September 25, 2018.
Faculty Approval by: Griffin Jardine, MD