Eye conditions: Refractive errors, lens disorders and glaucoma: Pathology review

Chapters:

Watch video only

Case study0:00–0:49

At the ophthalmology clinic, 61-year-old Pedro presents with vision impairment that has been progressive over the past couple of years.
He denies experiencing any pain. His past medical history is significant for type 2 diabetes mellitus.
Physical examination shows bilateral clouding of the lens. Next to him, 68-year-old Eileen comes in.
She complains that, about an hour ago she started experiencing excruciating pain in her right eye, accompanied by blurry vision and seeing halos around bright lights.
Eileen also tells you that she has since vomited twice. On clinical examination, her right eye is red, with a dilated pupil that fails to react to light.
Her left eye appears unremarkable.Based on the initial presentation, both Pedro and Eileen have some form of eye condition.

Physiology0:49–1:39

But first, a bit of physiology. If we take a closer look at a cross-section of an eye, we can see that it’s split into three different chambers: anterior, posterior, and vitreous.
The anterior chamber includes the area from the cornea to the iris. The posterior chamber is a really narrow space between the iris and the lens.
Finally, the much larger vitreous chamber includes the space between the lens and the back of the eye. Now, both the anterior and posterior chambers are located in the anterior segment of the eye, while the vitreous chamber is part of the posterior segment of the eye.
Both chambers in the anterior segment, that is, the anterior and posterior chambers, are filled with a clear watery fluid called aqueous humor, while the vitreous chamber is filled with a clear but thicker fluid called the vitreous humor.
Okay, let’s start with what’s probably the most common group of eye conditions, so refractive errors. Normally, when the eye is in a relaxed state, the refractive power of the cornea and lens help focus light onto the retina.

Refractive errors1:39–3:32

The retina is like a movie screen and the distance from the projector is the axial length of the eye. If it’s too close or too far from the projector, the image will end up looking blurry or out of focus.
When the lens and cornea can focus light perfectly on the retina, it’s called emmetropia. In hyperopia, also known as farsightedness, the axial length of the eye is too short for the refractive power of the cornea and lens, so the light ends up focusing behind the retina.
Hyperopia can be corrected with convex or converging lenses. In myopia, also known as nearsightedness, the axial length of the eye is too long for the refractive power of the cornea and lens, so the light focuses in front of the retina.
Myopia can be corrected with concave or diverging lenses. In astigmatism, there is an abnormal curvature of the cornea, which results in various refractive power at different axes.
Astigmatism can be corrected with cylindrical lenses. Finally, there’s presbyopia, where increasing age causes changes in the lens’s curvature, as well as a decline in the elasticity of the lens and the strength of the ciliary muscle, which normally controls accommodation of the lens to see objects at different distances.
As a result, presbyopia impairs accommodation or focusing on near objects, which can be corrected with magnifying reading glasses.Okay, let’s switch gears and discuss cataracts.

Cataracts3:32–6:14

This refers to clouding or opacification of the lens and it can be congenital or acquired. The main risk factors for congenital cataract include congenital infections.
For your exams, these infections can be remembered with the acronym TORCH, which stands for Toxoplasma, Other infectious agents, usually syphilis; Rubella; Cytomegalovirus, and Herpes simplex virus.
Other risk factors for congenital cataract include genetic conditions, such as trisomies 13, 18 and 21, Marfan syndrome, Alport syndrome, Refsum disease, myotonic dystrophy, neurofibromatosis type 2, and inborn errors of metabolism like galactosemia.
For your exam, remember that galactosemia can be type I caused by a deficiency in galactose-1-phosphate uridyltransferase; or type II which is caused by a deficiency of galactokinase.
Type I is the more common type so it’s also called classic galactosemia. Here, excess circulating galactose is converted to galactitol by the enzyme aldose reductase.
Galactitol then accumulates in the lens, creating a hypertonic environment that pulls in water, results in the swelling of lens fibers until they rupture, and this is called osmotic cellular injury.
Now, when it comes to acquired cataract, risk factors include advanced age, usually above 60, smoking, excessive alcohol use, eye trauma and infections, exposure to UV light, prolonged use of medications like glucocorticoids, and diabetes mellitus.
For your exams, note that the mechanism behind cataracts in diabetes mellitus, is similar to that in galactosemia. So, when there’s hyperglycemia, the excess circulating glucose is converted to sorbitol by aldose reductase.
Sorbitol then accumulates in the lens, causing osmotic cellular injury. Now, the main symptom of cataract is painless visual impairment that’s often bilateral and progresses slowly over many years.
For your exams, bear in mind that congenital cataract may also manifest with leukocoria or “white pupil”, which is an abnormal white reflection from the retina of the eye, also called a white pupillary reflex.
Remember that another cause of leukocoria is retinoblastoma. Diagnosis of cataracts includes slit lamp examination, which shows loss of lens transparency, and treatment is surgical removal of the lens nucleus.Another high-yield ophthalmologic condition is glaucoma.

Glaucoma6:14–11:35

Normally, the aqueous humor is secreted by the ciliary epithelium into the posterior chamber; then flows through a narrow space between the front of the lens and the back of the iris, and through the pupil to the anterior chamber.
From here, the fluid flows out of the eye through the trabecular meshwork, goes down into a circular channel, called the canal of Schlemm, and, finally, into the aqueous veins.
A small fraction of the aqueous humor follows the uveoscleral pathway, draining across the uvea and sclera to get reabsorbed by orbital vessels.
In glaucoma, part of the trabecular meshwork becomes partially or completely blocked. Now, there are two types of glaucoma: open- and closed-angle.
First, there’s open-angle glaucoma, which receives its name from the fact that the angle between the cornea and the iris is “open.” This is the most common type, especially in black individuals, as well as those with advanced age or family history.
Now, open-angle glaucoma can be primary, in which case the cause is unknown, or secondary to another condition, where the drainage system slowly gets clogged over time.
Common causes include a build up of white blood cells such as in the case of uveitis; red blood cells, in the case of vitreous hemorrhage; or even retinal elements, in the case of retinal detachment.
In all cases, there’s a gradual increase in the intraocular pressure, or IOP for short. Initially, this results in atrophy of the outer rim of the optic nerve, decreasing the peripheral vision.
Over time, as the IOP increases even more, there’s continued damage to the optic nerve, eventually leading to a loss in central vision as well.Then there’s closed-angle glaucoma, also called angle-closure glaucoma or narrow-angle glaucoma, which receives its name from the fact that the angle between the iris and the cornea is narrowed.
Again, closed-angle glaucoma can be primary or secondary. In primary cases, for unknown reasons, the lens is enlarged or gets pushed up against the iris.
On the other hand, secondary cases are caused by hypoxia from retinal diseases, like diabetes mellitus or central retinal vein occlusion.
This hypoxia induces neovascularization or growth of new blood vessels in the iris, which is pushed anteriorly, closing the angle.
Another secondary cause of closed-angle glaucoma common in the elderly is taking muscarinic (musk-kr-in-ic) blockers like atropine (Atro-pinne).
These medications can cause mydriasis, or pupil dilation, thus reducing aqueous humor outflow. In both primary and secondary cases, the result is that the drainage system gets blocked just like with open-angle glaucoma.
Now closed-angle glaucoma can be acute, in which case the blockage causes a rapid and sharp increase in intraocular pressure, and this is an ophthalmologic emergency.
In chronic closed-angle glaucoma, the pressure increase is more gradual and less severe but it will also lead to continued damage to the optic nerve over time.Symptoms of open-angle glaucoma include painless vision loss that progresses from peripheral to central.
Chronic closed-angle glaucoma is initially asymptomatic but can also progress into peripheral to central visual field loss.
In contrast, for acute closed-angle glaucoma, you should know that it is a true ophthalmologic emergency that can lead to the abrupt onset of severe eye pain, eye redness, a dilated, non-reactive pupil, blurry vision and seeing halos around lights, as well as frontal headaches, nausea and vomiting.
For the diagnosis of glaucoma, tonometry can be used to assess for increased intraocular pressure. Visual field testing can also be done.
Optic nerve damage should also be assessed either through imaging or by direct observation. Treatment focuses on medications that decrease the pressure in the eye.
This can be done in a couple of ways. First, we can decrease the production of aqueous humor with medications like beta-adrenergic receptor antagonists like timolol, and carbonic anhydrase inhibitors like acetazolamide.
Next, we can increase the outflow of aqueous humor through the uveoscleral pathway with prostaglandin analogs like bimatoprost and latanoprost.
Other medications can be used to increase the outflow of aqueous humor through the trabecular meshwork, such as cholinomimetics like pilocarpine and carbachol, or decrease its production, such as alpha adrenergic agonists like epinephrine, apraclonidine, or brimonidine.
For your exams, what’s absolutely necessary to remember is that in closed-angle glaucoma, alpha agonistsare strictly contraindicated, since they can cause mydriasis and reduce aqueous humor outflow even more.
Finally, refractory cases of glaucoma can benefit from laser treatment, like trabeculoplasty, in which a laser is used to open the trabecular mesh network, and iridotomy, where a tiny hole is punched in the iris.

Review11:35–12:17

All right, as a quick recap, disorders that cause refractive errors include hyperopia, myopia, astigmatism, and presbyopia; and they can be corrected by wearing the corresponding eyeglasses.
Cataracts refers to opacification of the lens and can be congenital, which causes leukocoria, or acquired, which presents with painless, progressive vision loss.
Glaucoma is a condition where the aqueous humor flow is blocked, and can be open- or closed-angle, each of which can be primary or secondary.
Closed-angle glaucoma can be divided into chronic and acute, which is an ophthalmologic emergency. Okay, back to our cases.

Summary12:17–13:05

61-year-old Pedro presented with painless, progressive vision impairment. This complaint, together with the bilateral clouding of the lens found on physical exam, should make you think of cataracts.
Other clues include his age and past medical history of diabetes mellitus, which are risk factors for acquired cataracts.
On the other hand, 68-year-old Eileen came in, complaining of acute onset of severe right eye pain, blurry vision, and seeing halos around lights.
In addition, she has since been vomiting. And along with the physical examination revealing right eye redness and the dilated, non-reactive pupil, the diagnosis of acute closed-angle glaucoma is highly likely.
This was then confirmed with fundoscopy, which showed increased intraocular pressure, and treated with medications in
Eye conditions: Refractive errors, lens disorders and glaucoma | Osmosis