If someone can explain the effects of alpha and beta on the eye and its relation to glaucoma that would be great.
(I tried understanding it from First Aid and googling, but I just down understand it)
Disclaimer: I was a tech for a glaucoma specialist in a metropolitan area for 3 years, and I may have enjoyed writing this explanation a little too much.
First, you need to know that glaucoma involves (usually) increased intraocular pressure because of the amount or accumulation of aqueous fluid. B2 receptors in the ciliary body produce aqueous when stimulated, aqueous enters the posterior chamber (the area between the lens and iris= "inflow tract"), which then drains through the pupil and into the anterior chamber (the area between the lens and the cornea = "angle"), which then drains through the trabecular meshwork, into the canals of schlemm, to the episcleral vein and then goes back to the general circulation. Ideally, the rate of production should equal the rate of drainage.
2 types of glaucoma:
Closed/Narrow Angle Glaucoma (means the ciliary epithelium is causing the lens and iris to stick together) so there is pressure/fluid buildup in the posterior chamber. These patients might not have elevated intraocular pressure b/c that is measuring the pressure of fluid in the anterior chamber, which is not the problem here. -- This type is either chronic, but usually is an acute/emergency attack and is precipitated by pupil dilation; At the ciliary muscle, B2 stimulation overrides the M3 stimulation and causes the muscle to relax and leads to dilation (for distant vision)- this pulls the zonular fibers and flattens the lens and makes the posterior chamber even smaller. Also, when the iris radial muscle (alpha1) is stimulated, the pupil dilates and closes the angle as well (this is why you don't give Epinephrine to someone with closed angle glaucoma). Closed angle glaucoma is treated usually with pilocarpine or carbachol because they stimulate M3 receptors (contraction of the iris circular muscle- this pulls the trabecular meshwork away and increases the amount of aqueous drained, the ciliary muscle also has M3 but these are only for accomodation), First Aid also says you can use physostigmine or echothiophate (these would be longer acting because of the anticholinesterase effect- long duration of M3 stimulation), but in reality - these really aren't used, maybe echothiophate, but rarely and only in serious conditions.
The more common type is Open Angle Glaucoma: either the trabecular meshwork (M3) is obstructing the canal of schlemm and causing accumulation of aqueous in the anterior chamber OR the ciliary body is producing (a2) or releasing (B) too much aqueous and it can't be drained quickly enough. You have high intraocular pressure, but usually no eye pain because accomodation is not affected.
You can treat this by:
-alpha2 agonists to vasoconstrict the ciliary body and prevent excess production of aqueous
-beta blockers to stop the ciliary body from releasing too much aqueous
-prostaglandins to vasodilate the canals of schlemm and increase outflow
-direct/indirect cholinergics to increase outflow (M3)
-if the person's intraocular pressure is super high you'll likely also give a carbonic anhydrase inhibitor to decrease synthesis of aqueous in the ciliary body
(there are also combined a2 agonists/ b2 blockers and b2 blockers/ CI inhibitors for someone who has a really high IOP)
Ultimately selection depends on what type of glaucoma (open or closed), and if it is open, you need to know if it is due to overproduction or undersecretion. I don't think on the USMLE they would expect you to differentiate this, they'd probably just ask drug mechanism or contraindications /side effects (ex, Beta blockers could have systemic effects, prostaglandins cause iris to darken and lashes to lengthen) Also they could ask about opiods which cause miosis because of central parasympathetic stimulation and used to be used in eye surgeries.
