glaucoma is too much aqueous due to blockage of trabecular meshwork outflow or uveoscleral outflow
where is AH secreted into normally?
what does AH resemble?
what is the measurement of AH?
what's AH's composition?
more glucose in AH than blood
more ascorbic acid in AH than blood
more lactic acid in AH than blood
LESS protein in AH than blood plasma
AH is more HYPERTONIC than blood
what is the most important risk factor for glaucoma development?
what ocular structure does AH supply?
cornea and lens, as well as their waste carried by AH
how is AH different from blood?
due to 2 physical characteristics of anterior segment:
1. there's a BAB (blood aqueous barrier) (at ciliary epithelium and endothelium)
2. active transport of substances by ciliary epithelium (the NPE of ciliary body actively secretes the aqueous humor)
how is AH formed?
active secretion (main way)
what enzymes does non-pigmented epithelium have?
what do the enzymes in NPE do?
they push the ions (Na, K, and Cl) so water can follow
what does acetazolamide do?
there are aqueous suppression drugs that inhibit carbonic anhydrase
then bicarbonate can't leave so, acetazolamide decreases aqueous production
are there neurostimulation of NPE to produce aqueous humor?
how is neurostimulation done?
alpha 2 and beta 1 receptors.
the sympathetic nervous system and parasympathetic nervous system are both involved in stimulating howflow but sympathetic nervous system has more of an impact-> this is why beta blockers and alpha2-agonists are good Tx for glaucoma b/c they inhibit aqueous production.
when id AH made the least?
asleep b/c sympathetic nervous system is not stimulated
what are the factors that are associated with decreased AH secretion?
diurnal (less secretion when sleeping)
short term secretion decrease when exercise
decrease in BP
increase in IOP by aqueous secretion (body will counteract)
Note: AH production does NOT change from stystem BP change! This is b/c AH production is an ACTIVE process and can only go so fast as its enzymes and channels permit