Tonometry and IOP Flashcards
aqueous production mechanisms
- active secretion
- ultrafiltration
how does active secretion control aqueous production?
controls carbonic anhydrase
how does ultrafiltration control aqueous production?
controls IOP/BP pressure balance
increased IOP = ___ rate of ultrafiltration
decreased
how does ultrafiltration control IOP/BP balance?
controls by lowering BP in capillaries of the ciliary processes
why is ultrafiltration control of aqueous production not used clinically?
due to the concomitant lowering of blood flow to the optic nerve head (ONH) which can worsen glaucoma
describe aqueous flow from posterior chamber to anterior chamber
- formed in ciliary processes
- posterior chamber
- through lens (iris diaphragm)
- anterior chamber
aqueous outflow pathways and %
- trabecular outflow (65-80%)
- uveoscleral outflow (20-35%)
aqueous convection currents in AC
- aqueous is warmer in deep AC
- warm aqueous rises
- approaches peripheral AC
- aqueous cools in peripheral AC
- aqueous drifts downward in the more anterior AC
most high IOP and open angle glaucoma (particularly COAG) is caused by:
an obstruction within the trabecular meshwork
relationship in episcleral venous pressure and IOP changes is:
1:1 (1mmHg increase in episcleral pressure = 1mmHg increase in IOP)
causes of increase episcleral venous plexus pressure
- valsalva
- increase in intrathoracic pressure
- taking a breath and holding it
- lifting, straining, coughing
- gonioscopy
- carotid cavernous fistula
- sturge-weber syndrome
uveoscleral outflow pathway
iris face -> iris stroma -> ciliary body/uveal tract -> suprachoroidal space -> choroidal veins
is uveoscleral outflow pressure (IOP) dependent?
no
is trabecular outflow pressure (IOP) dependent?
yes
ciliary muscle contraction causes ___ TM outflow and ____ uveoscleral outflow
- increased TM outflow
- decreased uveoscleral outflow
how do anticholinergics dilate the pupil?
they block Ach receptors on the sphincter which temporarily inactivates the pupillary sphincter muscle
list of the classes of glaucoma meds
- cholinergics
- sympathomimetics
- sympatholytics (beta blockers)
- carbonic anhydrase inhibitors (CAIs)
- prostaglandin analogs
list of anticholinergics used clinically (from weakest to strongest)
- tropicamide
- cyclopentolate
- scopomine
- homatropine
- atropine
mechanism of action for cholinergic drugs
stimulates a contraction of the ciliary muscle, particularly the longitudinal fibers which insert into the TM
when anticholinergics block the ciliary muscle, it causes:
cycloplegia
when anticholinergics block the pupillary sphincter, it causes:
pupil dilation
increased tone (ciliary spasm) can increase aqueous outflow rate via trabecular meshwork outflow path, and can ____ IOP
decrease
how can cholinergic (pilocarpine) affect ciliary tone and IOP
increase tone (ciliary spasm), increase aqueous outflow rate, decrease IOP
decreased tone (ciliary spasm) can decrease aqueous outflow rate via trabecular outflow path, and can ___ IOP
increase
how can anticholinergics affect ciliary tone and IOP
decreased tone (cycloplegia) can decrease aqueous outflow rate via trabecular outflow path
significant IOP spike in a susceptible patient can cause:
CRVO/ BRVO
differential diagnosis of post-dilated IOP spike
- angle closure
- plateau iris
- cycloplegic effect of the mydriatic agent
- pigment release into AC
difference in time for angle closure vs. plateau iris
- angle closure usually takes hours to onset
- plateau iris can take minutes
steps in the pathogenesis of angle closure (by pupillary block mechanism)
- mid dilated pupil
- relative pupil block
- increase in IOP in PC
- iris bombe (anterior bowing of iris)
- angle closure (only in preexisting narrow angles)
angles at risk
grade 1 (<1/4) grade 2 (1/4)
effect on aqueous flow of glaucoma med cholinergics (pilocarpine)
causes ciliary spasm, increases aqueous outflow through TM
effect on aqueous flow of glaucoma med sympathomimetics (epinephrine, dipivefrin)
stimulates B2 sites in TM, increases aqueous outflow in TM pathway
effect on aqueous flow of glaucoma med sympathomimetics (bromide, apraclonidine)
stimulated alpha2 sites in ciliary body, decrease aqueous formation, also increases uveoscleral output
effect on aqueous flow of glaucoma med sympatholytics (beta blockers-timolol, levobunolo, cartelol)
block B2 sites in ciliary body, decreases aqueous formation
effect on aqueous flow of glaucoma med CAIs (dorzolamide, brinxolamide)
block carbonic anhydrase in ciliary body, decreases aqueous formation via active secretion
effect on aqueous flow of glaucoma med prostaglandin analogs (lataniprost, travaprost, bimatoprost)
loosen the extracellular matrix in ciliary muscle, increases uveoscleral outflow rate
Definition of glaucoma
A group of disorders where progressive damage occurs to the retinal ganglion cell axons and is clinically evident in the optic nerve and retinal nerve fiber layer
In glaucoma, the OHN and RNFL damage is directly due to
Retinal nerve fiber (ganglion cell axon) death
What is not clinically evident in open angle glaucoma?
No clinically evident aqueous outflow obstruction on gonioscopy
