Tonometry and IOP

Question 1

aqueous production mechanisms

Answer 1

• active secretion

- ultrafiltration

Question 2

how does active secretion control aqueous production?

Answer 2

controls carbonic anhydrase

Question 3

how does ultrafiltration control aqueous production?

Answer 3

controls IOP/BP pressure balance

Question 4

increased IOP = ___ rate of ultrafiltration

Answer 4

decreased

Question 5

how does ultrafiltration control IOP/BP balance?

Answer 5

controls by lowering BP in capillaries of the ciliary processes

Question 6

why is ultrafiltration control of aqueous production not used clinically?

Answer 6

due to the concomitant lowering of blood flow to the optic nerve head (ONH) which can worsen glaucoma

Question 7

describe aqueous flow from posterior chamber to anterior chamber

Answer 7

• formed in ciliary processes
• posterior chamber
• through lens (iris diaphragm)
• anterior chamber

Question 8

aqueous outflow pathways and %

Answer 8

• trabecular outflow (65-80%)

- uveoscleral outflow (20-35%)

Question 9

aqueous convection currents in AC

Answer 9

• 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

Question 10

most high IOP and open angle glaucoma (particularly COAG) is caused by:

Answer 10

an obstruction within the trabecular meshwork

Question 11

relationship in episcleral venous pressure and IOP changes is:

Answer 11

1:1 (1mmHg increase in episcleral pressure = 1mmHg increase in IOP)

Question 12

causes of increase episcleral venous plexus pressure

Answer 12

• valsalva
• increase in intrathoracic pressure
• taking a breath and holding it
• lifting, straining, coughing
• gonioscopy
• carotid cavernous fistula
• sturge-weber syndrome

Question 13

uveoscleral outflow pathway

Answer 13

iris face -> iris stroma -> ciliary body/uveal tract -> suprachoroidal space -> choroidal veins

Question 14

is uveoscleral outflow pressure (IOP) dependent?

Answer 14

no

Question 15

is trabecular outflow pressure (IOP) dependent?

Answer 15

yes

Question 16

ciliary muscle contraction causes ___ TM outflow and ____ uveoscleral outflow

Answer 16

• increased TM outflow

- decreased uveoscleral outflow

Question 17

how do anticholinergics dilate the pupil?

Answer 17

they block Ach receptors on the sphincter which temporarily inactivates the pupillary sphincter muscle

Question 18

list of the classes of glaucoma meds

Answer 18

• cholinergics
• sympathomimetics
• sympatholytics (beta blockers)
• carbonic anhydrase inhibitors (CAIs)
• prostaglandin analogs

Question 19

list of anticholinergics used clinically (from weakest to strongest)

Answer 19

• tropicamide
• cyclopentolate
• scopomine
• homatropine
• atropine

Question 20

mechanism of action for cholinergic drugs

Answer 20

stimulates a contraction of the ciliary muscle, particularly the longitudinal fibers which insert into the TM

Question 21

when anticholinergics block the ciliary muscle, it causes:

Answer 21

cycloplegia

Question 22

when anticholinergics block the pupillary sphincter, it causes:

Answer 22

pupil dilation

Question 23

increased tone (ciliary spasm) can increase aqueous outflow rate via trabecular meshwork outflow path, and can ____ IOP

Answer 23

decrease

Question 24

how can cholinergic (pilocarpine) affect ciliary tone and IOP

Answer 24

increase tone (ciliary spasm), increase aqueous outflow rate, decrease IOP

Question 25

decreased tone (ciliary spasm) can decrease aqueous outflow rate via trabecular outflow path, and can ___ IOP

Answer 25

increase

Question 26

how can anticholinergics affect ciliary tone and IOP

Answer 26

decreased tone (cycloplegia) can decrease aqueous outflow rate via trabecular outflow path

Question 27

significant IOP spike in a susceptible patient can cause:

Answer 27

CRVO/ BRVO

Question 28

differential diagnosis of post-dilated IOP spike

Answer 28

- angle closure - plateau iris - cycloplegic effect of the mydriatic agent - pigment release into AC

Question 29

difference in time for angle closure vs. plateau iris

Answer 29

- angle closure usually takes hours to onset | - plateau iris can take minutes

Question 30

steps in the pathogenesis of angle closure (by pupillary block mechanism)

Answer 30

- mid dilated pupil - relative pupil block - increase in IOP in PC - iris bombe (anterior bowing of iris) - angle closure (only in preexisting narrow angles)

Question 31

angles at risk

Answer 31

``` grade 1 (<1/4) grade 2 (1/4) ```

Question 32

effect on aqueous flow of glaucoma med cholinergics (pilocarpine)

Answer 32

causes ciliary spasm, increases aqueous outflow through TM

Question 33

effect on aqueous flow of glaucoma med sympathomimetics (epinephrine, dipivefrin)

Answer 33

stimulates B2 sites in TM, increases aqueous outflow in TM pathway

Question 34

effect on aqueous flow of glaucoma med sympathomimetics (bromide, apraclonidine)

Answer 34

stimulated alpha2 sites in ciliary body, decrease aqueous formation, also increases uveoscleral output

Question 35

effect on aqueous flow of glaucoma med sympatholytics (beta blockers-timolol, levobunolo, cartelol)

Answer 35

block B2 sites in ciliary body, decreases aqueous formation

Question 36

effect on aqueous flow of glaucoma med CAIs (dorzolamide, brinxolamide)

Answer 36

block carbonic anhydrase in ciliary body, decreases aqueous formation via active secretion

Question 37

effect on aqueous flow of glaucoma med prostaglandin analogs (lataniprost, travaprost, bimatoprost)

Answer 37

loosen the extracellular matrix in ciliary muscle, increases uveoscleral outflow rate

Question 38

Definition of glaucoma

Answer 38

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

Question 39

In glaucoma, the OHN and RNFL damage is directly due to

Answer 39

Retinal nerve fiber (ganglion cell axon) death

Question 40

What is not clinically evident in open angle glaucoma?

Answer 40

No clinically evident aqueous outflow obstruction on gonioscopy