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OHP I > Tonometry and IOP > Flashcards

Tonometry and IOP Flashcards

1
Q

aqueous production mechanisms

A
  • active secretion

- ultrafiltration

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2
Q

how does active secretion control aqueous production?

A

controls carbonic anhydrase

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3
Q

how does ultrafiltration control aqueous production?

A

controls IOP/BP pressure balance

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4
Q

increased IOP = ___ rate of ultrafiltration

A

decreased

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5
Q

how does ultrafiltration control IOP/BP balance?

A

controls by lowering BP in capillaries of the ciliary processes

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6
Q

why is ultrafiltration control of aqueous production not used clinically?

A

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

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7
Q

describe aqueous flow from posterior chamber to anterior chamber

A
  • formed in ciliary processes
  • posterior chamber
  • through lens (iris diaphragm)
  • anterior chamber
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8
Q

aqueous outflow pathways and %

A
  • trabecular outflow (65-80%)

- uveoscleral outflow (20-35%)

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9
Q

aqueous convection currents in AC

A
  • 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
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10
Q

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

A

an obstruction within the trabecular meshwork

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11
Q

relationship in episcleral venous pressure and IOP changes is:

A

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

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12
Q

causes of increase episcleral venous plexus pressure

A
  • valsalva
  • increase in intrathoracic pressure
  • taking a breath and holding it
  • lifting, straining, coughing
  • gonioscopy
  • carotid cavernous fistula
  • sturge-weber syndrome
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13
Q

uveoscleral outflow pathway

A

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

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14
Q

is uveoscleral outflow pressure (IOP) dependent?

A

no

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15
Q

is trabecular outflow pressure (IOP) dependent?

A

yes

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16
Q

ciliary muscle contraction causes ___ TM outflow and ____ uveoscleral outflow

A
  • increased TM outflow

- decreased uveoscleral outflow

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17
Q

how do anticholinergics dilate the pupil?

A

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

18
Q

list of the classes of glaucoma meds

A
  • cholinergics
  • sympathomimetics
  • sympatholytics (beta blockers)
  • carbonic anhydrase inhibitors (CAIs)
  • prostaglandin analogs
19
Q

list of anticholinergics used clinically (from weakest to strongest)

A
  • tropicamide
  • cyclopentolate
  • scopomine
  • homatropine
  • atropine
20
Q

mechanism of action for cholinergic drugs

A

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

21
Q

when anticholinergics block the ciliary muscle, it causes:

A

cycloplegia

22
Q

when anticholinergics block the pupillary sphincter, it causes:

A

pupil dilation

23
Q

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

A

decrease

24
Q

how can cholinergic (pilocarpine) affect ciliary tone and IOP

A

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

25
Q

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

A

increase

26
Q

how can anticholinergics affect ciliary tone and IOP

A

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

27
Q

significant IOP spike in a susceptible patient can cause:

A

CRVO/ BRVO

28
Q

differential diagnosis of post-dilated IOP spike

A
  • angle closure
  • plateau iris
  • cycloplegic effect of the mydriatic agent
  • pigment release into AC
29
Q

difference in time for angle closure vs. plateau iris

A
  • angle closure usually takes hours to onset

- plateau iris can take minutes

30
Q

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

A
  • mid dilated pupil
  • relative pupil block
  • increase in IOP in PC
  • iris bombe (anterior bowing of iris)
  • angle closure (only in preexisting narrow angles)
31
Q

angles at risk

A 
grade 1 (<1/4)
grade 2 (1/4)
32
Q

effect on aqueous flow of glaucoma med cholinergics (pilocarpine)

A

causes ciliary spasm, increases aqueous outflow through TM

33
Q

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

A

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

34
Q

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

A

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

35
Q

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

A

block B2 sites in ciliary body, decreases aqueous formation

36
Q

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

A

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

37
Q

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

A

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

38
Q

Definition of glaucoma

A

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

39
Q

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

A

Retinal nerve fiber (ganglion cell axon) death

40
Q

What is not clinically evident in open angle glaucoma?

A

No clinically evident aqueous outflow obstruction on gonioscopy

OHP I (14 decks)

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