Ocular Disease II Mt 2

Thin Ks --> false low
Think Ks --> false high (LASIK pts will have a false low reading due to thinner corneas)

Temporal wedge defects (nasal radial fibers) DO/CAN cross horizontal midline

GLC dx may be made of a basis of: structural damage OR functional loss OR high risk

Cupping w/o pallor inside cup until later is highly specific for GLC.
Pallor of the rim tissue outside cup is non-GLC optic atrophy

Beta blockers do not work at night

Scleral canal size directly related to ONH & cup size

A 1 mmHg increase in intraocular pressure (IOP) results in a 10% increased risk for glaucoma (GLC) damage. Glaucoma is a disease that damages the optic nerve, often caused by increased pressure in the eye. Studies have shown that even a small increase in IOP can significantly increase the risk of developing glaucoma and experiencing damage to the optic nerve. Therefore, a 1 mmHg increase in IOP corresponds to a 10% increased risk for glaucoma damage.

Zone Beta is closer to ONH & has large chorodial vessles
Zone Alpha is more peripheral & is the irregular pigmented outer edge of Beta

50% sensitivity due to 1) substantial IOP variation in GLC pts, 2) varing susceptiblty of different pts to IOP-related damage

70-90% specificity --> most normals (non-GLC) show IOP

- Hypothyroidism --> not a vascular issue, messes with the TM
- High BP --> aggressively lowering BP is probably worse than high BP bc then you risk compromising the ON perfusion; however, long term high BP increases risk of GLC due to increased risk of arteriosclerosis & other vascular diseases
- Diabetes --> vascular compromise

corneal edema --> false low
corneal scarring --> false high

For RNFL eval, want LOW MAG or else you will likely think there is a defect when there is not. For ONH eval, you want HIGH MAG so you can see details

The greatest overlap of receptive fields is found in the PM bundles. Receptive fields refer to the area in the visual field that a single neuron responds to. When receptive fields overlap, it means that multiple neurons are responding to the same area, providing a more detailed and accurate representation of that particular region. In the case of PM bundles, the overlap of receptive fields is the highest, indicating a higher level of visual acuity and sensitivity in that area.

Af. Am. + Hispanics --> POAG
Chiese + Viet + Eskimo --> lower risk for POAG, but higher risk for ACG

This is actually a disadvantage of FDT/Matrix since these perimeters bottom-out at 0dB, whereas W/W perimeters can go into the negative numbers to show the relative change between the pt's different VF tests.

If you are providing care for a pt for the first time and you notice a slit defect, it would be best to monitor at this point. Since you have no idea about the change/progression of the condition, it would be too soon to treat, and it could be a pseudo-defect. If they have cooresponding ONH damage, then it would be a good idea to treat.

Dr. Comer indicated that pachymetry will most likely become the standard of care, but at this point (as least legally) it is W/W perimetry

Denser 79%
Increased size 53%
New VF in same hemifeld 50%
Improvement 2% (temporary)

If a pt does not have good direct light responses, always do near reflexes. Near reflexes should NOT be quicker than light reflexes

Parapapillary atrophy can precede GLC ONH damage by years. It is most commonly associated with age and is not a very strong sign for GLC. It is more common in DIFFUSE ONH damage & LTG. DDx RPE crescent

Opposite! Structural damage can precede functional changes by years (pre-perimetric GLC)

Focal damage is most likely to occur in the inferior area of the ON.

At least 3 the 1st year & 3 the 2nd year to determine rate of progression and RO rapid progression

For every 40 microns thinner central corneal thickness (CCT) than normal, there is a 70% increased risk for glaucoma (GLC) damage. This means that as the CCT decreases by 40 microns, the risk of GLC damage increases by 70%. This relationship suggests that thinner CCT may be a risk factor for developing glaucoma.

The correct answer is 2% because it is the percentage of normal patients who have a C:D (Cup-to-Disc) ratio greater than 0.7. This means that out of all the normal patients, only 2% of them have an optic cup size that is more than 70% of the optic disc size.

Superior & inferior LC coorespond to the arcuate bundles. Larger diameter fibers (M cells) pass through superior & inferior poles (theory that M cells are affected 1st in GLC, which is the basis of FDT technology)

Most early GLC VF loss occurs centrally, and later in the periphery

Drance hemes are common, but transient. Precedes ONH damage / VF loss by years. Indicates chronic vascular insufficiency...future damage is coming

I-Care is portable & does not require anesthetic, however it is still applanates and therefore is susceptible to IOP inaccuracies due to corneal biomech factors

Occur in nasal VF because arcuates are affected which are in the temporal retina. Can also occur beyond 20 deg superior.

Many eyes w/ drance hemes develop a focal notch at the location of drance heme & cooresponding VF defect

Need to do pachymetry before the cornea is touched (before GONIO & TONOMETRY)
Need to do imaging before pachymetry

At least 3 hours after waking up
At least 3 months after cataract sx
At least 3 6 months after refractive sx

Diffuse Axon Loss:
- generalized cup increase (ROUND)
- generalized RNFL drop out
- general depression of VF
- Tritan CV defect
- increased latency & amp on ERG
- often in younger pts & higher IOPs

Focal Axon Loss:
- ONH damage in localized regions (notching, vertical cup enlargement, occasionally temporal rim)
- RNFL loss localize to arcuate bundles (slit defects, wedge defects)
- Focal VF loss; arcuates damaged most often (nasal step, paracentral scotomas)
- often in elderly, normal/slightly elevated IOPs

Drance hemes, also known as flame-shaped hemorrhages, are typically seen in the retina and can be indicative of various underlying conditions. The given answer options include DM (diabetes mellitus), anti-coagulant use, migraine, PVD (peripheral vascular disease), and AION (anterior ischemic optic neuropathy). These conditions are known to be associated with the development of drance hemes. However, it is important to note that this list is not exhaustive, and other conditions such as CRVO (central retinal vein occlusion) and cardiovascular disease can also cause drance hemes.