1-2,3,4 - Glaucoma Flashcards
Describe organisation of RNFL
- Name RNFL area responsible for central vision
1) Central fibres near ONH are straight but more peripheral RNFs are arcuate. Never cross the horizontal raphe.
2) Papillomacular bundle.
lamina cribrosa role in glaucoma?
- How does it separate the optic nereve?
- Which part of VF gets defects more commonly?
It is a network of collagen fibres which are fenestrated and have pore/gaps that nerve fibres (GC axons) travel through. NFs before reaching lamina cribrosa are unmyelinated (pre-laminar) whilst those past lamina are myelinated (post-laminar)
- Superior and inferior VFs. Lamina cribrosa pores are stretched and enlarged which makes them structurally thinner thus more susceptible to damage.
Mechanical glaucoma physiology?
- Role of axoplasmic transport?
- Distortion to lamina cribrosa (seen as buldging posteriorly or inward) causes thinning. Distorted fenestrations disrupts nerver fibres (suffocation/squished), so nutrients can’t access area. Nerve fibres apoptose without nutrients which shows as neuralretinal rim thinning.
- 2 way communication between RGC bodies and synaptic terminal. This is done via microtubules and neurofilaments. Two ways are called
-> Anterograde (for proteins and lipids etc…)
-> Retrograde (for trophic factors which develop neurons) - Deficits in neutrotrophic factors supply meaning RGCs will apoptose.
Mechanical theory: High IOP compresses the lamina cribrosa which misaligns and distorts it. Prevents retrograde axoplasmic flow of neurotropin so apoptosis occurs. However, not all glaucoma has high IOP and reducing IOP doesn’t always work.
Describe RNFL loss in glaucoma
- Imaging RNFL loss is easier w/ what setting?
- “Floor effect”?
- Arcuate, respects horizontal midline.
- Use red free (green) filter. This has shorter wavelength and lower tissue penetration which is good for imaging RNFL which is superficial.
- VF loss corresponds to opposite area in RNFL organisation e.g. Superior temporal VF loss means inferior nasal RNFL loss.
- Floor effect is when VF loss so bad you can’t measure the progression anymore.
Optic Nerve Head examination shows what features if glaucomatous?
- NRR?
- Cup?
- Pale, atrophic, and thin NRR
- Larger, deep cup
Selective RGC loss theory?
- Evidence for?
- Against?
- Idea that larger cells are more affected due to larger axons which are more vulnerable.
- This is proven with preferential VF loss in superior and inferior RNFL which are where M cells are, and sparing of papillomacular bundle which is where P (midget) cells are.
- However, studies also show sizes of RGCs vary (midget cells aren’t always smaller) and studies show both types have reduced count in glaucoma.
Vascular Theory of glaucoma?
Loss of blood supply going to optic nerve causes apoptosis. This can be due to:
- High IOP disrupting BVs
- Vascular autoregulation disrupted e.g. sleep apnea
- Systemic haemodynamic changes e.g. low BP
This degenerates lamina cribrosa and reduces retrograde axoplasmic flow of neurotropin leading to apoptosis.
Neurotoxic theory of glaucoma?
Excess glutamate -> overstimulate receptors -> too much intracellular Ca2+ released + inflammatory and neurotoxic factors -> Apoptosis.
POAG must have all of the following conditions:
- Causes?
- IOP levels?
- Level of damage?
- Symptoms?
- Angle?
Pathophysiology?
- Not caused by other disease (Primary)
- IOP increase unknown cause
- IOP > 21mmHg at least once
- RNFL or ONH damage
- VF loss (unless pre-perimetric)
- Open AC angle
- Slow, bilateral usually (w/ asymmetry)
- Due to TM structural abnormalities e.g. plaques, fusion, thickening…
NTG
- Risk factors?
- How to diagnose it?
- Glaucoma but IOP consistently lower than 21mmHg
- Vascular risk factors e.g. systemic hypotension or sleep apnea
- Diagnosis of exclusion (rule out other diseases first). Examples of other diseases with VF defect and abnormal ONH is brain tumour compressing on ON.
2 mechanisms of Primary Angle Closure. Describe them.
- Iris physically blocks TM
- Severe + acute
Relative Pupillary Block: - Iris and lens contact and form seal (a.k.a. posterior synechiae)
- AH cannot flow from PC to AC
- Build up of pressure causes iris to bow anteriorly (iris bombe)
- Iris contracts with TM and closes it.
- Under slitlamp, optic section on iris is curved due to bowing of iris. Pupil is also distorted due to iris stuck in odd spots.
Non-pupillary Block: - Anatomic factors e.g.
- Plateau iris config (iris is placed anteriorly)
- Thick iris
- Anteriorly rotated ciliary processes
Iris ends up close to TM so likely for irido-trabecular contact.
Note: Mixed mechanism can occur where both pupillary and non-pupillary block can occur.
Stages of primary angle closure?
PAC suspect
- high risk but not yet closed
- Irido-trabecular contact in 2 or less quadrants
-No PAS (Peripheral Anterior Synechiae meaning permanently adhering iris to angle)
- Normal IOP and ONH
PAC
- Irido-trabecular contract in 3 or less quadrants
- Raised IOP but normal ONH (Not yet glaucoma)
PACG
- Has glaucoma now, optic neuropathy.
Signs/symptoms of PAC?
- Very painful
- Nausea/vomit
- Poor VA (6/60 or worse)
- Very high IOP spike (>50mmHg)
- Circumlimbal conjunctival hyperaemia
- Corneal Oedema
- Shallow AC angle
- Classic mid-dilated, vertically oval pupil
Note: Fellow eye may show occludable angles
Predisposing risk factor of primary angle closure?
Partial dilation can cause acute angle closure. Can be due to mydriatics, medications, or dim illumination. Can even happen hrs after dilating when drug starts to wear off so iris is mid-dilated. This is rare and usually avoided by testing anterior chamber angle prior to dilation.
Describe Pigment Dispersion Syndrome
-> Iris happens to be bowed posteriorly so closer to lens
-> Iris rubs against zonules of lens (the strings attached to the lens).
-> Iris pigmented epithelium releases granules
–> Granules compromise TM AH outflow (seen as TM hyperpigmentation)
–> Land on corneal endothelium to form Krukenberg spindle pattern
–> Land on anterior lens to form Scheie stripe pattern.
- Slit lamp shows transillumination of iris as rubbing off pigment off iris will let light through it.
- Can be primary or secondary disease.
