Age related macular degeneration Flashcards
Presentation/clinical features of ARMD?
Present with subacute onset of visual loss:
- progressive, central visual loss
- reduced visual acuity
- reduced vision at night / hard to adapt to dark settings
- visual disturbances fluctuate day to day
- visual changes: flickering/flashing lights, glare around objects.
- loss of contrast sensitivity
Common PC: letters are jumping/ reading line is distorted/wavy.
Risk factors for ARMD?
Advancing age
Smoking
FHx and genetics
Ethnicity - caucasian
Other PMH - CVD, HTN
Ocular characteristics - light iris, hypermetropia/long sighted
Other RF = ones associated to CVD —> HTN, DM, hyperlipidaemia.
Investigations for ARMD?
- slit-lamp microscopy –> to identify any pigmentary, exudative or haemorrhagic changes affecting the retina which may identify the presence of ARMD. This is usually accompanied by colour fundus photography to provide a baseline against which changes can be identified over time.
- fluorescein angiography is used if neovascular ARMD is suspected, as this can guide intervention with anti-VEGF therapy. This may be complemented with indocyanine green angiography to visualise any changes in the choroidal circulation.
- ocular coherence tomography is used to visualise the retina in three dimensions because it can reveal areas of disease which aren’t visible using microscopy alone
Management for ARMD?
Dry ARMD:
- self monitor using Amsler grid
- attend eye appts routinely
- reduce RF - check BP, reduce CVS risks, protect eyes from UV A and B
- prevent progression with anti-oxidant vitamins A,C,E, zinc
Wet ARMD:
- anti-VEGF = prevent progression of wet ARMD
- Laser photocoagulation = slow progression when new vessels formed.
What is drusen?
- Undigested cellular debris from the degeneration of retinal pigment epithelial (RPE) cells —> this accumulates = drusen.
- yellow/white in colour
- builds up between RPE and Bruch’s membrane
Signs of ARMD on:
1) Amsler grid testing?
2) Fundoscopy?
1) Amsler grid testing = line distortion.
2) Fundoscopy = presence of drusen.
What are the types of drusen?
Hard drusen = small, hard, solid deposits
Soft drusen = larger soft deposits
Compare dry ARMD and wet ARMD?
Dry ARMD:
- non-exudative
- atrophic
- gradual vision loss - years, decades.
- more common
- fundoscopy shows drusen at the macula
- less aggressive
Wet ARMD:
- exudative
- neovascular
- rapid vision loss over days/weeks
- less common
- fundoscopy shows macular odema
Pathophysiology of dry ARMD?
1)Get drusen build up
2) Get atrophy of RPE —> leads to gradual atrophy of photoreceptors —> reduced visual acuity, reduced contrast sensitivity —> gradual loss of vision.
Differential Dx for ARMD?
- Refractive error
- Corneal disease
- Cataract
- Primary open-angle glaucoma
- Posterior vitreous detachment, vitreous haemorrhage, or retinal detachment
- Cerebrovascular disease —> amaurosis fugax, stroke, TIA
- Retinal arterial occlusion or retinal venous occlusion.
- Medication induced e.g. chloroquine, hydroxychloroquine, isoniazid, thioridazine, isotretinoin, tetracycline, or ethambutol.
- Pituitary tumour and papilloedema.
Why can drusen build up lead to hypoxic state and inflammation?
Drusen builds up between RPE and Bruch’s membrane. So as it accumulates, it separates these two layers.
—> so nutrients and O2 can’t be delivered = hypoxia, inflam.
Why can drusen build up lead to hypoxic state and inflammation?
Drusen builds up between RPE and Bruch’s membrane. So as it accumulates, it separates these two layers.
—> so nutrients and O2 can’t be delivered = hypoxia, inflam.
What is the role of VEGF in ARMD?
Has a role in conversion of dry ARMD to wet ARMD.
- VEGF = a mitogen, get increased vascular permeability.
Here is how it leads to wet ARMD:
Start w/ dry ARMD —> drusen builds up —> inflammation —> macrophages at area to help with this —> macrophages produce VEGF —> VEGF signalling cascade —> increases vascular permability/ make more vessels so get neovascularisation —> wet ARMD
What is the role of VEGF in ARMD?
Has a role in conversion of dry ARMD to wet ARMD.
- VEGF = a mitogen, get increased vascular permeability.
Here is how it leads to wet ARMD:
Start w/ dry ARMD —> drusen builds up —> inflammation —> macrophages at area to help with this —> macrophages produce VEGF —> VEGF signalling cascade —> increases vascular permability/ make more vessels so get neovascularisation —> wet ARMD
Pathophysiology of wet ARMD?
1) VEGF stimulated blood vessels extend through Bruch’s membrane
2) fluid and blood leak behind and into the retina
3) forms fibrous scar tissue
4) scar tissue = get central vision loss
