6 - Opth - Retinal disease - AMD

Question 1

features of AMD

Answer 1

usually >70y
usually bilateral
progressive central vision loss
10% of over 65s

Question 2

RFs

Answer 2

age, smoking, HTN, high cholesterol, UV exposure

Question 3

Drusen - what? why? may lead to?

Answer 3

In BOTH types of AMD

yellow/white build up of extracellular material betwenn thickened Bruch’s membrane and RPE

Due to axonal degen and calcium deposition

may lead to irregular appearing edge of optic disc

Question 4

Ix of AMD

Answer 4

VA
reading speed
Amsler grid to assess distortion
Fundoscopy
Flourescein angiogram - bl ves and neovasc visualisation
Optical coherence tomography

Question 5

Dry AMD - description + percentage of cases

Answer 5

geographic/atrophic - 90%

Question 6

Features (non-fundoscopy) of dry AMD

Answer 6

central VA deteriorates - faces + reading difficulty
metamorphopsia (vision distortion)
central scotomas

Question 7

Fundoscopic features of dry AMD

Answer 7

hard (small well defined) and soft (large, poor defined) drusen
Focal RPE hyperpigmentation
RPE atrophy in advanced AMD - hypopigmentation + visible choroidal vessels

Question 8

MGMT of dry AMD

Answer 8

no Tx available, but slow progression
low visual aids
smoking cessation and vit supplements may slow progress

Question 9

Wet AMD - description + percent

Answer 9

neovascular/exudative - 10%

Question 10

3 main Features of Wet AMD

Answer 10

rapid loss of vision and development of scotomas

metamorphopsia

choroidal new vessels CNV - grow through Bruch’s to lie under retina

Question 11

Consequences of Choroidal new vessels

Answer 11

leak fluid, lipids and blood under retina

-degeneration and localised detachment of RPE, fibrous scarring (end stage)

Question 12

4 parts of MGMT for wet AMD

Answer 12

• intravitreal VEGF inhibitors
• photodynamic therapy
• laser photocoagulation
• surgery

Question 13

Intravitreal VEGF i - line? examples? mechanism? combined with?

Answer 13

• first line
• bevacizumab (avastin, ranibizumab (lucentis)
• dec cell proliferation, vessel formation and vascular leaks
• -> improved VA in 1/3rd - most of the rest maintain current vision
• may be combo with PDT

Question 14

Photodynamic therapy - what is used? mechanism? repeated when? combo?

Answer 14

• IV verteporfin + phototherapy slit lamp
• activvated verteporfin, causing thrombosis and occlusion of abnormal vessels
• 3 monthly intervals
• may be combo with anti-VEGF Tx

Question 15

Laser photocoagulation- only if? how? high what rate?

Answer 15

• only if lesion away from fovea (risk of sight loss)
• destroys bl vessels and prevents further neovascularisation
• high relapse rate

Question 16

Surgery - main part + one of these two options

Answer 16

vitrectomy + submacular excision of CNV
+ either of
- replacement of RPE, OR movement of fovea to overlie normal RPE