Let's learn about age-related macular degeneration: Introduction, clinical types, pathogenesis & treatment. Few fundoscopic images are also added for extra learning. Happy Learning!

1. Ophthalmology
- Fundoscopic images
- Age-related macular degeneration

2. Fundoscopic images

3. Normal Fundoscopic exam

4. ISNT rule
• Gradual decrease or no change in rim width at the following
position order: inferior (I) ≥ superior (S) ≥ nasal (N) ≥
temporal (T)

5. Diabetic retinopathy-Non proliferative
Cotton wool spot
White spots d/t
nerve fiber infarct
Dot
hemorrhages

7. Macular degeneration
Drusen
Irregular pale yellow
deposits at macula

8. Age-related macular degeneration
(AMD)

9. Introduction (AMD)
• Disease of the retina, affects the macula
• Usually in people aged 60 years and older.
• Leading cause of blindness (irreversible) in elderly
• When advanced, destroys central vision that we use to look
straight ahead (necessary for recognizing faces, reading
books, using mobile phone screens, watching TV, sewing,
preparing food, driving, safely navigating stairs and
performing other daily tasks we take for granted)
• If macula damaged, picture is there but fine points not clear.
• Fortunately, the peripheral vision remains intact.

10. Types of AMD
• Based on presence/absence of neovascularization, 2 forms:
• Dry AMD (Atrophic/Non exudative)
 Neovascularization absent
 Presence of drusen in early stage (insoluble extracellular
aggregates in Bruch membrane, d/t build-up of waste products from
photoreceptor metabolism)
 Geographic atrophy of retinal pigment epithelium (RPE) in late
stage, characterized by areas of degeneration of RPE cells &
overlying photoreceptors
• Wet AMD (Exudative)
 Choroidal neovascularization present
 Characterized by presence of angiogenic vessels that presumably
originate from choriocapillaries & penetrate through Bruch
membrane beneath RPE
 Leakage of fluid & blood from these vessels
T/T: Anti VEGF therapy (ranibizumab), photodynamic therapy

11. Early AMD
• Irregular pale yellow deposits at macula (Drusen)
Drusen

12. Normal Vs Dry & Wet AMD

13. Dry AMD
• Defective mitochondria
(decrease energy production, increase ROS-cell death)
• Toxins accumulate (Hallmark)
(Lipofuscin-non degradable debris, accumulates in RPE
with aging, forms ROS in presence of light- toxic to RPE
cells)
• Autophagy induction to eliminate intracellular components
that abnormally accumulate
• T/T
 No definite treatment
 Antioxidant vitamin & Zn supplementation

14. Dry AMD

15. Wet AMD
Complement activation
- Genetics
(Decrease function of
complementary regulatory
genes, CFH- excess
complement activity)
Oxidative stress
- Environmental factors
• Smoking
• Decrease dietary intake of
antioxidants, zinc
Increase VEGF-A by RPE
Angiogenesis
Recruit leucocytes,
proangiogenic
macrophages
- C3a & C5a-potent
chemotactic factors

16. Wet AMD

17. Amsler Grid
• Amsler grid can be given to patients with early AMD (& any
other patients over 60 years of age) for self-testing
• Help person spot macular defects early
• If an Amsler grid unavailable, can test themselves for
distortion by looking at a straight edge or a right angle, such
as a door frame or window, with one eye at a time.
• Someone with macular degeneration may see some or all of
the following:
• Straight lines that appear wavy or bent
• Boxes that differ in size or shape from the others
• Lines that are missing, blurry or discoloured
• Dark areas at the centre of the grid.

18. Amsler grid for self-testing

19. References
• Ambati J, Fowler BJ. Mechanisms of age-related
macular degeneration. Neuron. 2012;75(1):26-39.
https://www.ncbi.nlm.nih.gov/pmc/articles/PMC34
04137/#R115
• Mathenge W. Age-related macular
degeneration. Community Eye Health.
2014;27(87):49-50.
• Robbins & Cotran Pathologic Basis of Disease, 9e