Overview of functioning of eye • What is macula and it’s function • Age related macular degeneration • Pathophysiology of AMD • Risk factors • Types of AMD • Signs and symptoms of AMD • Diagnosis of AMD • Treatment and management of AMD Macula lutea is the specialized area of retina located at the posterior pole. • It contains fovea Centralis, which is much specialized and sensitive area in the centre of Macula • Foveola is the shining pit in the central floor of the fovea ,contains a great number of cones(light sensitive photoreceptors) responsible for bright vision • Macula is present in the centre of retina and is specialized for the central vision, pinpoint vision , i.e in reading ,driving etc • While the peripheral retina Gives the side images not the pin point images

1. Age related macular
degeneration
Presented by : Nimra Saleem
Roll no. 202008 DR AWAIS IRSHAD

2. Learning objectives
• Overview of functioning of eye
• What is macula and it’s function
• Age related macular degeneration
• Pathophysiology of AMD
• Risk factors
• Types of AMD
• Signs and symptoms of AMD
• Diagnosis of AMD
• Treatment and management of AMD

3. Overview

4. Macula and its function:
• Macula lutea is the specialized area of retina located at the posterior pole.
• It contains fovea Centralis, which is much specialized and sensitive area in
the centre of Macula
• Foveolais the shining pit in the central floor of the fovea ,contains a great
number of cones(light sensitive photoreceptors) responsible for bright
vision
• Macula is present in the centre of retina and is specialized for the central
vision, pinpointvision , i.e in reading ,driving etc
• While the peripheral retina Gives the side images not the pin point images.

7. Age related macular degeneration
• “It is a degenerative disease of the macula causing irreversible loss
of vision”
• It is the most common cause of irreversible visual loss and blindness
worldwide
• It mostly effect people after 50years of age.
• Incidence ranges from 9-25% at ages between 65 and 75 years .
• Macular area comprise only about 2.1% of the retina and the
remaining 97.9% (peripheral field )remains uneffected by the disease.

8. Risk factors of AMD
• Age
• Drusen formation at posterior pole
• Race: more common in white individuals; Caucasians
• Heridity ; family history
• Hypertension
• Smoking, doubles the risk because it reduces the level or circulating anti
oxidants
• High cholesterol
• Obesity – abdominal obesity, specially in men
• Low dietary fish intake , exposure to sunlight, drug (aspirin increase risk of
neovascular AMD

9. Pathogenesis
• The major abnormalities in the pathogenesis of ARMD are seen in
photoreceptors, retinal pigment epithelium (RPE), bruch’s membrane
and chorio capillaries.

10. Types of ARMD
• Atrophic (dry, non vascular) • Exudative (wet, neovascular)

11. Atrophic ARMD (Dry/non-neovascular)
• It is the most common form ,comprising about 90% of ARMD cases
• It is caused by progressive atrophy of photoreceptors,RPE and chorio
capillaries
• Clinical features:
• Symptoms
• Gradual impairment of central vision over a period of months or years
• Patient may complain of distorted vision and difficulty in reading
• Both eyes are usually effected but often asymmetrically
• Signs are variable and depend upon stage

12. Stages of dry ARMD
• Early stage (asymptomatic)
• Well defined small drusen
• Focal hyper pigmentation
• Intermediate stage (some visual loss)
• Less defined large soft drusens
• Sharply circumscribed small circular areas of RPE atrophy associatedwith
variable loss of choriocapillaries
• Advance stage( significantvisual loss)
• Geographical atrophy (dry ARMD) _ atrophic areas enlarges , coalease with
each other within which pre existing drusens disappear and choroidal
vessels become visible

13. Diagnosis
•history
• Typical clinical fundal findings
• Fundus florescin angiography show window defects characterized by
hyper florescence

14. Exudative ARMD( Wet /neovascular)
• It comprise only 10% of ARMD cases
• Clinical features
• Symptoms:
• Sudden onset of central visual loss usually with Metamorphosia
• Positive scotoma may be present due to hemorrhages
• Signs are variable and depend upon stage.
• The choroidal neovasularization (CNV) ,Originating from
choriocapillaries,grow through the defectsin the bruch’s membrane
into the sub RPE and sub retinal spaces.

15. Types of CNV
1. Sub RPE CNV (type 1) : The leakage and bleeding cause pigment
epithelium detachment PED which may be
• Serous PED – an orange dome shaped elevation with sharply delineated
edges
• Hemorrhagic PED – A dark red Dome shaped elevation with well defined
outline
• FibrovascularPED – An orange shape elevation with more irregular surface
and edges
• 2 . Sub neurosensory CNV( type 2): the CNV occur between RPE and
sensory retinal space . The membrane appears as grey –green or pinkish
yellow lesion

16. • 3. Retinal angiomatous proliferations (RAP) (type 3):
• On examination it appears as red discoloration,often associated with
retinal exudate . It arises from deep capillary plexus of the retina . It is
now treated as variant of CNV in ARMD
• The leakage and bleeding from CNV leads to exudation and
hemorrhage in macular area .
• 4. fibrous disciform scar at the mecula is formed due to the
resolution Of Exudative and hemorrhagic maculopathy

19. Diagnosis
• History
• Typical clinical fundus findings
• Fundus florescin angiography is important for the detection and
precise localization of choroidal neovascular membrane in relation to
the fovea Centralis

20. Treatment and management
1. Antiangiogenic therapy
I.E intra vitreal anti VEGF (1st choice) , intravitreal steroids( triamcenolone
acetonide) may improve retinal thickness and decrease vascular exudation in
selective cases.
2. Argon laser photo coagulation
It is effective in early and selected cases
Indicated in extrafovael, and not used in foveal CNVM
3. Photodynamictherapy
Transpupillary thermotherapy
4. Surgery