1. Retina, Vitreous, Choroid
1.1. Retinal Vascular Diseases
1.1.1. Diabetic Retinopathy
1.1.1.1. Non-proliferative
1.1.1.1.1. Findings
1.1.1.1.2. Treatment
1.1.1.2. Proliferative
1.1.1.2.1. Treatment
1.1.2. Central Retinal Vein Occlusion
1.1.2.1. Ischemic
1.1.2.1.1. Multiple Splinter
1.1.2.1.2. Blot hemorrhage
1.1.2.1.3. Soft exudates
1.1.2.2. Non-ischemic
1.1.2.3. Treatment
1.1.2.3.1. Retinal Photocoagulation
1.1.3. Central Retinal Artery Occlusion
1.1.3.1. Findings
1.1.3.1.1. Sudden painless loss of vision
1.1.3.1.2. Fundoscopy
1.1.3.2. Treatment
1.1.3.2.1. Immediate lowering of eye pressure
1.1.3.2.2. Improve intraocular blood flow
1.1.3.2.3. Done within 5 minutes of attack
1.2. ARMD
1.2.1. Neovascular
1.2.1.1. Sudden onset, central
1.2.1.2. Choroidal Neovascularization
1.2.1.3. Treatment
1.2.1.3.1. Laser photocoagulation
1.2.1.3.2. Photodynamic Therapy
1.2.1.3.3. Anti-VEGF
1.2.2. Non-neovascular
1.2.2.1. Gradual, painless deterioration of vision
1.2.2.2. Hallmark: Drusen
1.2.2.3. Geographic atrophy
1.2.2.4. Management
1.2.2.4.1. Education and monitoring
1.2.2.4.2. Lifestyle modification
1.3. Retinal Detachments
1.3.1. Rhegmatogenous
1.3.1.1. Symptoms
1.3.1.1.1. Flashes
1.3.1.1.2. Floaters
1.3.1.1.3. Wavy vision
1.3.1.1.4. Visual field cuts
1.3.1.2. Management
1.3.1.2.1. Laser photocoagulation
1.3.1.2.2. Scleral buckling
1.3.1.2.3. Proliferative vitreoretinopathy
1.3.2. Non-rhegmatogenous
1.3.2.1. Tractional
1.3.2.1.1. Causes
1.3.2.1.2. Treatment
1.3.2.2. Exudative
1.3.2.2.1. Causes
1.3.2.2.2. Treatment
1.4. Retinitis Pigmentosa
1.4.1. Type 1: Rods First
1.4.2. Type 2: Cones First
1.4.3. Symptoms
1.4.3.1. Nigh blindness
1.4.3.2. Visual field contraction
1.4.3.3. Blurring of Vision
1.4.3.4. Cataract
1.4.4. Fundoscopy
1.4.4.1. Vitreous cell opacity
1.4.4.2. Arteries narrowed
1.4.4.3. Diffuse pigmentation
1.4.4.4. INtraretinal perforation
1.4.4.5. Optic disc pallor
1.5. Vitreous Hemorrhage
1.5.1. Symptoms
1.5.1.1. Floaters
1.5.1.2. Sudden BOV
1.5.1.3. No history of trauma
1.5.2. Management
1.5.2.1. Retinal Exam
1.5.2.2. Ocular ultrasound
1.5.2.3. Bed rest, head elevated
1.6. Toxoplasmosis
1.6.1. Congenital
1.6.2. Acquired
1.6.3. Treatment
1.6.3.1. Antibiotic Intraocular Injection
1.6.3.2. Oral Antibiotics
1.6.3.2.1. Clindamycin
1.6.3.2.2. Sulfadiazine
1.6.3.2.3. Pyrimethamine
1.7. HIV Retinopathy
1.7.1. Findings
1.7.1.1. Cotton wool spots
1.7.2. Management
1.7.2.1. Gancyclovir
1.7.2.2. Foscarnet
1.7.2.3. Intravitreal implants
1.7.2.4. Vitreoretinal surgery
1.8. Vogt-Koyanagi-Harada Syndrome
1.8.1. Presentation
1.8.1.1. Symptoms
1.8.1.1.1. Sudden BOV
1.8.1.1.2. Photophobia
1.8.1.1.3. Floaters
1.8.1.1.4. Headache
1.8.1.1.5. Neck stiffness
1.8.1.1.6. Tinnitus
1.8.1.2. Findings
1.8.1.2.1. Retinal edema
1.8.1.2.2. Retinal detachments
1.8.1.2.3. Retinal vasculitis
1.8.1.2.4. Optic disc edema
1.8.2. Treatment
1.8.2.1. Systemic Steroids
1.8.2.2. Immunosuppressives
2. Optic Nerve
2.1. Papilledema
2.1.1. Presentation
2.1.1.1. Findings
2.1.1.1.1. Optic disc edema
2.1.1.1.2. Increased ICP
2.1.1.1.3. Bilateral
2.1.1.1.4. Blurred disc margin
2.1.1.1.5. Swollen veins
2.1.1.1.6. Dilate, tortouos retinal vein
2.1.1.1.7. Non-spontaneous venous pulsation
2.1.1.1.8. Symptoms
2.1.1.2. Causes
2.1.1.2.1. Brain tumors
2.1.1.2.2. Intracranial trauma
2.1.1.2.3. Meningitis
2.1.1.2.4. Hydrocephalus
2.1.2. Management
2.1.2.1. Treatment of underlying cuase
2.2. Optic Neuritis
2.2.1. Presentation
2.2.1.1. Usually unilateral
2.2.1.2. Inflammatory edema
2.2.1.2.1. Anterior: Papillitis
2.2.1.2.2. Posterior: Retrobulbar Neuritis
2.2.1.2.3. Retina: Neuroretinitis
2.2.1.3. Swollen optic disc
2.2.1.4. Hyperemic
2.2.1.5. Blurred margins
2.2.2. Management
2.2.2.1. IV Corticosteroids
2.3. Anterior ischemic optic neuropathy
2.3.1. Presentation
2.3.1.1. Sudden, painless, non-progressive BOV
2.3.1.2. Elderly
2.3.1.3. Comorbidities
2.3.1.4. Hemifield defect
2.3.1.5. Unilateral
2.3.2. Management
2.3.2.1. Treatment of underlying disease
2.3.2.2. Steroids
2.4. Toxic neuropathy
2.4.1. BOV
2.4.1.1. Slowly, progressive
2.4.1.2. Symmetrical
2.4.1.3. Bilateral
2.4.2. Presentation
2.4.2.1. Impaired color vision
2.4.2.2. Swollen optic disc
2.4.2.2.1. Early: Hyperemic
2.4.2.2.2. Late: Pallor
2.4.2.3. Use of ethambutol
2.4.3. Treatment
2.4.3.1. Discontinue drug use
2.5. Optic Atrophy
2.5.1. Long-standing damage
2.5.2. Nerve degeneration
2.5.3. Poor prognosis
2.5.4. White iotic nerve
3. Error of Refraction
3.1. Presentation
3.1.1. Headache
3.1.2. BOV
3.1.3. Squinting
3.1.4. Tearing
3.1.5. Head turn
3.2. Myopia
3.2.1. Near-sighted
3.2.2. Long eyeball
3.2.3. Steep Cornea
3.2.4. Focal Point: Front of Retina
3.2.5. Management
3.2.5.1. Spectacles
3.2.5.1.1. Concave
3.2.5.1.2. Divergent
3.2.5.1.3. Negative
3.2.5.2. Contact Lens
3.2.5.3. LASIK
3.2.5.4. Phaskic LOL
3.2.5.5. Clear lens extraction
3.3. Hyperopia
3.3.1. Far-sghted
3.3.2. Short eyeball
3.3.3. Flat cornea
3.3.4. Focal point: behind retina
3.3.5. Management
3.3.5.1. Spectacles
3.3.5.1.1. Convex
3.3.5.1.2. Convergent
3.3.5.1.3. POsitive
3.3.5.2. Contacts
3.3.5.3. LASIK
3.4. Astigmatism
3.4.1. No single point
3.4.2. Management
3.4.2.1. Spectacles
3.4.2.1.1. Cylindrical
3.4.2.2. Contact lenses
3.4.2.3. LASIK
3.4.2.4. Toric IOL
3.5. Presbyopia
3.5.1. > 40 years old
3.5.2. Problem with accomodation
3.5.3. Management
3.5.3.1. Reading glasses
3.5.3.1.1. Convex
3.5.3.1.2. Convergent
3.5.3.1.3. Positive
3.5.3.2. Compromised contact lenses
3.5.3.3. LASIK-SUPRACOR
4. Cornea
4.1. Transmission of Light Disruption
4.1.1. Corneal Scars
4.1.1.1. Microbial Keratitis
4.1.1.1.1. Symptoms
4.1.1.1.2. Management
4.1.1.2. Corneal Trauma
4.1.1.2.1. Abrasions
4.1.1.2.2. Lacerations
4.1.1.3. Exposure Keratopathy
4.1.1.3.1. Comatose
4.1.1.3.2. CN 7 Palsy
4.1.1.3.3. Lid and orbital deformity
4.1.1.3.4. Acute proptosus
4.1.1.3.5. Nocturnal exposure
4.1.1.3.6. Lagophthalmos
4.1.1.4. Lid Margin and Lash Disorders
4.1.1.4.1. Trichiasis
4.1.1.4.2. Trachoma
4.1.1.4.3. Chronic Blephritis
4.1.1.4.4. Epiblepharon
4.1.1.4.5. Entropion
4.1.1.5. Congenital
4.1.1.5.1. Peter's Anomaly
4.1.1.5.2. Dermoid Cyst
4.1.1.5.3. Infantile Glaucoma
4.1.2. Corneal Edema
4.1.2.1. Endothelial Dystrophy
4.1.2.1.1. Congenital Hereditary Endothelial Dystrophy
4.1.2.1.2. Fuch's Endothelial Dystrophy
4.1.2.2. Surgical Trauma
4.1.2.2.1. Anterior Segment Intraocular Surgeries
4.1.2.2.2. Mechanical Contact
4.1.2.2.3. Noxious Chemical
4.1.2.3. Increased IOP
4.1.2.3.1. Glaucoma
4.1.2.4. Treatment
4.1.2.4.1. Medical
4.1.2.4.2. Lower IOP
4.1.2.4.3. Topical Corticosteroid
4.1.2.4.4. Supportive
4.1.3. Endothelial Damage
4.1.4. Corneal Deposits
4.1.4.1. Lipid Keratopathy
4.1.4.1.1. Etiology
4.1.4.1.2. Treatment
4.1.4.2. Calcific Band Keratopathy
4.1.4.2.1. Etiology
4.1.4.2.2. Management
4.1.4.3. Corneal Staining
4.1.4.3.1. Symptoms
4.1.4.3.2. Management
4.1.4.4. Metabolic Disorders
4.1.4.4.1. Systemic mucopolysacharidoses
4.1.4.4.2. Sphingolipidoses
4.1.4.4.3. Mucolipidoses
4.1.5. Corneal Melt
4.1.5.1. Characteristics
4.1.5.1.1. Corneal Irregularity
4.1.5.1.2. Border melts
4.1.5.1.3. Central area thinning
4.1.5.1.4. Peripheral neovascularization
4.1.5.2. Management
4.1.5.2.1. Treat underlying etiology
4.1.5.2.2. Surgical
4.1.6. Corneal Tumors
4.1.6.1. Dermoid Choriostoma
4.1.6.1.1. Superficial
4.1.6.1.2. Inferotemporal limbus
4.1.6.1.3. Smooth, elevated, fleshy
4.1.6.1.4. Fibrous with hair and sebaceous glands
4.1.6.2. Corneal Transplant Neoplasia
4.1.6.2.1. Translucent
4.1.6.2.2. From limbus to cornea
4.1.6.2.3. Fimbriated or scalloped border
4.1.6.3. Pterygium
4.1.6.3.1. Wing-shaped, triangular
4.1.6.3.2. Vision obstruction
4.1.6.3.3. UV light exposure
4.1.6.4. Management
4.1.6.4.1. Surgical Excision
4.2. Refraction of Light Disturbance
4.2.1. Corneal Epithelium and Tear Film
4.2.1.1. Deficient Tear Volume
4.2.1.1.1. Keratoconjunctivitis sicca
4.2.1.2. Tear Quality Abnormalities
4.2.1.2.1. Tear Film
4.2.1.2.2. Management
4.2.1.3. Toxic Keratitis
4.2.1.3.1. Causes
4.2.1.3.2. Treatment
4.2.2. Corneal curvature
4.2.2.1. Keratoconus
4.2.2.1.1. Etiology
4.2.2.1.2. Management
4.2.2.2. Corneal Distortion
4.2.2.2.1. Peripheral scars
4.2.2.2.2. Pterygium
5. Cataract
5.1. Signs and Symptoms
5.1.1. Blurring of Vision
5.1.2. Glare
5.1.3. Image Blur
5.1.4. Distortion
5.1.5. Altered Color Perception
5.1.6. Decreased VA
5.1.7. Black lens opacity
5.2. Diagnostics
5.2.1. Swinging Flashlight
5.2.2. Direct Ophthalmoscope
5.2.3. Slit-lamp Biomicroscope
5.3. Treatment
5.3.1. Congenital Cataract
5.3.1.1. Simple aspiration
5.3.1.2. Lensectomy
5.3.2. Adult Cataracts
5.3.2.1. Intracapsular cataract extraction
5.3.2.2. Extracapsular cataract extraction
5.3.2.3. Small incision catarct surgery
5.3.2.4. Phacoemulsifications
5.4. Complications
5.4.1. Intraoperative
5.4.1.1. Iris prolapse, iris trauma
5.4.1.2. Post capsule rupture
5.4.1.3. Descemet membrane tearing
5.4.1.4. Dropped nucleus
5.4.1.5. Expulsive hemorrhage
5.4.2. Post-operative
5.4.2.1. Glaucoma
5.4.2.2. Corneal edema
5.4.2.3. Wound leak
5.4.2.4. Inflammation
5.4.2.5. Retinal detachment
5.4.2.6. Endophthalmitis
5.4.2.7. Cystoid Macular Edema
6. Glaucoma
6.1. Signs and Symptoms
6.1.1. Open Angle Glaucoma
6.1.1.1. Asymptomatic onset
6.1.1.2. Trabecular meshwork obstruction
6.1.2. Angle Closure Glaucoma
6.1.2.1. Painful BOV
6.1.2.2. Iriidescent vision
6.1.2.3. Headache, nausea
6.1.2.4. Red eye
6.2. Diagnosis
6.2.1. Slit-lamp biomicroscopy
6.2.2. Tonometry
6.2.3. Gonioscopy
6.2.4. Fundoscopy
6.2.5. Visual Field Exam
6.2.6. ONH Evaluation
6.3. Treatment
6.3.1. Medical
6.3.1.1. Aqueous Humor Suppresion
6.3.1.1.1. Beta-blockers
6.3.1.1.2. ALpha-adrenergic agnosit
6.3.1.1.3. Carbonic Anhydrase Inhibitor
6.3.1.2. Increased Outflow
6.3.1.2.1. Parasymphatomimetics
6.3.1.2.2. PG Analog
6.3.1.3. Decreased Vitreous Outflow
6.3.1.3.1. Mannitol IV
6.3.1.3.2. Glycerol PO
6.3.2. Surgical
6.3.2.1. Laser
6.3.2.1.1. Iridotomy
6.3.2.1.2. Gonioplasty
6.3.2.1.3. Trabeculoplasty
6.3.2.1.4. Cycloablation
6.3.2.2. Incisional
6.3.2.2.1. Trabeculectomy
6.3.2.2.2. Shunts and filtration device