Optho Flashcards
Layers of eye
Fibrous tunic (sclera, cornea) - Corneo-scleral layer
Vascular tunic (iris, ciliary body, choroid) - Choroid (uveal) layer
Retina (pigmented, neural layers)
- Retinal layer with nuclei lined up in pigmented layer (outermost layer abutting choroid layer)
- Retinal pigmented layer= Cells also have phagocytic components to clean up retinal cells that turn over
Chambers of eye
Anterior chamber=
- Space defined by cornea, iris, lens
- Filled with Aqueous humor
Posterior chamber=
- Spaced defined by iris, lens, zonule fibers, ciliary body
- Filled with aqueous humor
Vitreous chamber=
- Space defined by lens, zonule fibers, retina
- Filled with gelatinous vitreous humor (water, glycosaminoglycans)
Development of eye
Interaction of ectoderm and mesoderm (neural tube)
- Diencephalon–> optic vesicles (grow out from brain)
- Optic vesicles fold in to form optic cups
Optic cups:
- Inner layer= retina
- Outer layer= retinal pigment epithelium
Optic vesicles–> induce lens–> induce cornea from ectoderm
Mesoderm: forms vascular, muscular, connective tissues
Organization of Retina
OUTERMOST 1. Retinal pigment epithelium 2. Rod/Cone photoreceptor outer segments 3. Outer limiting membrane 4. Outer nuclear layer (photoreceptor cell bodies) 5. Outer plexiform layer 6. Inner nuclear layer 7. Inner plexiform layer 8. Ganglion cell layer 9. Nerve fiber layer 10. Internal limiting membrane INNERMOST
Basic layers:
- Retinal pigment epithelium
- Photoreceptors= phototransduction (light to neural activity)
- Interneurons= process neural signals
- Ganglion cells
Specializations of retinal layer:
- Optic disk/papilla (optic nerve, blind spot)
- When looking at something, blind spot in one eye compensated by other side/brain - Fovea= back of retina in line with visual axis
- No blood vessels (gets nutrition from surrounding area)
- All cones- least amount of refraction through retina
- Cells spread to form pit–> maximal visual acuity - Ora serrata:
- Anteriormost border of neural retina
- 10 layers collapse to 2= pigmented epithelium (no rods, cones, ganglion)
Organization of anterior eye (choroidal layer, corneo-scleral layers)
Iris= regulates light entering eye
- changes size of pupil
- via sympathetic innervation of dilatory pupillae
- Parasympathetic constrictor pupillae
Cilliary body= regulates fine focus
- Adjusts shape of lens
- Parasympathetic ciliary muscle
Ciliary process= aqueous humor production
Zonule fibers
- Fine ligaments connecting ciliary body to lens
Anterior Chamber angle of eye
Limbus= point of transition from sclera to cornea
Sclera= Opaque, dense connective tissue covering posterior 5/6 of eye
- Insertion site of extraocular muscles
Cornea= Transparent avascular cover over anterior 1/6 of eye
- Primary refractive element of eye
Canal of Schlemm= largest channel of trabecular meshwork
- Drains aqueous humor
- Blockage–> glaucoma
Organization of Iris
Anteriormost specialization of retinal layer
- Regulates amount of light entering eye by changing size of pupil
Sympathetically innervated dilator pupillae
- Myoepithelial cells derived from Retinal Pigmented Epithelial layer (RPE)
Parasympathetically innervated constrictor pupillae smooth muscle
Highly vascular loose connective tissue and pigmented cells
Inner surface lined by pigment cells (neural retinal layer)
Organization of cornea
Five layers:
- Stratified squamous non-keratinized corneal epithelium
- Bowman’s (basement) membrane
- Regular connective tissue= substantia propria (stromal layer)
- Descemet’s (basement) membrane
- Simple squamous corneal endothelium
Organization of lens
Biconvex transparent avascular tissue
- Provides fine focus for visual image
- Changes shaped via ciliary muscle
Outer capsule= connective tissue
Anterior epithelial cells= differentiate into elongated fiber cells
Opacities= cataracts
Organization of eyelid
Protects exposed surface of eye
- Outer surface= thin skin
- Inner surface= conjunctiva (stratified columnar epithelium with goblet cells)
Contains:
- Tarsal plate (fibroelastic connective tissue)
- Orbicularis muscle
- Large sebaceous Meibomium glands
- Small sebaceous Zeis glands
- Moll sweat glands
Lacrimal glands
Secrete tears
- Tubulo-alveolar serous glands
- Large lumens, few ducts
- Looks similar to pancreas (no Islets of Langerhans)
Diabetic retinopathy: mechanisms of hyperglycemic damage
Diabetic retinopathy= microvascular disease due to chronic hyperglycemia
Mechanisms:
• Thickened basement membranes:
- Hyperglycemia–> protein synthesis (glycoproteins, part of BM)–> increased thickness–> hindered diffusion
• Sorbitol toxicity (Aldose reductase)
- Converts glucose–> fructose and sorbitol
- Enter cells, do not leave well–> osmotic effects
- Inhibit aldose reductase–> decrease cataracts, pericyte loss, nephropathy, neuropathy
• Glycosylation (HbA1c)
- Higher affinitiy for O2 than normal hemoglobin–> less O2 released to tissues
• Erythrocyte abnormalities
- Glycosylation of the red blood cell membranes makes them more rigid
- Increased plasminogen and macroglobulins impede RBC rouleaux formation and cause clumping
- Both of these mechanisms impede blood flow through capillaries
• Platelet abnormalities
- Diabetic platelets are “stickier”
- Diabetic platelets aggregate faster in response to thrombin, ADP, epinephrine, and collagen
• Circulatory abnormalities
- Hyperglycemia impairs autoregulation of blood flow
- So, for example, in response to hypoxia, blood flow is not increased enough
Earliest findings of capillary damage
- Thickened basement membranes
- Pericyte dropout
- Pericytes are contractile cells which regulate flow through capillaries - Microaneurysms
- Degenerate and leak
- See hard exudates, macular edema
Non-proliferative Diabetic Retinopathy (NPDR)
Confined within retina: • Dot and blot hemorrhages • Microaneurysms • Cotton wool spots • Venous beading (sausage veins) • Hard exudates • Macular edema
Grade from Mild to Severe:
- Mild= small microaneurysms; leak dye
- Moderate= more dot and blot hemorrhages
- Moderately severe= see marked hard exudates, soft exudates (cotton wool spots)
- Severe= increased hemorrhages, dilated/beaded veins, intraretinal microvascular abnormalities
Macular ischemia= loss of capillaries supplying fovea
- Cause of vision loss in NPDR
Proliferative Diabetic Retinopathy
Worse prognosis
• With time, increasing capillary nonperfusion causes retinal hypoxia.
• In some cases, growth factors like VEGF stimulate the growth of new vessels (PDR)
• Neovascularization of the disc (NVD)
• Neovascularization elsewhere (NVE)
The NEW fragile vessels tend to bleed.
• Fibrous tissue grows along the vessels.
• When the fibrovascular tissue and vitreous contract, the vessels bleed.
• Further contraction can also cause retinal detachment and blindness.
Vitreous traction
- Abnormal blood vessels tether gel and pull on vitreous–> retinal detachment
Symptoms of macular edema
- Blurred vision
- Distortion
- Difficulty with night vision or reading
- Diabetic macular edema is the leading cause of vision loss in diabetic patients, decreased vision in working Americans
Predictors for severity of diabetic retinopathy
TTractional Retinal Detachment Risk Factors: Severity depends on • Duration of the disease • Age of onset • Glycemic control (A1C levels > glucose level) • Blood pressure control • Serum lipid levels
Risk factors: • At onset: No retinopathy • After 5 years: 25% • After 10 years: 60% • After 15 years: over 80% with some DR over 25% with PDR ** After 25 years: nearly all diabetics have some D.R.
- Severe retinopathy in children is rare.
- As a general rule, the years one has diabetes before puberty do not count as regards the development of retinopathy.
- So, assuming puberty at 12, any child whether he got diabetes at 1, 2, 3, or 8, would not be expected to develop retinopathy until age 17.
Prevention of diabetic retinopathy
• Control of glucose - Glycemic control - HbA1c < 7.1 delayed onset of retinopathy, nephropathy, neuropathy • Control of blood pressure • Control of blood lipids • Control of sodium intake
Focal Laser treatment
Used for diabetic retinopathy
- Beam stops some of vascular growth
- Leaves small focal visual defects
- 3 years post-treatment, risk of doubled visual angle (20/40 to 20/80) decreased by 50%
Other treatments for diabetic non-proliferative retinopathy
- Intravitreal corticosteroids
• Injections (triamcinolone)
• Implants (fluocinolone, dexamethasone + PLGA intravitreal delivery for 35 days)
- Complications: increased IOP, endopthalmitis (infection), cataracts - Other pharmacologic treatments
• Anti-VEGF drugs
- revolutionized diabetic retinopathy
- VEGF activity correlates with degree of diabetic retinopathy
- Drugs: Macugen, Avastin (antibody to VEGF), Lucentis (fragment of Ab), Eylea (fusion protein)
• Protein Kinase C Inhibitors - Parsplanavitrectomy (remove vitreous humor)
Treatment of Proliferative diabetic retinopathy
- Panretinal laser photocoagulation
- Apply laser to entire midperipheral fundus
- Complications
• Slight decrease in vision
• Slight decrease in night vision
• Slight decrease in peripheral vision - Vitrectomy surgery
- Used in patients with non-clearing vitreous hemorrhage
- Tractional retinal detachment
- Complications: major procedure, eyes/patients have poor risks, costly
Tractional Retinal Detachment
Cut adhesions between vitreous and retina
- Adhesions cause vitreous to pull on retina–> retinal detachment
- Correct tractional retinal detachment
- Remove scarred tissue overlying retina (from previous laser surgeries)
Causes of Red Eye
- Conjunctivitis
- Discharge - Keratitis (inflammation of cornea)
- may have discharge
- Painful
- Decreased vision
- pupil size may change - Iritis
- Painful
- may have Decreased vision
- Unequal pupil - Acute angle closure glaucoma
- Painful
- Decreased vision
- Dilated pupil
Uncommon:
- Pterygium
- Episcleritis
- Scleritis
- Dacryocystitis
Conjunctivitis
Chief complaint: foreign body sensation
Types:
- Viral:
- watery discharge
- tender palpable preauricular node
- recent URI
- Highly contagious
- Spread by eye-hand-eye contact
- Hand washing is of critical importance
- Treatment: Cool compresses and lubricating drops for most cases - Allergic:
- itching
- Stringy, white discharge
- See bumps on underside eyelid
- Associated with atopic disease
- Treatment: cool compress, topical antihistamine, NSAID, mast cell stabilizer, systemic antihistamines (only if NOT dry eye) - Bacterial:
- purulent discharge
Gram +
- Staph aureus and epidermidis
- Strep pneumoniae
- Strep Groups A & B
- Corynebacterium diptheriae
Gram -
- Hemophilus influenza
- Pseudomonas aeruginosa
- Neisseria gonorrhoeae and meningitidis
Culture with conjunctival swab
Treatment:
- topical antibiotic drop (polymyxin/trimethorpim, moxifloxacin, gatifloxacin, besifloxacin, azithromycin)
- Topical antibiotic drop (erythromycin, bacitracin)
** in hyperacute conjunctivitis, need to rule out GC (gonococcal conjunctivitis) by gram stain
Red eye in infants
- Ophthalmia neonatorum (neonatal conjunctivitis)
- Dacryocystitis
- Congenital glaucoma
Causes:
- Chemical - silver nitrate: 10% incidence with silver nitrate
- Onset within 2-4 hours
- Duration 24-48 hours
- Treatment: Lubrication and close follow-up - Chlamydia
- Gonococcus
- Others (e.g. staph, strep, pseudomonas)
Prophylaxis:
- Erythromycin ophthalmic ointment
- Azithromycin gel drops
Chronic conjunctivitis
Chlamydia Blepharitis Toxic (medications) Molluscum contagiosum of the eyelids Allergic (seasonal or vernal/atopic) Factitious
Chlamydia conjunctivitis
Neonates and sexually active adults
- Can cause systemic disease in neonates (e.g. otitis, pneumonitis)
- Lasts weeks to months without treatment in adults
Treatment:
- Systemic tetracyclines, azithromycin, erythromycin for 3-6 weeks
Blepharitis
Inflammation of the eyelid margin
- Crusting of the eyelashes, typically worse in the morning
- Associated with dry eyes
- Clogged Meibomium glands (zits)
Treatment:
- Warm compresses
- Eyelid scrubs, antibiotic ointment
- Occasionally systemic tetracyclines, azithromycin
Topical fluorescein dye
- Vegetable dye picked up by areas absent of epithelium
- Appears green with cobalt blue light
- Extremely useful in diagnosing corneal abrasions, lacerations, foreign bodies, etc.
** NOTE: Be careful as serious corneal injuries and infections can also stain with fluorescein
Corneal problems
Trauma - Foreign bodies - Chemical burns Contact lens complications Bacterial ulcers Herpes simplex virus infections Other infections - (e.g. fungus, acanthamoeba, herpes zoster)
Contacts causing Red Eye
GPC (giant papillary conjunctivitis)
Tight contact lens syndrome
Toxic/allergic reaction to chemicals in contact lens solutions
Bacterial corneal ulcers (pseudomonas especially)
Acanthamoeba keratitis (uncommon parasitic corneal infection)
Treatment of corneal ulcers
Mild to moderate, peripheral
- Topical fluoroquinolones
1. Cipro= pseudomonas, staph, strep
2. Ofloxacin= broad spectrum
3. Levoflox= broad spectrum
4. Moxi, gati, besi= 4th generation - Good gram neg coverage
- Improved gram pos coverage
- better penetration
Moderate to severe, central
- Topical fortified antibiotics:
1. Tobramycin (15 mg/ml) q 30-60 minutes ATC alternating with
2. Cefazolin (50 mg/ml) q 60 minutes ATC
Herpes simplex keratitis
- Active infection:
- Classic tree branch pattern epithelial defect=dendrite
- Tx: topical and/or oral antivirals
* ** Made WORSE by steroids in active infection*** - Inflammation:
- Can cause corneal edema and inflammation inside the eye (iritis)
- Tx: topical steroids w/ anti-viral coverage
Iritis
Signs/symptoms: circumcorneal injection, photophobia
Secondary to blunt trauma, keratitis
Associated with systemic diseases (e.g. sarcoidosis, connective tissue disorders)
Idiopathic
Referral not necessary for following:
Conjunctivitis improving over 2-4 days
Tx: cool compresses and tears
Chalazion
Tx: warm compresses
Subconjunctival hemorrhage (nontraumatic) Tx: none
Steroid complications in eye
Glaucoma (in susceptible patients)
Cataract (dose related)
Enhances most active infections, especially:
- Herpes simplex infections
- Fungal infections
- Acanthamoeba infections
Concerning signs/symptoms in red eye
Danger symptoms:
- Decreased vision
- Pain
- Photophobia
Danger signs:
- Corneal fluorescein staining
- Corneal edema
- Circumcorneal injection
- Abnormal pupil size or reaction
- Abnormal eye pressure
Urgent conditions (referral to optho):
- Corneal infection
- Iritis
- Angle closure glaucoma
- Orbital cellulitis
- Trauma: Hyphema (blood in anterior chamber), Laceration
Vascular supply to eye
Choroidal artery= back of retina
Retinal artery, vein
Retinal vascular disease
- Artery Occlusions
- Vein Occlusions
- Hypertension/ Arterial Sclerosis
- Amaurosis Fugax
- Ocular Ischemic Syndrome
- Diabetes Mellitus
- Sickle Cell Disease
Types of retinal hemorrhages
Streak/flame hemorrhages
- Superficial
- Nerve fiber layer- gives streak configuration
- More with arterial disease (hypertension)
Dot and blot hemorrhages
- Deeper retina
- Outer plexiform layer- gives round configuration (“blot” larger than “dot”)
- More with venous disease (retinal vein obstruction)
Cotton Wool spots
- Small foci of fluffy retinal whitening
- Located in retinal nerve fiber layer
- Occur secondary to blockage of terminal retinal arterioles
Histopathology: Regions of axoplasmic damming in the nerve fiber layer
Hard exudates
- Discrete yellow deposits in the retina
- Located in outer plexiform layer
- Occur secondary to chronic leakage of lipids from incompetent retinal vessels (or subretinal neovascularization)
Branch retinal artery occlusions
= Blockage of retinal artery Edematous opacification of the retina : - Within hours/days - In the distribution of the affected vessel - Embolus may be visible
Causes: Emboli= #1 cause - Cardiac - Irregular heart rate - Cardiac valves - Carotid plaques - Hypercoagulability - High Blood Pressure
Types of emboli:
- Cholesterol “Hollenhorst plaques”
- Arise from carotid - Platelet-fibrin
- Associated with arteriosclerosis - Calcific
- Diseased cardiac valves
Central Retinal Artery Occlusion
= Sudden, painless visual loss
Retinal appearance:
- Opaque and edematous
- Cherry-red spot”= unobstructed choroidal vasculature (outer retina) in tact, retinal vasculature gone
- Visible intact choroidal vasculature beneath the foveola
Causes:
- Atherosclerosis (Majority)
- Arterial spasm (e.g. migraine)
- Dissecting aneurysm
- GIANT CELL ARTERITIS= 1% of cases (rare, but can become bilateral quickly)
Management
- No good therapy exists
- If within 24 hrs
- Anterior chamber paracentesis (withdraw fluid from front of eye)
- Ocular massage (pressing on eye dilates arterioles)
- Lower intraocular pressure
- Carbogen (5% CO2, 95% O2)
Complications (more common in central occlusions):
- Iris neovascularization: Due to ischemic retina; Usually 3-4 weeks later
- Laser treatment required
Branch retinal vein occlusion
Within one sector or retina; occur where vein and retina cross frequently:
- Superficial hemorrhages
- Retinal edema
- Cotton-wool spots -
- Dilated and tortuous vein
- Corresponding artery narrowed and sheathed
Risk factors:
- Age 60-69 most common
- Hypertension
- Cardiovascular disease
- Increased BMI at age 20
- Glaucoma
- Hypercoaguable states (esp in younger patients)
Causes of visual loss
- Macular hemorrhage
- Macular edema
- Capillary occlusion (macular ischemia)
Management:
- Macular edema
- Laser
- Intravitreal triamcinolone or antiVEGF agent - Neovascularization
- PRP to ischemic area
Central Retinal Vein Occlusion
= Dilated and tortuous retinal veins all 4 quadrants - Optic disc swelling - Intra-retinal hemorrhages - Macular edema - Cotton-wool spots
Pathogenesis:
- Throbosis of central retinal vein at or posterior to the lamina cribrosa
Risk factors:
- Age (90% > 50 y.o.)
- Hypertension
- Diabetes
- Glaucoma
- Hypercoaguable states (especially in young patients)
Management:
- Family medical doctor to manage
- Hypertension
- Diabetes
- Elevated cholesterol
Treatment:
- Neovascularization: Laser (panretinal photocoagulation- permanent, shirinks vessels)–> avoid glaucoma by catching before vasculature moves into angle
- Macular edema: Intravitreal triamcinolone; Anti VEGF agents (temporary)
Ocular effects of systemic arterial HTN
Grade I (chronic)
- Retinal arterial narrowing
- Straightened retinal arteries
Grade II (chronic)
- Retinal arterial narrowing
- Straightened retinal arteries
- Arteriovenous nicking at AV crossings (vein underneath artery–> squished)
Grade III (acute)
- Retinal hemorrhages
- Cotton-wool spots
- Hard exudates
- Diastolic BP > 110-115 mmHg
Grade IV (malignant hypertension)
- More severe grade III changes plus:
- Optic disc swelling (elevated margins)
- Diastolic BP > 130 mmHg
- Systemic prognosis is poor
Pearls:
- Grade I changes from aging alone
- Fundus findings not helpful in managing htn unless Grade III or IV
- Only Grades III and IV adversely affect the vision; Rx: treat the hypertension
- For Grade III and IV changes- move on it!
