Ocular Disease Flashcards
Sclerotic Scatter
Get it aligned and then look with naked eye
Optic section
Depth
Conical beam
Dark adaption
Specular reflection
Oculars and beams at equal angel
Indirect illumination
Look off to the side
Is blanching in chemical burns bad or good?
Bad. Indicates ischemia.
Which is the most bad ocular burn?
Alkali. More prevalent too.
Corneal erosion
Can have mitotic pupil and mild anterior chamber reaction
Commotion Retina
Bruising of the retina OS. White. Resolves in 24-48 hours.
Berlins edema
Commotion retina in the macula
Can you do gonio on a hyphema?
No. Wait 1 month post injury to avoid re bleed.
Vossius ring
Pigment on lens due to lens hitting iris. Trauma.
Iriodialysis
Breaking at iris root. Will see a wide band of CB. Monitor for angle recession glaucoma due to damage of TM.
Orbital fracture
Most common to occur in maxillary bone in posterior medial. Crepitus, pain, diplopia, restriction. infraorbital hypesthesia, angle recession, etc.
Gonio and orbital fracture
None for 4 weeks
Blowing nose and orbital fracture
don’t do it for 48 hours after trauma.
Purtscher’s Retinopathy
Occurs with CPR or strangulation. Diffuse retinal hemorrhages, exudates, and cotton wool spots.
Choroidal rupture
Temporal to ON. Concentric to ONH. Risk of CNVM. Occurs with trauma.
Preseptal cellulitis
Most common. Occurs secondary to skin trauma like bug bites or acute hordeolum. no pain to mild tenderness, eyelid edema, no orbital congestion, ptosis, warmth.
Orbital Cellulitis
An infection posterior to septum. Can occur from a sinus infection. Will have diplopia, EOM restriction, APD, eye pain, malice, reduced color vision, diplopia.
What can orbital cellulitis cause
meningitis or cavernous sinus thrombosis
What can diabetics and immunocompromised get?
mucormycosis.
How to tell if preseptal or septal.
Preseptal will not have decreased VA, Pain on eye movements, fever, proptosis, EOM restriction.
Thyroid Eye Disease (Graves)
Females. MG correlation. TSH receptor antibodies attacking EOMs and can also affect thyroid gland. Tendon sparing. IM SLO.
Signs with TED
Unilateral or bilateral proptosis, upper lid retraction, edema. Decreased color vision, EOM restriction, APD.
What is the most common cause of proptosis in middle aged patients
Graves
Greatest risk factor for the development of Graves?
Smoking
Grading system for TED
NOSPECS. No signs or symptoms. Only signs but no symptoms (Dalrymple’s side-lid retraction), Soft tissue involvement (such as lid edema and conj. chemosis) Proptosis EOM involvement. Corneal involvement, Sight loss due to EOM compression.
Von Graffe sign
Lid delay on down gaze
Where does the thyroid patient have difficulty looking?
No looking up. The IR must relax.
Lochner’s Sign
Globe lag compared to lid movement when looking up
Normal exopthalmetry for adults
12-22 caucasians. 12-18 Asians. 12-24 African americans.
Carotid Cavernous Fistula
Abnormal communication between arterial and venous system. Common with closed head trauma. Build up of venous fluid with bruit, pulsatile proptosis, ocular bruit. Can also have loss of facial sensation or CN 3,4,6 palsy.
What goes through cavernous sinus
3,4,6V1,V2. V3 and 7 do not go through.
Cavernous Hemangioma
Most common benign orbital tumor in adults
Capillary hemangioma
Most common benign orbital tumor in kids
Rhabdomyosarcoma
Most common primary pediatric orbital malignancy
Neuroblastoma
Most common secondary malignancy. From abdomen.
Optic nerve glioma
Most common intrinsic tumor of the ON. NF type 1.
Mengingioma
Most common benign brain tumor
Dermoid cyst
Often in ST quadrant. Will have proptosis.
Neurofibroma
Tumor of astrocytes. Associated with NF.
Neurilemmoma (schwannoma)
A benign tumor of Schwann cell
What is seen with orbital tumors commonly
Progressive vision loss, APD, proptosis, diplopia.
Idiopathic Orbital inflammatory syndrome (orbital Pseudotumor)
Young to middle aged. Inflammatory process that can affect anything in the eyes. Have acute unilateral red eye, diplopia, or decreased vision. Can have fever, nausea, and vomiting. Proptosis or EOM restrictions, perioribital swelling, CHEMOSIS, lacrimal gland enlargement, increased IOP, decreased corneal sensation. Tendons WILL be inflamed.
Chemosis
Typically with allergic symptoms. However, if no itching and uliateral consider Idiopathic orbital inflammatory syndrome
Tolasa hunt syndrome
idiopathic orbital inflammation that affect cavernous sinus or SOF. Acute and painful exopthlamplegia to ipsilateral palsies on CN 3,4,6. Loss of sensory can also occur.
What do you suspect with bilateral orbital psuedotumor?
Systemic vasculitis.
Ocular Rosacea
Affects sebaceous glands (meiobomian). Has telengectasia. Can cause Ocular surface disease (phlyctenules, SPK, corneal neo, staph marginal keratitis) and dry eye syndrome.
Contact dermatitis
Type 4 reaction. Acute periorbital swelling, redness, and itching. 24-72 hours.
Ocular Cicatrical Pemphigoid
Type II reaction. Cell-mediated. Old female. conj. basement membranes are attacked. Symblepharon (bulbar to palpebral), ankyloblepharon, conj fibrosis and scaring. Destroys meiobomina, goblet, and accessory lacrimal gland=severe ocular surface disease.
What drugs can cause OCP
Pilocarpine, epinephrine, Timolol (PET)
Stevens-Johnson Syndrome
Type III hypersensitivity. Affects mucus membranes. Drugs (sulfa) or infectious agents can cause.
Stevens-Johnson Syndrome Acute signs/symptoms.
Will have a systemic prodrome of fever, malaise, and vomiting. Followed by skin lesions and ocular lesions (pseudomembranes, bilateral conj, endopthalmitis)
Chronic Steven-johnson
Entropion, ectropion, trichiasis, Mebomian gland damage, symblepharon, conj. keratinization. Ulcers, neo, scars.
Seborrheic vs. staph belph
Seborrheic has less lid inflammation, more oily, greasy scales, and more eyeglash loss and misdirected growth.
Chalazian
Chronic, steril inflammation of meiobomian gland. Ask about acne rosacea or seborrheic dermatitis
Hordeolum
Acute and hot. Ask about acne rosacea and seborrhea dermatitis. An acute staph infection of the eyelids
Internal hordeolum
meiobmoian glands
External hordolum
Glands of Zeiss or moll
Floppy Eye Lid Sydrome
Associated with Sleep apnea, NAION, normotensive glaucoma
Benign Essental Belpharospasm
Both eyes. Orbitularis, procures, and corregatio.
Meige syndrome
BEB and lower facial abnormalities
Myokymia
orbicular oculi only. Unilateral.
Basal Cell Carcinoma
Telengectasia. Rodent ulcer. Most common. Lower and medial most common
Squamous cell carcinoma
Comes from actinic keratosis. No telengectasia. More likely to metastasize
Order of most likely to metastastize
Malik mel–>Sebaceous gland–>squamous–>basal
Keratocanthoma
Look like BCC or SCC but will grow and then shrink.
Sebaceous gland carcinoma poor prognosis
Greater than 2mm
Dacroadentitis
Acute–>staph. Chronic–>sacred. S-shaped ptosis in acute. Can have swelling of preauricaular lymphadopenathy.
Canaliculitis
Pouting punch. Most common culprit is Actinomyces isralies (yellow sulfur granules). Will have a smoldering red eye. Will have pus or blood with palpitation.
Dacryocystitis
Lacrimal sac infection. Often occurs with nasolacrimal duct obstruction (kids) or involutional stenosis (aging). Selling below the medical canthal tendon. More pain and swelling than with cannaliculitis.
What to do with dacryocystitsi
Do not refer for treatment or irrigate. Start treatment first.
Nasolacrimal duct stenosis. M or F.
More common in females
Jones 1 testing
Put in dye and should drain out. Positive=patent=good.
Jones 2 testing
Nasolacrimal irrigation with saline following a negative Jones 1 test.
Conj. cyst
common benign fluid filled sac on conj.
Conj concretions
Superficial deposits in conj.
Conjunctival nevus
Presents puberty or early adulthood. Inclusion cysts are diagnosis for conj. nevus.
PAM (primary acquired melanosis)
Older patient. Flat and indistinct. Premalignant tendencies.
Conj. melanomas
happen in caucasians. Come from PAM. Thickness of lesion is prognosis. Metas. to liver.
Conjunctival intraepithelial neoplasm
Most common conj. malignancy. Can progress to squamous cell carcinoma.
PAM vs. CIN
PAM goes to melanoma. CIN goes to squamous cell carcinoma.
Conj. squamous cell carcinoma
Rare and slow growing. Comes from CIN. Caucasians.
Conj. Granuloma
Inflamed area within the conj. stroll tissue. Occurs with retained FB etc. Symptomatic or FB symptoms
Types of bacterial conjunctivitis
Simple bacterial conjunctivitis or Gonococcal
Cause of simple bacterial conjunctivitis in kids
h. influenza
Cause of simple bacterial conjunctivitis in adults
s. aureus or s. epidermis
Simple bacterial conjunctivitis
Acute onset of redness that usually begins in one eye and become bilateral. Eyelids stuck together upon wakening. Symptoms typically subside in 10-14 days without treatment. Discharge is typically mucopurulent. Corneal signs and pre auricular lymphadenopathy are rare.
Among all age groups what is the most common cause of simple bacterial conjunctivitis
S. aureus.
Gonococcal conjunctivities
hyper acute purulent discharge. conj. chemises with pseudomembrane, papillary reaction, pre auricular lymphadenopathy, and tender and swollen eyelids. Also evaluate for chlamydial infection.
How is gonorrohea conjunctivitis different than simple bacterial conjunctivitis?
G. has pseudomembrane and pre auricular lymphadenopathy.
Adenoviral conjunctivititis
Include Acute nonspecific follicular conjunctivitis, pharyjgoconjunctival fever, and epidemic keratoconjuntivitis. Most common from upper respiratory tract infections. Highly contagious for 12-14 days.
Acute non-specific follicular conjunctivitis
Most common. Diffuse red eye, follicles and mild discomfort. Mild cold.
Pharyjgoconjunctival Fevere (PCF)
Swimming pool conj. Very contagious. Follicular conj, mild low grade fever, and sore through. Corneal rarely involved.
Epidemic Keratoconjunctivitis
Most serous. Pain and corneal involvement occurs. Clinical symptoms occur 8 days after exposure. SPK is common during acute phase and Supepitelial infiltrates are common in the 3rd week when the active portion of the disease has stopped. Pre auricular lymphadenopathy is present and almost always has pseudomembranes.
What is pathognomonic for EKC
Palpable node in patient suspected of adenovirus. Will also has pseudomembranes.
Molluscum Contagiosum
Rare. DNA Pox virus. Umbilicate waxy nodules. If see multiple think HIV.
Allergic Conjunctivitis
Type 1 hypersensitivity (both seasonal and perennial). Chemises, papillae, itching, tearing.
Vernal Keratoconjucntivitis
Very rare and affects males under the age of 10. Occurs 2-10 years before resolving around pubutery. Those predisposed to atopic conditions. Seasonal outbreak with warm month.
Classic signs with Vernal
prominent papillae on limbus (truants dots) or upper conj (cobblestone). Can also have corneal involvement that begin the SPK and eventually coalesce into late erosion with shield ulcers.
Atopic keratoconj. vs. vernal
VKC prominently on conj and cornea. Allergic on outer eyelids and skins.
Atopic Keratoconj.
Common in young to middle age adults with a history of atopic conditions. AKC in not seasonal. Type 1 + 4. Prominent outer eyelids, dennie’s line (extra crease under eyes), and atopy shiners. Papillae are classically more inferiorly. Keratinous more common.
What is interesting about the papillae in Atopic keratconj.
Inferior more common.
Papillae
Occur with allergies, bacteria, and nonspecific reaction. PAPILLAE. is vascular.
Follicues
Lymphocytes. CHAT. Chlamydia, Herpes, Aden, Toxic.
GPC
Contact lens wear. Mechanical trauma and immune response to contact lens deposits. Symptoms more severe when remove lenses.
GPC is characterized by papillae that are ____
> 1 mm for giant papillae by >0.3 mm in GPC
Corneal Neovascularization
Chronic hypoxia. Watch for superior panned.
Corneal neovasculaization are larger than _____ mm
1.5
Corneal warpage
Alteration in corneal shape due to cl.
Superior limbic keratoconjunctibitis
occurs with CL, CL hypersentivitity, and TED. Papillary reaction and corneal filaments are rare when due to CL hypersensitivity to solution vs. TED.
3 and 9 o’clock staining
Most common complication of CL wear. Due to low riding cl.
Complication of low riding cl
3 and 9 staining
complication of high riding cl
corneal warpage
Superior Epithelial Arcuate Lesion (SEAL)
Too tight CL.
Chlamydial Adult Inclusive Conjunctivitis
Rare. D-K. Chronic smoldering. 5-14 days after inoculation. Have acute follicular conj that become chronic. Can persist a year if not treated. Have follicles and inferior palpebral conjunctivitis. Pre auricular lymphadenopathy. Corneal involvement can also occur.
Ophthalmia Neonatorum
Acute conj in newborns from any source. Chalmydia is the most common cause
Chlamydial Trachoma Conjunctivitis
Serotype A-C. Trachoma is the leading cause of blindness. Early have follicular conjunctivitis on the superior tarsal conjunctiva, lymphadenopathy, and mild superior pants. late they have arlt line (white scarring of the superior lid) and herberts pits (depression on the Limbal conj after resolving gimbal follicles) Leads to distortion of the lids and ulceration due to trichiasis.
Phlyctenular Keratoconjunctivitis
Common in teenage years and females. Type 4 hypersentivitiy. Tearing foreign body sensation, and itching occurs. Can be located on conj (pink and fleshy and near limbs) or cornea (near limbs and white and fleshy with adjacent conj injection).
What conditions should you ask about with phlyctenual keratoconjunctivitis
TB, Blepharitis, or cane rosacea.
Ligenous Conjunctivitis
Rare. Starts in childhood. Associated with systemic plasminogen deficiency. Thick, white, woody membrane plaques. Plasminogen does the breakdown of fibrin.
Parinaud’s Oculoglandular SYndrome
Cat scratch fever is number one. Tularemia, TB, and Syphilis too. Red eye, foreign body, Unilateral granulomatous follicular palpebral conj with pre auricular and submandibular lymphadenopathy.
Why is Parinaud’s oculoglandar syndrome easy to catch?
It is unilateral granulomatous uveitis and very swollen lymph nodes.
Phthiriasis Palpebrarum
Crab louse on lash. Unilateral or bilateral. Range from mild itching to blurred vision. Mild to severe chronic follicular conjunctivitis and preauriciular lymphadenopathy.
How to tell lice from demodex
Lice on lash. Demodex in lash.
Pterygium/Pinguculum
UV and chronic dryness are number one cause.
Pingueculum
yellow-white deposit adjacent to the limbus
Pterygium
Fibrovascular growth of bulbar conj that extend into the cornea and destroys Bowmans. Lead to WTR astigmatism.
Stocker’s line
Iron deposits on leading edge of ptergyium.
Episcleritis
Normally sectoral. Recurrence is common. Unilateral. Can get with UCRAP or Idiopathic. Mild discomfort.
Scleritis
F>M. Divided into necrotizing and non-necrotizing. Very painful. Thin sclera. Frequently bilateral.
Non-necrotizing
Diffuse: most common. Nodular: deep focal painful injected immobile nodule
Nectortizing with inflammation
Worst kind. Occurs with severe autoimmune disease.
Nectrozing w/o inflammation
Slceromalcia Perforano. Occurs in patients with RA. Complete lack of symptoms.
Scleritis vs. episcleritis
Scleritis is more serious. Episcleritis doesn’t have much pain. Scleritis has a blue hue. Scleritis is bilateral and diffuse. Scleritis is much less common.
How to differ scleritis from epi with phenylephrine
2.5% phenyl will blanch with conj. with episcleritis. 10% will blanch the superficial episcleral vessels (episcleritis less red). Scleritis will still be red.
Axenfeld’s nerve loop
Congenital abnormality where ciliary nerve loops are visible in sclera.
Acute vs. chronic uveitis
Acute is 3 weeks or less. Chronic is greater than 3 weeks.
What do worry about with uveitis
Cataracts, CME, PS, PAS.
Early what will happen with the IOP
decreased
What else can you have in uveiis
hypopyon, keratin precipitates.
What suggests granulmoatous
Mutton fat KPs and iris stroll nodules
Mutton Fat Kps
collection of macrophages and look greasy
Koeppe Nodules
WBC at pupillary margins. Granulomatous and non
Buscacca nodules
WBC within any part of stroma. Granulomatous.
Common Cause of granulomatous uveitis
Sarcoid, TB, Rarely sphyllis
Common cause of non-granulomatous uveitis
idiopathic, UCRAP.
Cyclic Membranes
Can be present in chronic uveitis. Fibrovascular membranes that extend into the ciliary body into the posterior chamber and involve lens
Common cause of posterior uveitis
toxo. Unlit.
Interstitial keratitis
stromal inflammation without primary involvement of the epithelium or endo. Get neo in stroma. Can get ghosting in late.
Causes of IK
syphyllis, tuberculosis, herpes simplex (SHiT)
Congenital trid
hutingtons teeth, deafness, IK.
Pars planitis
chronic intermediate uveitis characterizes by inflammation over the pars plans (snow banking). Not associated with systemic conditions.
Does posterior uveitis have to have WBC?
NO.
Most common cause of posterior uveitis
Toxo
If mother gets pregnant after infected by toxo will baby be infected?
NO
Toxo presentation
Will commonly have one chorioretinitiis scare with overlying vitritis. Headlights in fog.
Histo presentation
Fungal infection. Choroiditis with no vitritis. Multifocal punched out lesions in periphery, peripapillary maculopathy. NO VITRIFIES.
Stellate KP’s
Fuch’s heterochromic iritis and hepetic uveitis
Sarcoidoisis
Granulomatous uveitis. Diffuse vitiates with retinal vasculitis (cotton ball droppings)
Cytomegalovirus
Ocular infection in HIV. White patches of necrotic retina with hemorrhagic retinitis and vascular sheathing.
CMV vs. toxo
CMV has less vitirits and more intravitral hemorrhage.
SE of Sarcoidosis
dacryadentisis, DED, Bells, vasculitis and vitritis, and ON disease.
Coloboma
Most often IN. Failure of embryonic tissue to close.
Where do iris malignancy occur?
Melanocytes in the strma
Dellen
Dehydrated stroma. Due to elevated tissue next to it.
Filamentous Keratopathy
Mucus and epithelial cells. Caused by prolonged inflammation and DED>
SPK
BAK causes. Non specific inflammation of he cornea. Basically everything causes
Pathophysiology behind SPK
With the epi pump the K senses when 78% water is not in stroma. The Na is pumped out, K to the A, and Cl with water out. Loss of much of K can lead to cell death and SPK.
Thygeson’s superficial punctate keratopathy
20 year old with FB sensation but quiet eye. Have bilateral central opacities that look like bread crumbs and are intraepithelial and raised (also with Herpes). May be viral. Attacks and resolutions. Lasts for 10-20 years.
Neurotrophic keratatitis
Damage to V1. Big ulcer with no pain. V1 is not telling epithelium to regenerate.
RCE
Due to past abrasion or EBMD. Pain worse upon waking up.
Thermal keratopathay
SPK 6-12 hours after exposure to Vitamin C (less than 300). Affects epithelium and bowman.
Most common type of DED
Evaporative intrinsic
Aqueous deficiency dry eye
Sjogrens or non-sjogrens.
Sjogrens
Can be primary or secondary (triad)
Non-sjogrens dry eye
Can be primary (caused by age and ducts just not working as well) or secondary (something else affecting ducts like pemphigoid)
Criteria of DED
Hyperosmality (<308) and TF instability with symptoma
Tests for aqueous defiency
Schirmer, Lacrimal lake evaluation, phenol red
Schirmer one
No anesthetic. Looks at main and accessory tears. Normal is >10 mm in 5 minutes.
Schirmer two
Anesthetic so only looks at basal tears. Normal >5 mm in 5 minutes.
Phenol red test
Use a phenol red string. A normal result is >10 mm of wetting after 15 seconds.
Flurzscene vs. lissamine/rose bengal
Flurzscene pools in epithelial defects. Lissamine and bengal stain dead and devitalized tears
Evaporative DED
More common. Can be intrinsic or extrinsic
Intrinsic Evaporative DED
Due to MGD
Extrinsic Evaproative DED
Due to seoncdary causes damaged MG. i.e. cl wear or vitamin A deficiency.
Vitamin A deficiency
Need for glycocalyx so cause Evaporative DED and can cause Bitots spot on the conj
Keratoconus
Corneal ectasia. + family history with AD. Begins around puberty. Damage to bowman layer and corneal thinning. Results in stroll collagen fibril displacement and corneal thinning and protrusion (due to MMP). T-DOME associated.
What ring do you get with Keratoncus
Fleisher
Vogt’s striae
Late in keratoconus. Vertical lines deep in stroma
Munson’s sign
lower lid protrusion with downsize with Keratoconus.
Rizzuti’s sign
Conical reflection on the nasal cornea when light shown temporally with keratoconus.
Hydrops
Tears in descemets. Occurs with all corneal ecstaias.
Pellucid Marginal Degeneration
Less symptoms. Doves on cornea. High ATR astigmatism. Can also get hydrops
Keratoglobus
Thinning of the cornea present at birth
Names for Epithelial Basement membrane dystrophy
Map-dot, Cogans, Fingerprint, ABMD.
What is the most common anterior dystrophy
EBMD.
EBMD
Most commonly. Slightly more common in F. Abnormal epithelial adhesion with excessive BM production which causes maturing epi to become trapped below. Will have negative staining (around elevation) of map-lines, dots, and/or fingerprints.
Meerman’s Dystrophy
AD. Rare. Extensive clear intraepithelial cysts.
Reins-Buckler Dystrophy
Affects Bowmans development and replacement with collagen. Bilateral sub-epithelial gray opacities that are more central.
Why is Macular dystrophy Unique
Only AR corneal dystrophy
Macular dystrophy
Stromal dystrophy. AR. Have mucopolysaccharide deposits in stroma and progresses to all of cornea.
Granular Dystrophy
AD. Stromal dystrophy. Hyaline deposits. Rarer erosions.
Avellino dystrophy
Rare granular dystrophy variant. Granular and lattice deposits.
Lattice Dystrophy
AD stromal dystrophy. Amyloid deposits in stroma.
What do granular, avenillo, and late dystrophies have in common
All are a result of TGFB1 mutation. Macular is NOT.
Schneider’s Dystrohy
Stromal dystrophy. Correlated with high cholesterol.
Fuchs Endothelial Dystrophy
AD. More common in old females. Posterior lamina is produced excessively (guttate) and results in decrease in endo cell density and pleomorphism and polymegthism. If less than 500 cells will get stroll edema with chance of bullae.
Posterior Polymorphous Dystrophy
AD. Metaplasia of endocells where they can migrate into the angle and cause glaucoma. Can have vesicles (hallmark) band lesions, and diffuse opacities.
Characteristics of Dystrophies
bilateral, symmetric, central, no neo, associated family history
Anterior Dystrophies
Cogans (EBMD), Messman’s, Reis Buckler
Stromal Dystrophies
Macular (AR), Granular (Avellino), Lattice. TGFB1 associated last three. Schneider’s.
Posterior Dystrophies
Fuchs, Posterior polymorphic dystrophy.
Megalocornea
X linked. Males. 13 mm or greater HVID
Microcornea
Less than 10 mm HVID. Almost always hyperopic.
Cornea plana
Very flat cornea.
Haab’s Striae
horizontal lines that form due to cracks in descemets with congenital glaucoma.
Posterior Embryotoxon
Anterior displaced Schwalbe’s line.
Axenfeld Anomaly
PE+ angel abnormalities + increased glaucoma risk
Rieger anomaly
PE + angle anomalies + increased glaucoma risk + iris stromal abnormalities
Rieger Syndrome
PE + angle abnormalities + increased glaucoma risk + Iris stromal abnormalities + systemic abnormalities
Peters Anomaly
Rare condition where patients are born with white central corneal opacities with iris adhesions
What is an ulcer
Epithelial defects with SEI
How to tell sterile from infectious ulcer
Sterile will have very small stain. Bacterial will stain entire lesion.
Bacterial Keratitis
Most common infeciotus keratitis. Common with CL wear.
Pseudomonas Aeuruginosa
The most common gram - associated with bacterial keratitis. Has a thick green discharge, hypopyon, a dense stromal infiltrate, and can perforate the cornea within 24 hours.
Who can invade an intact cornea epithelium
CNHL. Corynebacterium diphtheria, Neisseria Gonorrhea and meningitides, Haemophilus, and Listeria.
How will an infectious corneal ulcer stain with fluorescent
1:1.
How will a sterile corneal ulcer stain with fluorescne
Less than 1:1
Fungal Keratitis
Trauma with vegetative matter.
Agar for fungal
Sabouraud’s agar. SO MUCH FUN ON MY SAB.
Candida
Normal floral. If see an infection think immunocompromised or chronic corneal disease. Similar appearance to bacterial ulcer.
Aspergillus and Fusarium
Culprit with vegetative trauma. Feathery borders with starlight lesion.
Acanthamoeba Keratitis
Rare parasitic infection associated with inadequate contact lens hygiene. Can invade if epithelium is damaged. Culture performed with non-nutrient agar with heat killed E. Coli. Starts with intense pain with barely any signs and then can have radial keratoneuritis with a ring ulcer.
Chocolate agar plates
For Haemophils and Niseria
Herpes Simplex Virus
Can affect the epithelium, Stroma, or Endo
Epithelial disease due to HSV
Due to direct invasion of corneal epithelial cells by HSV. Can have corneal vesicles (SPK like), Dendritic ulcers, Geographic ulcers (similar to dendritic ulcer but wider), and marginal ulcers (close to limbus).
Dendrite staining in HSV
Edges stain with rose bengal. Flurzscene pools in dendrite.
Neurotrophic Keratophaty
Also occurs with HSV. Can have a neurotrophic ulcer as well. Differed from geographic as it has smooth borders and inferior.
Stromal disease with HSV
IK (also with SHiT Syphilis and TB). Infiltrate in stroma with diffuse neovascularization, an immune rings, stomal thinning, and scaring. No involvement of the epi or endo.
Necrotizing Stromal keratisi
Rare keratitis from direct invasion of stroma. Results in severe inflammation in stroma and perforation.
Endothelium disease with HSV
Disciform Keratisis. Secondary stromal edema due to immune reaction within endo. Focal, disc-shaped, stromal edema with overlying keratic precipitates. No neovascularization in stroma.
Herpes Zoster Virus
Chickenpox is first infection.
Pre-zosters
Prodrome. Want to tx here so less chance of post.
Active zosters
Does not cross the midline. Have a pseudo dendrite. Uveitis. Hutchinson’s sign.
Post Zosters
Pain that lasts one month after Zosters.
Staining in HSV and HZV
HSV will stain the entire dendrite with flurzscene and edges with lissamine. HZ with stain borders only as it is elevated.
Mooren’s Ulcer
Rare condition. Older Men. No systemic disease associated. Typically uliateral. Painful vasculitis of the gimbal blood vessels that leads to necrosis and peripheral ulcerative keratitis that goes around. Associated with hepatitis C viral infection or hookworms. Classic presentation is unilateral peripheral crescent shaped gray infiltrate that progresses to an ulcer.
Staph Marginal Keratitsi
Very common. Due to body attacking staph aeurus. on lids. Type III hypersentitivy. Will have infiltrates at 2,4,8,10.
Collagen Vascular Disorders
Peripheral marginal ulcers or thinking due to collagen vascular disorders like RA, Lupus. ETC.
Fleshier ring
Iron at base in keratoconus
Hudson Stahli line
Iron found at the junction between the middle and lower third of cornea
Stocker’s line
Iron on the leading edge of ptergium
Ferry’s line
Iron with bleb
Band keratophaty
Calcium deposits within Bowman’s layer
Terrin’s marginal dystrophy
30 year old male. SN bilateral thinning with vascular that can lead to perforation. Idiopathic.
Salzman
60 YOF. Wearing a blue bowtie. Blue nodules on bowman. Hyaline deposits.
Band Keratopathy
Calcium deposit in bowmans. Can be due to uveitis, DED, trauma, gout, and hyper calcium, sarcoidosis, and renal failure. Normally asymptomatic. Swiss cheese pattern.
Unilateral arcus
Rare and associated with carotid disease on the side WITHOUT the Arcus.
Crocodile Shagreen
Can be in Descents or Bowmans.
Corneal Farinata
Flour dust in the cornea. Due to aging or AD.
How many does do sCL wearer need to be out of their lenses before surgary
3-14 days
How long do topic soft and rigid CL need to be out of their lenses before surgery
14-21 days
how many um per Diopter
15
How much stromal bed should be left after LASIK
250
Conductive Keratopathy
Used to shrink collagen with presbyopia, low hyperopia, and residual astigmatism after other surgeries. Must be repeated in 3 years.
Infections with refractive surgery
typically frame + or mycobacteria.
Complications in steep corneas
button holes
complications in flat corneas
free caps
When can you fit patients in CL after refractive surgery
8-12 weeks
Diffuse Lamellar Keratitis (DLK or Sands of the Sahara)
fine, granular sand like parties between the flap and stroma.
What is the most common complication of LASIK
Epithelial ingrowth
Epithelial ingrowth
Occurs 1 month post op. Faint gray line or deposits near the flap.
Retreatment
Occurs in 3-6 months post. 0.75D or more in an unhappy patient or worse than 20/30
Nuclear Sclerotic
Most common aging cataract. Can cause a myopic shift (helps with near vision)
Cortical cataract
Radial spoke like opacities that commonly induce a hyperopic shift.
Anterior sub capsular cataract
Directly under the anterior lens capsule
Posterior sub capsular cataract
located directly in front of the posterior lens capsule. Affects near vision worse than distance. Occurs with systemic or topical steroids.
Infant cataracts
rubella and galctosemilia
Early cataracs
MAD wilson. Myotonic dystrophy, atopic dermatitis, DM. Wilson.
Epicapsular stars
Residual remnants of the tunica vasculosa lentil and are small star shaped pigment deposit on the anterior lens capsule.
Potential Acuity Meter (PAM)
Look at how much the acuity is affected by cataracts
Brightness Acuity Testst (BAT)
Look at glare and cataracts
Average axial length
24 mm
How much RE does 1 mm correspond to
3D
What meds should you report before cataract surgery
Flomax, anticoagulants, prostaglandins.
Intracapsule cataract extraction
All of cataract and capsule. Must wear very large glasses to correct.
Extracapsule cataract extraction
Remove lens and keep capsule. Put lens back in. Need a big inceision
Acute Post-operative Endophthalmitis
Very serious. Most are staph epidermis.
Delayed Post-operative Endopthalmitis
Within a week to a month after surgery. Fungal is commonly delayed.
Toxic anterior segment syndrome
A sterile inflammatory rections due to chemical exposure during surgery. 12-48 hours after surgery. Must rule out endopthalmitis.
Most common SE in cataract surgery
PCO, and CME.
Posterior Capsule Opaciciciation (PCO)
Commonly occur 2-6 months post. Due to equatorial epithelial cells migrate to the posterior capsule
Elshnig Pearls
The PCO seen in children
Irvine-Gas’s Syndrome
CME due to cataract surgery. 6-10 weeks following surgery.
CME on FA
petaloid leakage.
Elevated IOP in Cataract sugery
Due to retained viscoelastic or steroid responder.
3 mirror lens
Only reversed.
D mirror
Angle
Trapezoid
Equator
Square
Ora
Asteroid Hyalosis
Normal with aging. Does not affect the Vision. Calcium-phosphate in the vitreous.
Synthesis Scintillians
Rare and occurs after vitreous hemorrhage, surgery, or uveitis. Unilateral golden brown cholesterol crystal.
Posterior Vitreous Detachment
Vitreous syneresis causes vitreous to detach from retina. Can cause ERM, vitreomacular traction, macular hole, weiss ring, retinal heme, retinal breaks (atrophic hole or tractional tear).
Shafer’s sign
retinal pigment epithelium in the vitreous after a retinal tear.
Causes of PVD
Age, DM, Myopia
Pre-retinal/Viteral hemorrhage
Can occur with pre-retinal neovascularization with a PVD. Ask about DM and HTN. Do a B-scan if the vitreous cannot be seen.
CRVO
Risk with HTN, diabetes, cardiovascular disease, open angle glaucoma. The artery compresses the vein and cause turbulent blood and a thrombus forms. Will have painless unilateral vision loss. Will then release VEGF and can cause neovasclarization in the angle (90 day glaucoma)
CRVO and POAG
If get a CRVO the NFL is poor and will be poor in the other eye. Check the other eye for POAG.
Collateral Veins
Occur several weeks to months. Help to get blood out of the eye.
Threatens to vision with CRVO
macular disease and neovascular glaucoma.
Ischemic and non-ischemic CRVO
Ischemic is 10 disc diameters
Where are BRVOs most common
ST.
What do you do if BRVOs occur at areas that are not AV crossings
Evaluate for vasculitis.
CRAO
Amaurosis fugal-unilateral vision loss. Common from the heart.
Which does CRAO come from
Embolis
Where does CRVO come from
Thrombus
Which emboli is worse
Calcific. It is bigger so obstructs more and more likely and from the heart.
Hollenhurst
Cholesterol emboli. From carotid arty and smaller so not as scary as calfic.
What tests should you run on a patient with CRAO or BRAO
Carotid doppler and EKG.
Giant cell arteritis
Can also cause a CRAO.
Cilioretinal artery
Can save vision with a CRAO.
Signs with CRAO
Superficial whitening of the inner retinal layers with a cherry red spot and an APD. Will return to normal color after perfusion is restored.
When do you get irreversible damage
After 90 minutes.
Do you get 90 day glaucoma with CRAO
no as retina is dead so doesn’t release VEGF
BRAO
patient will have a permament VF loss.
When to see a patient with no diabetic retinopathy
1 year
Mild to moderate retinopathy when do you see back
6-12 months
NPDR or PDR
Repeat every 2-4 months
What is the greatest risk factor for patient with type I diabets
Duration of disease
Risk of Mild progressing to PDR
5%
Risk of Moderate progressing to PDR
15%
Risk of severe processing to PDR
50%
Rules for Severe NPDR
- 4 quadrants of dot blot hemes. Venous needing in 2 quadrants. 1 quadrant of IRMA. Must meet one of the criteria.
Very severe NPDR
75% chance of progression. Two or more of the criteria in 4.2.1 rule. 4 dot blot heme quadrant, 2 venous needing, 1 IRMA.
High risk for vision loss with PDR
Neo of the disc greater than 1/4 within 1 DD, NED or NEA with sub retinal or intravitreal heme.
Threats to vision with diabetic retinopathy
macula or neo.
Macular disease with DR
Can have ischemia or edema. Send for FA to differentiate
CSME criteria
- retinal thickening with 500 um 2. hard exudates within 500 um with adjacent thickening 3. 1 DD of thickening within 1 dd
Threats to vision with Neovascularization with DR.
Worry about Pre-retinal/vitreal heme, neo glaucoma, or tractional RD.
Stage 1 of Hypertensive Retinopathy
- mild to moderate diffuse narrowing of retinal arteries.
Stage 2 of hypertensive retinopathy
stage 1 plus focal constrictor al retinal vasculature (nicking) and exaggeration of the ALR
Stage 3 of hypertensive retinopathy
Stage 2 plus CWS, retinal hemes, hard exudates (star) and retinal edema
Stage 4 hypertensive retinopathy
Papilledema (malignant HTN)
Elschnig Spots
choroidal infarcts that occur in severely hypertensive patients
Secondary HTN conditions
Diabetes, Vein occlusion, NAION, N. palsy, macroanyrusm.
Retinal Macroanarysm.
Unilateral focal area of dilation in a retinal with multilevel hemorrhages from a ruptured aneurysm with surround exudates.
Macular star
Exudates around the macula in a star pattern with HTN.
Ocular Ischemic Syndrome vs. Venous Stasis in REtinoapty
OIS is if the front of the eye is also affected. Venous stasis retonpathy if the back of the eye is only affected.
OIS
Occlusion of the ICA or ophthalmic artery secondary to atherosclerosis or GCA. Symptoms include granular vision loss, dull pain, amaurosis fugal. Will see unilateral dot blot hemorrhages int he mid periphery with dilated non-tortious retinal veins. Can have possible neo of the dic or anterior segment. Associated with systemic HTN, DM, and cardiac disease. Will have gradual VA loss in one eye.
Hyper viscosity REtinopathy
An increased resistance to blood flow secondary to elevated levels of plasma. Most common cause is hyperglobulinema.
Interferon Retinopathy
Looks similar to DR. patients getting interferon. Follow every 4-6 months patients on interferon.
Vascular sheathing
An inflammation of vessels. Characterized by exudates around the vessels. Occurs with syphyllis and sarcoidosis.
Idiopathic Juxtafoveal Retinal Telengectsia
Idiopathic abnormal perivofeal capillaries in the JXF region.
Coats’ disease
Males less than 20 years old. idiopathic peripheral retinal disease. Will progress to a total exudative retinal detachment. Will have decreased vision, leukocoria, strabismus. Will have marked hard exudates (diagnostic). Dilated telengectasia of vessels that have a lightbulb appearance and can progress to neovascular glaucoma.
Leukocoria
white reflex secondary to fibrovascular scaring secondary to tractional RD with ROP
Retinoblastoma
Most common intraocular malignancy in kids. Bilateral is heritable. Unilateral is non-heritable.
Differentials for leukocoria
Call the retina rude. Coat’s disease, toxo, ROP, RB.
Malignant choroidal nevus
TFSOMUHHD. Thickness (>2 mm), fluid (sub retinal), orange pigment, Margins, Ultrasound hallow, halo absent, diameter large.
Risks for ARMD
white, older, smoking, hyperopia, hypercholesterimia.
Nonexudative ARMD
Sick RPE with druse and RPE abnormalities (modeling). Worry about geographic atrophy. Could get PED due to build up of druse.
Risk of going from nonexudative to wet AMRD
Multiple soft drusen, hyper pigmentation, smoking, HTN.
wet macula edema
neovascularization. Can be blood under the RPE (Sub-RPE heme) can be blood under the Retina (sub retinal heme). Can be plasma under the RPE (Pigment epithelial detachment) or plasma under the retina (serous retinal detachment).
Type of CNVMs
Classic: well defined membrane. Occult: not well defined
What are more CNVMS
Predominately classic.
Central Serous Choroidopathy
Young middle aged males with type A personality. Localized macular serous detachment. Will have a smokestack appearance. Can also have a hyperopic shift. Improve in 1-3 months.
Histo
Chorioditis, multiple lesions, periparpillary, macula. No VITRITIS>
Pathological Myopia characterization
<6 or 26
Lacquer cracks
Streaks from the macula.
Epiretinal membrane
Occur from a PVD when glial cells are lost behind on the ILM.
MILD vs sever epirretinal membrane
mild=celophane Sever=macular pucker
Who is more effected by macular hole
Women.
Stages of Macular hole
- impending hole with loss of foveal depression and a yellow spot or ring around the fovea 2. round, small, full thickness hole with psuedooperculum 3. Large full thickness hole with operculum. Watzke allen sign. 4. PVD occurs.
Macular photostress test
Normally less than 60 seconds.
Albinism
Mutation in genes that make melanin. Foveal hypoplasie.
What is the most common retinal dystrophy
RP
RP
Progressive loss of RPE. Night blindness and peripheral vision loss.
RP triad
Retinal bone spicules, arterial attenuation, waxy nerve pallor.
Stargardt’s Dystrophy
AR. Kid ARMD. Have VA loss worse than what is seen in the back of the eye. Will have pisiform yellow flecks bilateral. Late stages will have bulls eye and salt and pepper changes.
Choroidermeia
X linked recessive. Deficiency in rap gernyl-geranyl transference. Have night blindness and peripheral vision loss. Have progressive atrophy of the RPE and choriocapillariis.
What could night blindness be due to
RP, CHoridoremia, or gyrate dystrophy.
Cone Dystrophy
Slowly progressing central vision loss. Late can have bull’s eye macular appearance etc.
Things with bulls eye maculopathy
Stars can’t handle the color. Starboard’s, chloroquine, hydroxycholorquine, thiadizein, cone dystrophy
Lukocoria
Call the retina rude. Coats, toxo, ROP, RB.
Best’s Disease
AD. Due to accommodation of material in the RPE. Patient will have big retinal signs with mild VA loss (opposite to stargardts)
Stage 1 bests
Pre-vitelliform. Abnormal EOG with normal funds in symptomatic patients
Stage 2 bests
Vitelliform. Egg yolk macular lesion apprear
Stage 3 bests
Pseudohypopyon. Lesion can become absorbed with little to no effect on vision
Stage 4 bets
Vitelliruptive. The eye yolk starts to break up and a scrambled egg appearance results. Mild vision loss expected
Stage 5 bests
End stage. Moderate to severe vision loss due to choroidal neo, hemorrhage, atrophy, or macular scarring.
Gyrate Atrophy
AR. Bilateral chorioretinal degeneration due to orinithin aminotransferase deficiency. Will have night blindness (RP and CHoriodremia too).
Rhegmatogenous RD
Caused by a retinal break (hole or tear) that allows vitreous into the sub retinal space.
Risk factors for rehmatogenous RD
Myopia and lattice degernation and PVD
Atrophic holes
Round or small full thickness defects that are NOT associated with vitreoretinal traction and therefore have a low risk for subsequent detachment. Holes are caused by chronic atrophy of the sensory retina. Most likely to be temporal.
Retinal tears
Caused by vitreous traction. Can be flap tears or percolated.
Flap tears
The flap is present because of uneven vitreous traction and the vitreoretinal traction persists so greater risk of detachment.
Operculate tears
The initial vitreoretional traction results in an even and symmetrical tear. No longer traction.
Acute RD
Convex wavy retina with clear sub retinal fluid that does not shift with body position. Shafter’s sign may be present.
Chronic RD
Pigment demarcation line will be present.
Most common location for retinal breaks and BRVO
Superior temporal.
Lattice degeneration
Educate about RD. Lateral is an area of peripheral thinning. Inner portion is atrophic and outer has an adhesion to the vitreous. More commonly ST.
Non-rhegmatogenous RD
Not caused by a break in the retina. Can be serous (exudative) and tractional.
Exudative RD non-Rhegmatogenous RD
Caused by subregional disorders (CH BALA) that damage the RPE and allow fluid to accumulate under the retina.
Tractional Non-rhegmatogenous RD
Caused by Dr. VOS.
Age related retinoschisis
splitting of the OPL and INL. Most commonly IT. Have an absolute field defect. Outer wall breaks are more dangerous.
Angoid Streaks
Breaks in bruch by PEPSI. Occur at the disc.
Toxocariasis
Will have optic nerve edema, RD, vitrifies, endopthlamitis, subretinoal granulomas.
Central Areolar Choroidal Dystrohpy
AD condition with bilateral large areas of geographic atrophy in the macula.
Acute Posterior Mulitofcal Placoid Pigment Epitheliopathy
Occurs after a viral infection. bilateral, yellow sub retinal lesions. Disc edema and RD can occur. resolves in a few weeks.
Ocular hypertension
IOP greater than 21 on consecutive visits in a patient without glaucomatous optic neuropathy.
Risks for Ocular Hypertension conversion to POAG
Age, race, family history, thin corneas, IOP (only one we can control)
POAG
glaucomatous ON damage that occurs with IOP greater than 21 with VF defects and an open angle.
What rim does glaucoma typically damage first?
The vertical rims.
Pseudo exfoliative Syndrome
Secondary open angle glaucoma. Abnormal white flaky deposits all over in body and in eye. Can have sampaolesi line due to pigment released when deposits rub on posterior iris epithelium (also with pigment dispersion). Associated with poor pupil dilation and increased risk of lens sublimation.
Pigmentary Dispersion Glaucoma
more common in caucasians, myopes, and males. Higher anterior chamber pressure that cause iris to bow back and rub against zonules. Cause pigment shedding. Will have transillumination defects in mid periphery, kruckenberg’s spindle, and samploswi line.
Angle Recession glaucoma
Due to trauma. Have a wide open angle with a recessed iris and wide ciliary body band.
Normal Tension Glaucoma
POAG where IOP is normal. Females have a greater risk. Also higher risk with vascular disorders.
Who is dance hemes most common with
Normal tensive POAG.
Who gets exfoliative glaucoma
Myopes and males. Caucasions
What race is more likely to get psuedoexfoliative and pigment dispersion glaucoma
Caucasians.
Primary angle closure glaucoma
Occurs as a result of posterior pressure pushing the peripheral iris anteriorly into contact with the TM.
Who gets pupillary block most common
Hyperopes. Asians and Eskimos
When are patients at greatest risk for pupillary block
When pupil reaches mid position of dilation.
Plateau Iris
Anterior positioned ciliary processes push iris forward into contact with the TM. Slit lamp and gone show o flat iris plane, a normal anterior depth, but a convex peripheral iris.
Sub acute Angle closure
Get a closure of the angle without symptoms as occludes and then opens Should expect with PAS and progressive ON damage and VF loss
Acute angle closure
Is angle closure causing an acute elevation in pressure and patient symptoms. Can have pain, vomiting, hazy cornea, glacuomflecken, corneal edema.
Glucomflecken
Anterior sub capsular opacities from high IOP causing epithelial cell death
Greatest threat to vision with angle closure
CRAO.
Mixed method glaucaom
Patients that suffered an acute angle closure are more likely to have POAG now
Neovascular glaucoma
DR VOS. Recognize with rubeosis of the iris. The fibrosis tissue with the neo is what causes glaucoma. Can block TM or pull iris into contact with TM
Uveitis Glaucoma
Caused by PAS (iris to TM) or PS (iris to lens). PS will only cause an elevation if there is an iris bombe (360 degrees) and pupillary block which move iris anterior into contact with TM.
Congenital glaucoma
Bilateral and males. Development abnormality in TM.
Bupthalmos
Enlarged eye as a result of congenital glaucoma.
ICE syndromes (iridocorneal endothelial) syndromes
Disorders characterized by abnormal corneal endothelium that grows onto the iris or in the angle. More common in Females
Essential Iris Atrophy
Iris thinning with resulting heterochromia, polycoria, correctopia, and ectropion uvea.
Chandler’s syndrome
The corneal endo with have a beaten metal appearance with corneal edema and correctopia
Iris-Nevus Syndrome (rogan reese)
Nodules will be present on anterior iris surphase
Glaucomatocylitic Crisis
Posner-Schlossmai syndrome. Acute trabeculitis that result in an acute elevation. There will be few cells in the anterior chamber and gonio will have an open angle.
Fuchs’ Heterochromic Iridocylctitis
Chronic, non-gram, low grade anterior units and stellate keratin precipitates. Will have iris heterochrima and iris/angle neo. Patient have an increased risk of glaucoma and cataracts.
Photolytic glacuoma
Occurs when hyper mature cataract leaks material into the anterior chamber and result in blockage of aqueous outflow through the TM.
PSD
Absolute value. Higher means more vision oss
MD
Lower means more general depression.
