EXAM Flashcards
Risk factors for myopia:
Increased near work
Low light exposure
Low outside activity
Unbalanced diet
Genetics (0:10%, 1:20%, 2:40%)
Management for myopia:
Glasses/CLs
Orthokeratology (OrthoK)
Photorefractive keratectomy (PRK)
Laser-assisted in situ keratomileusis (LASIK)
Daily atropine 0.125%
Myopia risk reductions:
Outdoor presence without base myopia(1h/week = 2% myopia loss)
Gaze breaks + longer working distance (decreased accomodative lag)
Myopia prevalence
Greater in females, greater in Asia 36-50% M/F 5-15 years
High myopia complications:
-6D:
Rhegamatogomous detachment
Macula degeneration (Myopic maculopathy)
Glaucoma
Cataract
Tilted disc
-20D:
Nerve damage
High hyperopia complications:
AAGC
Crowded ONH
Presbyopia (accomadative amplitude) with age:
10 AA~12D
40 AA<3D (presbyope)
50 AA~0D
Spherical change with age
0 = +2D
2 = +1D
40 = 0D
70 = 1D
80 = 0D
Lens protein changes with age
Post-translational crystallin: antioxidant decline (Glutathione enzyme loss) > denaturing > oxidation
Conformational changes: Oxidation > cross-links > aggregates
Loss of chaperone function: leads to loss of antioxidant capacity
Homeostatic factors in lens:
Ion transport (NA/K ATPase)
Water transport (Aquaporin 4)
Antioxidant (Glutathione)
Cataract formation factors/pathophysiology:
Oxidative damage (radicals/mitochondrial loss > less ATP > poor ion regulation)
Defence loss (less glutathione / ascorbic acid > less radical removal / O2 level change)
Metabolic / osmotic disturbance (cell stress reduces ATP > NaK ATPase / Ca ATPase disregulation > Na / Ca influx)
Calpain activation (Ca increase > calpain overactivation > crystallin proteolysis)
Post translational modification (UV/glycation > DNA damage/change)
Antioxidant loss leading to cataracts:
Loss of homeostasis in lens > Less antioxidant glutathione > ^Reactive O2 species from mitochondria > DNA damage > Defective crystalin protein formation > denatured crystalins scatter light
Cell repair:
alpha crystallin is chaperone to refold misfolded crystallins.
Misfolded proteins can be destroyed via Calpain (activated via Ca)
Transcription of stressed cells will decrease/end leading to apoptosis of damaged cells
Nuclear cataracts pathophysiology:
UV, Diabetes (glucose > glycation), Corticosteroids
Oxidation > ^ oxidised tryptophan (protein amino acid) > Chromophore production (milliard product) > chromophore cross links with crystallin > browning
Nuclear cataract on vision:
Myopic shift (RI change)
Blur
Tritan defect (blue light blocked)
Glare
Cortical cataract pathophysiology:
Metabolic disturbance, lens damage
NaK ATPase dysfunction > Na influx / overhydration > crystallin aggregation
Cortical cataracts on vision:
Loss of contrast
Astigmatism (localized RI change)
Nocturnal VA loss
Most common age related
Glare
PSC pathophysiology
Defective epithelium fiber production > defective cell migration to C1 > opacity formation
Age related PSC irreversible
Hypoglycaemia / corticosteroid induced PSC reversible
PSC on vision
Rapid development, vacuoles appear and disappear
VA loss
Contrast loss
Glare
Myopic shift
Cataract management
Surgery IOL implant:
Phacoemulsification: lens removed by ultrasound
IOL placed with lens capsule retained for internal barrier
Cataract surgery complications
Posterior capsular opacity: 2y post-op 1/2 Px epithelial cells proliferate over IOL, fixed by laser
Dislocated IOL
Rupture: leads to prolapse of vitreous into ant. chamber
IOP increase
Endophthalmitis (vit./aque. Inflammation from infection)
Cortex fragment remains (poor iol rotation for toric lenses)
Cataract progression without surgery:
AAGC (most common co-morbidity) from lens pressure on iris
morgagnian cataract (lens breaks)
DED definition:
Multifactorial disease of tears / ocular surface resulting in discomfort, visual disturbance, tear film instability, ocular surface damage. Accompanied by increased osmolarity of tear film and ocular surface inflammation
DED risk factors:
Age (>40 years)
Sex (^woman)
Race (^Asian)
CL wear
Environment (wind, pollution, humidity)
Screen use
Vit A deficiency
Surgery (Lasik)
Drugs (birth control)
Causes of ADDE:
Sjogren’s (primary/secondary)
lacrimal deficiency, lacrimal duct occlusion, reflex block, systemic drugs (antidepressants, birth control, pain killers), neurological (parkinsons)
Causes of EDE:
Most common
Intrinsic: meibomian oil def. lid def. low blink rate, drug action Accutane(acne medication)
Extrinsic: Vit A def. Topical drug preservatives, CL’s, ocular surface disease (allergies)
Sjrogren’s on dry eye
Autoimmune disorder against lacrimal gland (and salivary) decreasing secretion (ADDE) and slight MGD (EDE).
Occurs independently (primary), or with (secondary) disorder:
RA, systemic lupus/sclerosis
DED treatment severity level 1
Education of DED/diet
Local environment change
systemic drug elimination (caffiene/smoking)
Eye drops (lipid for MGD)
Lid hygiene/compress
DED treatment severity level 2:
Viscous eye drops (overnight lacrilube)
Tea tree oil for demodex
Punctual occlusion / moisture chamber
NSAID Diclofenar sodium 4/day
Short term topical corticosteroid Fluramethalone 4/day (month)
DED treatment severity level 3:
Oral secretagogue, serum drops, soft bandage/ridgid scleral CLs
DED treatment severity level 4:
Topical corticosteroid long term, membrane graft (damaged cornea), surgical punctal occlusion, surgical transplant/lid)
General vicious cycle
Hyperosmolarity > inflammation (proteases/cytokines) > goblet/epithelial damage > tear film instability > reduced TBUT > hyperosmolarity
Vicious cycle in depth
Loss of aqueous or evaporation > hyperosmolarity > epithelial irritation > Mitogen-activated protein kinase (MAPK) activation > inflammatory mediator release (IL-1/MMPs) > Matrix metalloproteinases damage epithelium / goblet cells > epitheliopathy (corneal epithelium loss) / tear instability > reduced TBUT > hyperosmolarity
Preservatives and their effect in dry eye
Benzalkonium chloride
Epithelial cell apoptosis, corneal nerve damage / poor wound healing, decrease tear film stabilit and decrease goblet cell density.
Liquid production of tear layer (glands/constitution)
Lipid - Meibomian in tarsal plate: cholesterols/esters
Aqueous - lacrimal gland (ion/water/protein): lysozyme (Amicrobial), IgA (immunoglobin)
Mucous - Goblet cells: MUC1/4/16 (membrane bound glue to glycocalyx to epithelium)
Aqueous layer content:
Mostly Water/ions
2%: lysozyme (antimicrobial), lactoferrin (immune), tear lipocalin (viscosity, viral inactivation), IgA
Lipid layer content:
Cholesterol, fatty acid, phospholipids
Mucin layer content
MUC 1/4/16 (membrane bound with galectin glue to glycolax mucin layer)
MUC5AC (forms gel instead of mucin strands > prevents scatter)
Conjunctival squamous cell carcinoma:
Malignant Extensive vascular fleshy growth.
Usually extending from limbus to fornix or cornea
SCC pathophysiology:
UV to epithelium > proliferation > mutation > atypical epithelial cells
Atypical cell proliferation > tumour formation (vascular)
BCC pathophysiology:
UV to stem cells > malignant proliferation
SCC opposed to BCC identification
Less common, more aggressive, high metastasis risk
Often with hyperkeratosis (cutaneous horn formation)
Arises from actinic keratoses
Erythematous (red)
Ulcers and bleeds
BCC opposed to SCC identification
More common, low metastasis risk
Superficial: Red patch
Nodular: white/pink nodule
Sclerosing: white patch
Ulcerative: pearly rolled edges with vessels and central ulceration
Squamous cell carcinoma treatment
Alcohol epitheliectomy (cornea), lamella scleroconjunctivecotomy (conj.), cryo (remaining bulbar components)
Usually wont spread globally unless immunocompromised
Mitomycin C / interferon prevent regression
Conjunctival Nevus:
Benign melanocytes in stroma. (10yo-30yo when notices)
Small elevated lesion, variable pigmentation, interpalpebral limbus.
<1% chance of formation to malignant melanoma
Primary aquired melanosis:
Melanocytes near basal epitheilum.
Brown pigment, scattered through conj. (usually Caucasian)
Atypia melanocytes =50% risk malignant melanoma
Conjunctival Malignant melanoma:
Commonly ~60yo from PAM, otherwise nevus/de novo.
Melanocytes penetrate conj. Stroma
Pigmented vascular elevation, anywhere on conj./cornea
Metastases to facial lymph, brain, lung, liver commonly
Non-malignant choroid/retina lesions:
Congentical hypertrophy of the retinal pigment epithelium (CHRPE)
Choroidal naevi
Uveal melanoma:
Usually from separate tumour metastasis (Female breast cancer, or male lung cancer)
Otherwise malignant melanoma (from nevi 5%)
50% further metastasis (1/2 die in 8 months)
60% metastasise to liver (then lung 25%/bone/brain)
Uveal melanoma risk factors:
Light iris/skin colour
Choroidal nevi
(Asia) 45 - (europe/males) 60 yo
Cooks (cooking oil), welders (carcinogenic gas)
Iris nevi (5% malignancy), choroidal nevi (0.0005%)
Choroidal naevi likelihood to from malignancy
> 2mm depth
5 mm width (1.5 disk diameters)
Orange lipofuscin (fatty acid/lipid accumulation)
Irregular boarders
Serous RD
Uveal melanoma treatments:
Enucleation, or Radiotherapy:
Brachytherapy, iodine-125 plaque near lesion
Proton beam/steriotactic radiotherapy: (large/close to ON tumor)
Transpupilliary thermotherapy (heating via contact lens)
Causes of ptosis:
Disinsertion of LPS (most common)
Myasthenia gravis / Graves (muscular)
Horners (sympathetic)
CN3 palsy
Globe retraction / eyelid swelling
Fatigue/trauma
Disinsertion of LPS:
Lid dehiscence/aponeurotic ptosis
LPS tendon less from tarsal from rubbing, CLs, trauma/surgery
Low lid, high crease, normal range of motion
Myathenia gravis:
Autoimmune against acetylcholine receptors of striated muscle.
Fatigue, facial weakness, ptosis (LPS weak)/diplopia.
Cognan’s lid twitch (upper lid overshoot on upgaze)
Curtaining/enhanced ptosis (contralateral drooping/elevation)
Myathenia gravis testing
Ptosis worsening towards end of day
Ice pack decreases acetylcholinesterase function > increases Ach > decreased ptosis
Pseudoptosis
Ptosis appearance unrelated to lid function
Dermatochalasia most common
CN 7 facial palsy (brow muscle loss)
Causes of anisocoria:
15-30% Physiological (asymmetric inhibition of edinger-westphal)
Horners
CN3 palsy
Adies tonic pupil
Pharmacological
Pupil damage
Acute angle glaucoma
CN3 palsy:
Lesion to CN3, often unilateral
Ptosis, mydriasis (depending on cause), down and out turn, headache.
Aberrant regeneration > miosis
Third nerve eye innervation:
Oculomotor nerve has somatic voluntary, and automatic fibers
Somatic: LPS, SR/MR (adducts)/IR/IO (elevates when adducted)
Automatic: sphincter pupillae / ciliary
Parasympathetic pathway for iris:
Afferent: Optic nerve > split at chiasm > optic track > split before LGN > sup. Colliculus > pretectal nuclei (processed) > both edinger-westphal nuclei.
Efferent: Edinger-westphal nuclei > CN 3 > ciliary ganglion > with short ciliary nerves > iris sphincter
Sympathetic pathway for iris:
1st neuron: hypothalamus > spinal cord > ciliospinal centre of bulge and waller
2nd neuron: ciliospinal > stellate ganglion (lung apex) > superior cervical ganglion (jaw)
3rd neuron: superior cervical g. > internal carotid > cavernous sinus > SO fiss. > CN 5 V1 (nasociliary div. Of ophthalmic) > long ciliary nerves > iris dilator
Also innervate mullers / facial
Tonic pupil/ Adie’s
Post ganglionic parasympathetic denervation,
Poor light constriction, good convergence constriction
Worm like redilation/constriction from partial denervation
Initially dilated pupil, long term mitotic pupil (abberant nerve regeneration)
Mainly young women
Pharmacological drugs that effect pupil:
Mydriasis: Scopolamine (motion sickness), ipratropium (asthma), nasal spray, antiperspirant, jimson weed/herbals
Miosis: pilocarpine (IOP decrease/Glauc.), prostglandins (IOP decrease/glauc.), opioids, clondine (Glauc.), insectisides
Pilocarpine pharmacology and DDX:
Muscarinic agonist for neuromuscular junction of sphincter, upregulates receptor number > hypersensitivity > constriction.
Dilute pilocarpine (0.5-0.15%) > tonic pupil constriction
Pilocarpine (1-2%) > no constriction in pharmacogically induced
Horners testing with cocaine:
Cocaine hydrochloride (10%), blocks norepinephrine reuptake in presynaptic terminal
Horners will fail to dilate after 60 minutes from lack of norepinephrine release
Horners testing with apraclondine:
Apraclondine (0.5-1%), A-1 adrenergic receptor agoinist.
40mins Horners will have abnormal lid raise, pupil dilate
Normal eye remain unchanged, stronger effect on a-2 receptors downregulate noradrenaline
Requires denervation hypersensitivity
Horners denervation hypersensitivity
Lack of Ca2 release into presynaptic terminal > reduced norepinephrine release > upregulation of a-1 adrenergic receptors
Takes 7 days of horners presence
Horners lesion localization
1% hydroxyamphetamine, ^norepinephrine release at neuromuscular junction for bilateral dilation.
First/second order neuron > no dilation
>48h following cocaine/apraclondine, hard to obtain
Hydroxyamphetamine:
Mimics norepinephrine, taken up by reuptake pump like NA.
Once taken into presynapse, causes release of NA from presynaptic terminal into synapse.
This requires stored norepinephrine in presynaptic terminal (third neuron), requiring functional neuron.
10 causes of red eye:
Infection
Vascular (hypertension/diabetes)
Autoimmune (eczema)
Neoplasia
Congenital
Nutrition (Vit A)
Latogenic (surgery)
Trauma (forign body)
Idiopathic
Age
Classifications of allergic conjunctivitis
Seasonal allergic (SAC)
Vernal kerato- (VKC)
Atopic kerato-(AKC)
Perennial allergic (PAC)
Contact blepharo-
Giant papillary (GPC)
SAC/PAC pathophysiology
Airborne allergen binding to IgE receptors in mast cells > degranulation of mast cells of MCt subtype > proinflammatory mediator release > eosinophil / basophil attraction
VKC pathophysiology:
Type I/IV hypersensitivity reaction, related to atopy (exzema)
Antigenic stimulation > lymphocyte activation (T-helper 2) with eosinophil infiltrate
Goblet cell increase > MUC5AC increase > abundant mucous
AKC pathophysiology:
Inflammatory disorder 20-50 years and male mainly
With atopic diseases 95% (dermatitis).
Type I/IV hypersensitivity, Reduction in MUC5AC
Contact blepharoconjunctivitis pathophysiology:
Type IV hypersensitivity
Partial antigen (hapten) binds proteins forming antigen > langerhans cells (type 2 MHC) present antigen to T helper 1 in lymph > T cells sensitize (week-months) > T cell present to ocular surface > cytokine/inflammatory cell accumulation
Unlike SAC/PAC, reaction to agent takes 2-3 days instead of 2-3 hours
GPC pathophysiology:
Mechanical damage to conj. Epithelium > Th2 lymphocyte resonse
Allergic component from CL/prosthetic deposits
Protein deposits serving as haptens (partial allergens) > type IV hypersentitivity
Symptoms shared by all allergic conjunctivitis:
Bilateral
Itching
Hyperemia
Photophobia
SAC specific presentation:
Sudden onset, associated with airborn antigen
Tearing, burning
Conj. Chemosis (swelling)
PAC specific presentation:
Mild, associated with DED
Tearing, burning
Conj. Chemosis (swelling)
Papiliary formation on tarsal conj.
VKC specific presentation:
Sticky discharge
Lid oedema
Type 1 (palpebral): giant tarsal papillae (7mm), cobblestone look on eversion
Type 2 (limbal/bulbar): gelatinous eosinophilic mounds (Trantas dots) at limbus
AKC specific presentation:
Tearing, madarosis (lask loss from scratching)
Eryhematous/swollen lids with eczema
Inf. Corneal punctate epithelial keratitis
Inf. Tarsal small pappillae (<1m)
Management of allergic conjunctivitis:
Avoidance of antigen
Artificial tears dilute agents
Topical drops;
Antihistamines
Mast cell stabilizers
NSAIDs (require ophthal)
Common topical treatment for allergic conjunctivitis:
Antihistamine levocabastine
Mast cell stabilizer Lodoxamide
NSAID Diclofenac sodium
Adenoviral keratoconjunctivitis:
Many manifestations, commonly epidemic keratoconjunctivitis (EKC) > Pharyngoconjunctivitis (PCF) > isolated follicular conjunctivitis
Commonly causes epidemics
Epidemic keratoconjunctivitis clinical presentation
Watery discharge, Hyperemia (pink eye), foreign body, photophobia
pain, chemosis, ipsilateral lymph adenopathy (swelling)
Pseudo/vascular membrane, symblephara (bulbar fuses lids), subepithelial infiltrates
Tarsal follicles, petechiae (blood spots), subconj. Hemorrhage
Complications of adenoviral infection (EKC):
Pseudo / vascular membrane formation in tarsal conj. Of fibrin exudate
Epithelial keratitis (infiltrates), immune reaction with viral antigens in corneal stroma, decreases corneal sensitivity, lasts weeks-years.
Bacterial superinfection of strep
Viral conjunctivitis DDX
Adenovirus > follicules/upper res. infection
HSV/HZV > unilateral / very painful, with dendritic keratitis
Varicella/zoster virus > fever
Picornavirus > hemorrhagic conjunctivitis in young Px
Molluscum contagiosum > follicular conjunctivitis / nodules at lid margin
Herpes simplex virus conjuntivitis clinical presentation:
Unilateral
Watery, preauricular lymph adenopathy, pain, burning, foreign body sensation.
Decreased vision, dendritic corneal lesions
Herpes zoster ophthalmicus conjunctivitis clinical presentation:
unilateral
Nose ulcer, injection, conj. Edema, petechiae (blood spot)
Branching corneal lesions with bulbs
HSV treatment:
Topical antiviral (trifluridine 1%)
Dosage x2 and oral if corneal/skin involvement
HZO treatment:
Resolves in 1 week
Antibiotic for bacterial protection
Cool compress / lubricants
Bacterial conjunctivitis causes
Gram-positive: streptococcus pneumoniae / Staphylococcus aureus (children)
Gram-negative: Pseudomonas aeruginosa / Haemophilus influenzae
Neisseria gonorrhoeae: hyperacute
Bacterial conjunctivitis clinical presentation:
Unilateral > bilateral 2 days
^abrupt than viral
Tearing, irritation, crusting, injection (most at fornix)
Mucopurulent Yellow sticky discharge (mattes lids/lishes)
Corneal ulceration, chemosis
Bacterial conjunctivitis treatment:
Self-limiting
Board-spectrum antibiotic Chloramphenicol reduces course / spread / ulceration
CLs to be removed
Fluroquinolone for corneal ulcers
Aminoglycosides have poor staph/strep coverage
Conjunctivitis DDX:
Pain, Photophobia, blur > refferal
Hyperpurulent dis. > gonococca
Mucopurulent dis. > bacterial
Serous dis. > Allergic (itching) / Viral (no itch)
Microbial keratitis risks:
CL overnight/extended wear > Hypoxia
Inadequate hygiene
Ocular/systemic disease (diabetes/mellitus)
Extended corticosteroid use
Surgery / trauma
DDX for bacterial keratitis:
Conjunctivitis
Dry eye
CLARE/CIL (contact induced inflammatory response)
Blepharitis (bleph can fall onto cornea and cause a non-infective immune response)
Mycotic keratitis
Corneal fungal infection of damaged epithelium
Filamentous (tropical): Fusarium
Yeast like (temperate): Candida
Mycotic keratitis clinical presentation:
Abrupt pain, photophobia, discharge, blur, ulcer, feathery satellite infiltrates
IOP increase from iris fungal mass
Acanthamoeba keratitis:
Rare protist corneal infection
Present in air, soil, fresh/tap water, hospital equipment, chlorinated pools
80% from CL wear (night/extended/submerged)
Acanthamoeba keratitis clinical presentation:
Extreme pain (sensory neuron focus), redness, epiphora, FBS, photophobia
Progression > ring/dendritic infiltrates (inflammtory in stroma) > Corneal ulceration /stromal abscess
Acanthamoeba treatment:
Topical drug cocktail against cysts
Biguanides (polyhexamethylese: PHMB) + diamidines (Hexamidine)
Hourly 0.2% of each then tapered
Bacterial keratitis:
90% of microbial keratitis, mainly from CLs
Caused by Pseudomonas aeruginosa (most common), Strep p. (ulcer in developing countries), Staph a. , serratia
Bacterial keratitis clinical presentation:
Pain, redness, photophobia, ulceration
Ring infiltrates
IOP increase / glaucoma
Hypopyon (neutrophil in Ant. Chamber)
Bacterial keratitis mechanism
Adhesion via adhesins
Invasion via proteases
Cytotoxic cornea damage
Stromal Necrosis and ring infiltrates
Bacterial keratitis drug treatments:
Broad spectrum antibiotics
Analgesics for pain
Cycloplegics for ciliary spasm
Antiglaucoma for IOP
Therapeutic CL for ulceration
Avoid NSAIDs (risk corneal melting)
Bacterial keratitis antibiotic treatments:
Broad spectrum antibiotics > Fluroquinolone mono/combination therapy
Antibiotic chloramphenicol (not pseud.)
Aminoglycoside Gentamicin > gram-neg
Cephalosporin > gram-pos
Fluroquinolone Ofloxacin > both bacteria via DNA/topoisomerase inhibition
Bacterial keratitis treatment procedure:
Fluroquinolone ofloxacin 3g/ml
Taper drops per day (24/d > 12/d > 6/d)
Antibiotic (based on likely suspect) drops at higher rate Topical cycloplegic Tropicamide for comfort and prevent synechiae
Cycloplegic can be avoided to reduce preservative load
Innate defences of cornea:
Tears > lactoferrin/lysozyme, immunoglobins (IgA/G), filtration, microbe dilution
Epithelia > Cytokine secretion (IL-a) on damage > immune response
Keratocytes > IL-6 synthesis > anti-microbial / healing
Corneal nerves > sensory reflex via substance P/Calcitonin > IL-8 > Neutrophils
Complement > Protein cascade in limbus
pH difference from tear film to stroma 7.4 > 7.6
Cells of innate immunity:
Neutrophils
Eosinophils
Macrophages
NK cells
Neutrophils:
Pass endothelial cells via diapedesis (adhesion receptors on endothelum)
Phagocytoses microbes
Eosinophils:
With IgE receptors and complement components
Activated via IL-3/5 > granulation
Macrophages in corneal defence:
Phagocytic / antigen presenting / Cytokine secretion
NK cells in corneal defence:
Large granular lymphocytic cells without antigen receptors
Recognize MHC1 > inhibition
Lyse cells poorly expressing MHC
Secrete TFN-a / IFN-a
Cells of acquired immunity
Langerhans cells
Cytokines
Langerhans cells of cornea:
Antigen presenters with MHC-2/1 antigens in limbal cornea
Recognize nonself antigen > processed > MHC transport to surface > T cell activation
MHC1 > CD8+ Cytotoxic T cell (kill microbe)
MHC2 > CD4+ T Helper cell (secrete cytokines)
Cytokine release in cornea:
TH1 > IL-2 / IFN-y, IgG/M/A synthesis
TH2 > IL-4/5, IgE synthesis
Contact lens complications:
Hypoxia
Microbial keratitis
Allergic / Toxic reaction
CL DED/Discomfort
CL-induces papillary conjunctivitis
Mechanical damage
CL Hypoxia induced changes:
Ocular/limbal erythema (redness)
Stromal oedema, vascularization, epithelial thinning, endothelial polymegethism (change in cell size), weakened immune defence.
Treatment for CL hypoxia:
Education on CL use/hygiene
Change to RGP CL (Increases Dk/t of O2)
Intermittent wear, CL discontinuing
Inflammatory CL changes/clinical presentation:
CL infiltrative events (CIE)
Contact lens-induced red eye (CLARE)
Pain, photophobia, keratitis, peripheral ulcers
Risk of non-infective CL inflammation:
30 day extended wear, Silicone hydrogel CLs, poor eye closure, tight lenses
Smoking > Infiltrates
Toxicity from CL solution
Non-infective CL inflammation treatment:
Self resolving in 21 days after cessation
Corticosteroids / antibiotics increase speed
CL hygiene education
CL induced papillary conjunctivitis CLPC risks:
Soft CLs (silicone-hydrogel)
Mechanical stimuli from poor CL fit
Long term wear > accumulation of lens deposits
CL induced papillary conjunctivitis (CLPC) treatment:
Daily CL change
Hydrogen peroxide CL solution
Enforce rinse-rub cleaning
Topical mast cell stabilizers / antihistamines > steroids
Cessation of CLs
Allergic / Toxic reaction to CL pathophysiology:
Uptake of small molecules from hydrogel material and CL solution > immune response
CL wear and dry eye
12 fold risk factor, 50% CL users experience EDE symptoms
Caused by meibomian blockage via mechanical trauma
Lid wiper epitheliopathy
CL friction on blink > palpebral conj. Irritates > abrasion on blink with ocular surface/CL > lissamine stain parallel to marx’s line (lid rim facing eye)
Treatment of CL related discomfort/dryness
EDE treatment > lipid lubricant, lid hygiene, compress, suppliments
Without EDE > Daily CL change, non-preservative solution, manage Demodex
Mechanical changes with CLs:
Blinking / eye rubbing / CL dislocation / insertion / removal / CL damage
Long term wear > Corneal sensitivity loss (with low O2)
Sup. Epithelial arcuate lesions (SEAL) > upper cornea lesion
Corneal warpage from poor fitting hard CLs
Types of microbes in CL related microbial keratitis:
Bacterial > most common Pseudomonas sp.
Fungal > commonly in tropical and agriculture
Acanthamoeba > Protozoan in water
Herpes simplex keratitis:
HSV type 1 > most common cause of infectious blindness in developed world
Infects any part of eye (epithelia > stroma > endothelia)
HSV 2 > STD related, keratitis in neonates
Commonly unilateral unless immunocompromised
HSV life cycle:
Membrane glycoproteins allow penetration of capsid through host membrane
Herpes viral entry mediator (HVEM) or nectin-1 delivers capsid to cytoplasm
DNA polymerase forms virons
Release via host heparanase
Enters latency by moving to trigeminal ganglion via corneal nerves
Exists in CD8+ T cells
HSV primary infection presentation:
Cold sores around sensory trigeminal innervation (mucosal membranes)
HSV reactivation:
HSV moves via anterograde axonal transport
Occurs at high sensory tissue (cornea/oral) via ophthalmic branch
Risk decreased by oral acyclovir
HSV reactivation triggers:
Stress, fever, UV, allergies, corticosteroids, laser treatment
immunocompromising
HSV epithelial keratitis clinical presentation:
Commonly unilateral unless immunocompromised
Pain, tearing, redness, FBS, DED
Dendritic keratitis > bulb-lesions/geographic ulcer (fluroscein)
Corneal denervation > neurotrophic keatopathy > corneal melt
HSV epithelial lesions:
Punctate keratopathy > dendritic keratitis (follow nerve plexus) > terminal bulb enlargement > geographic ulcer (central dead cells)
HSV epithelial lesion staining:
Fluorescein > central dendritic staining
Rose bengal/lissamine > edge lesion (dead cells)
Epithelial Herpetic keratitis DDX:
Misdiagnosed as acanthamoeba keratitis
HZO does not have terminal bulbs
Tested with PCR
HSV endothelial keratitis clinical presentation:
Disciform> most common, central oedema disc
Diffuse> wide oedema
Linear> limbal oedema
HSV stromal keratitis (HSK) clinical presentation:
20-50% of recurrent cases
Corneal vascularisation, stromal oedema/opacity, irreversible scaring
Necrotizing: stromal infiltration/ring, epithelial ulcer > corneal melt
Disciform: stromal oedema > neovascularisation
HSK treatment
3% topical antiviral Acyclovir ointment 5/day
Systemic analgesic ibuprofren (avoid topical to prevent corneal disturbance)
Avoid steroids (Cataracts / IOP increase)
HSV stromal keratitis treatment
Topical corticosteroid Prednefrin Forte 1% (6/day, 10 weeks)
With oral valaciclovir (antiviral)
Dosage increased with epithelial defects
Always tapered
HSK immune function:
Trigeminal virus reactivation > corneal innate immune signalling > cytokine/chemokines from stroma > 24h neutrophil/NK cell aggregation
Dendritic cells phagocytose virus > present antigen to lymph nodes > 7-21d CD4+T cells aggregate > IFN-g / IL-17 secretion
Inflammatory cells > corneal clouding
HSV endothelitis / uveitis clinical presentation:
Endothelial oedema / precipitates
High IOP (trabeculitis)
Iris atrophy
Immune cells in ocular HSV infection
Neutrophils > earliest responder, cause corneal opacity
Macrophage, NK cells > innate phagocytes
Dendritic cells > adaptive phagocyte
CD4+T cells > IL2/IFN, drive lesion development
CD8+T cells > controls recurrence via T cell receptor
Immune factors in ocular HSV infection:
Toll-like receptors > innate PAMP detector, drives cytokine production and opacity
Cytokine/Chemokine > IFN a/b stimulate antiviral genes, IFN y stimulates inflammation
Heparanase > removes harparan sulfate allowing virion release to other cells
HSV Corneal neovascularisation pathology:
Neutrophils form metalloproteases > extracellular matrix breakdown > vascularisation mediated by VEGF
Infection depletes VEGF receptors > increase in VEGF
Acyclovir HSV treatment:
Most common
Nucleoside analog > DNA polymerase inhibition > HSV replication inhibition
HSV enzyme can mutate for resistance
Highest HSV affinity > less toxicity for non-infected cells
Varicella zoster virus:
Contagious DNA virus; causes
Chickenpox (Varicella) > lifelong trigeminal infection
Shingles > reactivation of VZV
HZO skin lesions:
Vessicle rash, healed in 4 weeks
Follows CN V1 divisions (ophthalmic 1/2/3 = forehead/nose/chin)
Varicella zoster pathophysiology:
Enters upper res. > proliferates to pharyngeal lymph > skin (varicella)
HZO conjunctiva manifestation:
Membraneous / follicular response
Hyperemia / oedema
Resolving in 1 week
Antibiotics prevent bacterial infection
HZO corneal manifestations:
Punctate epithelial keratitis (focal lesions with fluroscein)
Tapered dendritic lesions
Photophobia, pain
HZO uvea manifestations
Usually unilateral
Iris atrophy/synechiae, IOP increase, cataract formation
HZV treatment:
Antiviral therapy > acyclovir, ganciclovir, famciclovir, (7d for HZ rash)
Analgesics > lidocaine (pain)
Intravenous acyclovir > ARN/PORN, immunocompromised
HZV acyclovir treatment procedure:
800mg orally per day
Administer within 72 hours of rash, for 7 days
VZV reactivation
Prodromal phase (fever/skin irritation) before activation
Activates with painful vascular lesions
