AED: Written Exam Prep [High yield cards only] Flashcards
How thicc is the tear film? Name the layers of the tear film from superficial to deepest, stating how thick each layer is
~7um thick.
Lipid - 0.1um
Aqueous - 7um
Mucoid - 0.05um
What does each layer of the tear film do?
Lipid - stabilizes tear film + reduces evaporation of tears
Aqueous - provides moisture, nutrients, O2 to tissue + removes waste and acts as a flushing mechanism
Mucoid - stabilizing + wetting agent. Anchors tear film to corneal epihtelial cells
How is the tear film replenished with blinking? Describe the mechanism
The meibomian gland produces lipids. The lids close to meet each other. As the lids open again, the upper lid draws up the lipid into a lipid layer. So a new lipid/oil layer is placed on the tear film with each blink.
Name the 4 main ocular allergy presentations
Seasonal conjunctivitis
GIant papillary conjunctivitis (GPC)
Vernal keratoconjunctivitis (VKC)
Atopic keratoconjunctivitis (AKC)
Of the 4 main ocular allergy presentations, which have the potential to be sight threatening?
VKC and AKC
Of the 4 main ocular allergy presentations, what is the key differential for GPC?
Large papillae in a CL wearer
How does VKC vs AKC differ in terms of:
A: onset?
B: sex incidence?
C: seasonal variation?
A: 1st decade vs 2nd/3rd decade
B: Males vs no preference
C: Spring vs perennial
How does VKC vs AKC differ in terms of:
D: discharge?
E: conj scarring?
F: horner trantas dot presence?
D: thick mucoid vs watery clear
E: Moderate incidence vs Higher incidence
F: Commonly seen (incl. shield ulcers) vs Rare (in AKC)
How do VKC vs AKC differ in terms of:
G: corneal neovascularisation?
H: presence of eosinophils in corneal scraping?
G: not present unless 2ndary to infectious keratitis vs generally common
H: more likely vs less likely
Describe the features of Grades 1-4 of GPC
Grade 1 [preclinical] = slight conj redness z fine papillae + no symptoms
Grade 2 [mild] = mild injection, 0.3-0.5mm papillae z mild symptoms
Grade 3 [moderate] = moderate injection, 0.5+mm papillae z increasing CL awareness
Grade 4 [severe] = severe injection, 0.75+mm papillae z lens intolerance
When using steroids for the 4 main ocular allergic presentations. What steroids do you use for each and how often?
Seasonal: FML iBD-iQID (2x-4x a day) for 2 weeks (iQID for one week, iBD for next)
GPC: FML iBD-iQID short term in more severe cases of GPC
VKC: FML/Flarex iBD-iQID
AKC: Flarex/Maxidex iTDS-Q2h with aggressive taper (3xday to every 2 hours)
What symptoms would you expect with an ocular IgE mediated allergic eye disease? (9)
Intense itchiness, “red eye”, conjunctival chemosis (swelling/oedema of conj), blurred vision, mucus discharge, lid thickening, giant or “cobblestone” papillae, limbal infiltrates, SPK, corneal ulcer, etc.
In what general type of ocular presentations would you expect papillae (2)?
Allergic
Bacterial
think “pABillae”
In what general type of ocular presentations would you expect follicles? (3)
Chlaymdia
Toxic
VIral
How can you manage seasonal conjunctivitis? (8)
allergen avoidance, topical AH/MCS or combos incl. vasoconstrictors, astringents, oral AHs, cold compress, topical steroids (if MCS don’t work, FML 2wks -> iQID wk, iBD wk) follow up (px request)
(also topical NSAIDs, topical cyclosporin A, artificial tears)
*(generally since it’s usually mild just try some antihistamines and you’re pretty good)
How can you manage VKC? (7)
Allergen avoidance,
Topical MC inhibitors (patanol iBD, Zatiden iBD), Corticosteroids (FML/Flarex iBD-iQD with follow up one week after),
Topical NSAIDs (Acular iQID),
Topical cyclosporin,
Referral for superficial keratectomy to improve resolution of shield ulcer
How can you manage AKC? (8)
same as VKC but more aggressive steroid use.
Allergen avoidance,
flushing of conj/hypoallergenic bedding,
topical AH/MCS/NSAIDs as per VKC,
Corticosteroids (aggressive. Flarex/Maxidex iTDS to Q2h with aggressive taper) [topical to reduce itch/inflammation], topical cyclosporin,
px must avoid eye rubbing,
follow up regularly and as tx mode dictates (see VKC)
How can you manage GPC? (4)
MCS for several months [if less severe] {patanol iBD, zatiden iBD},
topical steroid short term [if more severe] (FML iBD-iQID),
advise px on CL care, overwear and non preserved solutions,
consider new CLs such as dailies, removal of sutures
When does VKC most commonly manifest?
b/w 5-25yo
Where does VKC most commonly affect?
usually affects superior tarsal conj
In which of the 4 main ocular allergy presentations are patients likely to be atopic?
VKC and AKC
What does the limbal presentation of VKC look like? (4)
Limbitis
Limbal papillae
Horner Trantas dots
Pseudogerontoxon (cupids bow) in area of previously inflamed limbus
Which of the 4 main ocular allergy presentations is not associated with corneal damage of some kind?
Seasonal conjunctivitis
Compare bacterial ulcers with bacterial infiltrate in the following categories:
A: how common?
B: how painful?
C: location?
A: ulcers = rare; infiltrate = more common
B: ulcers = painful; infiltrate = less painful
C: ulcers = central; infiltrate = peripheral (more likely to be peripheral)
Compare ulcers with infiltrate in the following categories:
D: how does the staining compare?
E: AC reaction?
D: ulcers = staining mirrors infiltrate; infiltrate = staining smaller in size than infiltrate
E: ulcers = AC reaction present; infiltrate = no ac reaction
Compare ulcers with infiltrate in the following categories:
F: conjunctival reaction?
G: number of lesions?
F: Ulcers = generalised conj reaction; Infiltrate = sector conj reaction
G: Ulcer = single lesion; Infiltrate = sometimes multiple
In specific terms, how do you treat bacterial ulcers? (4). Which tx is the gold standard?
Freq. dose Ocuflox/Ciloxan (if small otherwise)
Dual fortified antibiotics [Gold std.]
Cefazolin 50mg/ml + Gentamycin 15mg/ml OR tobramycin 15mg/ml alternate each drop q1h
If above fails: lab testing to reveal bac. Resistance than Vancomycin 25mg/ml instead of cephazolin
If meet “1-2-3” guideline: Monotherapy z Fluoroquinolones 2 drops every 15 minutes for 6 hours 2 drops every 30 minutes for 4 hours until resolution
What is the “1-2-3” guideline? What should you do if an ulcer doesn’t meet this criteria?
“1” = 1+ or less cellular response AC; “2” = infiltrates 2mm or less in diameter; “3” = ulcer at least 3mm from visual axis. If ulcer doesn’t meet criteria or no improvement in 24 hours —> refer
How do you treat bacterial infiltrates? (2 basically)
If marginal (CL wear): Stop CLs, monitor, antibiotic [depend on cause. If infection], steroid [if infl], combo,
If bleph assoc. infiltrates: tx bleph, tx cornea z steroid z potential antibiotic cover, if no improvement consider oral doxy
Should you patch bacterial corneal ulcers? Explain
Never patch [creates env. for replication
In simple terms, what is the treatment for a bacterial ulcer?
Fortified antibiotic or fluoroquinolone
Compare Infectious vs Non-infectious ulcerative keratitis in the following categories:
A: Pain/redness/discharge
B: Association with CL wear
C: Location
A: More vs less
B: Assoc. vs Not assoc.
C: More central vs more peripheral
Compare Infectious vs Non-infectious ulcerative keratitis in the following categories:
D: Level of infiltrate
E: Level of AC reaction
D: More infiltrate vs Less infiltrate
E: Significant AC reaction vs mild or no AC reaction
When in doubt, how should you treat ulcerative keratitis?
treat as infectious
What are the signs of EKC? (9)
Acute onset
Unilateral, follicular conjunctivitis z ipsilateral node
Often becomes bilateral
Haemorrhagic conjunctivitis
Pseudomembrane or membranous conjunctivitis
No respiratory involvement
Watery, uncomfortable eye
Conjunctivitis 1-2wks
Corneal involvement (fine SPK from onset. Epi. Opacities at 7 days. SEI at 14 days; SEI persistent!)
What are the signs of PCF? (7)
Follicular conjunctivitis
Often bilateral
Often preauricular lymphadenopathy 3-4 days after onset
Eyelid oedema
May have pseudomembranes
May have keratitis (30% cases) incl. diffuse SPK + subepithelial infiltrates [rare in pCF]
What is the DDx for PCF? (4)
EKC, molluscum contagiosum conj., allergic conj., topical drug hypersensitivity
How can you manage EKC (during infectious period) (4)
If infectious period: supportive (vasoconstrictors, cold compress);
povidone iodine?;
cidofovir in future;
steroids maybe but not really? (prophylaxis/SEI Flarex BD to QID z slow taper
Also: Prevention: in office hygiene/sterilisation; px education
What can you additionally do to manage EKC (post infectious period)? (1)
If post-infectious period: STEROIDS useful in reducing SEI and improving VA
When would darryl use steroids in the management of EKC?
[Timing of steroid use = key to management of EKC!!] “I use steroids after infectious period is over” – Darryl Guest
How can you manage PCF? (7)
Optom hygiene + educate px
GP referral (to stay home)
Contagious for ~2/52
Povidone-iodine?
No antiviral agent proven effective
Palliative: cold compress, artificial tears/irrigation, relief of pharyngitis + fever (z Nurofen)
Steroid if severe inflammation [Flarex BD to QID z slow taper]
When would you follow up a patient with PCF? What should you monitor here?
Follow up: resolves usually in 7-14 days so see in this timeframe. Monitor for corneal involvement. May need topical steroid.
What are SEI?
SEI = sub-epithelial infiltrates = pale little islands of WBCs that are recruited by the limbus to reach the stroma
In which condition are SEI persistent? EKC or PCF?
EKC
Why would SEI be persistent? How can we counter this persistence?
sub-epithelial infiltrates = pale little islands of WBCs that are recruited by the limbus to reach the stroma. Sometimes the WBCs stay behind instead of migrating back. This is what it means when SEI is persistent. Can be persistent for up to a year. Steroids can be used to act as a messenger to tell the WBCs to go back to the limbus
What is a great diagnostic difference to tell apart ECK and PCF?
Amount of infiltrate. If you have more infiltrate present it’s EKC
What is the diagnostic rule of thumb for using different types of discharge for diagnosis of ocular presentations? (4)
Watery = viral/allergic
Mucoid (ropy) = allergic
Purulent = acute bacterial
Mucopurulent (ropy purulent) = mild/chronic bacterial or chlamydial
What are the signs of (NON-gonococcal) bacterial conjunctivitis? (5.5)
Conj hyperaemia (esp. in fornices. Clearer area around limbus useful diagnostically)
Mild SPK (only if inflammatory)
Mild papillary reaction
Mucopurulent discharge
Lid crusting, phylectenules (small vesicles), corneal marginal infiltrates (staph. A.)
What are the signs of gonococcal conjunctivitis? (5)
Marked conj hyperaemia, chemosis (conj oedema), Papillary reaction z lid swell
Often preauricular lymphadenopathy
Purulent discharge
Corneal involvement? – risk of perforation
How do you manage (NON-gonococcal) bacterial conjunctivits? (4)
Self-limiting, monitor, quicker with antibiotic
Bathing with NaCl (if little/no corneal involvement)
Broad spectrum antibiotics z/zout ointment @night 7-10days [chloramphenicol, aminoglycoside]
Follow up: 3-5days then 7-10 days
How do you manage gonococcal bacterial conjunctivitis? (5)
REFER – often systemic so IM CEPHALOSPORIN and/or ORAL FLUOROQUINOLONE indicated
Adjunct tx with topical fortified aminoglycoside or fluoroquinolone
Irrigate to remove discharge
Oral azithromycin for co-existing chlamydia
Describe CIN and it’s features (5). What causes it? What does biopsy show?
Local conj squamous ep. Metaplasia + plemorphism
Cells can become keratinised
Cause: HPV, excess UV
BV ‘strawberry spots’ more marked
More lush feeder vessels
More likely in immune compromised + elderly
Biopsy: plemorphism + metaplasia; Contained by BM – no invasion of stroma. Note how it’s stopping at the limbus when you see it?
How can you definitely differentiate CIN from malignancy?
OCT
Should you perform surgery on CIN. Why?
Yes. Due to biopsy findings but lack of stromal invasion —–consider “pre-malignant”
—-If untreated high chance of malignancy
How does UV cause a papilloma or CIN?
NB: UV denatures the DNA of the epithelial cells causing excess proliferation – this is how papillomas can form.
What is SCN?
When CIN breaks through basement membrane (BM) and invades underlying substantia propria (stroma)
Describe the appearance of SCN (4)
Appearance: as for CIN BUT non-motile as anchored by stromal invasion
Malignant lesion with pleomorphism + keratin
May see ulceration with white plaques
Small haemorrhages common due to BV involvement
Describe the 3 main characteristics of a malignant neoplasia
- Promote keratinisation (leukoplasia): NB: non-neoplastic sites will ALSO do this
- Produce a thickening/growth of a tissue layer
- Spread to involve other layers: these will be underneath the conj epithelium (i.e. stroma neoplasia that remain with it’s original tissue layer [e.g. CIN] are called carcinoma in situ. These are often considered pre-cancerous)
Define intraocular immune privilege
sites in the body where foreign body tissue grafts can survive for extended or indefinite periods of time, whereas similar grafts placed at conventional body sites are acutely rejected.
LIst 3 key pieces of evidence for intraocular immune privilege/no excessive immune response within blood ocular barriers
- Success of corneal transplantation (foreign tissue placed in anterior chamber is not rejected)
- Unrestricted growth of allogenic (non-self) tumour cells in the eye
- Aqueous and vitreous fluids inhibit inflammatory cells in vitro
How high are the levels of TGFbeta in the eye compared to other tissues? What is the role of TGFbeta?
• TGF-beta2 in high levels in eye – not so in most other tissues
- TGF-beta2 expression inside eye plays a role in inhibiting immune response (eg: disarming of T cells that cross PE and induction of TGF-beta2 expression)
What is TGFbeta expressed by in the eye?
Expressed by pigmented cells of the eye: RPE, PE of the ciliary body and iris
What is the role of alphaMSH?
Alpha-MSH inhibits macrophage activation and promotes production of anti-inflammatory factors
- Thus, even if T cells make it into the eye, alpha-MSH shuts it down
What are the 3 mechanisms behind intraocular immune privilege?
- Physical Barrier
- Inhibitory microenvironment
- Active regulation of immune response
How do physical barriers contribute to the intraocular immune privilege? (2)
Efficient BRB
No efferent lymphatics
What is ACAID?
ACAID (AC acquired immune deviation): immune privilege that inhibits immune defense mechanisms that could lead to damage to sensitive ocular tissue (based on expression of immunosuppressive factors on ocular tissue and in ocular fluids)
How does ACAID work?
the eye derived antigen elicit a T-regulation skewed and response in which DTH is suppressed
How does active regulation of the immune respone contribute to intraocular immune privilege? (2)
ACAID
Expression of Fas ligand in cornea, iris, and CB epithelium
How does the expression of Fas ligand contribute to intraocular immune privilege? Explain the mechanism
The expression of FAS ligand actively induces infiltrating Fas+ T cells to undergo apoptosis (through binding to death-receptor pathway)
In general terms, how does the appearance of papillae and follicles differ?
Papillae: raised with a flat top and with hard, flat topped central vessels [“flattened nodules + central vascular cores”]
Follicles: yellowish-grayish white, discrete round elevations of the conjunctiva with surrounding vessels
[“small, dome-shaped nodules without a prominent central vessel”]
What is conjunctival papillae made up of? What does this indicate?
accumulations of eosinophils and basophils. Indicates an allergic response
Is the central part of a follicle vascular or avascular?
avascular, but dilated blood vessels may surround the base and sweep over the base over convexity
Describe the pathogenesis behind how a papillae forms
Papillae are formed by mixed inflammatory infiltrate producing a raised elevation of the conjunctival epithelium
Describe the pathogenesis behind how follicles form
Accumulation of WBCs within the palpebral conjunctiva
Describe the histological appearance of papillae
closely packed, flat-topped projections, with numerous eosinophils, lymphocytes, plasma cells, and mast cells in the stroma surrounding a central vascular channel.
How do follicles and papillae differ in colour?
whereas a papilla clinically appears more red on its surface and more pale at its base, a follicle appears more pale on its surface and more red at its base
due to the blood vessels
Describe the histological appearance of follicles. Where are the follicles found? What do they consist of?
Histologically, a lymphoid follicle is situated in the subepithelial region and consists of a germinal center, containing immature, proliferating lymphocytes; and surrounding corona, containing mature lymphocytes and plasma cells.
Where are the follicles in follicular conjunctivitis typically most prominent?
inferior palpebral and forniceal conjunctiva
Define Keratoconus
a progressive bilateral typically asymmetric non-inflammatory ectasia characterised by progressive thinning of the axial corneal stroma
Describe the histopathology of KC [in general biochem terms]
Cornea biochemically unstable: (50% ↓biochem resistance, ↓d cross-links b/w + within collagen fibres in ant. Stroma)
Describe the histopathology of KC [primary corneal changes] (3)
epi abnormalities + breaks in Bowman’s layer, stromal thinning, decemet’s breaks
Describe the histopathology of KC [epithelium]
basal cells degen., down-growth of epi basal cells into bowman’s membrane, thickened basement membrane like layer, breaks in bowman’s –> filled by eruptions of underlying stromal collagen, iron deposition in basal epi cells @ base of cone = Fleisher’s ring
Describe the histopathology of KC [stroma]
reduced # of collagen lamellae, reduced # of keratocytes, changes to gross lamellae organisation (compacted + loss of arrangement), reduced density of corneal nerves + thicker fibre bundles
Describe the histopathology of KC [descemet’s]
unaffected until very late disease. If break = acute corneal hydrops [is when aqueous enters corneal stroma and you get dramatic corneal oedema]
List the symptoms of KC (8)
Highly variable: None to severe; ↓d/blurred vision [distortion, ghosting, doubling]; ↑light sensitivity; flaring of lights; difficulty night vision; eye strain [squinting, headaches, uncomfortable vision]; dry eyes/irritated/itchy [assoc. allergy]; Hx eye rubbing
List the signs of KC (7)
- Clinical sign = reduced spectacle V.A
- Refraction + best corrected V.A: Myopia + High astig [oblique or against rule]; frequent changes in Rx,; Near acuity often better than expected from refraction + age
- Retinoscopy: irregular scissor reflex
- Opthalm: charleux oil droplet
- Keratometry: doubling/distortion of mires
- Corneal topography
- Pachymettry: reduced CCT
List the biomicroscopic findings of KC (6)
Vogts striae; Fleisher’s ring; Increased visibility of corneal nerves; Corneal stromal thinning; Munson’s sign; Apical scarring [superficial and/or deep opacities]
Describe the severity classifications of KC. List the K readings
Stage 1 = Forme Fruste (sub clinical)
Stage 2 = Early (<45D, >7.5mm)
Stage 3 = Moderate (45.0-52.0D, 6.50-7.50mm)
Stage 4 = Advanced (>52D, <6.50mm)
Describe stage 1 KC and how you’d manage
sub-clinical; corneal topo; spectacle VA 6/6+; SL normal; Minimal/no change topo; Mx = spec correction; soft standard disposable CLs
Describe stage 2 KC and how you’d manage
Dx typically topo [central k>47.2D, I/S index >1.4]; minimal distortion; SL may have striae + fleishers [or may not]; no corneal scarring; Mx = spectacles [may be normal or slightly reduced], consider SCLs(torics)/RGPs/hybrid CLs if slightly reduced. Also cross-linking amirite?
Describe stage 3/4 KC and how you’d manage
Poor spectacle VA; progressive myopic astig; SL often find striae, fleishers’, prominent ecatasia, scarring; Mx = CLs [RGP, Piggyback (RGP + SCL carrier), Hybrid, Miniscleral/scleral]. Also cross linking amirite?
Describe the 3 different morphologies of KC
Nipple cone (~45%): near corneal centre or inferior nasal [ideal for smaller RGP] Sagging/oval cones (~50%): larger, below centre or inferior temporal, 3mm- 5.5mm [small RGP will ride low, typically want miniscleral/hybrid lens] Globus cones (~5%): involving up to 75% of cornea [most challenging to fit]
How do we manage end stage KC?
corneal graft (either DALK or PK)
How does cross-linking work?
UVA irradiation + riboflavin to strengthen collagen. UVA exposure (370nm) of riboflavin releases free radicals which cause cross-linking formation b/w the amino acids on the collagen chains
Increased cross-links cause an increase in collagen fibre diameter; Inter-fibre cross-links increase space b/w collagen fibrils
Which KC patients would you get to do cross linking? (6)
MUST have progressive KC (documented) –> >1D increase in apical power over 12 months. Minimal corneal thickness of 400 microns. Absence of significant corneal scarring, No hx herpetic eye disease, Not pregnant or breastfeeding, No auto-immune disorders or impaired wound healing
What things should you consider when thinking about giving a KC patient a corneal graft? (3)
CL intolerance to a good fit; inability to fit CL by experienced fitter; corneal scarring that limits acuity and quality of life; bilaterally progressive disease with high risk of visual impairment (high risk of hydrops in both eyes)
How do you treat/manage blocked tear duct in infants? (4)
Most resolve within 12 months of age. (it's basically just a breakdown) Tx: Bathing Massage Topical antibiotic
What is the main complication that can occur from a blocked tear duct in infants? Define it
Dacryocystitis: Infection of the lacrimal sec, secondary to obstruction of the nasolacrimal duct at the junction of lacrimal sac
What should we tell relatives of infants with blocked tear duct?
“let the kid grow up as we do”
What is another complication that can occur from a blocked tear duct in infants?
Amblyopia. Could occur due to eye being shut all the time
Where does the HSV virus go after a primary infection?
virus enters latent phase in trigeminal + superior cervical ganglion
Describe how the cornea is affected in a 2ndary HSV infection
Cornea primary location
§ epithelial: punctate keratitis, dendritic, amoeboid,
and geographic ulcers
§ Metaherpetic ulcer (epithelial ulceration with no
live virus – generally non healing)
§ stromal: necrotizing and non-necrotizing
§ disciform
§ endothelial
Can a 2ndary HSV infection affect other areas in addition to cornea?
Also can affect trab. Mesh/uvea
Describe the features of a 2ndary HSV infection
unilateral, follicular conjunctivitis, ipsilateral lymphadenopathy, burning, tearing
Variable amnt. Pain depending on # of recurrences
Look for convenient skin lesions, hx or evidence of previous attacks, aggravating factors
SPK
Dendritic keratitis (dendritic ulcers)
Describe the features of a dendritic ulcer (4)
May be central or peripheral in location
Bud at the edges, which is where it stains z rose Bengal/lissamine green
You can have micro dendrites or larger ones
Corneal sensitivity is reduced, but pain still present –> the surface of the nerve is not working properly, but the nerve is still functional
Describe the features of HSV stromal disease
Blinding complication marked by stromal infl., uveitis, endotheliitis, trabeculitis, +/- epithelial involvement
Inflammatory reaction here is due to viral antigens but not due to active viral replication
Onset of stromal disease marks a serious new complication in the condition
How do you manage/treat HSV stromal disease? (8)
§ aggressively manage inflammation § frequent use of topical steroids with slow taper [flarex+predforte every hour – tapering off for months] § antiviral cover § Acyclovir ung five times a daywith taper as steroids are tapered § oral antiviral? § manage IOP as needed § cycloplegia for comfort § Can we prevent recurrences?
How do we treat HSV epithelial keratitis? (3)
- Acyclovir ung 5xday
- Debridement + patching acyclovir also potential tx
NB: NO TOPICAL STEROIDS IN ACTIVE HSV EPITHELIAL KERATITIS (DON’T USE THEM)
