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Sem1revcards > AED: Written Exam Prep [High yield cards only] > Flashcards

AED: Written Exam Prep [High yield cards only] Flashcards

1
Q

How thicc is the tear film? Name the layers of the tear film from superficial to deepest, stating how thick each layer is

A

~7um thick.
Lipid - 0.1um
Aqueous - 7um
Mucoid - 0.05um

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2
Q

What does each layer of the tear film do?

A

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

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3
Q

How is the tear film replenished with blinking? Describe the mechanism

A

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.

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4
Q

Name the 4 main ocular allergy presentations

A

Seasonal conjunctivitis
GIant papillary conjunctivitis (GPC)
Vernal keratoconjunctivitis (VKC)
Atopic keratoconjunctivitis (AKC)

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5
Q

Of the 4 main ocular allergy presentations, which have the potential to be sight threatening?

A

VKC and AKC

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6
Q

Of the 4 main ocular allergy presentations, what is the key differential for GPC?

A

Large papillae in a CL wearer

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7
Q

How does VKC vs AKC differ in terms of:
A: onset?
B: sex incidence?
C: seasonal variation?

A

A: 1st decade vs 2nd/3rd decade
B: Males vs no preference
C: Spring vs perennial

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8
Q

How does VKC vs AKC differ in terms of:
D: discharge?
E: conj scarring?
F: horner trantas dot presence?

A

D: thick mucoid vs watery clear
E: Moderate incidence vs Higher incidence
F: Commonly seen (incl. shield ulcers) vs Rare (in AKC)

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9
Q

How do VKC vs AKC differ in terms of:
G: corneal neovascularisation?
H: presence of eosinophils in corneal scraping?

A

G: not present unless 2ndary to infectious keratitis vs generally common
H: more likely vs less likely

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10
Q

Describe the features of Grades 1-4 of GPC

A

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

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11
Q

When using steroids for the 4 main ocular allergic presentations. What steroids do you use for each and how often?

A

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)

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12
Q

What symptoms would you expect with an ocular IgE mediated allergic eye disease? (9)

A

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.

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13
Q

In what general type of ocular presentations would you expect papillae (2)?

A

Allergic
Bacterial

think “pABillae”

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14
Q

In what general type of ocular presentations would you expect follicles? (3)

A

Chlaymdia
Toxic
VIral

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15
Q

How can you manage seasonal conjunctivitis? (8)

A 
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)

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16
Q

How can you manage VKC? (7)

A

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

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17
Q

How can you manage AKC? (8)

A

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)

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18
Q

How can you manage GPC? (4)

A

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

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19
Q

When does VKC most commonly manifest?

A

b/w 5-25yo

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20
Q

Where does VKC most commonly affect?

A

usually affects superior tarsal conj

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21
Q

In which of the 4 main ocular allergy presentations are patients likely to be atopic?

A

VKC and AKC

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22
Q

What does the limbal presentation of VKC look like? (4)

A

Limbitis
Limbal papillae
Horner Trantas dots
Pseudogerontoxon (cupids bow) in area of previously inflamed limbus

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23
Q

Which of the 4 main ocular allergy presentations is not associated with corneal damage of some kind?

A

Seasonal conjunctivitis

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24
Q

Compare bacterial ulcers with bacterial infiltrate in the following categories:
A: how common?
B: how painful?
C: location?

A

A: ulcers = rare; infiltrate = more common
B: ulcers = painful; infiltrate = less painful
C: ulcers = central; infiltrate = peripheral (more likely to be peripheral)

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25
Q

Compare ulcers with infiltrate in the following categories:
D: how does the staining compare?
E: AC reaction?

A

D: ulcers = staining mirrors infiltrate; infiltrate = staining smaller in size than infiltrate
E: ulcers = AC reaction present; infiltrate = no ac reaction

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26
Q

Compare ulcers with infiltrate in the following categories:
F: conjunctival reaction?
G: number of lesions?

A

F: Ulcers = generalised conj reaction; Infiltrate = sector conj reaction
G: Ulcer = single lesion; Infiltrate = sometimes multiple

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27
Q

In specific terms, how do you treat bacterial ulcers? (4). Which tx is the gold standard?

A

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

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28
Q

What is the “1-2-3” guideline? What should you do if an ulcer doesn’t meet this criteria?

A

“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

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29
Q

How do you treat bacterial infiltrates? (2 basically)

A

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

30
Q

Should you patch bacterial corneal ulcers? Explain

A

Never patch [creates env. for replication

31
Q

In simple terms, what is the treatment for a bacterial ulcer?

A

Fortified antibiotic or fluoroquinolone

32
Q

Compare Infectious vs Non-infectious ulcerative keratitis in the following categories:
A: Pain/redness/discharge
B: Association with CL wear
C: Location

A

A: More vs less
B: Assoc. vs Not assoc.
C: More central vs more peripheral

33
Q

Compare Infectious vs Non-infectious ulcerative keratitis in the following categories:
D: Level of infiltrate
E: Level of AC reaction

A

D: More infiltrate vs Less infiltrate
E: Significant AC reaction vs mild or no AC reaction

34
Q

When in doubt, how should you treat ulcerative keratitis?

A

treat as infectious

35
Q

What are the signs of EKC? (9)

A

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!)

36
Q

What are the signs of PCF? (7)

A

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]

37
Q

What is the DDx for PCF? (4)

A

EKC, molluscum contagiosum conj., allergic conj., topical drug hypersensitivity

38
Q

How can you manage EKC (during infectious period) (4)

A

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

39
Q

What can you additionally do to manage EKC (post infectious period)? (1)

A

If post-infectious period: STEROIDS useful in reducing SEI and improving VA

40
Q

When would darryl use steroids in the management of EKC?

A

[Timing of steroid use = key to management of EKC!!] “I use steroids after infectious period is over” – Darryl Guest

41
Q

How can you manage PCF? (7)

A

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]

42
Q

When would you follow up a patient with PCF? What should you monitor here?

A

Follow up: resolves usually in 7-14 days so see in this timeframe. Monitor for corneal involvement. May need topical steroid.

43
Q

What are SEI?

A

SEI = sub-epithelial infiltrates = pale little islands of WBCs that are recruited by the limbus to reach the stroma

44
Q

In which condition are SEI persistent? EKC or PCF?

A

EKC

45
Q

Why would SEI be persistent? How can we counter this persistence?

A

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

46
Q

What is a great diagnostic difference to tell apart ECK and PCF?

A

Amount of infiltrate. If you have more infiltrate present it’s EKC

47
Q

What is the diagnostic rule of thumb for using different types of discharge for diagnosis of ocular presentations? (4)

A

Watery = viral/allergic
Mucoid (ropy) = allergic
Purulent = acute bacterial
Mucopurulent (ropy purulent) = mild/chronic bacterial or chlamydial

48
Q

What are the signs of (NON-gonococcal) bacterial conjunctivitis? (5.5)

A

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.)

49
Q

What are the signs of gonococcal conjunctivitis? (5)

A

Marked conj hyperaemia, chemosis (conj oedema), Papillary reaction z lid swell
Often preauricular lymphadenopathy
Purulent discharge
Corneal involvement? – risk of perforation

50
Q

How do you manage (NON-gonococcal) bacterial conjunctivits? (4)

A

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

51
Q

How do you manage gonococcal bacterial conjunctivitis? (5)

A

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

52
Q

Describe CIN and it’s features (5). What causes it? What does biopsy show?

A

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?

53
Q

How can you definitely differentiate CIN from malignancy?

A

OCT

54
Q

Should you perform surgery on CIN. Why?

A

Yes. Due to biopsy findings but lack of stromal invasion —–consider “pre-malignant”
—-If untreated  high chance of malignancy

55
Q

How does UV cause a papilloma or CIN?

A

NB: UV denatures the DNA of the epithelial cells causing excess proliferation – this is how papillomas can form.

56
Q

What is SCN?

A

When CIN breaks through basement membrane (BM) and invades underlying substantia propria (stroma)

57
Q

Describe the appearance of SCN (4)

A

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

58
Q

Describe the 3 main characteristics of a malignant neoplasia

A
  1. Promote keratinisation (leukoplasia): NB: non-neoplastic sites will ALSO do this
  2. Produce a thickening/growth of a tissue layer
  3. 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)
59
Q

Define intraocular immune privilege

A

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.

60
Q

LIst 3 key pieces of evidence for intraocular immune privilege/no excessive immune response within blood ocular barriers

A
  • 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
61
Q

How high are the levels of TGFbeta in the eye compared to other tissues? What is the role of TGFbeta?

A

• 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)

62
Q

What is TGFbeta expressed by in the eye?

A

Expressed by pigmented cells of the eye: RPE, PE of the ciliary body and iris

63
Q

What is the role of alphaMSH?

A

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

64
Q

What are the 3 mechanisms behind intraocular immune privilege?

A
  1. Physical Barrier
  2. Inhibitory microenvironment
  3. Active regulation of immune response
65
Q

How do physical barriers contribute to the intraocular immune privilege? (2)

A

Efficient BRB

No efferent lymphatics

66
Q

What is ACAID?

A

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)

67
Q

How does ACAID work?

A

the eye derived antigen elicit a T-regulation skewed and response in which DTH is suppressed

68
Q

How does active regulation of the immune respone contribute to intraocular immune privilege? (2)

A

ACAID

Expression of Fas ligand in cornea, iris, and CB epithelium

69
Q

How does the expression of Fas ligand contribute to intraocular immune privilege? Explain the mechanism

A

The expression of FAS ligand actively induces infiltrating Fas+ T cells to undergo apoptosis (through binding to death-receptor pathway)

70
Q

In general terms, how does the appearance of papillae and follicles differ?

A

Papillae: raised with a flat top and with hard, flat topped central vessels
Follicles: yellowish-grayish white, discrete round elevations of the conjunctiva with surrounding vessels

Sem1revcards (19 decks)

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