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OPTOM III > OPTOM 353B > Flashcards

OPTOM 353B Flashcards

1
Q

Corneal layers and its characteristics

A

Epithelium –> 50um thick and Statified squamous epithelium

Bowmans layer –> Acellular + 10um thick + Dense collagen fibrils

Stroma –> 90% corneal thickness + Layers of Parallel collagen fibrils w keratocytes

Descemets membrane –> Basement membrane of endothelium + 10um thick + Hexagonal fibrils

Endothelium –> Single layer of very thin flat cells + Covers posterior Descements membrane + Major role in corneal hydration

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1
Q

Importance of the endothelium and what does it require

A

Major role in corneal hydration for transparency, it needs high energy in the single layer of cells for the pump-leak model to function

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2
Q

Function of eye lids

A

Decrease FB contact and light. 15000 blinks per day to remove FB and pathogens. Has pumps and renews tear fluid maintaining the optical surface

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3
Q

Lipid layer function

A

Stops aqueous evaporation

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4
Q

Aqeuous and Mucus layer function

A

Removes free floating microbes, FB and debris. Also has anti-inflam and anti-microbrial proteins like lysozymes

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5
Q

Characteristic of epithelium and function

A

Tight junctions reducing microbe penetration

Has nerve endings and anti-oxidant production

Minor role in corneal hydration

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6
Q

How often is the epithelium replaced

A

every 5-7 days due to rapid healing and cell migration

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7
Q

Keratitis

A

Cornea inflammation giving the cardinal signs and loss of function.

Inflammation signs like epithelial cell loss, immune cell infiltration, corneal swelling and neo-vas.

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8
Q

What does fluorescein staining indicate

A

Depth of local tear film, it stains disruputed cell-cell junctions. Also absorbs blue light and emits higher wavelength yellow-green light.

Staining is painless

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9
Q

What is SPK

A

Superficial punctate keratitis

Small pinpoint defects in superficial corneal epithelium and stains w fluorescein. Also assoc. w other ocular disorders

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10
Q

What do stromal infiltrates in the anterior stroma represent

A

Inflammatory cell migration form limbal vasculature and tear film, can be infectious/non-infectious, epithelium either intact/not-intact

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11
Q

Epithelial oedemas

A

Means endothelial dysfunction. Leads to epithelial bullae formation causing light scatter. More effect on vision compared to corneal stromal oedemas due to endothelial pump dysfunction. Results in decreased corneal transparency.

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12
Q

Corneal neo-vas.

A

Corneal pannus is the infiltration of sub-epithelium with fine blood vessels

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13
Q

What is mirobial keratitis

A

Bacteria/Virus infection from compromised epithelium. Corneal excavations w tissue necrosis. Sight threatening ; Only few bacteria can penetrate epithelium.

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14
Q

What can cause microbrial keratitis

A

Contact lenses, trauma and herpetic diseases

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15
Q

Microbial keratitis characteristics

A

Have FB sensation, photophobia and increased pain.

Epithelial defect gives mucopurulent discharge, secondary sterile anterior chamber reaction in the central or periphery

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16
Q

How does microbial keratitis occur

A

Bacteria colonises stromaa and becomes antigenic releasing enzymes and toxins resulting in immune reaction and inflammation

Then polymorphonuclear leukocytes aggregate and phagocytoses bacteria.

Stroma damage by bacterial enzymes seen

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17
Q

Factors that increase corneal infection risk

A

CL lens w pathogens on it. Mechanical microtraumas from CL —> Pathogens enter stroma —> Immune reaction and inflammation

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18
Q

Signs of Corneal Infection

A

Red eyes, epithelial defects, corneal opacification and hypopyon

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19
Q

What is PEDAL

A

Pain, Epithelial defect, Discharge, Anterior chamber reaction and Location ( usually central )

Acronym to identify lesions that are related to infections

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20
Q

Viral keratitis

A

Majourity population seroposutuve for HSV antibodies

HSV 1 for the face, lips and eyes

HSV 2 is genital herpes

Primary HSV 1 infection in childhood via droplet with mild fevers and remians dormant in the trigeminal ganglion and the virus activates later in life

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21
Q

What is HSK and its classification

A

Herpes simplex keratitis

Classification either epithelial, stromal and endothelial.

Epithelial –> Dendritic or geographic ulcer

Stroma –> Stromal necrotic and interstitial keratitis

Endothelial –> Disciform endothelitis

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22
Q

Epithelial HSK

A

Unilateral w reduced vision.

Signs –> Conjunctival injections, reduced corneal sensation, branching of dendritic ulcer where dendrites can coalesce giving geographic ulcers

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23
Q

Stromal necrotic HSK

A

Rare w tissue necrosis and viral invasion.

Signs –> Conjunctival injections, cheesy necrotic stroma, anterior uveitis w keratic precipitates ( KPs ) and a vascularised scar

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24
Q

Keratic precipitates

A

Seen in anterior segment inflammation. Punctate KPs are inflammatory cellular deposits on the corneal endothelium

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25
Q

New vs Old KPs

A

New –> White and round

Old –> Irregular, faded and pigmented

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26
Q

Endothelitis

A

HS reaction to viral antigen. Has gradual onset, painless w blurred vision

Signs –> Reduced corneal sensation + Epithelial/stromal oedemas + KPs local to underlying lesion + Anterior chamber inflammation + elevated IOP

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27
Q

What is HZO

A

Herpes zoster ophthalmicus, from VZV which is dormant in dorsal root ganglion and reactivates as herpes zoster

Gives painful skin rash in trigeminal nerve path. Nasocilliary nerve affected affecting the eye.

Prevalence increases w age

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28
Q

HZO signs and symptoms

A

Prodromal fever + headaches and Malaise giving vessicular rash over cutaneous branches of the opthalmic nerve where 50% people get epithelial keratitis within 2 days

Epithelial HZO giving a pseudo-dendritic appearance

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29
Q

Complications of long term HZO

A

Nerve damage giving palsie + Scarring giving ectropion and increased IOP from trabecular meshwork scarring + Chronic inflammation + Dry eye due to tear duct damage

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30
Q

Acanthamoeba Keratitis

A

Either active as Trophozoites or dormant as cysts

Infection associateed w risk factors like epithelial defects and soft contact lens wear –> hard to diagnose and often treated as smthn else

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31
Q

Acanthamoeba keratitis signs and symptoms

A

Excruciating pain from attacks on corneal nerves, photophobia and blurred vision

Conjunctival infections, epithelial and sub-epithelial infiltrates w enlarged abscesses seen

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32
Q

Fungal Keratitis

A

Leads to severe sight loss where corneal infections from yeast like candida

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33
Q

Fungal keratitis risk factors

A

Ocular trauma, topical steroid therapy and pre-existing ocular/systemic immuosuppressive diseases

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34
Q

Fungal keratitis signs and symptoms

A

Marked pain and photophobia as presentation where px presents wihtin weeks ratehr than days of red eye

Signs –> Corneal infiltrates and oedemas + Anterior chamber reactions and hypopyopn

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35
Q

What are degenerations

A

Assoc. w systemtic diseases + inflammation + Age + Thinning corneal tissue + Unilateral

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36
Q

What are dystrophies

A

Inherited corneal disease, Autosomal dominant + Bilateral/Symmetry/Early onset and progressive

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37
Q

What is Arcus Senilis

A

In elderly, has white perilimbal band w clear zone + Phospholipid/cholesterol deposition in stroma + Px asymptomatic w no treatment needed

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38
Q

What is Arcus Juvenilis

A

Rare + Small part of peripheral cornea and Assoc. w genetic high blood cholesterol

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39
Q

Vogt’s limbal girdle

A

Common and age related + Sub-epithelial degeneration + w/wo calcium deposits in nasal and temporal perilimbal cornea w no visual significance

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40
Q

What is Dellen and how does it occur

A

Localised thinning of peripheral cornea w the dehydration and compaction of cornea

From Tear film instability assoc. w scarring and vascularisation. Pooling of fluorescein seen but epithelium is intact

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41
Q

Band keratopathy

A

Uncommon calcium deposits in sub-epithelial, bowmans and anterior stroma due to age related, chronic ocular inflammation, metabolic disruption and hereditary

Vision affected is central and cuase ocular irritation and begins nasally or temporally, expands centrally

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42
Q

Terrien’s Marginal degeneration

A

Non-inflamm progressive thinning or peripheral corneal stroma superiorly + Lipid deposits between collagen layers + intact epithelium + Bilateral + Slow progression + Assoc. w Vascularisation + Decreased vision caused by irregular astigmatism.

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43
Q

What is Mooren’s Ulcer

A

Peripheral ulcerative keratitis that is uni/bilateral, has autoimmune response to stromal antigens

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44
Q

Mooren’s ulcer signs and symptoms

A

Redness, pain, photophobia and decreased vision. Epithelial defects and healing assoc. w thinning and corneal vascularisation

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45
Q

Rosacea Keratitis

A

Skin disease w itching and flushing of facial skin.

Has prominent blood vessels w butterfly rash patterns aggravated sun exposure w dry eye and blepharitis.

Assoc. w margincal keratitis and Neo-vas.

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46
Q

What is RCE

A

Recurrent Corneal erosion. syndrome.

From unstable epithelial to basement membrane, uni/bilateral.

Dystropic RCE assoc. w corneal dystrophies. Post traumatic RCE follows superficial corneal trauma.

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47
Q

RCE signs and symptoms

A

Has recurrent ocular surface pain, blurred vision and photophobia.

Localised epithelial injuries w microcysts after healing seen

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48
Q

Corneal dystrophies

A

Genetic abnormalities in corneal structure and funcrion. This is autosomal dominant and treatment involves corneal graft

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49
Q

Where can corneal dystrophies occur

A

Epithelial –> Epithelial basement membrane dystrophy + Messman’s

Stromal –> Reis-Bucklers + Granular + Lattice + Macular

Endothelial –> Fuchs endothelial dystrophy + Posterior polymorphous dystrophy

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50
Q

What is epithelial basement membrane dystrophy ( EMBD )

A

Autosomal dominant assoc. w recurrent corneal erosion syndrome affecting central cornea if involved

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51
Q

EMBD signs and symptoms

A

Epithelial cells poorly attached to basement membrane

Maps –> Multilaminar basement membrane extending into epithelium

Dots –> Deep epithelial cells migrating to surface and trapped under abnormal basement membrane

Fingerprints –> Folds of reduplicated basemenr membrane within epithelium

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52
Q

Meesman’s Dystrophy

A

Autosomal dominant w tiny cysts in epithelium, has minimal effect on VA but has recurrent erosions

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53
Q

Reis-Bucklers Dystrophy

A

Bilateral and starts from young age. Damage to bowmans layer and anterior stroma.

Sub-epithelial opacities central but most dense in mid-periphery. Has loss of hemi-desmosomes causing recurrent lesions

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54
Q

Granular dystrophy

A

Autosomal dominant w granular deposits of hyaline in central anterior stroma w clear zones in between.

Decreased vision when opacities are confluent and has recurrent corneal erosions

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55
Q

Lattice dystrophy

A

Has stromal amyloid deposits w poor epithelial adhesion. There is Type 1 and 2 autosomal dominant and Type 3 autosomal recessive

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56
Q

Explain the lattice dystrophy types

A

Type 1 AD –> Most common w fine branched lines in anterior or mid stroma w periphery spared

Type 2 AD –> Thicker lines and begins peripherally

Type 3 AR –> Coarser lines limbus to limbus

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57
Q

Macular dystrophy

A

Autosomal recessice w Mucopolysaccharide deposits in stromal keratocytes.

Corneal thinning and progressive visiion loss where px needs corneal transplant. Does not lead to RCES

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58
Q

Fuchs endothelial dystrophy

A

Progressive and more in women. Autosomal dominant but can be recessive.

Starts asa endothelial dystrophy and progresses to Fuch’s endothelial dystrophy where vision loss and has pain is epithelial bullae is present

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59
Q

Corneal Guttata

A

Collagen deposits on Descemet’s membrane, the Guttata is visible on slit lamp exam, w endothelial cell loss

Pleomorphism and Polymegathism seen

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60
Q

Stages of Fuchs endothelial dystrophy

A
  1. Guttata and thickening of descemets membrane from collagen deposits
  2. Progressive loss of endothelial cells causing breakdown in barrier function and active transport givng corneal oedema
  3. Denegerative pannus and scarring w permanent vision loss ( May need corneal graft )
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61
Q

Posterior polymorphus dystrophy

A

Autosomal dominant affecting descemets membrane and endothelium. Has bubble like lesions on endothelium and has band like lesions across the endothelium

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62
Q

What can posterior polymorphus dystrophy cause

A

Compromises endothelium, where there is abnormal endothelial cells growing into the angle giving glaucoma.

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63
Q

What is the cause of blindness in developed countries

A

Trauma from chemical burns, thermal, abrasion and UV

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64
Q

Corneal wound healing process

A

Endothelium heals fast, epithelial cells migrate to site in 4 hours.

Stromal injuries heal slowly. Descements ,embrane also heals slowly and scars easily.

Endothelium has limited miotic or regenerative capacity where cells change shape and spread to cover defect

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65
Q

Consequences of Alkali burns on eyes

A

More severe than acid burns as it penetrates cornea and anterior chamber. Alkali combines w lipids causing cell disruption

Sloughing of corneal epithelium seen, stromal cell necrosis leads to oedema or corneal stroma.

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66
Q

Keratoconus

A

Non-inflammatory cental or paracentral thinning of stroma giving progressive corneal potrusion and steepening resulting in myopia and astigmatism. Has reduced vision and corneal scarring

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67
Q

Keratoconus treatment

A

KC begins w progression between age 10-40.

Treat w rigid gas permeable CLs. Some px need corneal graft due to poor VA. Aim is to prevent progression and the need for graft

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68
Q

Why is there variation in keratoconus studies

A

Due to different study inclusion criteria and factors like genetic predisposition and environmental cofactors

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69
Q

Keratoconus associations and symptoms

A

Assoc. w –> Asthma, hay fever and eczema, presents as sporadic disorder

Symptoms such as decreased vision, has glare sensitivity, monocular double vision, itchy eyes and sometimes pain.

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70
Q

Irregular astigmatism

A

Non-uniform steepening of cornea w blurred vision or monocular diplopia.

From corneal denegerations, corneal surgery and trauma

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71
Q

Keratoconus signs

A

Corneal thinning, central/paracentral ectasia, steep keratometry readings, changing in refraction w increasing astigmatim and myopia. Also abnormal retinoscope reflex

Will see prominent corneal nerves, Vogt’s striae and fleischer’s ring

If KC is advanced then Munson’s signs seen and corneal hydrops

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72
Q

Types of cones in KC

A

Nipple, Oval anf Keratoglobus

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73
Q

What will we see in retinoscopy w px of KC

A

Scissoring or swirling reflex that is hard to neutralise.

Oil droplet sign seen in dilated pupils in Opthalmoscopy

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73
Q

What is Vogt’s striae

A

Vertical white ligns in corneal stroma or Descemets membrane, will see this under high magnification w white light. Could be from mechanical stress

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74
Q

What is Fleischer’s ring

A

Iron pigment ring deposits at base of cone in deep layers or corneal epithelium, seenw blue cobalt filter

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75
Q

Munsons’ sign

A

Advanced KC where superfical corneal swelling seen due to breaks in the bowmans layer.

Looks like a V shaped protrusion of the lower eyelid during a down gaze

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76
Q

Corneal hydrops

A

Ruptured descemet’s membrane allowing AH to flow into cornea giving swelling of stroma and epithelium.

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77
Q

Symptoms of Corneal hydrops

A

Px has sudden and painful vision loss. Gives corneal opacification w vascularisation

Leads to flattened cornea on respution so px may need corneal graft to improve vision

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78
Q

What is KC severity based on

A

The best spectacle corrected VA, Keratometry readings, inferior and superior differences in corneal pachymetry

There is forme Fruste keratoconus where ther eis non-inflammatory thinning of cornea w no clinical signs

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79
Q

What happens in KC ( Keratoconus )

A

Stroma becomes compact and fibrils are lost in anterior stroma. The thinning due to re-orientation of stromal collagen and reduced keratocytes in anterior stroma

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80
Q

KC etiology

A

Apoptosis from enzyme release follwing chronic epithelial injury

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81
Q

Function of Keratocytes

A

Maintain, repair of stroma and collagen/GP/GAGs synthesis. All maintains transparency

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82
Q

What do rigid gas permable contact wear do

A

Endothelial pleomorphism, polymegathism and thinning

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83
Q

Is KC and endothelial cell abnormality associated

A

Maybe as KC has ndothelial cell abnormalities, but most KC px also wear RGP CLs so the endothelium is not directly due to the disease

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84
Q

KC management

A

Spectacles, soft CLs, Rigid CLs, Intacs corneal implants, Corneal collagen cross linking and corneal transplant

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85
Q

Glx and CLs use in KC

A

Glx used in early stages, but does not correct irregular astigmatism.

Soft CLs drape over the cornea contour so not good for correction

RGPs treats moderate KC but w increasing cone height the RGPs become unstable or cause corneal scarring

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86
Q

Intacs and Corneal implants use in KC

A

Thin and semi-circular plastic ring segments inserted into corneal stroma under anaesthesia.

This flattens cornea and reduces distortion improving vision –> Gives reduced central K readings, Px selection also important

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87
Q

Corneal collagen cross-linking use in KC

A

Newer treatment slowing KC progression and strengthens corneal tissue. Involves corneal epithelium removal/Vitamin B/UVA light exposure and potential for endothelial damage

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88
Q

Corneal transplants

A

Done when cornea becomes very thin and no other treatments give good vision. in NZ, 50% of corneal grafts is for KC and close monitoring for graft rejection

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89
Q

What is PKP

A

Penetrating keratoplasty, for full thickness corneal transplant if significant stromal scarring or unknown endothelial status –> Has long post-op recovery time

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90
Q

What is DALK

A

Deep anterior lamellar keratoplasty, for partial thickness transplant. There is a selective transplant of corneal stroma where the stroma is involved but the endothelium is healthy which decreases risk of endothelial rejection

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91
Q

What is pellucid marginal degeneration

A

Rare, bilateral corneal ectasia. It is non-inflammatory w a peripheral band of severe thinning of the inferior cornea.

Thinner area is flatter but superior cornea is steepest w Severe VA reduction. The clear band of normal cornea separates thinned cornea from limbus.

92
Q

What is the conjunctiva

A

Thin transparent vascularised mucous membrane

93
Q

What does the conjunctiva consist of?

A
  1. Palpebral/Tarsal Conjunctiva –> Lines posterior aspect of eyelid and adherent to tarsal plate
  2. Forniceal Conjunctiva –> Loop between eyelid and globe
  3. Bulbar conjunctiva –> Covers globe surface, loosely attached to underlying Tenon’s capsule and inserts centrally ay corneoscleral limbus
94
Q

Where are Lymphatic vessels

A

In the superficial and deep plexus in the substantia propia

95
Q

Describe the medial and lateral lymphatics

A

Laterial is pre-auricular/parotid lymph nodes

Medial is submandocular lymph nodes

96
Q

Term for external ocular infection

A

Lymphadenopathy

97
Q

What is conjunctivitis, and its signs and symptoms

A

Inflammation of conjunctiva

Signs –> Discharge, chemosis, follicles, papillar and membranes seen

Symptoms –> Ocular discomfort, redness, discharge and lacrimation

VA unaffected

98
Q

What is the redness seen in conjunctivitis

A

Diffuse, involving entire conjunctival surface. Hyperemia seen due to increased redness of conjunctival blood vessels.

Injection seen due to vasodilation of conjunctival blood vessels where intensity increases going away from the limbus. Different to ciliary injection

99
Q

What is the discharge seen in conjunctivitis

A

Exudate from conjunctival epithelium from dilated vessels

Discharge quality depends on the causative agent such as if it is watery, mucoid, mucous-purulent and severe purulent

100
Q

What is the Chemosis in conjunctivitis

A

Macroscopic severe conjunctival swelling where protein rich exudtaes through the walls of inflamed blood vessels. This results in translucent blisters that protrude through the clsoed eyelid.

101
Q

What are the follicles in conjunctivitis

A

Supepithelial foci of hyperplastic lymphoid tissue within conjunctival stroma. Multiple slightly elevated yellow-white nodukes seen. It is avascular but assoc. w vascularisation and viral/chlamydial conjunctivitis

102
Q

What is the papillae in conjunctivitis

A

Conjunctival epithelial hyperplasia, has vascular core w various inflammatory cells that develop in the palpebral and limbal bulber conjunctiva

Has a non-specific inflammatory response where it is assoc. w CL wear and floppy eyelid syndrome

103
Q

What are the membranes in conjunctivitis

A

True membrane infiltrate superficial layers of conjunctival epithelium.

If removed then tearing anf bleeding will occur.

The cause of this is Steven-Jognson syndrome where pseudomembranes are coagulated exudates that is adherent to inflamed conuunctival epithelium which can be peeled away keaving epithelium intact. Due to bacterial conjunctivitis from S.Pyogenes

104
Q

Bacterial Conjunctivitis

A

Bacteria infection from contact w infected secretions such as S.epigermis/auerus/pneumoniae/influenzae.

Common and has muco-purulent discharge w eyelids often glued tgt upon waking. It is unilateral but becomes bilateral in couple days

105
Q

Viral conjunctivitis

A

AKA Adenoviral keratoconjunctivitis AKA Pink eye.

Due to adenocirus fiving pharyngoconjunctival fever ( PCF ) and Epidemic Keratoconjunctivitis ( EKC ). Very contagious w water discharge, follicles and lymphadenopathy.

Development to keratitis is common

106
Q

Viral Conjunctivitis process

A

Unilateral redness becoming bilateral very quickly, followed by corneal epitheliopathy. Finally subepithelial infiltrates after a week

107
Q

How is viral conjunctivitis spread

A

By respiratory or ocular secretions, so STAY at home until symptoms settled.

Frequent hand washing, avoiding touching eyes, and cover while sneezing recommended. Do not share towels and utensils.

This why sterilising equipment is important

108
Q

Allergic Conjunctivitis

A

Non-infectious conjunctivitis due to allergen reaction w contact to the conjunctiva

109
Q

Pinguecula

A

Denegeration of elastic tissue and collgen in the conjunctival stroma from response to chronic UV exposure and surface dryness

110
Q

What is seen in Pinguecula

A

Yellow-white elevated lesion on bulbar conjunctiva adjacent to limbus, it is more nasal than temporal but usually bilateral

Becomes larger if inflamed

111
Q

Pterygium

A

Fibromuscular subepithelial ingrowth of degenrative conjunctival stroma and can be transformed from a pinguecula

Enroaches the limbus onto the cornea invading the bowmans layer

112
Q

Pterygium characteristics

A

High vascular conunctival overgrowth extending onto the cornea. Deposits of iron seen in corneal epithelium at apex known as Stocker’s line. There is chronic irritation and vision impairment

113
Q

Conjunctivochalasis

A

Excess conunctival tissue between the globe and lower lid. It is benign and age related.

Bilateral, redundant bulbar conjunctiva that protrudes over lid margin in inferior bulbar conjunctiva.

Symptoms –> Dry eye and Epiphora

114
Q

Conjunctival Naevus

A

Melanocyte proliferation in junction of conjunctival epithelium and the supepithelial tissue

115
Q

Conunctival Naevus Characteristics

A

Benign, unilateral, solitary, flat or slightly elevated

Common in juxtalimbal location, less then 1% risk of malignancy

116
Q

Ethnic melanosis

A

Common in darker skin pigmentation. Similar to Narvi but its hypermelanosis w normal number of melanocytees. This is bilateral and develops in early years and stable in adulthood

117
Q

Conjunctival melanoma

A

Unregulated proliferation of atypical melanocytes w stromal invasion with serious malignancy

Black/grey solitary nodule located at limbus with high metastasis and reccurence rates

Can arise from pre-existing nevus but mostly from PAM ( Primary acquried melanosis )

118
Q

What is Primary Acquired Melanosis

A

Acquired unilateral condition of middle aged white individuals involving the limbus and bulbar conjunctiva.

119
Q

What are the types of PAM

A
  1. PAM w/o atypia –> Benign proliferation of normal melanocytes in basal conjunctival epithelium
  2. PAM w atypia –> Pre-malignant proliferation of atypical melanocytes in all epithelial layers, up to 50% chance of malignancy wihtin 5 years
120
Q

PAM management

A

Small lesions without nodules and vascularisation is monitored yearly.

Larger lesions of suspicion require excision. We want to get all the acquired melanotic lesions of the conjunctiva and reviewed by ophthalmologists

121
Q

Conjunctival papilloma

A

Proliferation of squamous epithelial cells in conjunctiva. The acquired benign tumours assoc. w HPV type 6 and 11 occuring in various locations.

122
Q

Conjunctival papilloma Characteristics

A

It is Sessile ( Rounder ) or pedunculated ( More bumpy ) morphology which is either uni/bilateral and found in juxtalimbal areas.

Symptoms depends on size and location and rarely undergoes malignancy

123
Q

Conjunctival Intraepithelial Neoplasia ( CIN )

A

Unregulated proliferation of atypical squamous epithelial cells in conjunctiva, most common ocular surface tumours

124
Q

CIN process

A

CIN –> Carcinoma in situ –> Squamous cell carcinoma

125
Q

CIN characteristics

A

Unilateral and slightly elevated within the interpalpebral fissure at the limbus. It is slow growing, where redness, FB sensation and mild irritation is seen in older white men.

126
Q

Subconjunctival Haemorrhage

A

The rupture of conjunctival blood vessels where blood accumulates between conjunctiva and episclera.

127
Q

How does subconjunctival haemorrhage occur

A

Mostly idiopathic, can be from surgery or trauma but liely from older ageS

128
Q

Subconjunctival haemorrhage symptoms

A

No pain but there is discharge and inflammation and it looks worse than it feels, there is spontaneous resolution in 1-2 weeks

129
Q

What is the outer tunic

A

Opaque, fibrous and protective outer layer of the eye that forms 5/6th of the connective tissue of the globe surface

130
Q

Anterior vs Posterior sclera

A

Anterior sclera becomes cornea at limbus

Posterior sclera fuses w optic nerve dural sheath

Thickness ranges form 0.3-1mm, thickest at posterior pole covered by fascial sheath

131
Q

What makes up the conjunctiva

A
  1. Episclera –> Loose and vascularised, connected to the tenons capsule
  2. Scleral Stroma –> Dense and fibrous collagen tissue that intermingles w networks of fine elastic fibres
  3. Lamina Fusca –> Innermost thin layer containing melanocytes that blends w the suprechoroid and supraciliary lamellae of the uveal tract
132
Q

Scleral Stroma Vascular Supply

A

It is Avascular so the blood comes from the episcleral vascular bed

  1. Superficial episcleral plexus that runs under the tenons capsule. The vessels are straight w radial configuration
  2. Deep episcleral plexus resting on superficial surface of sclera
133
Q

What overlies the anterior sclera also

A

Layers of conjunctival vessels

134
Q

What is episcleritis

A

Inflammation within Tenons blood vessels and episcleral

135
Q

Episcleritis classifications

A
  1. Simple episcleritis which is most common, can be sectoral or diffuse, and spontaneous resolution within weeks
  2. Nodular episcleritis that is tender with congested red nodules w localised injection. It lasts longer than simple episcleritis
135
Q

Episcleritis signs and symptoms

A

Idiopathic, unilateral affecting young to middle age adults. Ocular redness, discomfort, lacrimation also seen

136
Q

What is scleritis

A

Oedema and cellular infiltration of the entire thickness of the sclera.

Either infectious or non-infectious ( Most common )

137
Q

Who does scleritis affect more

A

Middle aged adults between 4-6th decade in life. More females affected non-infectioudly

Males affected infectiously

138
Q

Scleritis signs and symptoms

A

Acute or gradual onset of ocular redness and lacrimation, the ocular pain radiates to the forehead and interferes w sleep

VA reduced w photophobia

139
Q

Scleritis classification

A

based on anatomical sites of inflammation and its associated vascular changes

140
Q

Anterior scleritis

A

Either mostly non-necrotising or Necrotising w or w/o inflammation

141
Q

Anterior non-necrotising scleritis types

A
  1. Diffuse which is widespread vascular congestion and dilation assoc. w oedema. It resembles simple episcleritis, more in females in 5th life decade. Can recur
  2. Nodular which are local granulomatous inflammation that resemble nodular episcleritis. Nodules have deeper blue-red colour and tender to palpitation. Same age and concidence as diffuse. BUT 1/4 people get visual impairment
142
Q

Anterior necrotising scleritis types

A

With or Without inflammation

143
Q

Anterior necrotising scleritis with inflammation

A

Most severe and aggressive form of scleritis.

Goes from Distortion and occlusion of deep vascular plexus –> Scleral necrosis giving spread and coalesce w other necrotic areas –> Scleral thinning giving bluish tinge from increased visibility of underlying area

Onset is 60 Y/O, bilateral presentation and can result in loss of one eye. 25% mortality rate within 5 year onset.

144
Q

Anterior necrotising scleritis without inflammation

A

Goes from Necrotic yellow scleral plaques in uninflamed sclera –> Enlargement, spread, coalescence giving slow and progressive scleral thinning exposing underlying uvea –> Staphyloma formation occuring but perforation of globe rare

In women w longstanding rheumatoid arthritis, it is bilateral and painless w no effective treatment

145
Q

Posterior Scleritis

A

Scleritis primarily arising posterior to equator affecting women 2x more especially w those already w systemic disease. 85% get visual impairment

146
Q

Posterior scleritis presentation

A

Eyelid oedema, ptosis and diplopia. The fundus seen to have ONH swelling, mecular oedema, ERD and choroidal folds

It is bilateral in 35% cases

147
Q

Scleritis clinical examination

A

Record time, mode of onset, description of any associated ocular pain and discomfort and any underlying systemic issues

Slit lamp exam in daylight, diffuse lighting w ND filter and red free filter. Blanch w 1gtt phenylephrine 2.5%. Dilation performed to exclude posterior involvement

148
Q

What are the 3 lines of defence

A
  1. Barriers preventing infection
  2. General response to infection
  3. Immunity against specific pathogens
149
Q

What is the eyes 1st line of defence

A

The orbit, eyelid and blinking which stops microbe-cornea attachment

150
Q

What is the eyes 2nd and 3rd line of defence

A
  1. The vascularised conjunctiva ( B-cells and macrophages )
  2. Tears that contain plethora of antimicrobial molecules ( Lysozymes, Lactoferrin and transports WBCs )
151
Q

How does the eye being immune privileged affect its regeneration and immune response

A

Eye is evolved to limit inflammation, as it cant regenerate it preserves vision.

The privilege is due to lack of blood or lymph vessels in the eye, having the Blood retinal/aqueous barrier and immunosuppressive molecules

152
Q

What is Sympathetic ophthalmia and how does it occur

A

It is known as spared eye injury which is bilateral granulomatous uveitis

From injury to one eye causing intraocular inflammation meaning that the eye is no longer privileged as the eye is exposed to sequestered antigens to the adaptive immune response

153
Q

What happens in sympathetic ophthalmia

A

BE attacked by immune system via T4 HS which is T cell mediated. It manifests 5 days to several years form injury.

Untreated = Bilateral Blindness

154
Q

What does re-exposure to allergen do to the body

A

Each re-exposure to the allergen gives HS response that becomes faster and more severe each time

T1 HS is immediate or known as anaphylactic

T4 HS is delayed or cell-mediated via T cells

155
Q

What is the process of T1 HS and its time of onset

A

Onset within 30 mins of exposure, known as allergic reaction

  1. Sensitisation by allergen binding to IgE and then binding to mast cells and basophils
  2. Allergen re-exposure causes mast cell degranulation releasing inflammatory mediators

Plasma cells produce IgE

156
Q

What is Acute allergic conjunctivitis

A

Common T1 HS conjunctival reaction like pollen.

Either seasonal or perennial allergic conjunctivitis. And anaphylactic drug allergy

Hallmark is bilateral itchy eyes

157
Q

Acute allergic conjunctivitis Signs

A

Conjunctival injections, erythematous and oedematous lids, chemises and watery discharge

158
Q

What is the process and onset of T4 HS

A

Onset is 24-72 hours after allergen exposure such as poison ivy, Mantoux test and seen in transplant rejection

  1. Sensitisation by allergen that causes T-cell maturation
  2. Activation of mature T cells on re-exposure causing 2 responses either TH cells or cytotoxic T cells
159
Q

What is allergic contact dermatitis

A

Known as contact allergic blepharoconunctivitis which is non-infectious inflammation.

It is a T4 HS to eyedrops or cosmetics. Involvges skin like Eczematous dermatitis, periorbital oedema, erythema, skin lichenfication and peri-ocular itching w mucoid discharge

160
Q

What is Phylctenular Keratoconjunctivitis

A

T4 HS due to S.Aureus which is small pink-grey gelatinous nodules on the bulbar conjunctiva. It is composed of B cells and plasma cells.

Self resolves in 2-3 weeks and can extend into cornea

161
Q

What is Type 4b HS

A

A combination of T1 and T2 HS.

IgE and T cell mechanisms play a role where there is feedback cycle of chronic inflammation w elevated humoral response

162
Q

What is Vernal Keratoconjunctivitis ( VKC )

A

Severe ocular allergy that affects children and young adults where male is dominated

163
Q

VKC symptoms

A

Itchiness, lacrimation, photophobia and mucoid discharge

Worse in spring and summer so this is more seasonal than perennial

Has concomitant atopy like asthma

164
Q

What is Atopic Keratoconjunctivitis ( AKC )

A

Persistent and severe form on ocular allergies that develops in adult hood

165
Q

AKC symptoms

A

Like VKC but worse, this is more perennial than seasonal so this condition is worse in winte

166
Q

How is AKC presented

A

Atopic dermatitis and asthma. Also assoc. w sinal visual morbidity. AKC in tarsal conjunctiva seen as diffuse infiltration and scarring

167
Q

What is Giant papillary conjunctivitis

A

AKA mechanically induced papillary conjunctivitis. It is a Non-HS that has inflammation of the tarsal conjunctiva

168
Q

How is giant papillary conjunctivitis contracted

A

It is secondary to second CL wear, exposed sutures mucous fishing syndrome due to concurrent allergy that adheres w CLs and the surface of antigen foreign bodies

169
Q

Giant papillary conjunctivitis symptoms

A

Same symptoms such as VKC and AKC.

170
Q

T2 vs T3 vs T5 HS

A
  1. T2 is antibody mediated cytotoxicity
  2. T3 is immune complex mediated
  3. T5 is stimulatory
171
Q

What is associated with T2 HS

A

Auto-immune disorders and allergic reactions to blood transfusions and drugs via IgG/IgM which induces cell destruction

172
Q

T2 HS process

A
  1. Initial allergen contact w IgG/IgM produced by plasma cells that circulate around the body
  2. IgG/IgM - cell interactions such as phagocytosis, complement activation and ADCC
173
Q

What is Cicatricial pemphigoid

A

Known as Mucous membrane pemphigoid, it is chronic and sub-epithelial blistering autoimmune disease.

A T2 HS giving complement activation causing epidermic-dermis separation resulting in scars.

Occurs w older age w more females than males affected

174
Q

What is Ocular Cicatricial pemphigoid

A

Has non-specific symptoms of chronic bilateral conjunctivitis, also ask px about lesions on other body parts

175
Q

How is diagnosis of ocular cicatricial pemphigoid confirmed

A

With immunofluorescence of biopsy where IgG/A/M and C3 along basement membrane of conjunctival epithelium

176
Q

Stages of ocular cicatricial pemphigoid

A
  1. Early stage where conjunctivitis causes dry eye and papillary conjunctivitis
  2. Intermediate stages has forniceal shortening and the keratinisation of the caruncle
  3. End stage has severe conjunctival fibrosis and ankyloblepharon
177
Q

What is associated with T3 HS

A

Rheumatoid arthritis, serum sickness mediated by immune complexes which are antigen-antibody aggregations

178
Q

T3 HS process

A
  1. Antibody production from allergen contact causing immune complexes that circulate around the body
  2. Has Immune complexes that deposit in tissues which initiates immune cascade such as phagocytosis and complement activation

Larger immune complexes give higher risk of tissue damage

179
Q

What is Sjogren’s Syndrome

A

A T3 HS, systemic autoimmune disease affecting exocrine glands, can affect kidneys and the liver.

Affects women 9:1 in their 50s. This can be primary or secondary and assoc. w higher risk of malignant non-Hodgkin lymphoma

180
Q

Sjogren’s syndrome signs

A

Dry eye giving burning and FB sensation, crusting of eyelids and transient blurry vision. Can perform TBUT and phenol red threat test

Dry mouth with dry fissured tongue

Dry slim which is reduced sweating

Enlarged parotid gland seen

181
Q

What is T5 HS and its process

A

Mediated by antibodys.

  1. Antibody production on contact w allergen
  2. Antibody binding to cell surface activating cell function so it acts as agonist
182
Q

What does T5 HS ultimately do

A

Overstimulates cell function leading to cell destruction

183
Q

What is Grave’s disease

A

T5 HS, autoimmune disorder giving thyroid hormone overproduction resulting in hyperthyroidism. Triggered by AB production that reacts w TSH receptors

184
Q

Who does Grave’s disease affect and its signs

A

Women in their 50s

symptoms like unexplained weight loss, sweating palpitations and fatigue

30-50% of people w Grave’s disease have ophthalmopathy

185
Q

What is the TSH feedback loop

A

Pituitary gland produces TSH –> TSH binds to TSH receptor –> Stimulates hormone synthesis in thyroid cell –> Hormones produced bind to pituitary gland –> Regulates production of thyroid hormones in the pituitary gland

186
Q

What is Grave’s Ophthalmopathy

A

Thyroid eye disease ( TED ) is a common extra-thyroidal manifestation of Grave’s.

The TRAb reacts against TSH receptors on orbital fat and connective tissues

187
Q

What are the stages of Grave’s Ophthalmopathy and its signs

A
  1. Active inflammatory stage
  2. Fibrotic quiescent stage

Soft tissue will be inflamed where peri-orbital and lid swelling is seen w conjunctival hyperemia. Optic neuropathy also seen

188
Q

What are cataracts and its signs

A

Opacification to the lens where too much opacification leads to visual impairment

Cloudy and diminished lens is seen.

189
Q

What is used to evaluate cataracts

A

VA w std high contrast test

Px w cataracts also sensitive to glare

190
Q

How to assess cataracts

A

Via pupil dilation then performing direct opth, retinoscopy, slit lamp and photography for grading

191
Q

Treatments for cataracts

A
  1. IOL replacing cataract lens for treatment or couching which is an ancient technique.
    - ICCE ( Intra-capsular cataract extraction ) removes lens and surrounding capsule. IOL put in the anterior chamber
    - ECCE ( Extracapsular cataract extraction ) replaces ICCE where now the lens substance is removed w the posterior capsule left intact, the IOL here is placed in the posterior chamber
  2. Phacoemulsification which emulsifies by vibration and removed by suction, this is less invasive and has faster wound healing
192
Q

How is the lens transparent

A

Its avascular, no intracellular organelles, compact cortical fibre structure, RI matching in the nucleus and has microcirculation system transport

193
Q

How does the microcirculation system work

A

Active ion transport driving fluid fluxes, regulating cell volume, nutrient delivery, waste removal and maintaining RI gradient

194
Q

What are the cataract morphologies

A
  1. Anterior subcapsular ( ASC )
  2. Cortical
  3. Nuclear
  4. Posterior subcapsular ( PSC )
195
Q

Anterior sub-capsular ( ASC ) morphology

A

Opacity beneath anterior lens capsule, assoc. w fibrous metaplasia of lens epithelium due to injury to lens epithelium. This leads to formation of ASC fibrous plaques that wrinkles lens capsule and disrupts tissue order.

Least common location and due to ocular trauma

196
Q

Cortical opacity morphology

A

Involves anterior, posterior or equitorial cortex in inferonasal quadrant initially. Assoc. w biochemical changes to lens fibres giving fibre cell swelling from ionic imbalances

197
Q

What is the consequence of cortical opacities

A

Forms typical cuneiform or radial opacities which can progress to cortical liquefaction due to morgagnian globule formation from age and Diabetes.

Most common location but least visually significant

198
Q

What affect do cortical opacities have on the lens

A

Impairs regulation of fibre cell volume due to failed osmotic regulatory systems

Gives imbalance of in/outward water diffusion giving water accumulation, results in fibre cell swelling, water clefts and vacuoles showing a cuneiform and wedge shaped opacities.

Seen w retro illumination

199
Q

Nuclear opacity morphology

A

Seen in central lens from biochemical changes to lens fibres where modified crystallin proteins accumulate

200
Q

Nuclear opacity signs and symptoms

A

Yellow hue due to urochrome pigment deposition and gets brown when advanced. Age, UV and smoking are risk factors, it is also assoc. w myopic shift

201
Q

What is a major factor in getting nuclear opacities and how does it work

A

Oxidative stress due to light absorption by lens substance

Failed ROS scavenger system allows ROS to damage lens where GSH is main antioxidant so in nuclear cataracts the GSH is reduced

More ROS the more cross linking of lens crystallin proteins ( Protein aggregation ) giving refractive index mismatching and opacities

202
Q

Posterior Subcapsular ( PSC ) opacity morphology

A

In front of posterior lens capsule due to lens epithelial cell migration along the posterior capsule at the lens equator

203
Q

What does posterior subcapsular opacity do to the lens

A

Forms grainy PSC depositions. Diabetes and corticosteroid use increases the chance of this.

Even a little opacity will affect vision due to its density and location

204
Q

What is the WHO grading criteria for cataracts

A

NUC-1/2/3

  1. Cortical part more transparent than central part
  2. Even opacity throughout the lens
  3. Central worse than peripheral for opacity
205
Q

How is the grading for cataracts done

A

With retro illumination, we want to see if opacity has reached the central lens

Example : NUC-2 + Cen for grade 2 w central opacity

206
Q

What is LOCS III

A

Cataract grading system for research and is very detailed. Grading done w dilation to see the full cataracts

207
Q

Cataract etiology classification and its examples

A
  1. Acquired –> Senile, Traumatic, Toxic, Assoc. w systemic disease or Secondary
  2. Congenital –> Hereditary, Assoc. w syndromes and Intrauterine infection
208
Q

How does traumatic cataract affect people

A

Gives unilateral cataract in young people, 65% of ocular trauma gives cataract

209
Q

Types of traumatic cataracts

A

Penetrating, Blunt, Electric shock, Infrared radiation and Ionising radiation

210
Q

Penetrating Trauma

A

Sharp objects penetrates lens and lens capsule = Focal non-progressive opacities

211
Q

Blunt Trauma

A

Extreme force against the eye or face. The cataract takes days-years to develop. The Cataract is transient, static and progressive.

Rosette ASC/PSC opacity most common known as sunflower cataracts.

Concurrent Vossius ring may be present

212
Q

Electric Shock Trauma

A

Diffuse/milky-white opacity, Sometimes is snowflake-like opacities in stellate subcapsular distributionI

213
Q

Infrared radiation Trauma

A

IR exposure from heating glass or molten metal from an occupation aka glassblowers cataracts.

Opacities seen at any location and causes true exfoliation of anterior lens capsule

214
Q

Ionising radiation

A

High exposure to ionising radiation, generally PSC opacities seen so it takes months to years to manifest

215
Q

What is Toxic Cataracts

A

Associated w abuse of drugs or toxic substances

216
Q

Drugs that cause Toxic Cataracts

A
  1. Corticosteroids such as anti-inflammatory drugs like Prednisone. Only steroids w gluco-corticoid activity does this which gives PSC opacities. The duration and dose affects this
  2. Phenothiazines which are anti-psychotic medications. ASC deposits in stellate configuration. The opacities are Dose and duration dependent
  3. Amiodarone which is an anti-arrhythimic drug treating atrial fibrillation. Seen as punctate/yellow-white ASC opacities
217
Q

Causes of Systemic disease cataracts

A
  1. Diabetes mellitus
  2. Myotonic Dystrophy
  3. Atopic Dermatitis
218
Q

How does diabetes increase risk of cataracts

A

Cataracts that is 2-5x more common in DM px (Duration of DM and metabolic control). Adults have cortical/PSC opacities, children have snowflake like cortical opacities. This makes it difficult to assess the retina.

Osmotic stress from high glucose increases ROS which gives loss of lens fibres giving swelling and loss of cell volume regulation giving cataracts

219
Q

How does Myotonic dystrophy increase risk of cataracts

A

Multi-system disease of not being able to relax and muscle wasting. There is autosomal dominant inheritance where 1–% of the px get bilateral cataracts

220
Q

Myotonic dystrophy process

A

At 3rd decade the px will have fine iridescent cortical opacities known as christmas tree cataracts.

At 5th decade we will see cortical and PSC opacities and later on it will be hard to distinguish from typical cortical cataracts

221
Q

How does Atopic dermatitis increase risk of cataracts

A

Common form of chronic eczematous dermatitis ( T1 HS ). This is often bilateral and has shield like ASC plaque that wrinkles the anterior capsule

PSC opacities also common

222
Q

What is secondary cataracts

A

Cataract from other primary ocular diseases

223
Q

Causes of secondary cataracts

A
  1. Chronic anterior uveitis which is a common cause of secondary cataracts. Correlated to duration and severity inflammation and the corticoid steroid treatment. Gives ASC and PSC opacities
  2. Acute congestive angle closure
  3. Hereditary fundus dystrophies resulting in RP
224
Q

What are congenital cataracts

A

Present at birth but diagnosed later. Autosomal dominance inheritance giving chromosomal abnormalities, metabolic disorders and intrauterine infections. 2/3 cases are bilateral

225
Q

How to manage congenital cataracts

A

Find out the cause and determine visual significance. Should be surgically removed early if it is sight threatening otherwise is can lead to strabismus or amblyopia.

226
Q

What happens if congenital cataracts are not managed

A

Long term visual rehabilitation from aggressive ambylopia treatment, high powered glx or CLs or IOL implant when older.

227
Q

What is PXO ( Posterior capsular opacification )

A

A late complication of uncomplicated cataract surgery ( 25% cases ). The lens epithelial cells proliferate to re-colonise denuded regions of the anterior capsule and colonises previously cell-free posterior capsule.

228
Q

What is seen in PXO

A

Patterns of PCO such as vacuolated, fibrosis type, soemmering ring.

229
Q

How to treat PXO

A

Nd:YAG laser capsulotomy

OPTOM III (5 decks)

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