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OPTO3003 > MID SEMESTER EXAM > Flashcards

MID SEMESTER EXAM Flashcards

1
Q

Pathophysiology of emmetropisation:

A

Hyperopic defocus (not accommodated over) > decreases amplitude of neural response > altered signals pass RPE+Choroid > Scleral fibroblast gene expression altered > ECM remodelled > ^creep rate > elongation

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2
Q

Types of myopia:

A

Simple myopia: progresses 0.5D per year till 20 years
Pathologic myopia: excessive axial elongation > myopic maculopathy/ optic neuropathy
Pseudomyopia: over-reactive accommodation from ciliary spasm
Nocturnal myopia: poor visual cures > tonic accommodation > myopic blur (night driving)
Myopic shift secondary to cataracts

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2
Q

Theories for myopia development:

A

Dopamine: Decreased sun > poor activation of dopamine receptors in eye > myopic development
Hyperopic defocus: peripheral hyperopic defocus (accom lag / interior walls) > emmetropization process > axial elongation to resolve peripheral blur > foveal blur

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3
Q

Risk factors for myopia:

A

Genetic (7/20/40%) : Specific MYP genes or general emmetropisation/structure inheritance
Environmental (dopamine/peripheral blur) : time inside/study/education

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4
Q

Risk factors for myopia:

A

Genetic (7/20/40%) : Specific MYP genes or general emmetropisation/structure inheritance
Environmental (dopamine/peripheral blur) : time inside/study/education

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4
Q

Atropine myopia control:

A

0.05% daily (ATOM2/LAMP) muscarinic antagonist against sclera
Causes photophobia/blur/rebound, still needing glasses

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5
Q

OrthoK myopia control:

A

Steepens periphery/flatten centre via neg-pressure
ROMIO study > 50% reduction
Causes discomfort

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6
Q

Convergence process in accommodation:

A

Blur/disparity activates supraocular motor nuclei > innervating oculomotor nuclei > axons sent to medial longitudinal fasiculus > contraction of medial rectus via CN3 > convergence while accommodating

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6
Q

MF soft CL myopia control:

A

Plus power in periphery > hyperopic defocus correction
MiSight lenses have 55% reduction
Risk infection/requires compliance

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7
Q

Stellest myopia control:

A

Lenslets in peripheral lens reduces hyperopic defocus
Reduces myopic progression (in dioptres) by 50%
May be combined with atropine if significant progression
Very costly

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8
Q

Stable myopia control:

A

Specs
Soft CLs (daily-monthly)
RGPs
OrthoK
Laser(PRK/LASIK/SMILE)
Clear lens extraction

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8
Q

Hyperopia development:

A

Genetic factors causing poor emmetropisation, flat cornea, short axial length

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9
Q

Accommodation process:

A

Blur signal received by visual cortex > bilateral Edinger Westphal nuclei (CN3 oculomotor) in midbrain > preganglionic parasympathetic fibres move with CN3 to ciliary ganglion to synapse to postganglionic neurons > neurons travel with CNV1 ciliary nerves to ciliary muscle and pupillary sphincter muscle > activation of muscarinic receptors by Ach > contraction of ciliary muscle and sphincter muscle

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10
Q

Hyperopia and aging:

A

Latent becomes manifest as accommodation decreases. Noted increase in asthenopia (fatigue)
Commonly produces esophoria (sometimes tropia) > inward turn

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11
Q

Management of hyperopia:

A

Cyclopentolate > full hyperopia measurement
Education for small latent hyperopia
Specs for symptomatic (asthenopia/esophoria/strabismus/amblyopia/blur)

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12
Q

Lens anatomy:

A

Capsule: elastic membrane, binds zonules, molds lens
Epithelium: single layer cuboidal, equatorial mitosis, nutrient transport, secretes capsule
Fibers: formed from epithelia, contains crystallins a/b/y (soluble proteins with RI)

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13
Q

Mechanisms of cataract formation:

A

1: Cell proliferation/differentiation disruption (Growth factors)
2: Metabolic disturbance/osmotic regulation (Na/Ca)
3: Calpains
4: Post-translational modification (lens proteins)
5: Oxidative damage
6: Loss of defense mechanisms

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13
Q

Patho of cortical cataract:

A

Mechanisms 2/3
Dysfunctional Na/K from damage > NA/K homeostasis loss > Ca/Na influx > overhydration/ calpain activation
Crystallin proteolysis > soluble protein decrease (relative insoluble increase) > ray-like space opacify

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14
Q

Patho of nuclear cataracts:

A

Mechanisms 1-6
PTM glycation of tryptophan cause fluorescent chromophore
Cortex-nucleus barrier to glutathione

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14
Q

Patho of PSC:

A

Mechanism 1
DM / Cort. / age > Change in GF expression (FGF) > aberrant epith. Proliferation at germinative zone
Dysfunctional cells collate with adjacent fibers forming balloon cells
Poor Na/K atpase transport > swelling > vacuoles / extracellular granular material

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15
Q

Nuclear cataract effect on vision:

A

Myopic shift (protein aggregation)
Decreased VA/contrast sense
Tritan defect (blue blocked by yellowing additive PTM)

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16
Q

PSC effect on vision:

A

Decreased VA/contrast sense
Worse in day/near
Vacuoles in flux

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16
Q

Cortical cataract effect on vision:

A

Decreased contrast sense
Astigmatism (localised RI change)
Worse in night

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17
Q

Complications of cataracts surgery:

A

Post. Capsule opacity (PCO) 50% by 2y: proliferation/migration of remaining lens epith.
Dislocated IOL
Retinal tear
Endophthalmitis
Risk increased with DM/high myopes

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17
Q

Other types of cataracts:

A

Congenital (blue dot)
Trauma (Rosette)
Metabolic (myotonic dyst. > Christmas)
Disease (Uveitis > PSC)
Toxic (cort. > modified Na/K)

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18
Q

Aqueous layer formation:

A

97% of film from lacrimal gland (95%) / Krause & Wolfring
From inner/upper lid

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18
Q

Lipid layer:

A

Thin outer meibum layer from sebaceous glands in tarsal plate (Meibomian glands) secreted during blink
Prevent evapouration, acts as surfactant (spreads film)
Non-polar cholesterol, esters, phospholipids, alcohols

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18
Q

Aqueous layer Components:

A

Water, electrolytes, proteins, growth factors, pro-inflammatory interleukin cytokines (accumulate during sleep), Lysozyme, lactoferrin, urea, glucose, ions (Ca/Mg/Na/K), IgA

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18
Q

Aqueous layer function:

A

O2 > Cornea
IgA / Lactoferrin / Lysozyme > Antimicrobial activity
Maintain moisture of non-keratinized corneal epith.
Leukocyte transport after injury
Smoothens optical surface
Flushes debris

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19
Q

Types of mucins:

A

MUC1/4/16: membrane bound, with galectin glue to glycolax
MUC7 / MUC5AC: secretory to prevent strands of mucous (light scatter)

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19
Q

Mucin layer composition

A

Thinnest layer of mucus from goblet cells in conj. / plica semilunaris / glands of henle & Manz
Hydrophilic High mol. Wgt. Mucin glycoproteins (transmembrane or secretory)
Transmembrane mucins bind glycolax from corneal epith.
Secretory are soluble in aqueous forming gel

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20
Q

Mucin layer function

A

Turns hydrophobic corneal epith. Hydrophilic > corneal wetting
Attaches film to cornea, allows lubrication

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21
Q

Definition of dry eye disease (DEWS 2):

A

Dry eye is a multifactorial disease of the ocular surface characterized by a loss of homeostasis of the tear film, and accompanied by ocular symptoms, in which tear film instability and hyperosmolarity, ocular surface inflammation and damage, and neurosensory abnormalities play etiological roles

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22
Q

Causes of ADDE:

A

Sjrogren’s syndrome (autoimmune against exocrine glands)
Lacrimal gland dysfunction: Primary (age/genetics) or secondary (AIDS/Lymphoma)
Lacrimal gland duct obstruction
Alteration in stimulation (reflex block)

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23
Q

Causes of EDE:

A

Lid dysfunction:
MGD, poor closure, poor blink rate, damaged
Surface dysfunction:
Cls, lesions, Vit A def., allergy/infection

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24
Q

ADDE from secretion stimulation alteration:

A

Reflex hyposecretion from reflex sensory block (CLs/LASIK/herpes/diabetes) or reflex motor block (CN 7 lesion)
Blockage of para/sympathetic nerves to lacrimal gland
Decreased androgen from hormone loss (age)
Exposure to anti depressants/histamines/birth control

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25
Q

hyperosmolarity

A

Loss of aqueous or evaporation > hyperosmolarity > epithelial irritation > Mitogen-activated protein kinase (MAPK) & NFkB activation > inflammatory mediator release (IL-1 & TNF-1/MMPs) > Matrix metalloproteinases damage epithelium / goblet cells > epitheliopathy (corneal epithelium loss) > pain > reflex stimulation

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26
Q

DEWS step 1:

A

Education (condition, diet)
Environment change
Eliminated offending medication
Lubricant (lipid drops of MGD)
Lid hygiene/warm compress

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27
Q

DEWS step 2:

A

Non pres lubricants
TT oil for demodex
Punctal occlusion
Over night ointment
Chlorsig for bleph

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28
Q

Blepharitis:

A

Lid inflammation from Staphyloccal or dermatitis
Ant. Affects zeis glands/lash follicles (crusty scales) > bleph debris decreases tear quality
Pos. affects meibomian glands (meibum capping) > EDE + inflammatory mediator passage from lid

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28
Q

Schirmer test:

A

5mm fold in Whatman filter inserted under lower lid (temporal side), don’t touch cornea/lash
Px closes eyes over filter
Remove paper after 5min
<10mm without anesthesia / <6 with ana. Indicates abnormal

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29
Q

TFBUT:

A

NaFl instilled with Wratten #12 cobalt filter lens
Px blinks before holding eyes open
Timed appearance of black spots
<10s abnormal, repeated breakup in given area indicates localized surface abnormality

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30
Q

Non neoplasic lesions of the lids:

A

Hordeolum
Chalazion
Cyst of zeiss/moll
Epidermal inclusion cyst
Dermoid
Xanthelasma
Molluscum contagiosum

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31
Q

Benign lid lesions:

A

Verruca vulgaris
SC/BC papilloma
Actinic keratosis
Freckle
Naevi
Cap. Hemangioma
Port-wine stain
Pyogenic granuloma
Neurofibroma

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31
Q

Malignant lid lesions

A

BCC
SCC
SGC
Malignant melanoma

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32
Q

Lid BCC patho:

A

UV on pluripotent stem cells > tumor mutations > unregulated proliferation of abnormal basal cells
Patched mutations / Sonic hedgehog pathway: altered “patched/smoothend” genes > sonic signalling pathway upregulation > ^activation of genes for cell differentiation
Mutations in detox proteins: altered genes for glutathione-S-peroxidase enzyme > decreased skin oxidation defence
Mutation in p53 ts gene > unregulated abnormal cell growth (noted in 50%)

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33
Q

BCC signs/symptoms and treatment:

A

Superficial: red patch, may crust/sting
Nodular: pearly/translucent bump
Sclerosing: white scar area
Biopsy > +/- Moh’s

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34
Q

SCC patho:

A

UV > proliferation (^mutation) / gene alteration / immunosupression > p53 / melanocortin-1 receptor gene alteration > Immunosuppression, unregulated proliferation of squamous epith., decreased apoptosis

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34
Q

SCC signs/symptoms and treatment

A

Initial erythematous tender red nodule w/hyper keratosis
Develops with ulceration and expansion
Requires cryo + biopsy (solar keratosis)
+/- Moh’s for remaining lesion

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35
Q

Benign conjuntival lesions:

A

Pingueculu/pterygium
Psuedopterygium
Inclusion cyst/dermoid
Papilloma
Actinic keratosis
Cap. Hemangioma
Conj. Naevus
Racial melanosis
Ocular melanocytosis

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35
Q

OSSN patho:

A

HPV/UV > squamous proliferation > CIN (partial replacement) > SCC (dysplastic cells pass basement into stroma)

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36
Q

Conjuntival naevus:

A

Clustered melanocytes in basal epith. From UV/genetics
Solidary raised pigmented lesion, can develop with age
Usually asymptomatic, photography monitored for <1% malignant transformation

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37
Q

Malignant conj. Lesions:

A

OSSN
PAM
Conj. Melanoma

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38
Q

OSSN presentation:

A

Leukoplakic: localised thickening with white plaque
Papilomatous: highly vascular mass w/ corkscrew BV
Gelatenous: transparent thickening of squamous epith.

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38
Q

Parasympathetic pupil pathway:

A

Edinger Westphal > with CN3 (accommodative axons) > cavernous sinus > synapse at ciliary ganglion > with short ciliary via subarachnoid space > iris sphincter > bilateral / equal constriction

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38
Q

Afferent pupil pathway:

A

Retinal light input > Ganglion cell axions > optic tract > split at chiasm > split before LGN > sup. Colliculus > synapse with olivary pretectal nucleus.
Afferent (retina) / efferent (light reflex) integrated > ipsi/contralateral EW nuclei of CN3

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39
Q

Sympathetic pupil pathway:

A

1st neuron: hypothalamus > ciliospinal Centre of bulge and Waller (C8/T2)
2nd: preganglionic fibers pass stellate ganglion (lung apex) > sup. Cervical gang. (jaw)
3rd: postganglionic fibers plexus with carotid > cavernous sinus > SO fiss. With nasociliary of CN5 > long ciliary in suprachoroidal space > dilatory > mydriasis
Also innervate mullers. facial innervation splits before sup. Cervical G.

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39
Q

PERRLA examination (first test):

A

Pupils Equal Round Reactive to Light (direct/consensual) and Accommodative
1. Direct response: light activates ipsilateral EW (afferent) > ipsilateral pupil constriction (efferent)
2. Consensual: light activates ipsilateral EW > contralateral EW activation > contraction
Accommodative: Near response triad > visual cortex / pupillomotor Centre in midbrain response

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39
Q

Signs of choroidal naevus developing to malignant melanoma:

A

Documented growth
Blur, metamorphopsia, VF loss, photopsia
>5mm diameter, >1mm deep
Presence of orange lipofuscin
Located near OD
Associated serous RD

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40
Q

Causes of anisocoria:

A

Efferent pupil pathway dysfunction:
Physiological (EW asymmetric inhibition)
CN3 palsy
Adies tonic
Aberrant regen (CN3p / adies)
Pharmacological
Pupil damage (trauma/Sx)
AAGC

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40
Q

Horners syndrome symptoms:

A

Disruption of sympathetic innervation to pupil dilator / mullers / ciliary body / facial sweat glands.
Causes Miosis / partial ptosis (1mm) / anhidrosis (not 3rd order) / accommodative excess / Conj. BV dilation
Congenital cases > Lighter/Darker Brown/Blue eyes

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41
Q

RAPD examination (second test):

A

Swinging flash test for Relative Afferent Pupil Defect.
No RAPD: equal constriction W/O radiation excluding Hippus
Mild: affected pupil constricts and redilates
Moderate: affected pupil does not change, then dilates
Severe: immediate dilation of affected pupil

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42
Q

CN3 palsy symptoms:

A

Mydriasis: Pia BV compression > pupillomotor fiber ischemia
Full ptosis: sup. Levator innervation loss
Down/out turn: Sup/Inf/medial rectus, inf. Oblique innervation loss
Thunderclap headaches

42
Q

Causes of CN3 palsy:

A

Pupil involving: compressive lesion/aneurysm on pia BV for parasym. fibers
Pupil sparing: DM/HT > main trunk ischemia
* Giant cell arteritis (temple pain) / Pos. communicating artery aneurysm / cavernous fistula common
Myasthenia gravis imitates pupil sparing palsy

43
Q

Common causes of horners syndrome:

A

1st : brainstem/spinal disease (vascular/tumor), diabetic neuropathy
2nd: Pancoast tumor, carotid/aortic aneurysm, neck lesion
3rd: carotid aneurysm, cavernous sinus mass, cluster headaches

44
Q

Common pharmacologic mydriasis/miosis:

A

Tropicamide: Muscarinic antagonists > Ach receptor block > sphincter paralysis
Phenylephrine: adrenergic 1 agonist
Pilocarpine: muscarinic agonist > Ach receptor upregulation > miosis
Apraclondine: Alpha agonist > dilation (weak a1, strong a2)
Tamulosin: Alpha antagonist > adrenaline receptor block > dilator paralysis

44
Q

Types of ptosis:

A

Myogenic (MG, simple congenital, blepharophimosis)
Neurogenic (CN3, horner, marcus gunn)
Mechanical
Aponeurotic (LPS disinsertion)
Pseudooptosis

44
Q

Assessing anisocoria greater in light:

A

Greater in light > parasym. Loss > CN3 palsy / adies
0.1% pilocarpine > great constriction of affect pupil in early adies (<2w) from Ach upregulation
1% pilocarpine > constriction of CN3 palsy
Faliure to constrict > pharmacological/atrophic mydriasis

44
Q

Measuring ptosis:

A

Margin reflex distance: 4mm from corneal reflex and upper lid
Palpebral fissure: difference between eyes: 2/3/4mm mild/moderate/severe
Levator function: pressure brow, measure upper lid change from downgaze and upgaze (15mm normal)
Upper lid crease: distance between lid margin and crease in downgaze (8mm normal)

45
Q

Assessing anisocoria greater in dark:

A

Greater in dark > sym. Loss > horners/aberrant regen (CN3/adies)
0.5% apreclonidine > pupil dilation of affected eye. Requires 1w post onset for a1 upregulation
1% hydroxyamphetamine > dilation of affected eye if 1/2 order neuron lesion (release of 3rd neuron noradrenaline)

46
Q

Myasthenia gravis:

A

Autoimmune disorder > auto antibodies against Ach receptors of striated muscle > weakness
Causes limb weakness, lack of expression, ptosis +_ diplopia worsening over the day.
Tested via 1minute upgaze, or ice pack for 2m (improves neurotransmission)

47
Q

Functions of the conjunctiva:

A

Connect lids to eye (enclosed sac)
Mucin/aqueous production
Immune function (Macrophages, langerhans cells)
Mediates passive/active immunity

47
Q

DDX red eye:

A

CL related: CLARE/CLPU/GPC/Tight lens syndrome/DED
Corneal defect: Keratitis/abrasion/erosion/FB
AC disease: Uveitis/AACG
Wall inflammation: Scleritis/episcleritis/conjuntivitis
Orbital cellulitis/sub. Conj. Heam.

48
Q

Structure of conjunctiva:

A

Epithelium: columnar W/ goblet apocrine glands and langerhan immune cells
Substantia propria: lymphoid layer (neutrophil/mast/Tcells) and fibrous layer (BV/nerves)

49
Q

Types of allergic conjunctivitis:

A

SAC/PAC
Atopic
Vernal
GPC

49
Q

Signs of conj. Inflammation:

A

Hyperaemia: from prostglandin release
Oedema: serous leakage from BV tight jun. via prost. release
Membranes: pseudo/true
Cicatrisation: scarring
Follicles/papillae

49
Q

Follicles and papillae:

A

F (viral/toxic): lymphocyte hyperplasia at fornix/tarsal > grey (macrophage) masses
P (bac./allergic): epith. Hyperplasia w/ infiltrate mast cells/eosinophils/fibroblasts > tarsal vascular cobblestones

50
Q

Types of infectious conjuntivitis:

A

Bacterial (hyper-/acute/chronic)
Adenoviral (follicular/PCF/EKC)
HSV
Chlamydial (adult inclusion/trachoma)
Fungal / parasitic / protozoan
Neonatorum

51
Q

Actue bacterial conjuntivitis

A

Gram+: Staph/strep aureus/pneumoniae
Gram-: haemophilus
Burning, mucopurulent, diffuse hyperemia, papillae
Associted fever/respiratory infection
Self limiting 3w, chlorsig .5% qid 1w reduce symptoms

51
Q

Types of discharge in conjunctivitis:

A

Watery (viral/acute allergic): serous exudate / tears
Mucoid (chronic allergic / DED): mucoid from inflamed goblet cell
Mucopurulent (chlamydial / bacterial): mucoid and pus (leukocytes)
Purulent (gonococcal): pus

51
Q

Adenoviral conjuntivitis:

A

FAC/PCF/EKC
Epiphoria, hyperemia, ocular discomfort
Follicles
Superficial punctiate keratitis
Lid oedema
Preauricular lymph adenopathy
Associated URTI

51
Q

Types of non-infectious conjunctivitis:

A

Toxic follicular
Molluscum contagiosum
Stevens-johnson syndrome
Graft vs. host disease
Ocular cicatrical pemphigoid
Sup. Limbic kerato-

51
Q

EKC management:

A

Self limiting 1-3w.
Practice good hand hygiene
Cold compress / lubricants (comfort)
Topical cortico. (flarex 0.1% qid) for corneal subepithelial infiltrates

52
Q

Herpes simplex conjuntivitis

A

Common HSV-1 (ocular) initial infection (<5yo).
Irritation, Watery, follicles, preauricular lymphadenopathy, HSV vessicles (lids),
Dendritic ulcer
Self-limiting 1-2w
Corneal involvement > acyclovir 3% 5/d 1w
No steroids

53
Q

Acute inclusion conjuntivitis:

A

Chlamydia trachomatis bacteria serotye D-K (1-2w incubation)
Unilateral hyperemia, watery, purulent
Large follicles w/papillary hypertrophy (tarsal conj.) > pannus
Swolen preauricular lymph
Rare SPEE/stromal infiltrate/limbal swelling
GP systemic azithromysin 1g.

54
Q

Trachoma cause/symptoms:

A

C.trachomatis bacteria serotype A/B/C
Initial infection (1w incubation) > mild mucopurulent conjuntivitis
Recurrent infection > active chronic inflammation
Late stage > inactive inflammation

54
Q

Trachoma active inflammation:

A

Irritation, DED, blur
Follicles w/papillary hypertrophy > pannus
Thickening of tarsal conj.
SPEE, limbal follicles

54
Q

Trachoma treatment:

A

Initial infection > self limiting
Recurrent > single dose of azithromycin 20mg/kg up to 1g

54
Q

Molluscum contagiosum conjuntivitis:

A

Poxvirus nodules containing intracytoplasmic inclusions toxic to conj.
Common 2-4yo
Lid umbilated nodules
Conj. Hyperemia, follicles, mucoid
Self limiting 3-12m, lid nodule excision if needed

54
Q

Trachoma inactive inflammation:

A

Cicatrical fibrosis of conj. > entropion > corneal scarring
Fibrosis/fusion of conj. > symblepharon
Tarsal scarring > white lines (arlt’s line)
DED from meibomian/goblet loss

55
Q

VKC patho:

A

Severe in spring, males under 20 w/atopy
Exposure to allergen (pollent/dust) > type 1 HS reaction w/T-cell activation > IgE binding > mast cell degranulation > histamine/prostglandin release > itch/pain and BV dilation
Profuse burning, ropey mucous, itching
Dissuse papillary hypertrophy w/mucous deposits
+/- tarantas dots, corneal pannus/SPEE, sheild ulcer

55
Q

SAC/PAC patho:

A

Seasonal/year long exposure to allergen (pollen) > type 1 immediate HS reaction > allergen binds IgE on mast cells > degranulation > histamine/prostglandin release > itch/pain and BV dilation
Causes hyperemia, tearing, mucoid discharge, lid oedema, chemosis, papillary response
Associated nasal symptoms

56
Q

AKC patho:

A

Rare, atopy related, >20y, resolves by 50
Allergen exposure > type 1 / 4 HS reaction > activation/infiltration of T cells > severe chronic inflammation
Severe itching, mucoid, hyperemia, chemosis, macerated lids, narrow fissure, chronic bleph., papillae
+/- cicatration > symblpharon, SPEE > erosions

56
Q

Ocular defences:

A

Lids: physical/flushing
Tear film: IgG/A, lactoferrin, lysozyme
Cornea epith.: immunoglobins (IgG/A) defer microbe adhesion
Mucin: trap microbes
Innate immune: complement protein system
Tight junctions: prevent passage

57
Q

GPC patho:

A

Allergic/mechanical reaction, associated atopy / CLs
Primary: type 1 HS reaction to alleregens
Secondary: environmental antigens adhere to mucus/proteins on CLs > repeated contact w/tarsal conj. On blink
Irritation, itching, hyperemia, Papillae, mucous
+/- debris on CLs, loss of CL tolerance (symptoms worsen after CL removal)

57
Q

Allergic conjuntivitis treatment:

A
  1. OTC vasoconstrictor: oxymetazoline 20mg/spray
    1. Histamine antagonist Levocabastine HCl 0.05%
    2. Mast cell stabilisers lodoxamide 0.1%
    3. Combined (2/3) Ketotifen Fumarate 0.025% (Zaditen)
    4. NSAIDs ketorolac 0.5%
      Cool compress, shower before bed, avoid allergen
58
Q

Process of microbial keratitis:

A

Loss of defence (glycolax loss) > breach in integrity allowing microbial colonisation (usually staph)
Antigen-antibody immune reaction > immune cell influx (neuto/macro) > stromal infiltrate
Stromal collagen degraded via microbial Enzymes (proteases) > thinning/scarring
Damage continues until microbe is removed

58
Q

CL risk of keratitis:

A

1/proportional to Dk/t value
Least with RGP lenses
From hypoxia > bacterial/epithelial adhesion
CL related lesions (CLARE/CLPU) > epith. Break > microbial vulnerability
Usually gram- psuedomonas aeruginosa

59
Q

Risk factors for keratitis:

A

CLs
Sx/trauma
DED/bleph
Co-infection (acanthamoeba/HSV)
Blink dysfunction
Immunosuppression
Immune loss (DM/malnutrition)

60
Q

Signs of keratitis:

A

BV dilation (prostglandins)
Corneal oedema (prostaglandins)
Discharge: water/mucopurulent > CNV activation/bacteria
Pain (severe/increasing)
Epith. Defect (microbe induced apoptosis/immune infiltrates)
AC reaction (Low IOP from low ciliary secretion, or high IOP from trabecular block)

60
Q

Bacterial keratitis symptoms:

A

Pain severe/increasing
Soggy infiltrate, centrally
Hyperemia, oedema, mucopurulent
+/- Ac reaction (low IOP, hypopyon)

60
Q

Fungal keratitis symptoms:

A

Pain gradual onset
Hyperemia, photophobia, mucopurulent (bac superin.)
Filamentuous: feathery
Yeast ligh: button

61
Q

Acanthamoeba keratitis symptoms:

A

Following days of incubation.
Early stage:
FBS, blur, photophobia, signigicant pain (radial keratoneuritis), epiphora, epith. Hazy
Late stage (weeks): stromal “wessely” infiltrates, extreme pain, hyperemia

61
Q

Acanthamoeba patho:

A

Corneal epith. irritation > mannose glycoprotein upregulation > Acan. trophozoites adhere via acanthapodia > protease MIP133 release > epith. Cytolysis > stromal invasion / degregation
Immune neutro/macro. Influx > immune proteases > ring infiltrates
Acan. Cluster nerves > immune/anti-microbial response > form dormant cysts

62
Q

Fungal keratitis patho:

A

Ahesion following epith. Dysfunction > proteolytic enzyme release > epith. Necrosis > stromal collagen dissolution
^size > poor neutophil phagocytosis
Usually present with bacterial co-infection

62
Q

Acanthamoeba keratitis risks:

A

Present in water sources
Poor CL use > biofilm build up
Secondary to damage/HSV

62
Q

Symptoms of HSK:

A

Hx prior HSK
FBS, photophobia, epiphora, blur, hyperemia
desensitization
Dendritic lesion
IOP increase (trabeculitis)
Lid HSV vessicles

63
Q

Acanthamoeba treatment:

A

Cease CLs and see ophthal.
Cocktail of polyhexamethylene biguanide (PHMB) with Hexamidine 0.1% and Neomycin tapered from hourly>quaterly from 2-6 months

63
Q

Management of bacterial keratitis:

A

Fluoroquinolone mono w/ciprofloxacin 0.3%
Q10m for first hour > qhour for 24h > review > qhour for 24h > q2hour
Unresponsive/complex needs referal

63
Q

Fungal keratitis treatment:

A

Ophthal referal
Topical natamycin 5% per 1/2hour for 24h then qid for months
Paired BS antibiotics prevent co-infection
Cycloplegic for ciliary spasm
Never steroids (increase fungal replication)

64
Q

CL complications:

A

Hypoxia
Neovasc
CL asso. DE
3-9 stain
Sup. Epith. Arcuate lesions (SEALs)
Tight lens syndrome
Toxic/allergic keratoconjuntivitis
CL asso. GPC
CL asso. Acute red eye (CLARE)
Culture neg. Periph. Ulcer (CNPU/CLPU)
Microbial keratitis

64
Q

CL corneal hypoxia:

A

Low Dk/t CLs, sleeping
Hypoxia > anaerobic respiration > ^LA (low pH)/ATP loss > pump dysfunction > oedema
Causes blur, pain, photophobia, tearing, corneal haze, stromal thickening
Requires CL ceassation, lubrication, refit higher Dk/t lenses

65
Q

CL corneal neovasc

A

Extended wear of low Dk/t lenses, sleeping
Hypoxia > conj. Vessel growth
Visual extension of conj. Vessels
Requires refit of Cl with hight Dk/t
Switch to daily lenses

65
Q

CL associated dry eye:

A

CLs split tear film / absorb moisture > Tear instability
Causes FBF, tearing, burning, worse at end of day
Requires lubricants, lens change/cessation

66
Q

3/9 oclock staining of CLs

A

Mechanical abrasion of RGP on limbus, abnormal blink
Causes intolerance, gritty, punctate epith. Loss at 3/9
Requires education on light blinking, lubricants, refit

67
Q

Tight lens syndrome:

A

Tightnening of CL during wear
Causes pain, photophobia, blur, hyperemia, satining limbus
Requires cessation, lubricants, prophylactic antibiotic (epith. Break)

67
Q

Toxic/allergic CL conjuntivitis:

A

Acute chemical toxicity from peroxide solution / preservatives in solution > type 1 HS or type 4 (long term)
Causes acute pain on insertion, hyperemia/chemosis, diffuse epithelial punctate stain w/ scattered infiltrates
Requires cessation, non-pres lubricants

68
Q

CL associated GPC patho:

A

Allergic type 1/4 of tarsal conj. To antigens coating CL, or mechanical abrasion on blink > activation of mast/eosinophil/basophil > ^ cytokine/GF > fibroblast stimulation > Collagen production > Papillae

69
Q

CL associated GPC signs and management:

A

Irritation, hyperaemia, CL intolerance (worsens without wear), papillae on sup/inf tarsal conj. Mucous
Requires cessation (1mo), change cleaning regieme

69
Q

CL associated acute red eye (CLARE)

A

Sterile inflammation via colonisation of gram- psudomonas
Microbe adhereance > exotoxin release > antigen antibody response > inflammatory cascade > immune influc > infiltrates / hyperemia
Causes severe pain, photophobia, epiphoria, subepithelial infiltrates, SPEE
* No mucopurulent discharge
Requires cessation (days)

69
Q

CL associated microbial keratitis:

A

CL wear > microtrauma / O2 disruption / CL colonisation > (if glycocalax breached) microbe colonises cornea > stromal collagen degraded via enzymes

69
Q

Culture negative peripheral ulcer:

A

Sterial inflammation from gram + staph
Adherence > exotoxin release > Microbe adhereance > exotoxin release > antigen antibody response > inflammatory cascade > immune influc > infiltrates / hyperemia
Causes severe pain, photophobia, epiphoria, subepithelial infiltrates, SPEE
Infiltrates larger than epithelial defects, unlike microbial keratitis
+/- AC reaction
Requires cessation (days)

70
Q

Distinguish CPLU and MK:

A

PEDALS
Pain: severe, increasing
Epithelial defect: boggy (oedema) / pesudodendrites (acan)
Discharge: mucopurulent in MK
AC reaction:
Location: central ulcers are infective
Size: defects > 2mm infections

70
Q

HSV/VSV structure:

A

dsDNA
Icosahedral capsid
Viral glycoproteins on envelope

71
Q

Initial HSV infection:

A

Direct via secretions (cold sores) > epith. Replication > primary manifestation > blepharokeratoconjuntivitis > retrograde transport to trigeminal ganglion

71
Q

Causes of HSV reactivation:

A

UV (induced immunosuppression)
Trauma
CLs
Stress

72
Q

VZV initial infection:

A

Chickenpox
Rash, fever, malaise, pneumonia
Traves to dorsal root/CN sensory ganglia (retrograde)
Lies dormant

72
Q

Herpes Zoster reactivation:

A

Loss of cell mediated immunity against virus (stress/age) > Shingles
Causes prodromal malaise, fever, fatigue, painful rash
HZO when virus travels opthalmic branch of CNV

73
Q

Clinical presentation of HZO:

A

Lid vessicles/edema/inflammation
Conjuntivitis w/ papillae/follicles/membranes
Epi/scleritis
Keratitis
Epitheliopathy (pseudo-dend.)
Uveitis
Optic neuritis
Post-herpetic neuralgia

73
Q

HSK Geographic ulcer:

A

Immunocompromised Px enlarged ulcer. Larger risk of co-infection
3% aciclovir ointment 5/d until re-epith.
Lissamine stains only periphery

74
Q

HSK dendritic ulcer:

A

Epithelial ulcer w/ stromal oedema, desensitisation, ^IOP
Limbal ulcer > ant. Stromal infil. (white BC)
Photophobia, slight hyperemia
Self limiting (3w), can be anaesthetised and debrided
3% aciclovir 5/d for 2w

74
Q

Metaherpetic ulcer:

A

Poor healing of geo. Ulcer
Lissamine stains central ulcer
Requires refferal

75
Q

Neurotrophic ulcer:

A

Spontaneous breakdown of epith. Secondary to nerve damage > poor GF delivery
From HSK, HZO, LASIK, DM
Appears as enlarged SPEE covering several layers of epith.
Requires topical lubricants per 2h w/ opthal refferal

76
Q

HSK stroma affliction:

A

Antibody cascade against inactive viral antigens
Nummular infiltrates, oedema, diffuse/focal opacity
Leads to stromal thinning, scarring, opacification, ghost vessels

77
Q

HSK necrotising keratitis:

A

Immune reaction to live viral particles in stroma
Neutrophil/macrophage influx > viral removal via proteolytic enzymes > stromal loss
Dense infiltrates, oedema, necrosis/melting/thinning

77
Q

Endothelial HSK:

A

Inactive viral antigens in endo. Post initial manifestation
Keratic precipitates, stromal oedema, ant. Chamber reaction/flare
Stromal white wessely ring > light haloes

78
Q

HSK keratouveitis:

A

Deeper infection leading to trabeculitis (^IOP), glaucoma, cataract
Noted endo. Precipitates, stromal oedema, descemets folds, synechiae, moth eaten iris atrophy
Requires refferal for cortico. Treatment

79
Q

Herpes zoster epithelial keratitis:

A

epith. Damage via invasion/replication/cell lysis
Initial punctate epith. Keratitis (several lesions of live virus)
Forms pseudo-dendrites (5d)
Requires 800mg acyclovir 1w

80
Q

Nummular stromal keratitis from HZO:

A

Antigen-antibody response > stromal neutrophil/macrophages
Several granular infiltrates, usually under epith. Ulcers
Requires FML qid w/ acyclovir 3%

80
Q

Corneal epithelium basement layer:

A

Collagen, proteoglycans
2 layers: ant. Lamina lucida attaches to basal epith. Via hemidesmosomes. Posteria lamina dens w/ anchoring fibrils of collagen to plaques in bowmans/stroma

81
Q

HZO keratouveitis:

A

T-cell mediated response in uvea
Causes blur (spasm)
Ant. Chamber flare/cells, iris synechaie, corneal oedema, trabeculitis (or blockage from white BC), iris atrophy
Requires pred-forte 1% per 2h, w/homatropine 2% (reduce spasm pain)

81
Q

Post-herpetic neuralga

A

50% by 70y
Inflammation/damage of sensory nerves from viral reactivation > dysfunction of unmylenated nociceptors
Light hypersensitivity via mechanical nociceptor stimulation > severe pain (allodynia)
Sporadic pain w/o stimulation
Zostarvax vaccine is in the works

81
Q

Corneal epithelium structure:

A

55um with 10 stratified layers at limbus and 5 over cornea
Superficial layer of non-keratinised squamous cells
Middle layers of polygonal wing cells
Basal layer of columnar cells attached to basement
Tight junctions/ desmosomes/ gap junctions laterally

81
Q

Herpes zoster disciform stromal keratitis:

A

Late stage (1mo) from type 1 and 4 hypersensitivity > upregulated immune response
Inflammation of stroma (full depth), immune ring
Limbal vascular keratitis > ^IOP
Requires pred-forte 1% per 2h (opthal)

82
Q

Bowmans membrane:

A

500um (90% cornea) of uniform collagen fibrils secreted by keratocytes (fibroblasts).
Fibrils form bundles (lamellae) spaced by glycosaminoglycans

83
Q

Corneal epith. Replacement:

A

Basal cell mitosis at palisades of vogt at limbus > wing cell formation > differentiate into squamous cells > slough into the tears
Complete epith. Replacement per week

83
Q

Corneal innervation and blood supply:

A

Innervated via short/long ciliary nerves of CNV1
Supplied via tears, limbal vasculature, aqueous

83
Q

Decemets membrane:

A

Endo. Basement.
Matrix of collagen fibrils, GAGs, proteoglycans secreted from endo.
Thickens throughout life and w/ endo. Stress

83
Q

Phases of epithelial wound healing:

A

Latent
Migration
Proliferation
Attachment

84
Q

Epithelial wound healing latent phase:

A

^metabolic activity
Damaged apoptosis
Gap junction loss, desmosome remodelling, hemidesmosome disconnection
Fibronectin matrix forms in lesion to aid migration

84
Q

Epithelial wound healing proliferation phase:

A

Proliferation/differentiation > density/structure restoration
Limbal cells produce amplifying cells forming basal layer
Gap/tight junctions reformed

84
Q

Epithelial wound healing migration phase:

A

Surrounding cells migrate via filapodia > monolayer
Multilayer migration follows w/ ^glycoprotein synthesis
Migration rate of 0.05mm/h

84
Q

Epithelial wound healing attachment phase:

A

Hemidesmosome reattachment
If lesion passes stroma, complex reformation take 1-3mo w/risk of corneal erosions

85
Q

Stromal wound healing:

A

Basement membrane disruption > cytokine influx (IL-1 / TGF-b) > IL-1 activation of kerocytes > differentiation to fibroblasts > migrate to lesion edge
Transforming GF-b activation of fibroblasts > diff. To myofibroblasts containing a-SMA > wound closure
Fibroblasts secrete new collagen/ECM > opacity > ECM organisation via specific apoptosis
Takes 3-4 years to remodel

85
Q

Complications in stromal wound healing:

A

Myofibroblasts apoptosis / fibroblast innactivation > transparent scar
Myofibroblasts can remain > excess ECM > hypercellular scar > refractive changes (a-SMA stress)

85
Q

Endothelial wound healing:

A

Initial loss of endo. Barrier / pump > water influx to stroma > opacity
Cell migration across lesion > polymegethism (^size) / pleomorphism (shape) > barrier restoration
Response after 6h, progresses at 1mm/day (usual 1w to heal)

85
Q

Barriers to corneal wound healing:

A

Nerve loss (DM/HSK) > substance-P/neurotrophic-GF loss
Basement membrane dysfunction (DM) > poor framework
Limbal loss (steven-johnson) > low epith. Production
Ocular surface inflammation (DED) > MMP-9 upregulation > epith. Damage
Lid abnormality > exposure > desiccation
Also hormone imbalance/CLs/malnutrition

OPTO3003 (18 decks)

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