Uveal

Iris pigmented layer at bottom

C/body pigmented epithelium at top facing stroma ie follow retina

But it is NPE facing posterior chamber that secretes aqeous

101 tuts
Target iop
=initial iop times [100-initial iop]/100-D
D =level of damage
Eg 15mmhg mild 12 mod 10 severe 6
30mm mild 27 mod 18 severe 15
40 mmhg mild 24 mod 21 severe 18

Eg dad
Target iop
=initial iop times [100-initial iop]/100-D
15[100-15]/100-6
15 times 85 ]/94
=13.56

Vis

What is chrpe.
2 types typical [may be single large] or multiple small
Atypical oval/pigment only one margin
Ass FAP OR
gardners[polyposis coli+osteoma esp mandlble+Fibromas/lipomas
AD starts adolescent ca colon 100% by 50 5q gene fap
Criteria 4 lesions
Or tuscat [medulloblastoma/glioma]
Chr&RPE
Position peripheral or juxtapappilary
Ass NF TYPE2
Ass RD/EM/CNM
Hamartoma of RPE
Jet black very rare

Systemic dx
Phacomatoses
Nf 1 presents as droopy eyelid,glaucoma ,encapholocoele pulsatingdt hypoplastic sphenoid wing,optic
nerve glioma
Nf ii deafness
Sturge weber glaucoma dt angle angioma and diffuse choroidal haemagioma
Death dt epilepsy from parietal haemangioma
Tuberous sclerosis
Path is fibroangioma
Death /mr/epilepsy dt brain astrocytoma
Or cardiac rhabdomyoma or
Kidney angiolipomas
Present with retinal astrocytoma in 50%
And papilloedema CN 6 palsy dt inc ICP
Von hippal
Very serious condition but eye innocous capillary haemagioma
Death renal cell cancer/phaeochro/cysts
Cerebellum haemangioblastoma

ALL AD EXCEPT sturge-weber sporadic

Racemose haemangioma
Direct comm no capillaries
Wybon masson ass similar lesions ipsilateral brainstem/post fossa/temp lobe that bleed
Epilepsy/haemorhage
Rx nil for ey lesions
Cavernous multiplexa
Retinal cavernous haemagioma + cutaneous lesions
Presentation
Vitous hx

Elastic degenerations
Marfan AD
15q fibrillin
Eye hypoplastic dilator/
Ectopia lentis/microshero/
Keratoconus/megacornea/prom nerves/plana
Angle anormaly
Myopia
Rd
Homocytinuria AR
Treat with B6 pyridoxine converts methionine/homocystine
Feature different from marfan is Mental retardation and thrombosis esp post partum
Cx osteoporosis
Eyes myopia/ectopic lentis/rd
Ehler danlos
recessive type 6 assos eyes
Hyperelasticity + bleeding diathesis
+ MVProlapse
Eye like marfan + angoid streaks
Pseudoxanthoma
Only eye manifestation angoid streaks
Dominent or recessive
Cf
Small pappules
Bleeding diathesis
Accelerated atheroma

Tap
5400um or less with classic cnv at least 50% of lesion
Must be subfoveal
Verteporfin light activated drug
When excited generates oxidants eg o- that can damage cellular components and occlude vessels of cnv
with minimal damage to surrounding
Result
61% of treated eyes lost less than 15 letters=3 lines
Vs 46% not treated
Diode laser 689nm 83sec
600mw/cm2
Vision testing in tap
5 letters per line and doubling resolution angle every 3 lines
5 lines = 25letters lost severe visual lose
ARGON macular pc study
EFCNM 200 to 2500um from faz centre
treatment svl at 1 year 25%
at 5 yrs 45%
Non Treated 40% 65%
Recurrence 50% at 5 years
Most ie 75% in 1st year
sub foveal
Treated 20% will lose 5 lines at 3 months vs only 10% if not treated
at 2 years it reverses 20% vs 40%

Recurrence high 50% at 2 years

Risk to fellow eye at time.
Small drusen 10% cnv at 5 years
Large drusen and focal clum[ps of rpe pigmentation 60% cnv at 5 years

Diagnostic
pons is round and has single basilar artery central often calcified
Anatomy
Nerve supply
4 short ciliary and 2 long ciliary
Both pierce sclera at optic nerve and travel perchoroidal space.
Short ciliary from ciliary ganglion
Which had input from sensory nasociliary via a short ramus,sympathetic to choroidal vessels via an input
from fibres around ica and parasympatheic from ocular motor ew nucleus via inferior division to iris
sphinter & ciliary body for accomodation /constriction
Long ciliary has sensory input nasociliary nerve to most of eyeball including cornea and ,sympathetic to
iris dilater via an input from fibres around ica
TMW
ENdothelial cells + stroma
Final exit is canal of sclemm ENdothelial cells
Form vacoules tranversing cell from base to apex to form channel
Main outflow
Others
Minor routes intercell channels
Or pinocytic vessicles ie active
From cos via 20 to 35 one every clock hour collector channels all round to deep scleral and episcleral
veins and finally anterior ciliary veins
Some directly to anterior ciliary veins
Via aquous veins
The ciliary blood vessels named so because they end up at cb
7 anterior from muscle branches form the greater arterial circle at cb and minor circle at iris
2 long posterior ciliary arteries from ophthalmic pierce scleral outside inserion of optic nerve and
travel to greater arterial circle at cb
Short posterior ciliary arteries from
ophthalmic are 7 and divide into 20 pierce sclera around optic nerve to CHOROID WHICH SHOULD BE
NATERAL CONTINUATION OF PIA(WHICH WAS BEIND SUPPLIED BY CRA AND OPHTHALMIC
Supplie prelamina optic nerve[nb post lamina supplied by ophthalmic /cra
Circle if znn is anastamosis small between pia CRA/choroidal short posterior artery.
But very small
Nb 20% pop has short ciliary branch to macular area coming of just tem to optic nerve
Surgical approach to orbit
1Subbrow
2lid crease
3superior nasal rim= as it says
Lower
1subcilial=lash line
2Medial inferior=external 3ethmoidectomyincision/lynch

#drugs
Chloroamphenicol
No recurrent erosions
Can use in kids
#lacrimal gland
Symblepharon
Miotics Pilo/phospline iodide/
B blockers eg timolol
Adrenalin
Actinomyces g+ bac penicillin
Chronic infection
Canaliculi are patent
Often has concretions
Mucocoele are orbital cellulitis never ir v rare

#Lids
Blepharospasm
Assosciation in addition to 1'/fb are basal ganglia red nucleus/ parkinson lesions
Eg wilson/huntingtons/tardive dyskinesia[from chronic neuroleptic use eg chlopramazine/halo]/tetanus
#Path and tumours
Lid tumours
Both are papilomas
1Solar keratoses =actinic may become a bcc or scc
It is hyperkeratotic with vascular stalk
Scaly,red/dry
2seborhoeic keratosis is slimy flat pigmented mass
Hyperkeratosis
Rx shave off
3?/keratoacantoma looks like locally invasion bcc!
Path looks like scc!
At chronic inflammation/burn
Rx excise/inject steroids
Locally invasive
Hyperkeratotic with crater/ ulcer rapidly growing
4Bcc
Most common tx
Rodent ulcer common site lower lid
Central crater or flat morpheoform that is difficult to dx
Sites
Most common
Lower lid followed by 1
2medial canthus
3Lateral canthus
4 upper lid
______ 4

-----------

2< 0 > 3 orbit

------------
______ 1
Sun exposure
Local spread not blood
Problem is orbital drainage invasion
Rx
Mohs = resect lammellae at a time with margin and send to histopathologist while on table to preserves
tissue
OR
Local excision wide margins including lacrimal apparatus if mohs unavailable
Radiotherapy palliative
what is bc naevus syndrome=
Multiple bcc at young age
+ neuro/skel/endo abnormalities
5MM
Same incidence as skin rare dt small area of lid
3 types superficial spreading
80% of cases
/lentigo maligna/nodular=hutchinson melanotic freckle 10%
1st 2 lateral spread but nodular vertical
Spread by blood early mets to liver spread
Maslows depth of invasion
Rx
Wide excision and ln removal if microscopic spread
6Scc
2nd most common
upper lid
Very agressive
I can talk about it
HPV / sun Hiv radiotherapy
Rx mitomycin
7Sebaceous c cx
From glands of zeiss or meibomian glands
or caruncle
May invade canaliculis structure
Recurrent meibomian cysts should alert to sebacous cx
Also chronic blepharoconjunctivitis
dx dont put in alcohol as mucous destroyed
Difficulties in dx
A MULTIFOCAL WITH SKIP LESIONS----therefore mohs unreliable
B SPREAD BLOOD /LN/LOCAL --- aggresive
25% die fRom metastasis
do fullthickness lid biopsy comes from deep
Use oil red Stain
fix with formalin NOT paraffin as it removes lipid.
Optics
Hypermetropia
Caused if lens is removed eg subluxation
Globe shortened eg compression cavernous haem
Cornea flattened
Retinal elevation eg csi
Accomodation failure eg cyclpent/atropine
Tricyclics/BOTULINIM
Drawing optics
Foward and up positive
REDUCED EYE distances FROM CORNEA
F1 -15.7
Principle plane/point 1.35
F2 24.13 ie on retina
Nodal point plane 7.08
Javel shiotz

Adjust object size to get a specific image size

Microscope
2 convex lens
Galeliean telescope
Convex object
Concave eye piece
Magnifys by increasi g angle subtended
1/v -1/u= 1/f2
Two rules
A ray from top of object passes thru principle point undeviated
A ray parallel to principal axis after refraction passes thru second princple focus in convex lens or away
from f2 in concave

The image formed by my glasses eg -2 diopter[ is 50 cm focal point] is always virtual erect and minified
and inside f2
A magnifying glass loupe 32 diopters [ 3cm focal point ] with object inside or near focal point will make
virtual erect magnified image outside focal point 1
This is principle of loupe causing angular magnification of 8times if held 25cm from eyes

if object at focal point image at infinity and virtual erect

If i wear presbyopic glasses of 2Diopters [focal length 50cm] and i look at object outside 50cm eg tv
image will be real inverted and outside F2
This is also way we use indirect 20diopter [5cm focal length] image is al and inverted

#glaucoma
Humphrey
What is percentage of reliability index ? 20%
False + trigger happy
False - inattentive or incorrectly plotted blind spot
Program 24 - 2 tests 54 point
2 mean that points on the
Merideans not tested and the grid is 6' points apart.
Statpac fast pac sita are threshold algorithms

Display
Greyscale -difrent tones 5db
Numerical--- no in bracket if below 5db and retested
Total dev patient vs age matched control
Pattern adjusted total for generalized depssion of cataract/miosis
Propability
0.5 to <5
Likelihood of chance less for lower p
Global indices
Work out difference as a single no
MD measure of overall field loss
PSD measure of localized loss taking into account generalized depression
More specific for glaucoma.
A positive no indicates worse deviation
Stf measures 10 points throughout test and compare
CPSD actually as PSD taking into account STF
What is glaucoma?
 Glaucoma hemifield test measures difference between superior/inferior field in mirror image points
 if there is a difference outside normal on 2 occasions
 CPSD less than 5% on 2 occasions
 Cluster of 3 or more non edge points PSD less than 5% and one less than 1% on 2 occasions

#lens
What causes cataracts
Anatomy
No space between fibres
Complex interdigitations
Cortex fibres converge =suture
Ant upright y
Post inverted y
Cataracts
Capsule
=bm
Focal thickening excrescences in lowes aniridia
Corona
= wartlike excrescences that are replaced by clumps of epithelium and look like granular debris in cortex
Post lentoconus thin lens bulges and opacifies
Ant lenticonus different cytoarch anormalies
Inorganic deposits
Copper in wilsons/igGgammopathy/myeloma
Blue green in subflower conf
Also exposure to mercury
Pxf easy
True exfoliation=delamination of layers of capsule
Dt IR/thermal
Epithelium
Glaucomflecken
Deg cell under ant capsule acute glaucoma
Necrosis/prol epithelium metaplasic cell that can make collagen --- iritis/atopic dermetitis/trauma
Iron fb iron in epithelium stain prussian blue]
Pscc dt age=
Disrubtion of mitosis/migration of equatorial epithelium
Migrate post swell=bladder/wedl
Dt steriods/iodizing radiation
Interuption of capsule eg cataract sx stimulates epithelium prliferation
To cover defect
Eg elschig pearls=globular semitransparent mass abherrent fibres
Soemmwring
= doughnut configeration of equatorial fibres after incomplete cortex removal in esp cong/aumatic
cataracts dt sequestraion of equatorial cells
Cortex

C
Structural changes
Sccc vacuolation of epithelium
Ascc epitelial metaplasia
Pscc dysplasis
Cortocal fibres swell
Types
capsular :glassbowers ir radiation/mercury = grey/alkali burn/chlorpramazine congenital ant polar
Post scc steriods/age/dm=cupudiform
Ant scc wilsons =green sunflower/pilo/glaucomflecen
Cortical congenital=blue dot or coronary/ age cuneform/
Nuclear congenital=lammelar or embryonal/sclerosis

Metabolic
All the hypos!
Gput/gk def
Hypopara causing hYpocal
Hypoglycaemia
Hypothyoroid
Wilsons
Lowes
Fabrys
Mannosidosis
Homocystinuria

ECTOPIA LENTIS
Subluxation= in lens fossa vs dislocation
Causes
Systemic=Mar/ed/wm/falmilial el/aniridia----
metabolic =homocystinuria/sufite oxidase def/hyperlys/
All are AR except marfan/aniridia AD
Ehler danlos is peculiar in that all types inheritence
Marfans
Features
Myopia
Flat cornea
Hypoplastic dilator muscle
Angle anomalies
MicroSpherophakia
Lattice
RD more common

#Cornea
What can u tell me about dystrophies
Epithelial meesman
Bowmans microcystic and cogan reese=honey comb
Macula
Granula no need for graft and periphery spare
Lattice
All auto recessive except macula ad
All except meesman& granular cause recurrent erosions
Hsk
Rx 3% acyclovir not 5%
Or trifuorthymidine or idoxuridine or vidardine
Nanopthalmos
<20mm > 7Diopters
Thick sclera
Prk
Indication
Keratoconus and irregular astigmatism
Somal haze dt trauma/inflammation
2nd cause bullous keratopathy
After serious infection mostly filamentous fungus that mostly scars with poor esponse to antibiotics
Tectonic to support globe
Most commonly corneal melt dt to RA
What is required for donor
 48 hours in moist pot
 1week in corneal sorage media at 4'c
 30 days organ culture
Principles of storage
Moist pot 2 days
then tissue culture [TC 199 dextran,ab] 1 week
then tissue culture[ with chondroitin sulphate;bicarb;aa;ab] 2weeks
then organ culture[? Kills ag presenting cells] 4 weeks
Cryopresevation liquid nitrogren up to 1year

Endothelial cell density 2300ccells/mm2

AGE IS not ci
Old arcus problem
Less than 1 year ectasia problem
Do hiv/hep B&C
Ci
JC;cmv;slow virus
Hepititis;rub;rabies;sepsis
Cancer
Glaucoma/ocular tx/uveitis/ocular sx
Age less 1 small steep>50ectasia
More than 65 low endothelial count
Death o than 6 hours
Corneal pigmentation
All structures all depths
EPITHELIUM
Iron from tears @ line corresponding lid closure=epithelium= hudson stahl line
Adrenaline @subepithelium/bowmans black
Verticella=vortex @ from point lower cornea epithelial gold dep dt
Amoidarione/chlopra/indomethacin/chloroquine/fabrys=sphingolipidosis with no alpha galactosidase A
Fleisher @ base of cone in keratoconus=iron in epithelium
Stocklers@epithelium of pterigium
Ferrys same but of trabbleb
STROMA
Crysiasis Gold purple@ ant stroma
Haemorrhage@ deep stroma=iron/haemosiderin
Descements
Copper=wilsons=kf @peripheral descements ass green sunflower cataract
Mercury preservative
Silver=argrosis both@ descements
Endothelium
Krukenburgs@endothelium is melanin
Lipid k
Stroma cholesterol/fa
With neovascularization
Causes
Any neovascularization
HSK
Trauma
Disorders of fat metabolism very rarely
Rx argon laser of bv
Hist
Lacuna spaces plus granulomatous infl.
Spheroidal=bietti=labrador
Anterior stromal lesions dt elastoid degeneration of collagen
No fat
Proteins give orange color=tryptophen/tyrosine/cysteine/cystine
Band k
Ca in sub epithelial/anterior bowmans
Clear space separates limbus
Small holes transmit nerves.
Can break epithelium ----pain
Causes idio/ppmd/age/phthysis/chronic uveitis/hypercalcaemia
Rx
Remove epithelum
Apply chelater eg na edetate/versenate
Eximer laser promising.
Infant corneal opacification
embryonal dysgenesis
Lens does not separate from surface ectoderm= Anterior clevage syndrome
Cornea does not differentiate=scleracornea
Endothelium does no form=ched
IEM
Mucopolysacharidoses
mucolipodosis
Gangliosidosis
Glycogen storage- von gierkes
Lowes
Cystinosis
Riley day

#neuro
Optpkintic nystagmus
Drum moved right to left
Left parieto-occ lobe sees and makes a slow pursuit
Left Fef frontal saccades fast back to right.
Nb both conhSlow purshuit by vestibular
Fast correction by brain stem/fef
Nb rotatory is dt vestibular
cniii
weber c niii contra hemi peduncle
Benedicts cniii + red nucleus=contr angoid streaks alateral tremor[red nucleus
Nonagel cniii+ ipsilateral ataxia [cerebellar peduncle]
Claudes= ataxia and tremor= bendicks and nonagel
The INO once and for all
Pupil response midbrain most dorsal
Vertical gaze midbrain dorsal
Convergence more ventral but still behind red nucleus
Cf
Do conjugate version test
 INO lesion and u cant move cniii on same side [no other lesion causes only mr palsy ] and
convergence normal =cogans posterior ino
 Bilateral ino and convergence abnormal =cogans anterior ino Wall eyes ino rostal ino+cn111
exotropia and ino
 Ino and pprf pons 1 and half
 pprf only conugate gaze palsy

Nystagmus
Parinauds
Anatomy midbrain
Posterior is superior coliculus
 Light reflex very posterior tectum
 Verical gaze centre a bit anterior
 near triad needs cortical input for accomodation/constriction/convergence
 All post to aqueduct
Problem verical gaze palsy with compensatory excessive lid retraction
Poor light reflex but good near constriction
Poor convergence ie with nystagmus and retraction of globe
Poor accomodation
Causes pineal gland tx or vascular anomalies kids
Adults
Ms cva metastases

Pupil
Horners
TESTS
Imagine 2 neurons
Once and for all!
Point 1~~~Cocaine 4% only dilates normal eyes by augmenting NA that is being produced already
Point 2~~~hydroxyamphetamine 1% only dilates if 2nd neuron is working by releasing NA into cleft
actively from nucleus
#strabismus
Hirshsprings
Pen torch oSmove and by herris the uinting will move as well until symetrical reflections got

Angle kappa is normally positive with fovea 5'degrees temporal to optical axis
Xince torch .light comes from fovea it is displaced temprally givinb a ;i gure of ESO normally.
Ressection is more effctive than recession
The lateral rectus has most field ie 90 so we canwMr 6mm
Sr 4mm
LR palsore for distance ie more palsy when looking far.
Rx
If you disinsert lateral SR&IR and attach to upper and lower poles of LR=hummelshem
lateral SR&IR split and attached to equator =jenson IE MUSCLES NOT CUT
Amblyopia
There are few fibres to lgb/cortex so crowding occurs and words are mo difficult than letters so ask to
read letters alone
Neutral density filters eg red free do not improve va

what is most common exotropia

Intermittent type
Mostly does no rq sx
3 types
 basic
 More exotropia at distance ie divergent excess dt to much acommodation
 More exotropia at near ie convergence insufficiency

Nystagmus blockage syndrome
Is a type of nystagmus but causes esotropia as eye physiologically tries to dampen fast phase
How to differentiate?
Nystagmus came first
Variable angles
Other neuro problems
Psedopalsy of abduction
Fixating eye abducts and non fixating eso
Likely amblyobia
A&V
A due to bilateral superior oblique overaction
V due to bilateral Inferior oblique overaction
A more exo on down gaze
V more exo on upgaze
Say exo because o
Rx bmr and faden since deciding on a particular eye is impossible

#Macula
Rerinoscishis
You will see senile type very common
Only 1% have or will dev Rd
70% are hyperopic and 33% are bilateral
It is a degeneration
So look for degenerations
Eg microcystic and white with pressure
 The split is at outer plexiform layer after cysts/oedema
Difference from Rd
 Smooth imobile Dome shaped no folds-- most important
 No high water marks ie pigmented demarcation linesareas at edges
 Beaten bronze appearance
 White with pressure on outer leaf
 White dots at ilm
Rd only if break in both leafs
Vs juvenile
Very rare
Split at nfl
Macula always involved eg CMO
Vitreous very deg like swiss cheese
Erg abnormal b wave
X linked
Ass goldman favre
Or ad wagners

Fleck retina
Remember vit a def and oxalosis as well
Deposits at RPE & hyperfluorecence
Most are AR
Blindness or scotomas do not occur
Central vision is variable kandori/albi have good cv

ERG
A wave photoreceptor inner segments
B MULLER ~~ BIPOLAR
A wave speared if condition is subtotal as a rule eg crao--- macula ok as supplied by choroid
Csnb---- cones ok
Retinoscisis --- not that serious
Lipid storage eg battens fovea ok
Or when macula is relatively ok

Bests
AD
Normal vision as a child
5 stages
Previtelliform
Reduced EOG normal
Vitelliform
10 years old
3 dd cyst of lipofuschin
Vision surprisingly good

Pseudohypon
Superior half RPE Atrophy
Vitelliruptive
15 years
Scrambled egg
End stage
Disciform
Histology
disgenerate pr in RPE/lipofuschin in RPE/lipofuschin in SRS
VS ADULTS
Presents at 50
Smaller lesions
Eog normal

Stages of macular holes (new - Gass 1995)

1A) foveolar detachment yellow dot
1B) foveal detachment yellow ring
2) early hole (<400 microns)
3) larger hole (>400 microns) +/- operculum
4) full thickness hole with PVD.
Ddx
Macular cysts=opl cysts/lammelar hole = coalasced cysts dt CMO
Pseudohole.
#vascular
Ischaemic Crvo
Very poor px dt ischaemic macula
Rubeosis iris in 50% at 2 to 4 months
So do prp only once it occurs
Non Ischaemic Crvo
Only 15% become ischaemic at 4 months and 33% at 3 years
va returns to close to normal in 50% only signs
Disc collaterals/pigmentary changes/epiretinal gliosis
Fu at 3 months and 3 years do fa to check for ischaemia
Rx CONTROVERSY HIGH INTENSITY BURN COLLATERAL BETWEEN RETINAL & CHOROID
RISKY CAUSES GLIOSIS/HAEM
BVO
Px good most recover va
If at 3 monthsand oedema
Do laser id
Nvd occurs in 10% and nve 25%
If occurs do prp
4 types
Watch macula
 1st order temp branch near optic disc
 Away from o/d but involving macula
 Minor macular branch only
 4 peripheral temporal branch not affecting macula
Coats
Spectrum
Spectrum is Lebers miliary aneurysms then telangiectasia[Similar to von hippel lindau]
and lastly exudation
Fa
Usually UNILATERAL but may show art/ven dilation both eyes
Nb affects both art/eyes
 Telangiectasia =are mostly macula and can cause macula star.
 Aneurysms sacular and periphery mostly temporal= Lebers miliary aneurysms
who?
Young boys 8 years old leucocora
Or adult coats with macular exudation
Exudative Rd
Rx argon laser
CSO
Fa
More common ink dot/smudge
Fluid from bd brb accumulate in sensory retina slowly
Less common smoke stack
Occurs with small RPE defect that changes the dynamic of leakage over time.
Small accumulation and later sensory retina fills and vertically to limit of RPE detachment
Later umbrellas into whole sensory retina
Ht vs arteriosclerosis=thickened calcified media
arteriosclerosis
grade1 minimal
2 veins deflect at av
3 copper wiring & veins taper at av and then dilate
4 silver wiring & bvo
Ht
1 generalized arteriole attenuation normal 1,2 to 1 a to v
2focal arteriole attenuation av nipping/venous tortuousity
3hx/exudates/cws/macular star
4 = maligmant ht ie disc swelling
Ophthalmic artery occlusion
Both cra/and ciliary b/s affected
Tf no cherry red st as macula and rest of retina affected
Delayed choroidal filling
Decreased a and b waves
Late it looks like rp
Va very bad
#retina
RP
Most common mode is AR[50%]
X and AD 25% each
Ar and x progressive severe visual loss
Ad it remains 6/18 ie good
What are electrodx tests
EOG lost early dt PR Lost
Later ERG defects both but Esp scotopic
Dark adaptation inc threshold of both esp rods
Rafsums
Phytanic acid in green veg/milk/
Def PA hydroxylase
Cf similar to thiamine[beri beri]
Ataxia/pn/cardiomyopathy/ichythosis/deafness/rp
Sticklers
Like marfans but more common
Also AD
CF
Vitreous lacuna/syneresis/veils
Myopia
Lattice/RD
Also pscc/coag
Two genes procollagen defect
Ddx
Goldmanfavre=reinoschysis+vitreous AR
Marfan AD
Juvenile retinoschysis XLR
Wagners=AD=sticklers without other systemic
Bulls eye
Chloroquine maculopathy
It affects RPE so EOG is affected and causes ring of hypopigmentation.
Screen for red scotoma 10 to 15' from fixation ie premaculopathy.
Also EOG ABNORMAL at this stage
So use these tests.
Also difficult accomodation.
Incidence proptional to cumulative dose rare if less than 300grams taken
Hydroxychloroquine less risk.
#uveitis
Ues
Idiopathic in middle aged Males
Effusion and hence thickened choroid & resultant RPE detachment
Except for dilated episcleral veins no abnormalities and iop normal do lammela sclerotomy but
va variable dt remissions/exacerbations
RPE Leopard spots fa normal
Pxf
Difference iris atrophy with pigmentory glaucoma
Pxf at margin dt fluff/lens deposits vs midperphery
Material is fibrilla proteoglycan like amyloid but no rxn with congo red
Like bm PAS + /eiosinophylic
Who ?scandanavians/blacks
Pds/pg
Rx
More resistant than poag
Pilo reverses mid periphery bowing
What is krukenbergs
Pigment phagocytosed by endothelium dt aqeous current
Fhu
Causes of dec va
PSSC
Vitreous opacities
Uveitis stellate white fillaments between whole cornea
Amslers sign
Steroids dont help as it is not inflammatory
Cause anterior segment ischaemia seen on fa
& hist hyalination of bv
Ddx heterochromia
1'
Trauma/infl 2' to atrophy
Waardenburgs & perry romburg? rare
Horners/siderosis/melanoma

Ampee
a vitritis with mutiple plaque like chorioretinal lesions dt viral infection
Ass thyroiditis/enteritis/erethyma nodosum/cerebral vasculitis.
Less than 25 males
Pg
Ischaemia/inflammation choriocapillaris and RPE causing poor choroidal flourecence on fa
Late the is transmission indicating RPE atrophy.
Px nil rx but va improves dramatically
Ddx
Serpiginous but over 45
But not placoid like but in all directions
When recovered Pohs
Birdshot
So
Type iv s antigen PR os/choroid/csf pineal gland
Link between cns eye correlates with ass vkhhla dr4 dw15
Hla a11 inc risk vs vkh b22
Koeppe=m/phages at margin
'in Coupe hangs head out'
Dallen fuchs= epitheliod m/phages between npe pe of cb & at bruchs=yellow white sts at
fundoscopy
Vkh=uveoencephalitis
Affects skin hair cns eye
Alopecia/poliosisvirtiligo
Meningism/encephalopathy/ear--deaf/tinnitis/vertiligo
Ant uveitis
Posterior uveitis
vk=skin ant uveitis hair
H = posterior uveitis + cns
#paeds
The accomodative esotropias
1refractive accomodative
Child is +4 to +7 and needs a lot of acommodation to see near
Magnitude between near/ar varies a little ie 10D
The are 2 subtypes that the esotropia is completely or partially corrected with correction
2non refractive accomodative
High AC/A
Accomodation may for unkmown reason be defective
Convergence may be excess for
for unkmown reason be defective
straight for distance eso for near
The difference is that where accomodation is a problem in the latter the near point is not
discenable ie remote.
So ask to est NPA
Aniridia
Either AD OR sporadic with system manifestations Then [sporadic]or alone[then AD}
If with system manifestations then deletion of 11q
These then mo like to have Wilms.
system manifestations = body hemihypertrophy
Mr/digital anomalies/hygonadism.

Glaucoma is infantile as it takes adhesions to cause it and only in 50%common cause of

blindness in 30-50% of pts
often developing before the age of 30
due to angle closure as well as mesodermal tissue in angle

millers = wilms+aniridia
system manifestations
Aniridia
1:100,000
AN1 (85%)
familial with isolated ocular manifestations in AD pattern with complete penetrance but variable
expressivity
2/3 of patients have affected parents
usually punctate cortical opacities needing surgery 30-40 yo
AN2 (13% )
del of short arm chrm 11p-
sporadic nonfamilial associated with Wilm's tumor (nephroblastoma)
may get visually significant nuclear cataracts
1/4 with Wilms tumor which is often diagnosed before age 5
GU abnormalities severe mental retardation
facial dysmorphism hemihypertrophy
long facies low set ears with poor lobes
prominent nose
Miller's syndrome
WAGR (Wilms tumor, aniridia, genitourinary abnormalities, mental retardation)
AN3 (3%)
Gillespies's syndrome, AR, with mental retardation and cerebellar ataxia
no Wilm's tumor, CT shows abnormal structure of brain
normal macula and optic nerve
ICE
Usually unilateral dx midd;e aged females
EIA
IN COGAN REES diffuse naevi prominent sl iris processes PAS usually ant to scwelbes/correctopia/nodules
CHANDLERS PAS
Endothelial dystrophy/ clouding
Glaucoma
What is diference
Iris processes vs pas
Flat small & fine vs Pas tented varous sizes
Ass HSK PCR has detected it and is similar eg sectoral atrophy/correctopia
Not genetic not HLA
#neuro
OKN
Need fef[saccades initiation]
Parieto-occipital[pursuits] eg infarct with homonomous hemi or organic blindness
Verical gaze centre ---dorsal midbrain lesion
Horizontal gaze centre ---- pontine lesion
infantile nystagmus --assymerical okn
Congenital nystagmus ---- inverse okn
Browns
Male = female
Taught so muscle
eye cant elevate on adduction
Cause
Cong recovers 7 years old
RA
Surgery not usually but if head tilt
Do so tenotony risk of so paresis

Duanes female and left more common

Duanes type 1
only one eye affected eg left
 Straight notice slight esotropia
 Left gaze palsy plus widening of palperpral fissue
 Right gaze narrowing
Ddx
Infantile eso
Mobius
Abducent palsy

Associations
Skeletal neuro facial abnormalitieseg undescended scapula
Eye coloboma/iris heterochromia /pupil membranescataract/ micro
IE ORBIT TO IRIS TO LENS
15% bilateral

type 111
like exotropia with no/very little adduction
Type 11
just reduced adduction
Rx only if significant head posture
Never get ablyopia
If amblyopia there is refractive error and will correct with glasses.
NEVER recess LR as uwill only cause restriction .
4th nerve palsy
Only on exits posteriorly and long intracranial path.
Common etiology
Anterior medullary vellum contusion in severe head trauma
Congenital has 2 distinct features
No cyclotorsion
Large vertical fusion
Both compensatory mechanisms
Ddx
Ie hypertopia
Mg/ted/oid/skew deviation of parinauds[vertical gazw centre
/atypical browns
So palsy
Rx
Harada ito
For excyclotorssion seen modtly in scwuired and not in congenital
transpose anterior tendon lateraly and anteriorly
If u overcorrect u can always go back
Does not cause browns as superior oblique tucking does.

#Surgery
Astigmatism&placido
Steep axix where flections closest and along short axis
How to treat post PRK astigmatism
A apai of corneal relaxing sincisions 120' long at both sides of steep axis 0.5mm inside g-h jxntxn
With compression times 3 sutures in flat meridean

Implants
 Medpor = high density porous polyethelene20mm ball for enucleation 18mm for eviseration
 Hydroxyappetite
 Porous allows ingrowth of host tissue and prevents extrusion
 Pore size 40 to 150um
Coveringmaterials
Merciline or dacron or vicryl mesh
Or sclera smooth easy implantation.
Risk prion jc dx
Viscoelastics
Solid when static fluid when dynamic
resists deforming by force and must be able to recover after deforming.
healon cant coat [high surface tension
Viscoat = NAH +CS
Chondroitin sulfate coats but not good viscoelastic + hyaluronate good viscoelastic
What is post enuc syndrome
Lower lid laxity
Shortening of inf fornix
Endophthalmos
Deep upper lid sulcus
29% extrusion rate with mercilene mesh and only 3% with hydroxyappetite because of deep ingrowth of
tissue

Ectropian
Kuhnt szymanowski
= excision of lateral pentagon + blepharoplasty ielateral triangle of skin as well excised
Endophthamitis
Genta inravitreally macula infarct
Cipro iv can give therapeutic level intravitreal
FA
Autofluroscence
Exudates
Astrocyte hamatoma
Od drusen
Lipfuscin
Flureceine 5ml 10% 500mg given
Anaphalaxis <1%

Things i forget

how do u approach Entropian

Weiss full thickness horizontal cut 4mm below
qiuckett
at 2/3 from medial canthus make 2 vertical cuts 4mm down and then 2 horizontal
Adress horizontal lid laxity by suturing margin
Adress entropian by everting
Jones very powerful procedure
Partial thickness cur at crease
Proceed like garankuwa everting procedure.

Facial block
3 places
Nadbath and rheman at stylomastoid foramen
O briens At 2/3 distance up from jaw angle to zygomatictemporal bone nb as it crosses neck of mandible.
Van lint At latral to lateral anthus deep t oo
All u must touch periosteum
Temporal artery biopsy
Below dermis and below superficial fascia=subcutaneous fat
It is in DEEP fascia of temporalis
It is from eca and it is terminal branch with parietal & frontal branches
before it is formed eca gives offmaxillary branch
Procedure
Look for hair line
Make circumlinear incision
Move away skin and dermis
Has anastamosis with ica via supraorbital and lacrimal artery of ophthalmic
Therefore wait to see if cf of stroke before tieing & cutting proximal/distal part
Cut 3cm
How to reverse p
alpha1 agonist:
phenylephrine, stimulates iris dilator to produce mydriasis
Reverses
alpha 1 antagonist:
dapiprazole (Rev-Eyes), inhibits iris dilator to produce miosis, no activity on ciliary muscle
or Thymoxamine[moxisylate]
Betaxolol betagen
Inc optic head perfusion so good in ltg.
Dcr=anas lac sac to middle meatus
Pack nose 2% lid plus 1 in 200 000 adrenalin or 4% coccaine
Cut skin 10mm medial to canthus
Find blunt dissection anterior lacrimal crest dont cut post canthal ligament.
Nb!vein is medially so dont pierce it!
Move sac away
Make a hole removing on both sides of crest ie mostly in lacrimal fossa
A good rule in sac sx is never have a bony margin closer than 5mm to common canaliculis as this may
close off canal.
Probe nld and feel where lacrimal sac is
Cut it vertical *****
CUt nasal musosa verically and then an h configaration
Ie
--- l---
l nasal musosa
--- l---
Ties together post flaps and close ant flaps
Close but reattac medial canthal lig to peristeum

Rop
Plus dx
 Pupil fails to dilate
 Vitreous haze
 Dilated /tortuous veins/arteries
 Inc preretinal/vit hx
Threshold means treat!
Plus dx
5 continous clock hrs or 8 non continous
Stage 3=extrareinal fvp or more in zone 1 or 2
The zones
Think in terms of radius
Z1 radius from optic nerve to twice distance to fovea
Z2 radius to nasal ora
Z3 radius to temporal ora
Stage
1 line
Ridge
Fv
Subtotal rd
Rd
rd sites
S
65% ST
15% SN
15% IT
10% IN

Fluid goes down & up on other side.

Screen less than 31 weeks or less than 1500g
Screen at 34 weeks/or 6 weeks post birth whichever earlier
Use 0.5 cyclopen
0.25% phenyl
Bottle we have in clinic is 2% cyclo and 1% phenyl
2 types cnm
Young pic sepeng---goes to sensory retina
Old armd -------flat remains under rpe
The sensory retina one will obviously fluresce late
Fluresceine

Kids
zinnat 250 bd
Gentamyvin 80 daily 3ml/kg
Augmemin 1,2 g tds

Sudafed 10ml tds

cephalosporins
1st:
cephalothin, cefazolin, cephalexin, cephradine: gram positives and negatives, do not cover enterobacter, Proteus
(except mirabilis), Psuedomonas, Bacteroides, Serratia, enterococci
2nd:
cefamandole, cefoxitin, greater gram neg coverage
3rd:
cefotaxime, moxalactam: cefotaxime penetrates blood-brain barrier better than other cephalosporins
How does scoline cause parslysis?
It takes up ach receptor nicotinic and remains until it is broken down. Its initial action is depolarization or
contraction.
It is broken down by cholinesterase which naturally ends its effect of relaxation.which we want
[Normally cholinesterase ends the effect of contraction of acetylcholine.] If someone is on eg phospotidyl iodide a
cholinesterase inhibitor the scoline will not be broken down and we will have prolonged relaxation.so stop
6 weeks before GA.
How does reversal work?
We use cholinesterase inhibitor to reverse non polarizing relaxant like vercuronium that competes with
ach.at nicotinic site.
It now allows more ach to form and compete /replace the vercuronium and cause normal muscle action
Path signs of cancer
A) Cell
1) increased N:C ratio
2) abnormal configuration (anaplasia)
3) darker staining (hyperchromasia)
4) abnormal mitotic figure
5) abnormal nucleus (indented, several nuclei)
6) loss of cell polarity
B) Tissue
1) loss of tissue polarity
2) increased mitotic figures
3) MICROBIOLOGY
Cultures
A) Bacteria
1) non-specific: blood agar
2) neisseria and hemophilus: chocolate agar (factor V and X - NAD and hemin) with 5% CO2
3) TB: Lowenstein-Jensen
4) anaerobes:
- thioglycolate
- Thayer Martin
5) after tx. with ABC's: brain-heart infusion

B) virus
1) animal/human cell lines

C) Chlamydia
1) McCoy fibroblasts
2) chlamydiazyme
3) Microtrac

D) Fungi
1) blood Agar
2) Sabouraud's ( without cyclohexamide - inhibitor of fungi)
3) brain-heart infusion

E) Acanthamoeba
1) non-nutrient agar with E.Coli overlay

Stains for infections

A) Bacteria
1) Gram
2) Giemsa

B) Virus
1) Giemsa
2) PAP

C) Chlamydia
1) Giemsa

D) Fungi
1) Gram
2) GMS
3) Calcofluor white
4) acridine orange

E) Acanthamoeba
1) Calcofluor white
2) acridine orange
3) PAS
4) Giemsa

F) TB
1) Ziehl-Nielson
2) acid-fast

G) filamentous bacteria
1) acid-fast stain

mmunohistochemical Stains
A) Epithelial
1) keratin
2) EMA (epitheliam mb antigen)
3) cytokeratins
B) Mesenchymal
1) Factor 8: vascular endothelium
2) vimentin: SM, fibrocytes, Schwann cells
3) MSA (muscle-specific actin): muscle
4) desmin: muscle
5) myoglobin: muscle
C) Neural origin/ neural crest
1) NSE: (neuron-specific enolase): nerve tissue tumors
2) GFAP: astocytes, Schwann cells
3) neurofilament: neurons
4) S-100: melanoma, neural tissue
5) HMB-45: melanoma

What is aberrent regeneration of CN III:nb the 111 rd cn supplies itself incorrectly?

results in
Move eyeball; down ----lid retracts or pupil constricts
Move eyeball Medial------lid retracts or pupil constricts this looks like argyl robinson !

:Pseudo von Grafe sign =lid retraction with downgaze -due to innervation of levator palpebrae by IR fibers Inverse Duane's
syndrome=lid retraction with adduction-due to innervation of levator palpebrae by MR fibers Pseudo-Argyll-Robertson pupil=light-
near dissociation due to innervation of pupillary sphincter by MR fibers Pupillary constriction on downgaze due to innervation of
pupillary sphincter by IR fibers

Mri
Suprasellar vs sella turcica
Eg craniopharangioma Suprasellar
Compresses ventricle and midbrain path eg parinauds may also have pituatory path
Most common non glial tx in brain in kids
2 to 80yrs
From stalk
Cystic most reliable approx 80% but not pathognemonic
Calcification in 65% may occur in aneurysm/sphenoid masses but rare in suprasellar meningioma or macroadenoma
Meningioma
may be sella or suprasellar arises
Diaphragma/tuberculum/dorsum sella
Dense homogenous unique
obtuse dural margins
Hyperostosis in 1/3 may be confused with craniopharyngioma

ICA intracavernous aneurysm Suprasellar

Macroadenoma sella
macroadenoma lobulted never calcification sella enlarged encases carotids abuts ica
Ms
T2 weighted --- demyelination plaques deep w /m paraventricular
RRMS plaques come and go
Conflicting studies as to whether correlation of mri findings to clinical
Obvoius that demyelination and subsequent axonal lose both are involved.
Rx ifn b1b and b1a and 8miu

Ivi all in 0.1ml

Gentamycin sulfate 0.1mg [40mg/ml]
Cefazolin 2.25mg[500mg]
Vancomycin hcl 1mg[500mg]
Clindamycin po4 1mg[600mg]
Miconazole 0.025mg[20ml of10mg/ml]
amph b 0.005mg[50mg]

Collagen
Cornea i
Vitreous ii
Lens capsule iv
Bm iv of cornea etc
Vitreous collagen is geatest density at base It is type II but has more galactoglucose chains and higher
content alanine
Zonules similar to vitreous collagen onlytightly packed and collagenase resistant
Lens capsule type 4 and probably the thickest Basment membrane ever
Cornea basement membrane type 4
Cornea stroma collagen diameter 24-30 nm abd periodicity 64nm mainly type I but all others too!

Dx
Ehler danlos type 3 cartlilage/joints
Why does can cataract cause rapd?
RAPD is dt sick optic nerve that is more potent from nasal fibres.
A cataract projects light temporally so causing less optic nerve stimulation and hence impression of
RAPD.
vf
1Centrocaecal dt optic atrophy with temp pallor dt nfl macularpapular bundle damage.
Common tobacco / alcohol amblyopia eg in cuba
Dec risk methionine diet/b12/b1 niacin b2 ribflavin & caretenoids
Rx daily B complex monthly imi hydroxycobalamin
Partly reversable
2 central scotoma and supertemporal defect= juntional scotoma[ ie nasal fibres damaged]
If the crossed macular fibres are involved the scotoma would be upper temporal paracentral
If you see a central scotoma always look at other vf.
Lesion is optic nerve near chiasm where opposite eyes nasal fibres are crossing.They do a funny
histological pattern in that the enter anteriorly into the other optic nerve =von willbrands knee
Lesion granuloma eg sarcoid
3Bitem hemianopia easy!
4
111 cn
Fascicle courses ventrally through the red nucleus and exits through the medial portion of the cerebral peduncles
lesions are usually of vascular or metastatic etiology
- causes 4 types of syndromes a. Nothnagel superior cerebellar peduncle~~ cerebellar ataxia b. Benedikt lesion red nucleus and
medial lemniscus~~contralateral loss of sensation, brain stem uncontrolled movements (rubral tremor,hemichorea, athetosis, and
ballismus)c. Claude ~~ combined d. Weber cerebral peduncle~~~contralateral spastic paralysis
Nonagel=cerebellar ataxia
Benedict=loss sensation[ml]/uncontrolled movement[red nuc]
Claude=cerebellum/basal ganglia/ml= above 2
Weber=peduncle spastic paralysis
noanthal walks with gait
C van damme gait and uncontrolled movements cant feel egg texture
Benedict cant feel egg texture
Weber brit in wheelchair

Rl vs bss vs bss+
Electrolytes more cl from other sources like Mg
Nacl 102 110 122
Kcl 4 10 5
Ccl 3 3 1
Mgcl 1.5 1
Na Ca K found by hartmann to keep muscles contracting.
Buffers: bss uses acetate/citrate while bss + uses bicarb/phosp
Nalac 28

Naacet 29
Nacit 6

Na2po4 3
Naco3 27

Bicarb is the most physio buffer but is not stable and when mixed only stable 6 hours
The pka= ph when it exists 50% split associated /dissociated
Additives bss+ has dextrose & glutathione
Dextrose 5
Glutathione[oxidized 0.3
Although Glutathione is needed as antioxidant in reduced form it is unstable so oxidized
form with ?benefit used
Dextrose allows longer nutritional support
Physical properties
Ph 6to7.2 7.4 7.4
Osm 207 305 305
NB
SALINE Has nacl 154 and osmo 290
Optics
Glasses correction is diopteric power of far point
To calculate accomodation take prints and test as close as possible vision and work out
diifernce between near and far point.
Normal 6 Diopters at 40 years and decrease 1 Diopters every 4 year older and increase by
half D every 4 year younger ie at 32 it is 8 at 12 years 9.5 at 68 only half D

8 10
12 9.5
16 9
20 8.5
24 8
28 7.5
32 7
36 6.5
40 -----6d
44 5
48 4
52 3
56 2
60 1
I will lose half diopter every 4 years until i hit 40 when i will start to lose 1 diopter every 4
years!
Other 3 ways ;
1 method of spheres Place a 3D lens in front of emmetropic or corrected eye ie make far point
33cm .Then use ruler to distsnce nesr point and work out difference
2

) BSS Plus
has:
1) glutathione
2) bicarbonate
3) glucose ?
- used in diabetics
- Fortified BSS Plus can be prepared by adding 3 ml of a 50% dextrose solution
- this is done to preserve clear lens in diabetics

Dystrophies

Inheritance Most AD
Cogans and fuchs -----sporadic
Ie common ones I see in clinic sporadic
Macular/gelatinous-----AR
Epithelium
Bm=cogan microcystic=map/dot/finferprint Not familial or progressive in 20s
Hist;Fibril protein between bm & bowman ----maps
Absent hemidesmosome---erosions
;Fibril protein between epithelium layers
Rx Nil
Meesman AD vacoules in epithelium = bubble paper
Rx not reqd.

Bowmans layer
Reis bucklers AD
No bowmans
Rx eximer/graft very necessary
Bowmans dystrophy ii= thiel behnke AD=honeycomb
Rx nil rqed
Central crystalile schnyder dystrophy
Central scintalating cholesterol /phospolipid
Rx eximer
So far all AD except 1st MDF/

Stromal
Lattice 12 3 amyloid
All AD
Grade from fine to course
Rx lamellae/PRK oftennil if fine type i
Granular AD
Hyaline
Rx lamellae/PRK
Avellino
Hyaline/ amyloid
Superficial snowflakes
Looks like Granular or Lattice often confused
Rx nil
Macular most common dystrophy
Iem keratin sulfate only corneal manifestations
2 types 1 11 depends on ag in serum to keratin sulfate
Only one of two AR
Hist closely packed collagen/abnormal aggregate GAGS
RX ONLY PRK but unfortunately WITH late recurrence.
Gelatinous drop like dystrophy
=ant stromal amyloid
AR like macula
Rx superficial keratectomy
Endothelial
PPD ENDOTHELIUM like epithelium AD BIRTH RX NOT NEEDED
CHED FOCAL LOSS ENDOTHELIUM AD OR AR BIRTH RX PRK EARLY
FUCHS EASY AD BUT MOST ARE SPORADIC!

Ched CHILDHOOD ad or ar
Ar at birth with thich opacified
Cornea and deprivation
nystagmus
Ddx cong glaucoma / peters/ corneal opac eg infectious,metabolic,forceps/

Ad in childhood slowly progressive

PPD PARENTHOOD ad
Vessicles and like ice ie angle/iris growth causing glaucoma

FUCH Fifties ad
Gutta ic inc glaucoma
 Quick refraction
eye>>>>>FAR POINT>>>>
slow fast neutral fast slow

dull bright brightest bright dull

Narrow wide no movement wide narrow

confusing!

A plus lens pulls neutral far point in!

For every diopter of accomodation we converge 3 to 5 say 4 prism diopter!
By taking a working distance eg .33m or 33cm i am effectively making it my far point! That i have chosen to bring
everything or neutrality to.
I must subtract this so my refraction gives the diopteric power of the far point
Focal length is half radius so diopteric power is 1\half of radius in meters

Magnification
Say of a 60D lens
=focal length of 16mm

Quick anatomy
MIDBRAIN
^ __ ^ superior collic
l O o o O l lgb & pretectal
l OO l E/W
l a a l nearreflxcentre
__________
nb cn111 exits anteriorly
Near reflex centre more ventral
Pupil reflex centre dorsal=pretectal
Cavernous sinus
_________
____l____l____ chiasm/ica
/ \ pit g / \ on
/ / \ \ tr
/ cs / \ \ v1/v2
l / sph si \ l
L _ /______ _ \___ l ica/ab
/ sph bone \

cowillis
\ \ \ / / aco &
\ \__\_/ / aca
===0 / /___ \ \0===mca
/ / \ \pca to bas

asaler
Iris lesions diff diagnosis
Cong
 eg brushfield=in downs areas of normal iris with ring of atrophy 10 to 20 spots
 Nf lisch nodules=pinhead size nest of naevus cells

Inflam
 busaka=at iris stroma/
 knoeppes=at pupil border = macrophages that may be giant or bechets
Infectious
 iridicyclitis/
 Fungal endophthalmitis
Deg
 eg sec atrophy hsimplex or essential
Tx of melanocytes
 Neavus = discrete nodules variable pigmentation also in neurofibromitosis & cogan
reeses type of ice vs chandlers=only iris atrophy mostly unilateral in middle age.
 Iris freckle=flat inc pigment but not no of melanoctes
 Malignant melanoma iris distortion esp inferior temporal variable pigment
 Tapioca melanoma=nodule may be ass with glaucoma
 Melanocytosis cong o/od unilateral ass with blue patches sclera mal potential
Tx of PE
 Iris pigment epithelium proliferation = black velvety plaques of hyperplasia often
seen esp by us after trauma
 Iris pigment epithelium cysts=both layers cyst and raise stroma may transilluminate
better when dilated b scan useful
 Epithelium invasion / cyst may be solid/serous follows stroma injury to protrude thru
stroma
 Medullary epitheloima rare on iris
Other
 Juvenile XGL= orange granuloma with cholesterol histocytes and giant cells plus
Touten=giant cells with chronic inflammatio Benign in first year of life may cause
hyphema Regress spontaneously may be anywhere else ass with glaucoma
Stromal tx
 leiomyoma/sarcoma
Malig tx
 metastatic,
 RB
 leukaemia
Aquired
 fb rxn

Nystagmus
How to examine
1Look at eyes
2Look at head posture used to dampen nystagmus [esp in congenital ]
Look at nystagmus in 1'position
--4 planes hor ver rotary see saw
--2 types of velocity jerky=fast and slow and pendular= equal velocity
--direction of fast [is correcting and not diseased movement
--size fine medium or course
4do ocular motility with object not pen at 1/2m for 5 sec mainly to see if size is
increased in each of 6 positions[in jerk it is increased if eyes turn to fast
phase side.]
5 check for dampening on convergence
6do cover test to elicit latent manifest nystagmus
7 do neuro exam if; Jerky or INO~~~~Cerebellar---disdiokinesis/dysmetria ie MOTOR
Pendular~~~~FOVEAL EXAM eg albinism/optic hypoplasia IE SENSORY
See saw~~~~Bitemporal hemianopia

Common types
1Jerk dt cerebellar lesion and inc when looking in dir of fast
phase
2down beat is fast dt cerviomed lesion eg arnold chiari ie low
down !
3 upbeat is fast dt pon/med 4th ventricle/cerebellar vermis
4 see saw when one eye elevates and intorts other depresses and
extorts dt chiasm lesions
5congenital
Is pendular with poor vision so check eye
Or if true congenital with ok vision than do 13 point check!
6convergence retractioxx dorsal mid brain /parinauds =part of
vertical gaze palsy
7ataxic nystagmus dt INO when abduction eye goes mad
8 latent nystagmus in infantile esotropia when eye is covered
9nystagmus and if it dampens on convergence it is an entity
called nystagmus blockage syndrome.

Genetics rp
Rhod chromosome 3=Rod 3 letters

Red and green chromosome x

Blue chromosome 7
Rhodopsin mutations
 Pro23hist=histadine sub with proline at 23 aa position
 Classic type 30% of AD type
 others pro34leu/his----less common but worse.
 Rds[ retinal deg slow]gene mutation codes peripherin
 AR rp is due to nonsense mutation in rhodopsin
LCA
Ar and at birth
Early normal and later like rp
 guanylate cyclase def no gtp to c gmp and isomerase all trans retinyl ester to retinol
Nb the genes are specific ie therefore no other organ involvment
Nd chro 17 and 1
Cone rod dys= central or inverse rp very early onset and lose central vision first otherwise looks like rp
Choroidaemia
x linked early looks like rp and later confluent cr atrophy
Gyrate high levels of ornithine ar inheritence later scalloped or gyrate atrophy def ornithine ketoacid
aminiacid def which can be assayed in skin fibroblast
Ushers 3 types all ar
Ataxia and sn deafnessall above ddx of rp
Rp pathology
Pigment lost from pr and deposits intraretinal along bv and superficially
arteiolar attenuation is sec change and waxy pallor of on is atrophy
Pscc unknown cause
Dust like part in vitreous= free melanin and macrophages with mealanin.
White dots at level of rpe = r,puntata albesens= rpe degeneration

Also exudative vasculopathy

Nb sectoral rp inf nasal is mostcommon
12 genes ad 16
ar 6
xl
either transduction rhodopsin peripherin or rpe itself

Physiology

Rhodopsin
T1/2 420 years,348 aa crosses 7 times
spectral differences due to amino acid difreences
C intracellular
close by has a phosphorylation site fxn inactivation
and 2 × palmitate fatty acids nearby fxn
P intra disc
close by has oligosaccharide residues nearby fxn maintain structure
tranducin binds inside disc
Visual cycle
photoreaction cis to trans
met i to ii ~~~last and unique only reversible reaction
this finally resulting in trans retinol that now allows binding of transducin.
that is activated rhodosin allows transducin to bind
Transducin
It is a G protein abg.

normally GMP is linked to a membrane G protein and when activated in dark is converted to CGMP that
keeps ion open.

Tranducin closes chanels of this type by;

Transducin binds and splits into active Phosphodiesterase that breaks down cGMP.

Inactivation of photocascade
1Activated Rhodopsin inavtvated by phosphorylation at its sites or attachment of Arrestin
2decreased Ca conduction stimulate recoverin that stimulatesGuanylate cyclase
dark current outer to inner current of Na
Remember: cells are - inside generally due to NA/K pump 3 Na out to 2 K inand the fact membranes are
more permeable to K moving out than Na in

Congenital nystagmus
Pt normal can see
Ie harmless /
13 points
1At birth
2Dampens convergence
3Horizontal
4Conj
5Null point
6Uniplanar
7All dir of gaze
Latent component
8No oscilopsia
9Paradox optokinetic response
10Diminished in darkness
11Binocolar
12Inc on fixation but dampen on convergence
13Head nodding=titubation
14Head tilt to null point
Nb neutral point is where nystagmus reversed vs null=no nystagmus

Atropine vs Phospholine iodide:

Atropine blocks accomodation ie antimuscuric
Phospholine iodide increase accomodation ie muscurinic ie inc fxn of ach

Phospholine iodide:
-is an acetylcholinesterase inhibitor which is used as a miotic agent
-can help patient with hypermetropic accommodative esotropia and patient with a high AC/A ratio
-causes contraction of ciliary muscle and iris sphincter resulting in an increa`z4qqsed accommodation for a given accommodative
effort and therefore less convergence
-side effects include: iris cysts (reduced with concurrent treatment with phenylephrine, cataract, retinal detachment and angle
closure glaucoma in adults.
-has systemic effect and can prolong the action of succinylcholine. Therefore, patients should not have succinylcholine or have to
stop the drops at least six weeks prior to surgery

Pathology
Oedema and exudates from damaged bv acc in plexiform layer
Protein pas + eoisonophilic=hard exudate
Subhyaloid hx boat shaped
Nfl hx=flame shaped
Deeper dot/blot
Roth spots=white centre bacteria/neutrophils
MA
Cws=infarct of nfl

Imc drugs
 cyclophos is n2 mustard cross links guanine doc WG MU OCP
Antimetabolites
 Folate antagonists methotrexate inhibits folate to tetrahydrofolate
 Purine analogue Azathioprine doc TED
 PYRIMIDINE ANAlogue 5FU
 Fungal cyclosporine inhibits T cells
 Mitomycin C
Anatomy
rectus muscles
12 mm posterior to insertion the rectus muscles penetrate posterior Tenon's capsule
which fuses with the intramuscular septum to form muscle sheath
tendon length: 4-8 mm long
muscle length: 40 mm
muscle width: 10 mm
horseshoe shaped insertion so hook them posteriorly
insertion from limbus is approximately:
5.5 mm (MR) 6.5 mm (IR)
7 mm (LR) 8 mm (SR)
Tendon
So tendon 2cm long muscle 1cm only
Io nil or 1mm
Mr small only 4mm
Lr long 9mm
MR
easiest to lose without attachments to obliques
tendon is only 4 mm long, therefore resection is often bloody

LR
Faden procedure ineffective since it already has long arc of contact
easiest to expose
if lost, look at the inferior oblique insertion
tendon is 9 mm long

superior oblique
SO muscle is the shortest EOM, only32 mm long, but the tendon is the longest at 20
mm
As it passes underneath the SR, it becomes attached to the SR muscle sheath
insertion is variable, but usually at the lateral border of the SR
vortex vein is located posteriorly
inferior oblique
IO tendon 1 mm
inserts almost directly over macula about 12 mm posterior to the lower LR insertion
inferotemporal vortex vein very close
nerve enters as IO passes below IR

Blood supply
30% of anterior perfusion by 2 long posterior ciliary arteries at 3 and 9 o'clock
70% by 7 anterior arteries in rectus muscles
LR only rectus muscle with one anterior ciliary artery, all others have two
after surgery, anterior ciliary arteries do NOT recannulate
because there are no posterior ciliary vessels superiorly and inferiorly, iris angiograms
are more disrupted when IR or SR are operated on
iris angiograms do not predict ischemia
older patients may be more prone to ischemia
perilimbal conjunctival vessels may play a role in circulation
Hasselheim /jansen for LR palsy works by splitting lr and attaching to SR & IR.
Squints
Weaken move away from insertion
Strengthen move to insertion

Brown's syndrome:
-caused by a taut superior oblique tendon
-slight downshooting on adduction is common and widening of the palpebral fissure on adduction
-the condition may resolve spontaneously and therefore surgery is not usually indicated
surgery include superior oblique tenotomy with silicone expander or superior oblique tenotomy with ipsilateral inferior oblique
recession to prevent post-operative inferior oblique overaction
Color vision fields
central 4 degrees: no blue; red & green only=fovea
4 to 20-30 degrees: trichromat=macula
30-70 degrees: dichromat (red-green blind)=equator
> 70 degrees: monochromat=peripheral

Interno
Goniotomy
Incision made at midpoint schwalbes & s.spur running for 120'
Trabecodyalysis=similar but incision made at schwalbes .and using flat part of knife TMW is
disinserted from scleral spur
Externo
Trabeculotomy
Do steps of visco and then enter schlems canal
Put trabeculotome right into canal and tear trabeculum to enter ac
Repeat procedure to the left.
Nb all 3 are to make a connection between ac and schlems canal
Anatomy of angle recession
Imagine ciliary body just below sclera.
Longitudinal fibres attached to s.spur.
Circular near stroma and oblique in between.
It is triangle and iris attaches anterior.
Anterior epithelium in contact with stroma and pigmented
post incontact aqueous and non pigmented and is blood aqeous barrier
Cyclodialysis is disinsertion of Longitudinal fibres of cb from s.spur
Angle recession is split between Longitudinal fibres &oblique/circular forcing ciliary body
anterior
Iridodialysis is separation of iris from ciliary body.
What is ICE
Iris navus,chandlers=corneal ,iris atrophy
What is uveoscleral flow
10%
Aqueous enters ciliary body into suprachoid and vortex veins
Other iris veins

Surgical limbus
2mm band with post limit over s.spur.
2 parts ant blue=betw bowmans and schelbes
Post white=betw schwalbes and spur
Anatomical limbus=ant limit isline joining bowmans & scwalbes and post limit is curved line
that is transition of corneal fibres & haphazard scleral collagen fibres

Eua use ketamine not isoflurane/halothane as they dec IOP.

What is icg
Indocyangreen
It is 98% bound so very little leaks and so detailed choroidal circulation seen.without blur of
leaked out dye
Absorbed at 805 and flur at 835nm
Used mainly choroidal pathology
The is also a better picture of choriod as it is more visible thru RPE & xanthophyl.
Why is fovea dark?
Choriodal circulation is v.important but choriodal fluorescein is blocked by 1RPE(taller and more
melanin)
2increased xanthophyl
3avascular
What is blood retinal barrier?
INNER---Retinal capp endothelial cells~~~~~ Allows bv to be seen
OUTER-- RPE~~~~~~~~ prevents free fluorescein into sensory retina.
Princples of fluorescein ?
Light excited short wavelength emits light long wavelength.eg blue makes green
490nm--->>>530
Medical retina .
What's CSO
Breakdown of RPE.
Young psychiatric adrenalin junkies.
Ass optic pit,coloboma,choroidal melanoma.
Swelling so correct with plus lens ie hyperopic short eye
May look like and all risks of myopia ie atrophy,cnvm etc.
Ffa smoke stack /ink blot.
Mx 60% recover 3months
80 ---6 and 100--- 1year
40% recurrence.
What is CMO?
+ ***Remeber this leakage from perifovealar capillary bed = Petaloid pattern of CMO
May be a vascular /non vascular cause
Muller cells intracelullar swelling reversable
The muller at outer plexiform/henles layer so the swelling is here
Treatment of CMO
1) NSAIDs (topical and po)
2) steroids (topical, subTenon's and po)
3) Diamox (po)

tip to check for IOO you must adduct eye!

tip to check for DVD COVER eye

Vertical squints
1 so/io palsies or overactions
2multiple muscles eg congenital fibrosis syndrome double elevator palsy,DVD,A & V PATTERNS
3 other's eg cn111 palsy TED, blowout fractures
What is IOA
Mostly bilateral associated with horizontal squints or SO paresis or idiopathic.
Clinically
Ass V PATTERN this can be understood by herrings law that dictates that if io is overactive the
superior rectus of other eye must also be overactive!!
SO underaction
Upshoot in adduction.
Obeys herrings law ie sr of other eye also active

Faden
For dvd does not obey herrings law
We recess superior rectus and then with non absorbable fix it 12mm post to globe.
Outcome causes no restriction but good cosmetic change in 1' position but restricts elevation
when moved to upgaze
Fxn restrict movement in direction

Io is recessed or weakened in ioo ie moved from insertion AT LOWER BORDER MR MIDDLE TO

IR BORDER NEAR INSERTION
SO is strengthened or moved closer to insertion by splitting into anterior and posterior part and
move anterior part near SR INSERTION