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Ophthalmology

Dhaval Patel

MD (AIIMS)

1st Edition

Explorer

Ophthalmology Post-PG Examination Guide


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Ophthalmology Explorer

Ophthalmology Post-PG Examination Guide

MD (AIIMS)Dhaval [email protected]

by ophthalmologyexplorer.blogspot.com1st edition, April 2014

This is a compilation effort from my preparation notes and other sources, thusany contributions or comments are welcomed in the effort to improve this book.Therefore, feel free to e mail me at-

[email protected]


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Ophthalmology Explorer Dhaval Patel MD

1

PREFACE

The CLASS is knowing what to say, when to say and when to stop.

Dear Friends,

If you are reading this, then either you are approaching your final ophthalmology exams

or you are preparing for further study courses in ophthalmology.

So first thing I want you to know is the course for this exam include all aspects of

ophthalmology in different amounts and nobody knows it perfectly. This preparation manual I

have prepared during my residency and added up while preparing for senior residency/

fellowship examinations preparation which may serve as a small guide to your preparation. It

will also serve as a good collection of facts which we might forget/neglect during overall MD/MS

exam preparation.

So whatever it may serve you, I am proud of what I have prepared and I feel it worth

sharring with all emerging ophthalmologist friends.

All the Best..!!

-Dhaval Patel MD


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INDEX

Exploring EYE .................................. 6

Basic Sciences ............................... 90

Optics & Refraction ......................... 122

Cornea ........................................ 160

Lens ........................................... 192

Glaucoma .................................... 205

Retina......................................... 226

Uvea .......................................... 264

Strabismus ................................... 275

Neurophthalmology ......................... 284

Oculoplasty .................................. 310

Community Ophthalmology ................ 337

Miscellaneous ............................... 342

Lateral Thinking ............................. 356

The Class Questions ....................... 364

Important History ............................ 369

Recalls from previous papers ............. 370


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3

Exploring EYE .................................. 6

AAO Color Codes of Topical Medication: 6

Age Related Changes ...................... 6

Aquaporins ................................... 7

Acquisition time.............................. 7

Axis and Angles ............................. 8

Bimodal Age Distribution ................... 8

Blocks ......................................... 9

Cell Cycle Phase Facts ..................... 9

Collagen Collection ....................... 10

Contents of Important Fluids ............ 11

Chromosomes for Eye .................... 13

Connexins .................................. 19

Craniosynostosis .......................... 20

Diameters .................................. 20

Drug Resistance ........................... 21

Dye for Eye ................................. 21

Electromagnetic Spectrum ............... 21

Evolutions of anesthetic techniques for

cataract surgery ........................... 22

FDA Approved Drugs ..................... 23

FDA Device Classification ............... 26

Field of View ............................... 27

First in Genetics ........................... 27

Fellow Eye Risk ........................... 28

Frequency of Probes ..................... 29

Genes ....................................... 29

Giant Cells .................................. 35

Growth Factors ............................ 35

Half Life ..................................... 36

HLA .......................................... 37

HLA wise Diseases ..................... 37

Disease wise HLAs ..................... 37

Host Cell Receptors ....................... 38

Host for Parasites ......................... 39

Hypersensitivity in Eye .................... 39

IHC Markers ................................ 40

Inheritence .................................. 41

Inside Retinal Layers ...................... 42

Interferons Therapy & Eye ............... 43

Intraocular Gases .......................... 44

Intracameral Dosages .................... 44

Intrastromal Dosages ..................... 45

Intravitreal Dosages ....................... 45

Intravitreal Implants ....................... 46

Iris Nodules & Pathology ................. 48

Laser Facts ................................. 48

Brief History .............................. 48

Instrument Wavelengths ............... 49

Therapeutic Wavelengths ............. 49

Laser settings for glaucoma ........... 50

Laser settings in Retina ................ 51


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4

Laser Parameters for PTK ............ 51

Modes of Laser ......................... 51

Laser Mediums ......................... 52

Laser Safety Classification ............ 52

Latest Drugs ............................... 53

Mechanism of Action ..................... 57

MIP .......................................... 58

MMPs ....................................... 58

Molecular Weights ........................ 59

MUCins ..................................... 59

NV % ........................................ 60

OCT Review ............................... 61

Optic Nerve Segments ................... 62

Orders of Abberations .................... 63

Percentages % Primer ................... 63

Phacomatosis .............................. 65

Principles ................................... 66

Radiation and Eye......................... 67

Rates ........................................ 67

Recurrence % .............................. 68

Refractive Indices ......................... 69

Resolutions ................................. 70

RB Stats .................................... 71

Racial predilection of Diseases ......... 72

Studies and Trials ......................... 72

DR ........................................ 72

DME ...................................... 74

ROP....................................... 76

ARMD .................................... 77

Vitreomacular interface (VMI) diseases ............................................ 81

Glaucoma ................................ 82

ON ........................................ 83

NAION .................................... 83

MISC ...................................... 83

Surface Tension ........................... 84

Specific Gravity ............................ 84

Surface Area ............................... 85

Survival Rates .............................. 85

Test Distances ............................. 86

Thickness ................................... 87

VEGF Facts ................................ 88

Vitreous cavity volume displacement ... 89

Water Content .............................. 89

Basic Sciences ............................... 90

Optics & Refraction ........................ 122

Cornea ....................................... 160

Lens .......................................... 192

Glaucoma ................................... 205

Retina ........................................ 226

Uvea .......................................... 264

Strabismus .................................. 275


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5

Neurophthalmology ......................... 284

Oculoplasty .................................. 310

Community Ophthalmology ................ 337

Miscellaneous ............................... 342

Lateral Thinking ............................ 356

The Class Questions....................... 364

Important History ........................... 369

Recalls from previous papers ............ 370


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6

Exploring EYE

AAO Color Codes of Topical Medication:

Based on the American Academy of Ophthalmology recommendations to the FDA to aid

patients in distinguishing among drops and thus minimize the chance of using an incorrect

medication

Purple Cap: Alpha-Adrenergic Receptor Agonists

Yellow or Blue Cap: Beta-Blockers

Green Cap: Cholinergic Agonists, Miotics

Orange Cap: Carbonic Anhydrase Inhibitors

Turquoise/Teal Cap: Prostaglandin Analogues

Red Cap: Mydriatic/ cycloplegic agents

Tan Cap: Anti-infectives

Pink Cap: Steroids/ Anti-inflammatory

Gray Cap: Nonsteroidal anti-inflammatories

Dark Blue: beta-blocker combination

Age Related Changes

Ganglion cell loss: 5000/year

Endothelial cell loss: 0.6%/year

Decrease in ACD due to increase LT: 20 microns/year

Age related loss of VF sensitivity: 1 db/year

15.6-μm decrease in choroidal thickness for each decade of life

LENS thickness increases 0.2 mm per 10 year .

20 year: 3.8 mm

40 year: 4.4 mm


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60 year: 4.8 mm

80 year: 5.2 mm

central anterior chamber depth decreases 0.01 mm/year

Aquaporins

Water channels are known as aquaporins and lens epithelial cells contain an abundance of

these.

MIP26 is believed to be a very old (and not very efficient) member of the aquaporin family

and is termed aquaporin O.

Types

o AQP0 (MIP) in lens fiber

o AQP1 in cornea endothelium, ciliary and lens epithelia and trabecular meshwork

o AQP2 is not present in eye and is restricted to the kidney collecting duct

o AQP3 in conjunctiva

o AQP4 in ciliary epithelium and retinal Müller cells

o AQP5 in corneal and lacrimal gland epithelia

AQP1 protects against vascular leakage by stabilizing the formed vessels.

NMO-IgG is a disease-specific autoantibody for neuromyelitis optica (NMO) and its target

antigen is aquaporin-4 (AQP4) water channel.

Acquisition time

Pentacam: 2 sec

OCT: 1 to 5 sec

Visante ASOCT: 3.3 sec

o Anterior segment scan ( 16×6mm): 256 A-scan/ 0.125 sec

o High resolution scan: 512 A-scan/ 0.25 sec


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o Pachymetry scan: 128 A-scans/0.5 sec

Dynamic light scattering DLS for lens pathology: 5 sec

CSLO: 1.6 sec

Axis and Angles

Axis of the Eye

FOVea

o Fixation Axis: This is a straight line that joins center of rotation of eyeball with fixation point

o Optical Axis: A line passing through center of cornea, center of lens and posterior pole ofretina is the optical axis of eyeball

o Visual Axis: A line joining point of fixation with fovea and passing through nodal point of

eyeball is called visual axis. Nodal point of eyeball is just anterior to posterior capsule of lens.

Fixation point is the point which is being seen with fovea at any particular moment.

o Pupillary Line: This is a straight line that passes through center of pupil

Angles of the Eye

o Angle Alpha is the angle formed between optical axis and visual axis. AOV

o Angle Kappa is the angle formed between visual axis and pupillary axis. KaVPa

o Angle Gamma is the angle formed between optical axis and fixation axis. GOF

POsitive angle Kappa results in pseudoeXotropia. K-POX

Bimodal Age Distribution

Craniopharyngioma (peaking in the first 2 decades and again in the years 50 to 70

Thyroid orbitopathy (for women occur from ages 40 to 44 years and 60 to 64 years; for

men from ages 45 to 49 years and 65 to 69 years)

Hodgkin's lymphoma (early peak at 15 to 35 years of age and a second peak after 50)


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Glaucoma in SWS: (early-onset/congenital-type and later-onset)

Ocular Trauma

Blocks

Facial Blocks: LOAN

van Lint‘s block: Blocking the peripheral branches of facial nerve

O‘Brien‘s block: Facial nerve trunk block at the neck of mandible

Atkinson‘s block: In it superior branches of the facial nerve are blocked by injecting

anaesthetic solution at the inferior margin of the zygomatic bone.

Nadbath block: facial nerve is blocked as it leaves the skull through the stylomastoid

foramen.

Other Blocks

Retrobulbar block was introduced by Herman Knapp in 1884

Peribulbar block was described in 1986 by Davis and Mandel

Cell Cycle Phase Facts

Thymocyte- T cells: G0 arrest

Stem Cells: G0 arrest

Endothelial Cells: G1 arrest

central zone epithelial cells of lens capsule: G0 arrest

In the G1 phase of the cell cycle, the RB-protein is hypophosphorylated.

In S, G2, and M, it is hyperphosphorylated.


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p53 mediates arrest of the cell cycle in the G1 phase after sublethal DNA damage

Rb gene arrests cells in the G1 or G1/S-phase of the cell cycle, and stops further

proliferation.

Mitomycin C acts on all phases of cell cycle.

Collagen Collection

Type 1: corneal stroma, tarsal plate

Type 2: vitreous

Type 3: ciliary process

Type 4: Descemet membrane, lens capsule, PNBZ, basal lamina of corneal epithelium

Type 5: Bowman membrane

Type 7: ABZ

Cornea total Collagen 15%

o fibrous collagens types I, II, III and V

Type I 50-55%

Type III ~ 1%

Type VI 25-30%

o non-fibrous collagen type IV

Type IV 8-10%

o filamentous collagens types VI, VIII, IX and X

o basal lamina of the epithelium contains type IV collagen

o Bowman‘s layer: type V

o predominant collagen (about 90%) of the stroma is type I

o Descemet's membrane contains predominantly type IV collagen, with about 10%

type V


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BM of ciliary process and ciliary muscles ECM: laminin and collagen types I, III, and IV

human trabecular meshwork: collagen types I and III and elastin

Juxtacanalicular Tissue: collagen type III but no collagen type I or elastin

steroid-induced glaucoma shows increase in fine fibrillar material stains for collagen typeIV in the subendothelial region of the Schlemm canal

anterior uveitis: reducing the density of collagen type I in the extracellular matrix of the

ciliary body leading to increase in uveoscleral flow

lamina cribrosa of the human optic nerve head: collagen types I through VI, laminin, and

fibronectin

Topical prostaglandin F2alpha treatment reduces collagen types I, III, and IV in the

monkey uveoscleral outflow pathway

Contents of Important Fluids

BSS: Na, K, Ca, Mg, Cl, Citrate, Acetate

BSS plus: ―+ HCO3, PO4, Glucose, Glutathione

Aqueous: ―+ Lactate, Ascorbate, Protein

M.K. Media (4days): Tc199, Dextran, PH 7.0-7.5, Osmolality 295-355, gentamycin sulphate

75-150 micro gm/ml, HEPES as buffer, Phenol red as indicator

K-Sol: Tc 199, MEM & Earles media, HEPES, Gentamicin, Chondroin sulphate 2.5%

Dexol: MEM, 1.35% Chondrotin Sulphate, 1mM Sodium pyruvate, 1mM non- essential

amino acids, Antioxidants, 1% dextran40.

Optisol GS: MEM, 1.35% Chondrotin Sulphate, 1mM Sodium pyruvate, 1 mM non-essential

aminoacids, Antioxidants, 1% dextran40, ATP, Iron, cholestrol, L-hydroxyproline, Vitamins, 2

antibiotics- Gentamycin, Streptomycin

Procell: MEM,1.35%chondrotin sulphate,1mM sodium pyruvate1mM,Non-essential

aminoacids,Antioxidants,Dextran40, Humen insulin 10 ug/ml & Human epidermal growth

factor hEGF 10ng/ml to improve long term endothelial survival after PKP

Eusol-C: Store at 4 deg.C, Dextran, Sodium Piruvate, Glucose, Essential & non-essential

aminoacids, mineral salts, Vitamins, Gentamin, hepes buffer, Bicarbonate, Phenol Red


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Organ culture medium: Fetal Bovine Serum, L-Glutamine, Earle's salts and 0.44%

Mercaptoethanol in addition to the other constituents present in most intermediate storage

media

Aqueous contents

Relative to plasma, aqueous humor has

o Slight hypertonicity and acidity (pH 7.2 in AC)

o Marked excess of ascorbate (15 times greater than arterial plasma)

o Marked deficit of protein (0.02% in aqueous vs. 7% in plasma)

o Only calcium and phosphorus are in concentrations of about one-half that in plasma.

o Chloride and bicarbonate vary from 20% to 30% above or below plasma levels.

o Sight excess of lactic acid

o Slight deficit of sodium, bicarbonate, carbon dioxide, and glucose

o Protein and antibodies in aqueous equilibrate with those in serum when a plasmoid

aqueous occurs with an anterior uveitis

o Albumin/globulin ratio is similar to plasma, although there is less gamma globulin

Tear contents

o Lipid layer

Wax, cholesterol, fatty acid esters

o Aqueous layer

Water

electrolytes (Na+, K+ Cl –, HCO3 –, Mg2+)

proteins (albumin, lysozyme, lactoferrin,transferrin, ceruloplasmin),

immunoglobulins (IgA, IgG, IgE, IgM)

cytokines

growth factors (EGF, TGF-α, TGF-β1, TGF-β2, bFGF, HGF, VEGF,

substance P)


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others (glucose, vitamins)

o Mucinous layer

Sulfomucin, cyalomucin, MUC1, MUC4, MUC5AC

o IgD has not been detected in any study of human tears.

Chromosomes for Eye

Chromosome 1:

Fuch‘s dystr ophy, COL8A2, AD

Posterior polymorphous dystrophy, PPCD2, AD

Stickler syndrome, COL2A, AD

Gelatinous drop like dystrophy, TYACSTD, AR

Schnyder corneal dystrophy, MJNFR, AD

EDS, EDS6, AR

Congenital glaucoma, GLC3B, AR

JOAG, Myocillin, AD

Stargardt‘s, ABCA4, AR

ARMD, CFH1

Usher syndrome, AR

Chediak higashi syndrome, LYST, AR

Leber‘s congenital amaurosis, RPE65, AR

Chromosome 2:

Congenital Glaucoma, CYP1B1, AR

Oguchi‘s disease, Arrestin, AR


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PXE, laminin/fibrillin, AR

Autosomal dominant drusen, EFEMP1, AD

Fleck dystrophy, PIP5K3, AD

Chromosome 3:

BPES 1 (with premature ovarian failure) and BPES 2 (without premature ovarian failure) are

caused by type 1 mutations in FOXL2 gene

Von Hippel –Lindau syndrome Inheritance is AD condition caused by a mutation of the VHL

gene clusterin

Retinitis pigmentosa, Rhodopsin, AD

Xeroderma pigmentosa, NER enzyme, AR

Alkaptonuria, homogentisate 1-2 dihydroxygenase, AR

Kjer autosomal dominant optic atrophy, OPA1, AD

Chromosome 4:

Axenfield Rieger syndrome, PITX2, AD

CSNB, PDE6, AR

Wolfram syndrome, WFS1, AR

Hurler syndrome, alpha L iduronidase, AR

Bietti dystrophy, CYP4V2, AR

Fraser syndrome, FRAS1, AR

Chromosome 5:

Treacher Collins syndrome (mandibulofacial dysostosis) Inheritance is AD with high

penetrance and variable expressivity, although 60% of cases occur with no family history

and are thought to arise by de novo mutation. The gene involved is the ‗treacle‘ gene

TCOF1 on chromosome 5q.


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Cri du chat syndrome (partial deletion of 5p)

Mutations in TGFB1 on chromosome 5 cause CDB1, CDB2, lattice type 1, lattice type 3A,

Avellino, and granular dystrophy. These are therefore allelic variants.

Chromosome 6:

Adult-onset macular vitelliform dystrophy is caused by mutation in the RDS gene on chrn

Dysromosome 6p, as well as the BEST1 gene in common with juvenile-onset Best

dystrophy.

VEGF

Pattern dystrophy, RDS/ peripherin, AD

Axennfeld reiger syndrome, FOXC1, AD

Chromosome 7:

Galactosemia classic, galactose 1 phosphate uridyl transaferase, AR

Pigment dispersion syndrome, AD

Chromosome 8:

Chromosome 9:

Lattice 2, gelsolin, AR

Nevoid BCC syndrome, PTCH, AD

Rilet Day syndrome, IKBKAP, AR

Chromosome 10:

Crouzon syndrome Inheritance is usually AD, but 25% of cases represent a fresh mutation.

The gene (FGFR2) has been isolated to chromosome 10.

Thiel behnke dystrophy, AD


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MEN2B, RET proto-oncogene, AD

Gyrate atrophy, OAT, AR

NTG-COAG, optineurin, AD

Chromosome 11:

Aniridia, peter‘s, AD keratitis, Axenfed reiger: PAX6, AD

Nanophthalmos, NNO1, AD

Best disease, 11q13 bestrophin, AD

FEVR, frizzled 4 gene, AD

OCA, TYR/OCA2, AR

CFEOM2: 11q13

Chromosome 12:

CFEOM-1:

Cornea plana, KERA, AR

CHSD, DCN, AD

Meesman dystrophy, KRT3, AD

Fundus albipunctatous, RDH5, AR

Chromosome 13:

Retinoblastoma, 13q14, AD

Sclerocornea, HCCS, AD

Microphthalmos, Trisomy 13

Congenital microcornea, AD

Oguchi disease, rhodopsin kinase, AR


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Late onset fuchs dystrophy, FECD2, AD

CFEOM-3

Chromosome 14:

Oculopharyngeal dystrophy Inheritance is AD caused by mutation on chromosome 14q.

Chromosome 15:

Marfan syndrome: FBN1, AD

Chromosome 16:

Posterior Polar Cataract: mutation of PITX3 gene

Macular dystrophy, CHST6, AR

Pseudo xantoma elasticum, ABCC6, AR

Fish eye disease, LCAT, AR

Tyrosenemia, tyrosine amino transferase, AR

Chromosome 17:

Meesman dystrophy, AD

NF1, NF1, AD

Cystinosis, CTNS, AR

Chromosome 18:

Edwards syndrome (trisomy 18)

Transthyretin


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Chromosome 19:

Chromosome 20:

CHED AD, CHED1 20911, AD

CHED AR< CHED2 20p13, AR

PPMD2, VSX1, AD

Chromosome 21:

Down syndrome (trisomy 21)

Homocystinuria: Inheritance is AR with the gene locus on chromosome 21q.22.3.

Chromosome 22:

NF2, NF2, AD

Sorsby dystrophy, TIMP3, 22q13, AD

Chromosome X:

XR

Fabry disease, alpha galactokinase

CSNB, calcium channels

Megalocornea, LTBP2

Coat‘s disease, NDP

FEVR, NDP

Retinitis pigmentosa, RPGR

Choroderemia, REP1

Norrie disease, NDP gene on chromosome Xp11.


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XD

Lowe syndrome, OCRL1

Alport‘s syndrome, COL4A3

Aicardi syndrome

Incontinentia pigmenti: NEMO gene on chromosome Xq28.

Ichthyosis, STS

Chromosome Y:

Connexins

At electrical synapses a cytoplasmic bridge is formed by specialized proteins called

connexins. Six connexins form a hexagonal tube that projects out of the plane of the

plasma membrane of one participating cell; this unit is called a connexon.

Connexin 43:

o gap junctions of lateral membranes of lens epithelial cells

o oculodentodigital syndrome

Connexin 46 and 50:

o Transmembrane proteins forming lens fiber gap junction is typically 16 nm thick

o connexin 50 or MP70 is most prevalent in outer cortical fibers, where it undergoes

age-related degradation to MP38, which continues in functional gap junctions.

connexin mutations can give rise to congenital cataracts

Connexin 50, connexin 37, and connexin 40 are all encoded by genes consisting of a single

exon on chromosome 1q21

A zonular pulverulent cataract has been localized to chromosome 13 near the connexin

46 gene.


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Craniosynostosis

SPOT:

Scaphocephaly: sagittal suture closure (aka 'dolichocephaly')

Plagiocephaly: unilateral Coronal suture (anterior) or Lamboid (posterior)

Oxycephaly: coronal suture plus any other suture, like the lambdoid

Trigonocephaly: metopic suture closure

Syndromes

Apert syndrome

Crouzon syndrome

Pfeiffer syndrome

Saethre-Chotzen syndrome

Diameters

Collagen fibres in corneal stroma: 25 nm diameter, 60 nm spacing between each pair

Collagen fibres in vitreous: 10 nm diameter

Lens fibre diameter: 10.5 um

Zonular fibres: 70-80 nm diameter, grouped into bundles of 5-50 um diameter

Cone diameter: 2 um with 0.3 um spacing

Cochet and Bonnet esthesiometer wire: 0.12 mm


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Drug Resistance

CMV UL97 mutations (a CMV DNA polymerase mutation that confers ganciclovir

resistance) were detected in 3% of patients treated with ganciclovir over 3 months and in

none treated less than 3 months.

Dye for Eye

Anterior Segment (Capsule staining)

o 0.5% indocyanine green

o 0.15% trypan blue (less costly when compared to the cost of ICG)

Posterior Segment

o ICG: ILM staining 0.05%

o IFCG: 0.05%

o TB: ERM stain 0.06%

o BBG: ILM staining 0.05%, 0.025%

o TA

o PB

o BrB

o NaF

Electromagnetic Spectrum

(part of spectrum which is important in ophthalmology)


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Ultraviolet C rays: This band is blocked by the ozone layer of atmosphere.

Ultraviolet B rays: This band is responsible for snow blindness and photo keratitis caused

by welding arc. Prolonged exposure to these rays can cause formation of pingicula and

pterigium.

Ultraviolet A rays: This band of UV rays is absorbed by crystalline lens and thus retina is

protected against their bad effects. Prolonged exposure to these rays causes cataract

formation. IOLs implanted during cataract surgery have chromophores [inhibitors of UV rays]

to protect retina against UV rays.

Visible Rays: VIBGYOR

Infrared A rays are responsible for macular burn in solar eclipse [photo retinitis].

Infrared rays B and C can cause corneal opacity and cataract formation on prolonged

exposure.

Evolutions of anesthetic techniques for cataract surgery

General anesthesia 1846

Topical cocaine 1881 Koller

Injectable retrobulbar cocaine 1884 Knapp

OrbicuIaris akinesia 1914 Van lint, O'Briens Atkinson

Hyaluronidase 1948 Atkinson

Peribulbar 1970 kelman (but not published)

Posterior peribulbar 1985 Davis and Mandel

limbal 1990 Furata et al.

Anterior peribulbar 1991 Bloomberg

Pinpoint anesthesia 1992 Fukasawa and Furata

Topical tetracaine 1992 Fichman

Topical plus intracameral 1995 Gills

No anesthesia 1998 Agarwal


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Cryoanalgesia 1999 Gutierrez-Carmona

Xylocaine jelly 1999 Koch and Assia

Hypothesis, no anesthesia 2001 Pandey and Agarwal

Viscoanesthesia 2001 Werner, Pandey, Apple et al

FDA Approved Drugs

Drugs Approved in 2012

Cystaran (cysteamine hydrochloride); Sigma Tau Pharmaceuticals; For the treatment of

corneal cystine crystal accumulation due to cystinosis, Approved October 2012

Jetrea (ocriplasmin); Thrombogenics; For the treatment of symptomatic vitreomacular

adhesion, Approved October 2012

Lucentis (ranibizumab injection); Genentech; For the treatment of diabetic macular edema,

Approved August 2012

Zioptan (tafluprost ophthalmic solution); Merck; For the treatment of elevated intraocular

pressure, Approved February 2012


Eylea (aflibercept); Regeneron Pharmaceuticals; For the treatment of neovascular (wet)

age-related macular degeneration, Approved November 2011


Zymaxid (gatifloxacin ophthalmic solution); Allergan; For the treatment of bacterial

conjunctivitis, Approved May 2010


Acuvail (ketorolac tromethamine); Allergan; For the treatment of pain and inflammation

following cataract surgery., Approved July 2009

Bepreve (bepotastine besilate ophthalmic solution); Ista Pharmaceuticals; For the treatment

of itching associated with allergic conjunctivitis, Approved September 2009

Besivance (besifloxacin 0.6% ophthalmic suspension); Bausch & Lomb; For the treatment

of bacterial conjunctivitis, Approved June 2009


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Ozurdex (dexamethasone); Allergan; For the treatment of macular edema following branch

retinal vein occlusion or central retinal vein occlusion, Approved June 2009

Zirgan (ganciclovir ophthalmic gel); Sirion Therapeutics; For the treatment of acute herpetic

keratitis, Approved September 2009


Akten (lidocaine hydrochloride); Akorn; For anesthesia during ophthalmologic procedures,

Approved October 2008

Astepro (azelastine hydrochloride nasal spray); Meda Pharmaceuticals Inc.; For the

treatment of seasonal and perennial allergic rhinitis, Approved October 2008

Durezol (difluprednate); Sirion Therapeutics; For the treatment of inflammation and pain

associated with ocular surgery, Approved June 2008


AzaSite (azithromycin); InSite Vision; For the treatment of bacterial conjunctivitis, Approved

April 2007


Lucentis (ranibizumab); Genentech; For the treatment of neovascular (wet) age related

macular degeneration, Approved June 2006


Macugen (pegaptanib); Pfizer / Eyetech Pharmaceuticals; For the treatment of wet age-related macular degeneration., Approved December 2004


Restasis (cyclosporine ophthalmic emulsion); Allergan; For the treatment of low tear

production., December 2002


Lumigan (bimatoprost ophthalmic solution); Allergan; For the reduction of intraocular

pressure in patients with open-angle glaucoma or ocular hypertension, Approved March

2001

Travatan (travoprost ophthalmic solution); Alcon; For the reduction of elevated intraocular

pressure in patients with open-angle glaucoma or ocular hypertension, Approved March

2001


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Valcyte (valganciclovir HCl); Roche; For the treatment of cytomegalovirus retinitis in patients

with AIDS, Approved March 2001


Betaxon; Alcon; For lowering IOP in patients with chronic open-angle glaucoma or ocular

hypertension, Approved February 2000

Quixin (levofloxacin); Santen; For treatment of bacterial conjunctivitis, Approved August

2000

Rescula (unoprostone isopropyl ophthalmic solution) 0.15%; Ciba Vision; For the

treatment of open-angle glaucoma or ocular hypertension, Approved August 2000

Visudyne (verteporfin for injection); QLT; For the treatment of wet age-related macular

degeneration (wet AMD), Approved April 2000


Alamast; Santen; pemirolast potassium ophthalmic solution, Approved September 1999

ZADITOR; Ciba Vision; Treatment for the prevention of itching of the eye, Approved July

1999


Alrex; Bausch & Lomb, Pharmos; Treatment for seasonal allergic conjunctivitis, Approved

March 1998

Cosopt; Merck; Treatment for glaucoma or ocular hypertension, Approved April 1998

Lotemax; Bausch & Lomb, Pharmos; Treatment for post-operative eye inflammation,

Approved March 1998

Salagen Tablets; MGI Pharma; Treatment for Sjogren's Syndrome, Approved February 1998

Viroptic; King Pharmaceuticals; Treatment for inflammation of the cornea in children due to

herpes simplex virus, Approved February 1998

Vitravene Injection; Isis Pharmaceuticals; Treatment for CMV in AIDS patients, Approved

August 1998


Acular (ketorolac tromethamine ophthalmic solution) 0.5%; Allergan; Treatment for

postoperative inflammation in patients who have undergone cataract extraction, Approved

January 1997


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Acular (ketorolac tromethamine ophthalmic solution) 0.5%; Allergan; Treatment for post-

surgical inflammation following cataract extraction, Approved November 1997

BSS Sterile Irrigating Solution; Alcon; Treatment during ocular surgical procedures,

Approved December 1997


AK-Con-A (naphazoline ophthalmic); Akorn; Over-the-counter combination

vasoconstrictor/antihistamine product for opthalmic use, Approved January 1996

Alphagan (brimonidine); Allergan; Treatment for open-angle glaucoma and ocular

hypertension, Approved September 1996

Ocuflox (ofloxacin opthalmic solution) 0.3%; Allergan; Treatment for corneal ulcers,

Approved May 1996

OcuHist; Pfizer; Over-the-counter antihistamine eye drop, Approved January 1996

Vistide (cidofovir); Gilead; Treatment for cytomegalovirus (CMV) retinitis, Approved June

1996

Vitrasert Implant; Chiron; Drug delivery system for the treatment of cytomegalovirus,

Approved March 1996

FDA Device Classification

3 classes of oph tha lmology devices

1. Class I devices (eg, refractometers, perimeters, sunglasses, visual acuity charts) are

usually considered minimal-risk devices. Although these devices are subject to general

controls, most of them are exempt from premarket review by the FDA. With few exceptions,

manufacturers can go directly to market with a class I device.

2. Class II devices (eg, phacoemulsification units, tonometers, vitrectomy machines, daily-

wear contact lenses) are usually considered moderate-risk devices. Class II devices are

those for which general controls alone are insufficient to ensure safety and effectiveness

and for which methods exist to provide such assurances. These devices, in addition to

general controls, are subject to special controls, which may include special labeling

requirements) mandatory performance standards, and postmarket su rveillance. With few

exceptions, class II devices requi re premarket review by the FDA.


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3. Class III devices (eg, excimer lasers, intraocular lenses, extended -wear contact lenses,

intraocular fl uids) are considered significant-risk devices that present a potential

unreasonable risk of illness or injury. Class III devices are those for which insufficient

information exists to ensure safety and effectiveness solely through general or special

controls. Class III devices cannot be marketed in the United States until the FDA

determines that there is a reasonable assurance of safety and effectiveness when usedaccordi ng to the approved indications for use. Most class III devices come to market

through the premarket approval (PMA) process and require an extensive review by the FDA

before approval is granted for marketing.

Field of View

Standard Fundus Camera: 20, 30 and 50 degrees

RetCam: 130 degrees

Optos: 200 degrees of retina (equator is at 180 degrees)

First in Genetics

Wow…!! It’s amazing that all of following diseases first described in each category has an eye

manifestation…!!! (Ref: Alex Levin MD, WEI, PA, USA )

1st AD: Piebaldism

1st AR: alkaptonuria

1st XR: red green colour deficiency

1st

XD: Incontigenta pigmenti

1st Mitochondrial: LHON

1st digenic: RP

1st trigenic: bardet biedel


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1st two-hit hypothesis: Retinoblastoma

1st contiguous gene deletion syndrome: anridia syndrome of wagner

Fellow Eye Risk

Keratoconus: 50% of normal fellow eyes will progress to keratoconus within 16 years

PXG: A patient with unilateral PXG and only PXF in the fellow eye is at high risk ( 50% in 5

years) of developing glaucoma in the fellow eye. A patient with unilateral PXG who does not

have PXF in the fellow eye has only a low risk of developing glaucoma in the normal eye.

Patients with advanced AMD (late ARM) in one eye, or even moderate vision loss due to

non-advanced AMD in one eye, have about a 50% chance of developing advanced AMD in

the fellow eye within 5 years.

In Age related Macular Hole, risk of involvement of the fellow eye at 5 years is around 10%.

In NAION, Involvement of the fellow eye occurs in about 10% of patients after 2 years and

15% after 5 years.

AAION affects 30 –50% of untreated patients of which one-third develop involvement of the

fellow eye, usually with in 1 week of the f i rst .

7% of patients with CRVO develop a nonsimultaneous venous occlusion of the fellow eye

within 2 years

The risk of any vascular occlusion in the fellow eye is estimated to be 0.9% per year .

The Macular Photocoagulation Study (MPS) reported that the 5-year risk of

neovascularization in fellow eyes of individuals with unilateral neovascular AMD was 10%

in those without large drusen and 30 –46% in those with large drusen

POHS with CNVM, 20% risk over a 2-3-year period of developing choroidal

neovascularization in the macula of the fellow eye

50-75% of patients with angle closure in one eye will have an attack in the fellow eye

often within 1 year (up to 10years) despite miotic treatment. Prophylactic laser iridotomy in

fellow eyes of patients presenting with unilateral acute PAC also appears to be safe and

effective in preventing acute PAC in 100%, and in preventing long-term rise in IOP in 89%


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Acute retinal necrosis may occur in the fellow eye in approximately 30% of patients at an

average interval of 4 weeks.

Chances of RD in fellow eye varies from 9-40%.

Frequency of Probes

USG: 10 MHz

Ultrasonic Pachymetry: 10-20 MHz

UBM: 50 MHz

HI-SCAN: 35 MHz

Genes

Genotypic heterogeneity: multiple genes causing single disease

Phenotypic heterogeneity: single gene causing multiple disease

PXF: LOX L1

BPES: FOX L2

Pterygium: KL-6

Lowe‘s syndrome: OCRL1 gene

TGFB1: aka BIGH3

o 5q31.2

o Protein produced by corneal epithelium

o Phenotypic heterogeneity

GREAT

Granular

Reis Buckler


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EBMD

lAttice

Thiel Behnke

PAX6, 11p13: phenotypic heterogeneity

o Aniridia

o Gillespe

o WAGR

Axenfield Reiger Spectrum (AD) – genotypic heterogeneity, multiple genes causing samedisease

o GJA1 (connexin 43) 6p21

o FKHL7/ FOXC1 6p25

o PITX2/ RIEG1 4q25

o RIEG2 13q14

o COL4A1 13q34

(MCQ: all except type question, so remember its Chromosomes 4, 6 and 13)

Fuchs: genetic heterogeneity

o Following all genes do cause Fuchs and other diseases mentioned below.

COL8A2: PPMD

SLC4A11: CHED

ZEB1: PPMD

PITX2: homeobox gene Peters, ARS, AN, Iris hypoplasia

KCNJ13: upregulates ZEB1


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Keratin genes: cytokeratin 12 + 3

o KRT3: 12q13 Meesman

o KRT12: 17q12 Stocker Holt

Keratoconus: VSX1, SOD1

Glaucoma Genes nosology:

o GLC is name given to primary gene loci byHUGO : Human Genome

Organisation, Geneva

o GLC1: open angle (only 10% pt): AD

Only 3 genes are known till now

GLC1A: JOAG 36%, POAG 4% 1q23-25 MYOC/TIGR

GLC1B: POAG 2q nI IOP

GLC1C: POAG 3q high IOP

GLC1D: POAG 8q23 high IOP

GLC1E: POAG/NTG 16% 10p14 Optineurin (OPTIc NEURopathy

INducing), nI IOP

GLC1F: POAG 7q

GLC1G: POAG 5% 5q WDR36 (WD Region 36)

o GLC2: close angle

o GLC3: congenital (>25%): AR

GLC3A: 2p21 CYP1B1, cyrochrome P450 gene

GLC3B: 1p36

GLC3C: 14q24

MYOC is responsible for 5.5% PCG

o Pigment Dispersion Genes: AD, 7q35


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o Pseudoexfoliation syndrome: LOXL1, 15q24-25

o Genes associated with MMP

MMP9 downregulated during acute PACG

SNP rs17576 of MMP9 at chromosome 20q11 is strongly associated withacure PACG.

o Genes Causing Early-Onset or Familial Glaucoma

CYP1B1, Cytochrome p450 Congenital glaucoma

LTBP2, Latent transforming growth factor beta binding protein 2

Congenital glaucoma

PITX2, Paired-like homeodomain 2 Axenfeld-Riegers

FOXC1, Forkhead box C1 Anterior segment dysgenesis

PAX6, Paired box 6 Aniridia

MYOC, Myocilin Primary open-angle glaucoma (juvenile and familial)

OPTN, Optineurin Familial normal-tension glaucoma

TBK1, TANK-binding kinase 1 Familial normal-tension glaucoma

LMX1B (9q34, glaucoma associated with nail-patella syndrome)

o Glaucoma Gene Testing

Congenital glaucoma CYP1B1, LTBP2

Anterior segment dysgenesis FOXC1, PITX2, PAX6

Primary open-angle glaucoma MYOC

Normal-tension glaucoma OPTN, TBK1, OPA1

Eyelid Tumors genes

o BCC:

Sonic hedgehog pathway

PTCH1 (patched 1): in BCNS or Gorlin syndrome

o SeCA:


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Muir Torre Syndrome

MMR- Mismatch Repair genes (MSH-2, MSH-6, MLH-1)

MSI- high frequency of Micro Satelite Imbalance

o Merkel Cell Carcinoma

MCPyV: Merkel Cell Polyoma Virus 70% cases

LTA: Large T Antigen binds to host proteins, forces cell into S-

phase

o Cutaneous Malignant Melanoma

C-KIT activating mutations chronic sun damage MM (Acral MM, Mucosal

MM)

BRAF activating mutations V600E (90%) Non chronic sun damage MM Nevi

P16INK4a-Rb pathway: loss of function mutation of CDKN2A Familial

melanoma (dysplastic nevus syndrome)

Melanocortin receptor (MC1R) varients increased risk of MM and BCC

independent of cutaneous pigmentation

ARMD

o Complement factor H gene (CFH): 1q32

o Apolipoprotein E: 19q13.2

o Many others..BIG BIG list!!

Retinal/Macular Dystrophies

o Best macular dystrophy BEST1, Chr11 AD/AR

o Stargardt disease ABCA4, Chr 1 AR

o Stargardt-like dominant macular dystrophy ELOVL4 Chr 6 AD

o Pattern dystrophy PRPH2 Chr 6 AD

o Sorsby fundus dystrophy TIMP3 Chr 22 AD


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o Autosomal dominant radial drusen EFEMP1 Chr 2 AD

o North Carolina macular dystrophy Unknown Chr 5 and 6 AD

o Spotted cystic dystrophy Unknown Unknown AD

o Dominant cystoid macular edema Unknown Chr 7 AD

o Fenestrated sheen macular dystrophy Unknown Unknown AD

o Glomerulonephritis type IICFH Chr 1 AR

Mutations of LHON

o 11778: 98% patients, VA < 20/200, worst prognosis

o

14484: 10-15% patients, high incidence of spontaneous VA recovery, best prognosis

o 3460: 8-15% of patients, high incidence of visual recovery, family history positive

Gene therapy: for LCA, RPE 65 gene, NEJM 2008 study, Lancet 2009

Ocular development genes:

o Sonic hedgehog

o Paired box

PAX2: (during optic vescicle, causes ocular-renal coloboma syndrome)

PAX6 (eye development)

o Other downstream genes CHX10, FKHL7 (6p15, forkhead transcription factor, ?

neural crest), PITX2

Genes causing Diabetes: ALR2, RHGE, TGF beta1

Uveal melanoma gene: DDEF1 gene, chromosome 8q

The ATP-binding cassette

o Subfamily A:ABCA

Adrenoleukodystrophy


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Zellweger syndrome

Stargardt disease (ABCA4)

Autosomal recessive retinitis pigmentosa

Cone-rod dystrophy

o Subfamily G: ABCG

ABCG2: limbal stem cells

Giant Cells

Langhans giant cells: peripheral ring of nuclei, associated with tuberculosis, sarcoidosis

Touton giant cells: midperipheral ring of nuclei surrounded by a peripheral ring of lipid,

associated with xanthogranu lomatous disease

Foreign body giant cells: randomly dispersed nuclei, associated with foreign material and

fungi

Growth Factors

INF-Y: decreases angiogenesis

PEGF: decreases neovascularisation

Angiopoeitin: decreases leakage

o Angiopoietins-1 –4 (Ang1 –4) form a family of growth factors involved in angiogenesis

o only Ang1 and Ang2 currently are known to have roles in ocular neovascular disease

o Endothelial cells are a primary source of Ang2 production where it is stored in

Weibel –Palade bodies (WPB) from which it can be released by a variety of stimuli

Myofibroblasts are derived from keratocytes under influence of TGF beta1.

HGF and KGF are predictor of corneal epithelial healing.

Keratocytes apoptosis is mediated by IL-1.


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PKC beta is most important in DR pathogenesis. It increases basement membrane

permeability.

Angiogenesis is regulated by a balance between VEGF and PEDF (pigment endothelium

derived factor), as evidence is emerging that PEDF may inhibit new blood vessel growth.

PDGF-B is a growth factor structurally related to VEGF. The contributions of PDGF-B to

angiogenesis are mediated largely through its effects on mural cells such as pericytes and

vascular smooth muscle cells.

Half Life

IVTA

o Normal eye: 41 days

o Vitrectomised eye: 16 days

o Aphakic eye: 6.5 days

PST

o Aqueous: 11 days

o Vitreous: 17 days

o Plasma: 25 days

Intravitreal Bevacizumab 1.25mg

o 4.32 days rabbit

o 5 days in humans

Intravitreal Ranibizumab 0.5 mg

o 3 days in monkeys

Strontium-90: 28 years


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HLA

HLA wise Diseases

A2: JIA

A11: Sympathetic ophthalmia

A29: birdshot chorioretinopathy (90-100% association)

B5, B12: behcet's dz

B7: toxoplasmosis, POHS, serpiginous choroidopathy, ankylosing spondylitis, APMPPE

B8: Sjögren‘s syndrome, sarcoidosis

B12: Ocular cicatricial pemphigoid

B13: sarcoidosis

B27: PAIR Ankylosing spondylitis (88%), Reiter‘s syndrome (85–95%), inflammatory

bowel disease (60%), psoriatic arthritis (also B17).

B51: behcet‘s disease, eales

Bw54: Posner-Schlossman syndrome, VKH?

DR2: POHS, intermediate uveitis, APMPPE

DR4: VKH, SO, OCP.

DR2/15: pars planitis and Multiple Sclerosis

Disease wise HLAs

Keratoconus: A9/10/12, B5/21

PXF: A1/33, B8

OHT progression to Glaucoma: B7/12

AMD: A3, CW02/07

Diabetic Retinopathy (DR) development: DR1/7

Diabetic Retinopathy (DR) proliferation: DR4, DQ8


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Retinal vasculitis: B44

Eales: B51, DR1/4

IU: B8/51, DR2

Pars Planitis: DR15/17/51

VKH: HLA-DR4 and HLA-Dw53 are more common in Chinese patients, HLA-DR1 and HLA

DR4 more common in Hispanic patients, and HLA DRB1 in Indian patients

SJS: significantly increased incidence of HLA-B12, HLA-Aw33, and DRw53

HSV EM: HLA-DQw3

TEN: HLA-B12

ocular lesions of SJS: HLA-B44

Birdshot choroidopathy: White, HLA-A29, 96%

Ankylosing spondylitis: White and asians, HLA-B27, 89%

Behçet's disease: Japanese, HLA-B5, 68%

Reiter's syndrome: White, HLA-B27, 80%

POHS: White, HLA-B7-77%, HLA-DR2-81%

Host Cell Receptors

Adenovirus type 37: CD46

Epstein –Barr virus: CD21

Herpes simplex virus: Heparan sulfate

Human cytomegalovirus: Heparan sulfate

Human papillomavirus: Integrin a6

Influenza virus: Sialic acid

Rhinovirus: ICAM-1

Vaccinia virus: EGF receptor


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Host for Parasites

Definitive:

o Toxoplasma gondii: domestic and wild cats

o Echinococcus granulosus: dog

o Taenia solium: human

Intermediate host

o Taenia solium: pig

o Toxoplasma gondii: animals including humans

o Echinococcus granulosus: sheep, cattles, pigs

o Francisella tularensis: rabbit, squirrels, cats, foxes, raccoons

o Brucellosis: veterinarians and abattoir workers

o Oncocerca volvulus: many species of black fly simulium

Both definitive and intermediate:

o

Taenia solium: human

Hypersensitivity in Eye

Gell, Coombs, and Lackmann‘s classification of Hypersensitivity Reactions

o Type 1: VKC, AKC, SAC, GPC

o Type 2: OCP, PV, DH

o Type 3: SJS, RA, SLE, PAN, RP

o Type 4: TB, WG, Contact dermatitis, herpes disciform keratitis, sarcoidosis, transplant

rejection


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IHC Markers

Melanoma markers: HMB45, melan A, tyrosinase, S-100 , MITF

Epithelial markers: Cytokeratins (CAM 5.2, AE1, AE3, CK7, CK20, involucrin, etc.)

Endothelial markers: Factor VIII, CD34

Muscle markers: Muscle specific actin (MSA), smooth muscle action (SMA), desmin,

myogenin

Neuroendocrine tumors: Chromogranin

Melanoma: HMB45, S100

Neural tumor : S100, Leu7

Fibrous histiocytoma: CD68

Spindle cell carcinoma: Cytokeratin

Rhabdomyosarcoma: Desmin, Vimentin, Muscle specific actin, Myoglobin, Myogenin,

MyoD1, Caveolin-3

lymphoid tumors

o CD3: T cells

o CD5: T cells, mantle cells, SLL/CLL

o CD10: follicular lymphoma

o CD20: B cells

o CD23: follicular dendritic cells

o Bcl-2: follicular, anti-apoptosis

o Bcl-1: cyclin D1, mantle cell

Retinoblastoma is positive for neuron-specific enolase (also found in aqueous of RB), class

III tubulin isotype (h4), microtubuleassociated protein 2 (MAP2), and synaptophysin; they

are negative for glial fibrillary acidic protein and S-100 protein

Retinal stem cell marker : nestin, CD 34

Mitosis specific marker in cornea: Ki67


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Limbus Stem Cells: CK 5/14+ve, CK 19+ve, P63+ve, Vimentin+ve, ABCG2, alpha-enolase

(5+14 =19)

Central Corneal Cells: CK 3/12+ve, Connexin 43+ve (3 x 4 = 12, 4.3)

Inheritence

All vitreoretinopathy are AD except

o Norrie XL

o XLRS XL

o Glodman favre AR

o Stickler AD but rarely AR

o FEVR AD AR XR

All MPSs are transmitted by the AR mode, except MPS II (Hunter sy nd rome) wh ich is

XR .

albinism inheritance

o All OCA are AR except ADOCA

o OA are XR.

All corneal dystrophies are AD except

o Macular AR

o Gelatinous droplike AR

o LCD type 3 AR


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o CHED type 2 AR

Microcornea: AD

Megalocornea: XR

Familial ectopia lentis is AD

Ectopia lentis et pupillae is AR.

Simple myopia and simple hypermetropia: AD

Inside Retinal Layers

The nuclei of the Müller cells lie in the inner nuclear layer , whereas the nuclei of the

photoreceptors lie in the outer nuclear layer.

The nerve fiber layer contains the axons of the ganglion cells.

The inner plexiform layer has axons of the bipolar and amacrine cells and the synapses

of the ganglion cells.

The outer plexiform layer has connections between the photoreceptors, horizontal cells,and bipolar cells.

The footplates of the Müller cells form the internal limiting membrane.

cell bodies whose processes project into the lateral geniculate and pretectal nuclei

ganglion cell layer

Müller's cell nuclei inner nuclear layer

Photoreceptors nuclei Outer nuclear layer

horizontal and bipolar synapses outer plexiform layer

amacr ine and bipolar cell synapses inner plexiform layer

storage of dietary vitamin A retinal pigment epithelium (RPE)

cell bodies whose processes form spherules and pedicles outer nuclear layer


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high baseline cyclic guanosine monophosphate (cGMP) levels and membrane

depolarization photoreceptor layer

flame-shaped retinal hemorrhages nerve fiber layer

dot hemorrhages inner nuclear layer

Hard exudates OPL

Soft exudates/ CWS NFL

Interferons Therapy & Eye

Alpha 2a: capillary hemangioma

Alpha 2b: papilloma

Beta 1a:

o Avonex: for MS, intramuscular, once weekly

o Rebif : for MS, subcutaneous, thrice weekly, EVIDENCE Trial

Beta 1b:

o Betaseron and Extavia: for MS, subcutaneous

Gamma

o chronic granulomatous disease, kidney tumors and leishmania and other parasites.


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Intraocular Gases

Physical characteristics

Intracameral Dosages

Vancomycin: 1 mg/ml

Cefazolin: 1 mg/0.1 ml

Cefuroxime: 1 mg/0.1 ml (ESCRS Study)

Gatifloxacin: 100 mcg/0.1 ml

Moxifloxacin: 100 mcg/ 0.1 ml

Amphotericin B: 5-10 mcg/0.1 ml

Irrigating fluid

o Vancomycin: 25-50 mcg/ml

o Gentamycin: 0.008 mg/ml

Adrenaline tartarate: 1:10,000 (0.1 ml of 1:1000 is diluted with 0.9ml)

Pilocarpine: 0.1 ml of the drug (25 mg/ml) is diluted in 0.1 ml ringer lactate

Gases Mol wt. Purity

(mole%)

Expansion Longevity

(days)

Nonexpansile

conc. (%)

Air 29 99.99 0 5-7 ----

SF6 146 99.9 1.9-2.0 times 10-14 18

C3F8 188 99.7 4 times 55-65 14


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Intrastromal Dosages

Voriconazole: 50 microgram/ 0.1 ml

Amphotericin B: 5-7.5 microgram/0.1 ml

Ciprofloxacin: 0.3 mg/0.1 ml

MMC: 0.02-0.04% for 15-30 sec to reduce post-operative interphase haze

Intravitreal Dosages

Antibiotics

o Vancomycin: 1mg/0.1ml

o Ceftazidime: 2.25mg/0.1ml

o Amikacin: 400 migrogram/0.1 ml

o Gentamycin: 200 migrogram/0.1 ml

Antifungals

o Voriconazole: 50-100micrgram/0.1ml

o Amphotericin B: 5 migrogram/0.1 ml

Antivirals

o Ganciclovir (Cytovene): 200 –400 mg/0.1 mL

o Foscarnet (Foscavir): 1200 mg/0.05 mL

o Cidofovir (Vistide): 20 mg/0.1 mL

Steroids

o Dexamethasone: 400 mcg/0.1 ml

o Triamcinolone acetonide: 1-4 mg/ 0.1 ml

Anti VEGFs

o Pegaptinib MACUGEN: 0.3 mg in 0.09 ml pre-filled syringe


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o Bevacizumab AVASTIN: 1.25 mg in 0.05 ml

1 ampoule: 0.2 ml

1 vial: 4 ml or 16 ml of 25 mg/ml

o Ranibizumab LUCENTIS: 0.5 mg in 0.05 ml

o VEGF Trap EYELEA: 0.05, 2, 4 mg in 0.05 ml

o SiRNA: 70-300 mcg

Intravitreal Implants

Dexamethasone intravitreal implant (DEX implant; Ozurdex, Allergan, Irvine, CA)

o delivers the steroid intravitreally for 6 months

o consists of poly (lactic-co-glycolic acid), a DEgradable polyester and

dexamethasone

o single-use applicator through a 22-gauge

o uveitis and macular edema caused by retinal vein occlusion

o 350 µg and 700 µg version

o Uses NOVADUR Delivery system

o GENEVA (dexamethasone implant) study: Global Evaluation of implantable

dexamethasone in retinal Vein occlusion with macular edema (GENEVA) study

Vitrasert ganciclovir implant

o poly(vinyl alcohol) and poly(ethylene vinyl acetate)

o delivers the medication for approximately 32 weeks (8 months) and has been

shown to halt the progression of CMV

o nondegradable

o 5/4.5 mg implant

o Releases 1 mcg/ hour

o Approaches concentration of 4 ug/ml intravitreal

Retisert fluocinolone implant


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o blend of the drug with poly(vinyl alcohol) and methylcellulose

o 0.59 mg pellet embedded in a nonbiodegradable scaffold designed to be implanted

in the vitreous cavity via a sclerotomy and anchored by a suture to the eye wall

o releases drug at steady state between 0.3 and 0.4µg/day for approximately 30

months

o used most commonly for treatment of chronic non-infectious posterior uveitis.

o Studied for DME also

Iluvien fluocinolone implant

o narrow cylinder 3.5 × 0.37 mm

o 25-gauge

o lowest dose format (0.2 µg/day)

o higher-dose (0.5 µg/day) system

o FAVOR (iluvien) study

I-vation triamcinolone implant

o helical screw coated with triamcinolone acetonide that delivers the drug intravitreally

for 36 months

o 25-gauge

o drug is entirely within the coating on the helical structure and not within the bulk of

the device

ECT CNTF Implant

o which allows the intravitreal implantation of a chamber containing live cells

programmed to release CNTF

o 1.5 ng/day

o possible efficacy for age-related macular degeneration (AMD) involving geographic

atrophy and for RP

o 2 years or more

ECT technology anti-VEGF implant

o NT-503


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o For ARMD

Brimonidine Intravitreal Implant

o Patients With Geographic Atrophy Due to Age-related Macular Degeneration

(AMD)

o This is a randomized, double-masked, dose-response, sham-controlled evaluation of

the safety and efficacy of brimonidine tartarate intravitreal implant in patients with

geographic atrophy from age-related macular degeneration. It is hypothesized that

the implant may promote the release of neuroprotective factors that may slow the

progression of retinal degenerative disease.

Iris Nodules & Pathology

Lisch nodule, neural crest hamartoma: NF 1

JXG nodules are composed of histiocytes and Touton giant cells: JXG

Koeppe nodules are collections of inflammatory cells, near pupillary margin: granulomatous

and non-granulomatous uvetis

Bassaca Nodules are seen at base: only in granulomatous uveitis (sarcoid, Tb, syphilis,

VKH); often look gelatinous

Brushfield spots are stromal hyperplasia: Downs syndrome

Berlin nodules are seen in angle: granulomatous uveitis

Laser Facts

Brief History

1917 - A. Einstein: Laser possible.

1958 - C.H. Townes, A.L. Schawlow: Theoretical basis for lasers.

1960 - T. Maiman: Built first laser.


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1963 - C. Zweng: First medical laser trial (retinal coagulation).

1965 - W.Z. Yarn: First clinical laser surgery.

Instrument Wavelengths

(Chronological order in nm)

SWAP: 440, blue light

Retinal Thickness Analyser RTA: green, 540-nm HeNe laser

Hertmann Shack‘s Aberrometer: 575 nm

HRT- CSLO: 670 diode

GDX-SLO: 780 diode

IOL Master: 780 diode

Lenstar: 820, SLD

Macular OCT (Posterior Segment OCT): 830

RNFL OCT: 810/850, SLD

AS-OCT: 1310, SLD

Swept Source OCT: 1050

Therapeutic Wavelengths

(nm)

Excimer laser: 193, Argon Fluoride (ultraviolet)

Excimer laser: 308, Xenon Cloride (ultraviolet)

Excimer laser trabeculostomy ELT: 308, Xenon Cloride

Argon blue-green: 488

Df Nd YAG: 512 (green)

ND YLF laser : 527 (in the treatment of diabetic macular edema)


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Argon green: 514

Yellow dye laser: 577 for DME

Krypton red or Dye red: 620-630

He Ne Gas laser: 632, for Laser interferometry

Rostaporphin PDT: 664 nm

Diode: 689, PDT (its verteporphin‘s peak absorption)

Ruby laser: 694, red

Infrared diode laser: 780, IOL Master

Transpupilary thermotherapy, DLCP: 810

subthreshold micropulse STMP diode 810nm: for DME

Intralase: Nd: YLF, wavelength is 1053 nm

Nd YAG: 1064

Ho YAG: 2100, used for laser thermokeratoplasty

Erbium YAG: 2940, for laser phacoemulsification

CO2 laser: 10600

Laser settings for glaucoma

ND YAG PI: 500u, 5-15mJ, 12ns pulse, 1-3 pulse/sec

Argon PI: 50u, 1000mW, 0.1-0.2s,

Laser pupilloplasty: 200u, 0.2s, 400mW

Laser sphincterotomy: 50u, 0.01-0.05s, 1.5W

ALT: 50u, 100ms, 1000mW

SLT: 400u, 0.5-1.2mJ

DLCP: 810 nm, 2 mm from limbus, 8 spots per quadrent, 2000 ms, 1200-2000 mW


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Laser settings in Retina

PRP: df NdYAG

o 200-500 micron spot size

o 200-500 ms

o 200-500 mW

Macular Grid Laser: df NdYAG

o 50-100 micron spot size

o 50-100 ms

o 50-100 mW

Laser Parameters for PTK

Fluence: 160 ± 10 mJ/cm2

Repetition rate: 5 Hz

Ablation rate: 0.20-0.35 mm per pulse

Ablation diameter: 5.5 –6 mm including a 0.5 mm transition zone

Ablation depths:

o Epithelium 40 mm (default value) or as determined by pachymetry

o Stroma: Depth of scar or opacity (postoperative corneal thickness should be at least

250 mm)

Modes of Laser

There are three modes of laser: continuous, Q-switched and mode-locked.

o Laser from continuous mode has a constant power and is measured in watts.

o Q-switched and mode-locked increases the energy by compressing the energy in

time and the energy is best measured in joules.


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o Mode-locked laser compresses the laser more than Q-switched laser and therefore

produces more energy.

Laser Mediums

Solid state lasers have lasing material distributed in a solid matrix, e.g., the ruby or

neodymium-YAG (yttrium aluminum garnet) lasers. The neodymium-YAG laser emits

infrared light at 1.064 micrometers.

Gas lasers (helium and helium-neon, HeNe, are the most common gas lasers) have a

primary output of a visible red light. CO2 lasers emit energy in the far-infrared, 10.6

micrometers, and are used for cutting hard materials.

Excimer lasers (the name is derived from the terms excited and dimers) use reactive gases

such as chlorine and fluorine mixed with inert gases such as argon, krypton, or xenon.

When electrically stimulated, a pseudomolecule or dimer is produced and when lased,

produces light in the ultraviolet range.

Dye lasers use complex organic dyes like rhodamine 6G in liquid solution or suspension as

lasing media. They are tunable over a broad range of wavelengths.

Semiconductor lasers, sometimes called diode lasers, are not solid-state lasers. These

electronic devices are generally very small and use low power. They may be built into larger

arrays, e.g., the writing source in some laser printers or compact disk players.

Laser Safety Classification

The International Safety Classification of Lasers divides the lasers into 4 groups. Group 3 is

subdivided into 3a and 3b. Class 3b and above is damaging to the eye and their powers are

5MW and above. All lasers used in ophthalmology are classed as 3b and above. Safety goggles

should always be worn by people in the vicinity.

Class I: Do not emit hazardous levels.

Class II: Visible light lasers that are safe for momentary viewing but should not be stared into

continuously; an example is the aiming beam of ophthalmic lasers, or laser pointers.

Class III: Unsafe for even momentary viewing, requiring procedural controls and safety

equipment.


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Class IV: Also pose a significant fire and skin hazard; most therapeutic laser beams used in

ocular surgery are in this class

Latest Drugs

Lampalizumab: new monoclonal antibody that inhibits complement factor D, which is a rate-

limiting enzyme of the alternative complement pathway, first positive treatment result for

patients with dry age-related macular degeneration and geographic atrophy.

Pazopanib is a small molecule lipophilic potent and selective multitargeted receptor tyrosine

kinase inhibitor of VEGFR-1, VEGFR-2, VEGFR-3, PDGFR-a/β, and c-kit that inhibits

angiogenesis.

o Pazopanib eye drops

o 5-10 mg/ml TID

o failed to reduce as-needed ranibizumab injections by ≥ 50%

AGN-150998:

o Designed Ankyrin Repeat Proteins (DARPins)

o Concept Study

o Selectively binds to vascular endothelial growth factor-A with high binding affinity.

ROCK inhibitors:

o Rho-kinase inhibitors (ROCK) novel drug in glaucoma

o human trabecular meshwork and Schlemm‘s canal cells to produce reversible

changes in cell shape, focal adhesions and decreases in stress of the actin fibers.

This resulted in an increase in permeability of the Schlemm cells‘ monolayer by 80%

o decrease intraocular pressure by 25% to 32% and have a duration of action of 10 to

12 hours

o ATS907, ATS8535, AR-12286, AR-13324, AMA0076

nitric oxide-donating prostaglandin F2-alpha analog BOL-303259-X

o comparable to latanoprost


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Aganocides: novel class of compounds that mimic the body‘s natural defense against

infection

o NVC-422 Phase IIb clinical trial to treat adenoviral conjunctivitis.

Voclosporin (Luveniq): novel immunomodulatory drug that inhibits the calcineurin

enzyme, was originally developed to prevent organ graft rejection and to treat autoimmune

diseases. The chemical structure of voclosporin is similar to that of cyclosporine A, but with

a difference in one amino acid, leading to superior calcineurin inhibition and less variability

in plasma concentration.

Mapracorat:

o selective glucocorticoid receptor agonist (SEGRA)

o similar anti-inflammatory and immunosuppressive effects as the glucocorticoids but

with a decreased potential of the steroid side effects

o Phase II study is evaluating its effectiveness in preventing the signs and symptoms

of allergic conjunctivitis. In addition, a Phase III study is underway for the

treatment of ocular inflammation after cataract surgery.

CF101: adenosine A3 receptor agonist

o Adenosine has been shown to inhibit leukotriene B4 (LTB4), which is part of the

arachidonic acid cascade for the synthesis of prostaglandins and leukotrienes

o For patients with moderate to severe dry eye

Lifitegrast: lifitegrast is a potent and selective small molecule drug being investigated for

the treatment of dry eye and ocular allergy. It inhibits T-cell inflammation by blocking the

binding of two key cellular surface proteins that mediate the chronic inflammatory cascade.

SMO Inhibitors (Smoothin): for advanced BCC

o Cyclopamine (SMO Inhibitors):


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naturally occurring sterol alkaloid, topical drug is in clinical trials

it is obtained from Veratum calnifornicum (rocky mountain corn lily) ingestion

of which causes serious malformation known as cyclopia and hence the

name given cyclopamine

o Vismodegib (GDC-0449):

Synthetic small molecule

Orally active

o Statins

o Vitamin D3

Downstream SHH pathway inhibitors

o Rapamycin (sirolimus)

Macrolide antibiotic

Inhibits MTOR in GLI1-transforme cells

No human stdies for BCC

o MYCN anti-sence oligonucleotides

No human studies for BCC

BRAF inhibitors: for Malignant Melanoma

o Sorafinib (pan BRAF)

o PLX4032 (V600E-BRAF)

C-KIT inhibiors

o Imatinib

Sutent: Sunitimab

o orally available multi-kinase inhibitor

o Inhibits c-Kit, VEGFR, PDGFR etc

o Activity against c-kit mutations that render OMs resistant to Gleevec


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o Synergistic effects with radiation and chemotherapy

o Combination of Sutent, tamoxifan, cisplatin

Tegretin (Bexarotene): for CTCL (Mycosis Fungoides)

FOVISTA: Binds PDGF-B, phase 3 trials going on for wet AMD and CNVM.

Natalizumab: alpha 4 integrin

NT- 501

o intra-vitreal implant is a Ciliary Neurotrophic Factor (CNTF) secreting encapsulated

cell device

o CNTF is a cytokine, which is a survival factor for various neuronal cells and seems to

prevent neurodegeneration.

o CNTF may act through the IL-6 receptor.

o A semi-permeable membrane encapsulates genetically engineered human RPE cells

that secrete CNTF. It prevents host antibodies and immune cells from entering the

device but allows nutrients to diffuse in, to nourish the cells within and CNTF to

diffuse out. This holds promise for retinitis pigmentosa and dry age related macular

degeneration

Bevasiranib (CAND5) is a siRNA which switches off VEGF production, but clinical effect is

not seen till the preexisting VEGF is cleared. It has a potentially longer duration of effectthan currently available anti-VEGF agents. It is well tolerated at multiple doses.

Vatalanib is a VEGF receptor tyrosine kinase inhibitor given orally.

Fenofibrate is drug of the fibrate class used to treat dyslipidemia. Raises HDL and lowers

LDL and triglycerides and typically is used in combination with a statin. It lowers lipid levels

by activating peroxisome proliferator-activated receptor alpha (PPARα). PPARα activates

lipoprotein lipase and reduces apoprotein CIII, which increases lipolysis and elimination of

triglyceride-rich particles from plasma.

Fenretinide in Dry AMD: This drug is an oral vitamin A binding protein antagonist and is

being studied in patients with geographic atrophy (GA).It halts the accumulation of retinol

(vitamin A) toxins through affinity for retinol-binding protein. One of the hallmarks of dry

macular degeneration is the accumulation of lipofuscin that is responsible for drusen

formation and geographic atrophy. One year interim data showed that fenretinide slowed the

growth of geographic atrophy lesions by 45% in the 300 mg dose.


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Copaxone (glatiramer acetate): weekly vaccination, Macular degeneration, Alzheimer‘s

disease and Multiple sclerosis

Citicholine (Cytidin-5-diphposphocholine): It is similar in action to levodopa. When

administered in adult patients with strabismic amblyopia (1gm\day i.m for 15 days), it has

showed improvement lasting over 6 months including improvement in contrast sensitivityand VEP.

Mechanism of Action

Local anesthetics block the generation and conduction of nerve impulses

General Anesthetics: multiple

Fluoroquinolones: bactericidal agents that act by inhibiting DNA replication. They have dual

targets, topoisomerase II (DNA gyrase) and topoisomerase IV

Tetracyclines: broad-spectrum antibiotics that inhibit bacterial protein synthesis by binding to

the 30-S ribosomal subunit of the bacteria

Aminoglycosides: inhibit bacterial protein synthesis by binding irreversibly to the bacterial

30S ribosomal subunit.

Glycopeptides (Vancomycin and teicoplanin): inhibit peptidoglycan synthesis in the bacterial

cell wall by complexing with cell wall precursors

Macrolides: bacteriostatic agents that inhibit bacterial RNA-dependent protein synthesis by

binding reversibly to the 23S tRNA of the 50S ribosomal subunits

Chloramphenicol: bacteriostatic agent that inhibits protein synthesis by binding reversibly to

the peptidyltransferase component of the 50S ribosomal subunit and prevents the

transpeptidation process of peptide chain elongation

SMX-TMP: competitively inhibit the bacterial modification of p-aminobenzoic acid into

dihydrofolate, and trimethoprim inhibits bacterial dihydrofolate reductase

Bacitracin and gramidicin: Bacitracin disrupts bacterial cell-wall synthesis by inhibiting the

dephosphorylation of a lipid pyrophosphate, while gramicidin interferes more with cell

membrane permeability

Polymyxins: interact with the phospholipids of the bacterial cell membrane, which increases

the cell permeability and disrupts osmotic integrity. This process results in leakage of

intracellular constituents, leading to cell death


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Trifluridine: potent inhibitor of thymidylate synthetase and therefore inhibits DNA synthesis

Vidarabine: interfere with the early steps of viral DNA synthesis and arrests the growth of the

viral deoxynucleotide chain

Acyclovir: inhibits viral dependant TK (thymidine kinase)

Ganciclovir: competition with deoxyguanosine for incorporation into viral DNA

Polyenes: binds esterols in the fungal cell wall, forming ‗blisters‘ and causing lysis of the cell

Imidazoles: affect the formation of ergosterol needed by the cell membranes by inhibiting

the enzyme lanosterol 14 α-demethylase

Caspofungin: inhibits synthesis of B(1,3)-D glucan,a component of fungal cell wall

MIP

major intrinsic membrane protein

The most abundant membrane protein of the lens is intrinsic membrane protein 26 (MP26,

MIP). It is a lens-specific single polypeptide with a molecular mass of 28,200 kDa (263

residues) that makes up about 50% of the lens membrane protein.

MIP26 is a member of the aquaporin (AQP) family, members of which transport small

molecules such as water and glycerol.

MIP26 is termed aquaporin O

A locus for autosomal dominant cataracts has been mapped to chromosome 12q12-14.1

near the MIP gene

MMPs

MMP 1: collagen 1,2,3

MMP 2,9: collagen 4,5,7 and laminin

MMP 3: GAGs and Fibronectin

Only MMP 2 is found in normal cornea.


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Molecular Weights

Sodium fluorescein: 376.27 daltons

Indocyanine green: 775 daltons

VEGF: 45kDa

Bevacizumab: 149 kDa

Ranibizumab: 48 kDa

Sodium Hyaluronate: 2 –5 million d

Chondroitin Sulfate: 50,000 d

Silicone oil: 28,000 (1,000 centistokes)

Air: 29

Sulfur hexafluoride (SF6): 146

Perfluoroethane (C2F6): 138

Perfluoropropane (C3F8): 188

PMMA IOLs: 2.5 to 3 million Da

Acylic IOLs: 80 000 to 140 000 Da

Botulinum toxin: 900 000 Da

MUCins

Mucins are classified by the nomenclature MUC1 –21 and are divided into secreted and

membrane-spanning categories

o Membrane-spanning mucins consist of a short intracellular tail, membrane-

spanning domain, and large, extended extracellular domain that forms the

glycocalyx.

o Secreted mucins are either gel-forming or small soluble.

Gel-forming mucins are large molecules (20 –40 million Da) secreted by

exocytosis from Goblet cells.

Small soluble mucins are secreted by the lacrimal gland.


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MUC 1, MUC 4, and MUC 16: apical surface of the corneal epithelium

MUC 5AC and MUC 2: aqueous layer of the tear film (membrane-spanning, gel-forming

mucins)

MUC16 protein levels decreased in conjunctival epithelium and increased in tears of

patients with Sjogren's syndrome

MUC1 splice variants also play a role in dry eye

MUC5AC is the gel-forming mucin forming mucous layer backbone

NV %

BRVO

NVI: 1

NVD: 10

NVE: 30

Ischemic BRVO

40% of patients with an ischemic BRVO develop NVE or NVD.

60% of the patients with NVE-NVD develop VH/PRH.

Ich CRVO

NVI: 50

NVD: 30-35

NVE: 20-25

NVG: 45

CRAO


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NVI: 20

NVD: 2

OIS

NVI: 67

NVD: 35

NVE: 8

EALES‘ DISEASE

NVI: 0.5-0.8 %

NVD: 10-18 %

NVE: 50 %

Sec RRD: 8-11 %

OCT Review

Time Domain OCT (TD-OCT)

o Light echoes from each time delay measured sequentially

o Slow acquisition speeds, high signal-to-noise ratio, poor view of the choroid

o 400 A-scans per minute, 6 B-scans per macula, 10-μm resolution

Spectral Domain OCT (SD-OCT)

o Light echoes from each time delay, all measured simultaneously (high-speed

spectrometer)

o Fast acquisition speeds, low signal-to-noise ratio, view to the choroid possible

o 52,000 A-scans per minute, 20-40 B-scans per macula (up to 100), 5-μm resolution

Enhanced Depth Imaging OCT (EDI-OCT)


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o Zero delay line (ZDL) positioned at the inner retina

o The further from the zero-delay line (ZDL), the lower the signal resolution.

o EDI moves the ZDL closer to the choroid; negative images when the ZDL is crossed.

o Thinner layers permit deeper tissues to be closer to the ZDL.

Full Depth or Combined Depth Imaging OCT (CDI-OCT)

o 100 B-scans averaged for a single line scan.

o 50 in standard SD-OCT mode and 50 in EDI mode

o Maximizes resolution of vitreoretinal and choroidal structures in a single scan

Swept Source OCT

o

Topcon DRI OCT-1 Atlantis

o Longer wavelength light source (1050 nm)

o Fast (100,000 A scans per second)

o Uniform sensitivity, allowing excellent visualization of structures from vitreous to

sclera in one scan

o Automated segmentation (7 layers)

o 100,000 A-scans per second, 1-μm resolution

o 12-μm wide scans (vs. 9- and 6-μm scans)

o Image depth of 2.6 mm vs. 1.9 mm for EDI—even more ideal for choroidal tumors

Optic Nerve Segments

Longest segment intraorbital

Shortest segment intraocular

Segment with the most variable length intracranial

Divided into three subsegments intraocular

Most vulnerable to indirect trauma intracanalicular


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Most redundant segment intraorbital

The only segment not bathed in cerebrospinal fluid intraocular

Orders of Abberations

0. Piston

1. Vertical and horizontal prisms

2. Myopia (positive defocus), hyperopia (negative defocus), Regular (cylindrical)

astigmatism

3. Coma, trefoil

4. Spherical astigmatism

5. rosette

6. pentacle, axial coma

Percentages % Primer

50% of patients with scleritis have systemic disease

Steroid-induced increases in intraocular pressure occur in about 6% of patients on topical

dexamethasone

30 –50% of individuals with glaucomatous optic nerve damage and visual field loss have an

initial intraocular pressure measurement less than 22 mmHg.

sporadic inheritance of aniridia need to be evaluated for Wilms‘ tumor, which is associated

with 25% of cases.

BCC 3% mortality rate

83% of macular holes are idiopathic, and 15% are due to some sort of trauma

Deuteranomaly is present in approximately 5% of the population; deuteranopia,

protanopia, and protanomaly in 1% each; and tritanopia or tritanomaly in only 0.002%.


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ACUTE ACG: 40 –80% chance of an acute attack in the fellow eye over the next 5 –10 years.

PPMD: Glaucoma is associated in 15%.

Axenfeld‘s syndrome is the anomaly with coincident glaucoma in 50% of cases.

Glaucoma in hyphema: Secondary glaucoma occurred in

o 13.5% of those eyes in which blood filled half of the anterior chamber,

o in 27% of those eyes in which blood filled greater than half of the anterior chamber,

and

o in 52% of

pg guide vvimp

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