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The Eye E-Book

The Eye E-Book

John V. Forrester | Andrew D. Dick | Paul G McMenamin | Fiona Roberts | Eric Pearlman


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Book Details


The Eye: Basic Sciences in Practice provides highly accessible, concise coverage of all the essential basic science required by today’s ophthalmologists and optometrists in training. It is also essential reading for those embarking on a career in visual and ophthalmic science, as well as an invaluable, current refresher for the range of practitioners working in this area.

This new fourth edition has now been fully revised and updated in line with current curricula, key research developments and clinical best practice. It succinctly incorporates the massive strides being made by genetics and functional genomics based on the Human Genome Project, the new understanding of how the microbiome affects all aspects of immunology, the remarkable progress in imaging technology now applied to anatomy and neurophysiology, as well as exciting new molecular and other diagnostic methodologies now being used in microbiology and pathology. All this and more collectively brings a wealth of new knowledge to students and practitioners in the fields of ophthalmology and visual science.

  • The only all-embracing textbook of basic science suitable for trainee ophthalmologists, optometrists and vison scientists – other books concentrate on the individual areas such as anatomy.
  • Attractive page design with clear, colour diagrams and text boxes make this a much more accessible book to learn from than many postgraduate textbooks.
  • Presents in a readable form an account of all the basic sciences necessary for an understanding of the eye – anatomy, embryology, genetics, biochemistry, physiology, pharmacology, immunology, microbiology and infection and pathology.
  • More on molecular pathology.
  • Thorough updating of the sections on pathology, immunology, pharmacology and immunology.
  • Revision of all other chapters.
  • More colour illustrations.

Table of Contents

Section Title Page Action Price
Front cover cover
The Eye i
Copyright page iv
Table of Contents v
Preface vii
Acknowledgements viii
1 Anatomy of the eye and orbit 1
Anatomical terms of reference 1
Osteology of the skull and orbits 1
General arrangement and features of the skull 1
Osteology of the orbit 1
The walls of the orbit 2
Features of the orbital roof 2
2 Embryology and early development of the eye and adnexa 103
Introduction 103
General embryology 103
Ocular embryology: general introduction 103
Genetic regulation of eye development 110
Eye field transcription factors 110
Periocular mesenchyme is derived from a mixture of neural crest and mesoderm 111
The neural retina and retinal pigment epithelium are derived from neuroepithelium 112
Axes in the neural retina 113
Retinal morphogenesis (Fig. 2-8) 114
Macula and foveal development 115
Peripheral retina 117
Development of retinal vasculature 117
Development of the retinal pigment epithelium 117
Optic nerve and disk development 118
Development of the fibrous coat of the eye 119
Development of the sclera 119
Development of the cornea 119
Development of the intraocular contents 120
Lens development (Fig. 2-13) 120
Development of the vitreous and hyaloid system 121
Development of the uveal tract 124
The choroid 124
The ciliary body 124
The iris 126
Development of the anterior chamber angle and aqueous outflow pathways 127
Development of the extraocular muscles 129
Development of the eyes and surrounding structures is influenced by the pattern of development of the skull, pharyngeal arches and face 129
Further Reading 129
Further Reading 129.e7
3 Genetics 130
Chromosomes and cell division 130
Chromosomes 130
Cell division 130
Mitosis (Box 3-1) 130
Meiosis: formation of gametes 131
Genetic makeup 132
Molecular genetics (DNA and genes) 132
How genes work: decoding DNA 133
Regulating gene expression is constantly active, has multiple pathways and is influenced by environment (epigenetics) 135
Ordering of DNA and accessibility for transcription 135
Non-coding RNA and RNA-binding proteins constantly regulate gene expression 135
Spliceosomes 135
Chromosome defects and gene mutations 135
Structural chromosomal abnormalities 136
Gene mutations 137
Clinical genetics 137
Autosomal inheritance 137
X-linked disorders 137
Mitochondrial inheritance 138
Multifactorial inheritance 138
Disease associations 139
Genetic polymorphisms 139
Population genetics 140
Gene frequency 140
Genetic linkage and linkage analysis 140
Linkage equilibrium and disequilibrium 141
Mendelian randomization identifies causal modifiable environmental risk to disease 141
Epigenetics (Box 3-7) 141
Understanding the human genome: DNA analysis 142
Cloning 142
Refining technology: molecular analysis of human genes and mutations 142
Southern and Northern blotting 142
DNA polymorphisms 143
Restriction fragment length polymorphism 143
Variable number of tandem repeats polymorphism 143
Polymerase chain reaction 143
Genomics, transcriptomics and proteomics 143
Finding and tracking the gene through families 146
Molecular biology and clinical medicine 146
Gene probes 146
Molecular and cell biology: controlling cell destiny 146
Using molecular biological technology to detect apoptosis 147
Gene therapy 147
Genes, cell differentiation and cell-based therapies 148
Molecular genetics and ophthalmology 150
The X chromosome 150
Retinitis pigmentosa (Fig. 3-13) 151
X-linked retinitis pigmentosa 151
Autosomal dominant retinitis pigmentosa 153
Choroideraemia 153
Norrie’s disease 154
Retinoblastoma 154
Albinism 155
Oculocutaneous albinism 155
Ocular albinism 155
Myotonic dystrophy 155
Mitochondrial inheritance 156
Leber’s hereditary optic neuropathy 156
Other mitochondrial disorders 156
Further Reading 156
Further Reading 156.e1
4 Biochemistry and cell biology 157
Introduction 157
The continuing advance of ‘omics’ 159
Cells and tissues 160
The cell 160
General structure 160
The plasma membrane 161
Endoplasmic reticulum and Golgi apparatus 164
Mitochondria 164
The nucleus 169
The intracellular matrix 169
Microfilaments. 169
Intermediate filaments. 173
Group 3 cytoskeletal fibres. 174
Septins. 177
Intracellular signalling mechanisms 177
The extracellular matrix 178
Extracellular matrix proteins determine the structural nature of the tissue 178
Non-structural proteins 184
Glycosaminoglycans occur in the extracellular matrix bound to core proteins as proteoglycans 186
Extracellular matrix molecules are intimately involved in cell adhesion 186
Epithelial and endothelial cells bind via transmembrane complexes to each other and to the basement membrane 189
Mesenchymal cells bind to the matrix via focal adhesion sites 189
Biochemical pathways that affect ocular function 189
Glucose metabolism and tissue glycation 189
Glucose enters cells by facilitated diffusion 190
Excessive levels of glucose may impair cellular metabolism 191
Excessive levels of glucose lead to glycation of proteins 191
Glucose and lipid metabolism 193
Oxidation/reduction and free radical production 193
Lipids and lipid peroxidation 194
The ocular surface 198
The tear film 198
Tear film lipids have unique characteristics 198
Lacrimal gland secretion provides the aqueous component of tears 199
The mucous layer stabilizes the aqueous layer by providing a hydrophilic contact surface 200
Tear secretion is under psychoneuroendocrine control 201
The conjunctiva 201
The epithelium is more than a simple covering layer for the conjunctiva 201
The conjunctival stroma is highly vascular and contains aqueous veins 202
The lids 202
Cornea and sclera 203
The cornea 203
Corneal transparency is a function of its relative acellularity and matrix structure 203
The epithelium. 203
Matrix factors affecting transparency: collagen. 204
Glycosaminoglycans. 205
Swelling pressure versus hydration. 206
Cellular factors affecting transparency: (1) keratocytes. 207
Cellular factors affecting transparency: (2) leucocytes. 207
Cellular factors affecting transparency: (3) the endothelium. 207
Transport of water out of the cornea is a dual process. 208
Optical factors affecting image formation. 209
Metabolism of corneal cells 209
Oxidative metabolism and glucose utilization. 209
Oxygen handling by the cornea. 209
Effects of contact lens wear on corneal physiology. 210
Cell turnover and wound healing in the cornea 211
The epithelium. 211
Limbal corneal stem cells. 211
The stroma. 212
The endothelium. 213
Vascularization. 214
Vitamin A and the cornea. 215
The sclera 215
Matrix factors. 215
Bulk fluid transport and the uveal effusion syndrome. 215
Uveal tract 216
The iris 216
Physiology 216
Blood flow in the iris 216
The ciliary body 217
Functions of the ciliary body 217
Blood flow in the ciliary body 217
Ciliary muscle and accommodation 217
Blood–aqueous barrier 218
Eicosanoids in the iris/ciliary body 220
Detoxification and antioxidation in the anterior segment 220
The cytochrome P450 system is the major drug detoxification (CYP) system in the eye. 220
The ciliary body is the main source of antioxidant systems in the anterior segment. 220
The choroid 221
Functions of the choroid 221
Vascular function. 221
Non-vascular functions. 222
Lymphoid function. 222
Aqueous humour dynamics 222
Aqueous humour is secreted by the ciliary body epithelium 222
Composition of aqueous humour 222
Neural/autonomic control of aqueous secretion 223
Cholinergic mechanisms are not involved in control of intraocular pressure 223
Adrenergic receptors regulate IOP via adenylate cyclase 225
Nucleotides and nucleotide receptors 225
Circadian regulation of aqueous humour formation 225
Is guanylate cyclase involved in intraocular pressure control? 225
Aqueous humour outflow from the eye 225
Control of outflow at the trabecular meshwork 226
Metabolism of trabecular meshwork cells 226
Uveoscleral drainage 227
Episcleral circulation 227
An intraocular pressure-independent link between aqueous production and aqueous outflow? 228
Does aqueous contain components that contribute to flow resistance? 228
The lens 228
Lens transparency 228
The epithelium 228
The organization of the lens fibre cells underpins the transmission properties of the lens 228
The crystallins 230
Cytoskeletal proteins of the lens 232
Membrane lipids and proteins 233
Extracellular matrix 234
Semipermeable membranes and physiology of the lens 234
Lens metabolism 235
Carbohydrate 235
Protein 235
Lipid 236
Redox systems in the lens microenvironment 236
Ageing in the lens and cataract formation 237
Reduced vision in cataract is caused by increased light scatter by lens proteins 237
Cataract formation is caused by any insult to the lens 238
Age-related cataract formation is multifactorial 238
Mechanism of age-related cataract formation: a failure of chaperone function 240
The vitreous 240
The vitreous body is a true connective tissue containing collagen, gags and cells 240
The matrix 240
Vitreous cells 241
Physicochemical properties of the vitreous gel 241
The viscoelasticity of the vitreous protects the retina during eye movement and deformations of the globe 241
Vitreous retards bulk flow of fluid and diffusion of small molecules 241
The retina 242
The neural retina is highly organized in layers 242
Metabolic function in the retina 242
Glucose metabolism in the retina 242
Protein metabolism in the retina 243
The retina contains a high content of lipid (20%) 245
Blood flow in the retina 245
The blood–retinal barrier regulates the passage of molecules into the retina 245
Retinal blood flow may be partly under autonomic control 245
Photoreceptors 246
Metabolism and turnover 246
Photoreceptor cell-specific proteins 249
Melanopsin comes of age 250
Photoreceptors are easily damaged but readily regenerate 251
The interphotoreceptor matrix is the biological glue for retinal adhesion 253
The retinal pigment epithelium 254
The RPE is a pluripotent cell 254
Photoreceptor function is critically dependent on a healthy RPE layer 256
The RPE is polarized with tight junctions, but transport is bidirectional 257
The chemistry of the visual response 258
Photochemical reactions in the retina 258
Rhodopsin, vitamin A and photoreceptor turnover 258
Phototransduction: the conversion of light energy to an electrochemical response 259
Phototransduction is a biological cascade 261
Does phosphoinositide metabolism have a role in phototransduction? 261
Renewal of photoreceptors is associated with accumulation of lipofuscin pigment in the RPE cells 261
RPE lysosomes contain a battery of enzymes capable of degrading complex lipid–glycoprotein aggregates 262
Synaptic events between photoreceptors and cells of the inner nuclear layer 262
Two types of bipolar cell 263
Neurotransmitters and neuromodulators 265
Glutamate is the major neurotransmitter in the retina 265
Horizontal and amacrine cells 266
Dopamine exerts a neuromodulatory effect on retinal function 267
Conclusion 268
Further Reading 268
Further Reading 268.e1
5 Physiology of vision and the visual system 269
Introduction 269
Do I have good vision? 269
Flicker can be used to determine limits of vision 271
Motion detection is also a feature of rod vision 271
Sensing colour 271
There are many hues but only three primary colours 272
Chromaticity is semiquantified ‘colouredness’ 272
Shape, form and depth perception (and more) help to ‘shape’ vision 273
Light detection and dark adaptation 273
What are the limits of detectable light? 273
Thresholds and the frequency of seeing 274
What is the minimal stimulus for vision? 274
Dark adaptation curve and retinal sensitivity 274
Melatonin and circadian rhythms 276
Are two small stimuli equivalent to one large one (summation)? 277
Spatial summation 278
Temporal summation 278
Detection of minimum stimulus for motion displacement 279
Binocular summation 279
Visual acuity and contrast sensitivity 279
Visual acuity is not simply a function of cone activity 279
Limits of and limitations on acuity 280
Contrast sensitivity 283
Does the retinotopic arrangement of fibres in the cortex have a bearing on acuity? 285
Best-corrected visual acuity: effects of external factors 285
Pupil size and visual acuity testing in infants 286
Eye movements 286
Binocular viewing and the probability theory of visual perception 287
Electrophysiology of the visual system 287
The electrical response is initiated by phototransduction 287
Electrophysiology of single retinal cells 288
How does the photochemical change in the receptor produce the spike discharge in the retinal neurone? 291
Retinal connections, circuitry and neurotransmitters 291
Retinal connections 291
Clinical visual electrophysiology 296
Resting potential and the electro-oculogram 298
The electroretinogram 298
The multifocal ERG 299
The visual evoked potential 299
Flicker 301
Colour vision 302
Colorimetry and colour discrimination 302
Different colours have different luminosity 302
Spectral sensitivity curves 302
Photochromatic interval 303
Cone thresholds 303
Colour detection requires more than one type of photoreceptor 303
Trichromatic theory of colour vision 303
Psychophysical evidence for three cone photoreceptors 303
Molecular evidence for three receptors 304
Convergence, Young–Helmholtz and Hering 305
Responses between photoreceptors and neural cells 305
Ganglion cell responses and opponent colour theory 306
Colour constancy 306
Colour blindness 307
Monochromatism 307
Dichromatism 308
Anomalous trichromatism 308
Achromatopsia 308
Visual perception 308
Monocular versus binocular vision 309
Positioning objects in space 309
Measuring by eye 311
Are two eyes better than one? 312
Stereopsis and depth perception 313
The horopter 313
Measuring stereopsis 314
Image disparity and stereopsis 317
Retinal rivalry and ocular dominance 317
Colour processing 318
Shape detection 319
Contribution of texture analysis and motion detection to depth perception 319
Division of labour in the visual system: parcellation and the human connectome 321
Imaging studies 321
The magnocellular and parvocellular pathways subserve different functions 321
The striate cortex and the prestriate cortex shuffle information between them in the build-up to a perceived image 322
Parcelling out the processing in V1 323
Is the visual cortex organized for hierarchical neural processing or for functional specialization? 324
Physiology of ocular movement 326
Types of movement 326
Uniocular eye movements 326
Binocular eye movements 327
Saccades 327
Pursuit 327
Control of eye movement 329
The fixation reflex 329
Oculovestibular reflexes are eye movement responses to positional changes in the relationship between the head and the trunk 329
Rolling eye movements are due to oculovestibular and oculocervical reflexes 330
The midbrain is a coordinating centre for reflex eye movement and connects input from multiple sources 330
The superior colliculus is involved in both perception and eye movement control 331
Cortical centres regulate complex eye movements 333
The cerebellum 334
Ocular movements during natural activity 335
Neural versus mechanical control of eye movement? 335
Conclusion 336
Further Reading 337
Further Reading 337.e1
6 General and ocular pharmacology 338
Introduction 338
Pharmacokinetics: drug trafficking in the body 338
Basic concepts 338
Drug absorption 340
The rate of passage (diffusion) through a cell membrane can be predicted by Fick’s law 340
Active transport 340
Drug absorption is dependent on a drug’s lipid solubility 340
Drug properties 340
The rate of drug absorption varies with the route of administration 341
Drug distribution 341
Drugs are metabolized to facilitate clearance 342
Metabolized drugs are excreted in urine and bile 343
Renal excretion 343
Glomerular filtration. 343
Secretion. 343
Reabsorption. 343
Biliary excretion 343
Pharmacodynamics: drug handling by the body 344
Drug–receptor interactions 344
Ion channels 344
Second messengers 345
Cyclic adenosine monophosphate (cAMP) 345
Calcium is a major mediator of cellular activity 345
Regulation of protein synthesis 346
Ligand–receptor affinity determines selectivity 346
Genetic control of drug handling influences response 346
P450 gene. 347
Ocular pharmacology: drug handling by cells and tissues of the eye 347
Mechanisms of ocular drug absorption 347
Factors influencing delivery of drugs to the eye 347
Routes of administration 347
Conjunctiva. 347
Precorneal tear film and cornea 348
Delivery methods of ocular medication 349
Residence in the conjunctival sac 349
Drug vehicles affect drug delivery 350
Solutions 350
Semisolids (ointments) 350
Slow-release preparations 350
Ocular inserts. 350
Collagen shields. 350
Soft contact lens. 351
Intravitreal inserts. 351
Advanced ocular delivery systems 351
New ophthalmic delivery system (NODS) 351
Particulates 351
Liposomes 351
Ocular iontophoresis 352
Intracameral and intravitreal administration 352
Intravitreal delivery of drugs has revolutionized care for vascular retinal disorders 352
Drugs administered systemically also penetrate the eye 353
Topical medications and preservatives 354
Reconstituting the tear film 354
Tear substitutes 354
Mucolytics 355
Ocular drugs and the autonomic nervous system 355
The parasympathetic system 355
Parasympathomimetics mimic the action of acetylcholine 355
Parasympathetic antagonists affect the pupil and ciliary muscle separately and are exploited therapeutically 356
The sympathetic system 357
The control of intraocular pressure is facilitated by similar and opposite effects of adrenergic receptors 358
Clinical control of intraocular pressure exploits the adrenergic system 359
The histaminergic system: histamine is released from conjunctival mast cells during allergic reactions 359
Antihistamines 360
Sodium cromoglicate 361
Eicosanoids affect multiple ocular functions 361
Serotonin: a potent neurotransmitter 363
Serotonin receptor subclasses mediate different effects 363
5-HT antagonists 363
Glucocorticoids 363
Immunosuppressant agents: combating ocular inflammatory disease 364
Biologics 365
Local anaesthetics: an integral part of ophthalmic examination and surgery 366
Local anaesthetics affect excitable membranes 366
Local anaesthetics have both local and systemic side-effects 368
Ocular toxicity from systemic administration of drugs 368
Uveal tract 368
Photosensitization 368
Oculotoxic drugs 369
Further Reading 369
Further Reading 369.e1
7 Immunology 370
Introduction 370
Overview of the immune system 370
Cells and molecules of the immune system 373
The myeloid system and innate immunity 377
Neutrophilic granulocytes 377
Myeloid mononuclear cells 377
Other granulocytes 378
The lymphoid system and acquired immunity 380
T cells 380
B cells 380
Blurring the margins between innate and adaptive immunity 381
Natural killer cells 381
Lymphoid tissue inducer cells 381
Innate lymphoid cells 382
Initial response of the host to injury (the innate immune response) 382
The acute inflammatory response 382
The acute inflammatory response goes through three phases: 382
Tissue damage and the release of mediators 382
Vascular changes 386
Leucocyte activation and adhesion to the endothelium 386
Adhesion of leucocytes to the endothelium thus involves a series of molecular events 386
Leucocyte migration into the tissues and chemotaxis 387
Phagocytosis and removal of damaged tissue and microorganisms 389
Activation of innate immune cells by microorganisms 389
NK, NKT and γδT cells also express PRRs and mediate innate immunity 390
Effector cells in the inflammation response 392
Resolution of inflammation 392
Chronic inflammation 393
The systemic response to acute inflammation: the acute-phase reaction 394
Development of adaptive immunity and immunological memory 395
Antigen recognition is made possible by antigen-presenting cells 395
T cells respond to antigen by clonal expansion 395
T and B cells participate in the effector response 396
How does the organism deal with intracellular antigen? 396
Effector mechanisms 396
Antibodies 396
All five antibody isotypes have similar basic structure 396
Special features of H and L chains 396
Antigen–antibody binding 397
Monoclonal and polyclonal antibodies 399
Cytokines are the effector elements released by cells during innate and adaptive immune responses 399
What makes a cytokine a cytokine? 399
Cytokines involved in specific immune reactions 401
Cytokines involved in lymphomyeloid cell maturation 402
Cytokine receptors and cytokine receptor antagonists 402
Some cytokines play a bigger role in inflammation than others 403
Chemokines and chemokine receptors 404
Complement 405
What is complement and what does it do? 405
Complement has the following effects: 405
The classical complement cascade 406
The alternative pathway 408
Collectin activation of complement 408
Cytolysis and the membrane attack complex 408
Regulation of complement activation 408
Complement activation is usually incomplete: implications for age-related macular degeneration 409
Cellular mechanisms of tissue damage 410
The delayed-type hypersensitivity reaction is the hallmark of cell-mediated immunity 411
Inflammatory (M1-like) macrophages cause tissue damage: alternatively activated (M2-like) macrophages are more likely to promote healing 411
Do cytotoxic T and NK cells induce cellular damage by making holes in the cell membrane? 412
Organization of the immune system 412
Functional anatomy of lymphoid organs 412
Bone marrow stem cells produce all blood cells 413
The thymus regulates T-cell development and maturation 413
Lymph nodes are designed for antigen trapping 414
The spleen receives antigen from all sources (lymphatics and blood) 415
Tertiary lymphoid organs 416
The mucosal immune system 416
The immune system as a police force 416
Dendritic cells are the major surveillance cells of the afferent lymphoid system 416
Trafficking of cells to and from the lymphoid system depends on specific cell surface adhesion molecules 418
What turns a lymphocyte on? 419
Where are memory cells found? 420
What turns a lymphocyte off? 420
T regulatory cells. 420
Antigen recognition 421
The APC makes the antigen recognizable 421
Processing by APCs is under tight cellular control 422
Making the antigen presentable: the MHC molecule as candy wrapper 423
The major histocompatibility system 424
What are MHC antigens and where are they found? 424
Organization of the MHC genes in the genome 426
Regulation and transcription of the MHC genes 427
T-cell activation 427
The TCR and antigen binding 427
The right time and the right place for T-cell activation 430
What are γδT cells and what is their role? 431
Superantigens 431
Antigens can be presented by other MHC and MHC-like molecules 432
Co-stimulation: presentation of antigen requires ‘help’ from other molecules 432
Co-stimulatory molecules 433
Getting the message across: cell signalling through the immunological synapse 435
Action of drugs on cell activation 437
B-cell activation 437
Antigens, B cells, and T cells: which does what? 437
Antigen recognition by B cells 437
B cells as antigen-presenting cells 438
B-cell differentiation 438
Antibody generation during B-cell ontogeny 439
Somatic mutations occur in the CDR of the V genes 439
Genetic control of antibody production 439
Immunological tolerance and autoimmunity 439
What is tolerance? 441
Sites of tolerance induction 441
Mechanisms of tolerance induction 442
Clonal deletion 442
Anergy 442
Active suppression by specific lymphocytes: T-regulatory cells 443
T-cell tolerance is different from B-cell tolerance 443
Failed tolerance 444
Autoimmune disease is the dysfunction or damage of tissue caused by immune responses to autoantigens 444
Parasitic infections persist by giving false signals to the immune system 444
Allergy and immediate hypersensitivity 445
Atopy, asthma and allergic eye disease 445
Mast cells and mast cell degranulation 446
Immunoglobulin and helper T cells 447
Mechanism of disease production in allergic disease 448
Mast cells also have a protective role 448
Organ and tissue transplantation 450
Tumours induce immune responses 451
The eye and the immune system 453
The innate immune system and the eye 453
The adaptive immune system and the first line of defence in the eye 453
Progressive ocular surface disease 454
Cicatrizing disease of the conjunctiva 454
Keratitis and ‘melting’ corneal ulcers 455
Inflammatory disorders of the orbit and sclera 456
The eye as a privileged site: what does this mean for the survival of corneal grafts? 457
Intraocular inflammation 459
The role of the immune system in ageing and degeneration in the eye 460
Conclusion 461
Further Reading 461
Further Reading 461.e1
8 Microbial infections of the eye 462
Introduction 462
Microbes in the environment 462
Host defences at the ocular surface 463
Physical barriers 463
Epithelium 463
Resident macrophages and dendritic cells in the cornea 464
Pathogen recognition receptors and recruitment of neutrophils 464
Toll-like receptors (TLR) 464
NOD-like receptors 464
C-type lectins 467
Neutrophils 467
Adaptive immunity to microbial infection 469
Ocular infections worldwide 469
Contact lenses 469
Viral infections of the eye 471
Herpes stromal keratitis 471
Primary infection. 471
Angiogenesis and lymphangiogenesis. 471
Latency. 471
Viral retinitis 472
Bacterial infections of the eye 473
Ocular surface 473
Pseudomonas aeruginosa virulence factors. 473
Streptococcus pneumoniae. 474
Staphylococcus aureus. 474
Contact lens-related corneal inflammation. 474
Bacterial endophthalmitis 474
Fungal infections of the eye 475
Corneal infection with Aspergillus and Fusarium 475
Contact lens-associated fungal keratitis. 475
Treatment of fungal keratitis. 475
Pathogenesis of fungal keratitis. 475
Corticosteroids. 477
Protozoan causes of ocular disease 477
Acanthamoeba keratitis 477
Acanthamoeba virulence factors. 478
Host response to Acanthamoeba. 478
Acanthamoeba as a ‘Trojan horse’. 478
Toxoplasmosis 478
Host response. 479
Ocular toxoplasmosis. 480
Helminth causes of ocular infection 480
Toxocariasis 480
Ocular infections in developing countries 480
Onchocerciasis (river blindness) 480
Life cycle and parasite burden 480
Pathogenesis 480
Endosymbiotic Wolbachia bacteria 481
Onchocerciasis control 481
Loa loa (loiasis, Eyeworm) 482
Trachoma 482
Trachoma in Australia 483
Conclusion 483
Further Reading 485
Further Reading 485.e1
9 Pathology 486
Introduction 486
Cell and tissue damage 486
Agents or conditions that can cause direct damage to ocular cells and tissues 486
Reduced oxygen supply 486
Physical agents 486
Chemical agents 487
Toxins 487
Viruses 488
Dysregulated immunity 488
Nutritional deficiencies 488
Genetic abnormalities 488
Chromosomal abnormalities 488
Single gene defects. 488
Mechanism of cell death 489
Necrosis 489
Apoptosis 489
Sublethal cell injury 490
Hydropic swelling. 490
Atrophy. 490
Hypertrophy. 490
Metaplasia. 490
Healing and repair 490
Healing in the cornea usually leads to a corneal opacity (scar) 491
Iris 492
Lens 492
Retina 492
Choroid 492
Sclera 492
Optic nerve 492
Inflammation 492
What happens in acute inflammation? 492
How does infection cause inflammation? 494
Bacteria 494
Pyogenic infection. 494
Chronic infection. 494
Viruses 495
Herpes simplex keratitis. 495
Herpes zoster ophthalmicus. 495
Acute retinal necrosis. 496
Progressive outer retinal necrosis. 496
Cytomegalovirus retinitis. 497
Chlamydia 497
Fungi 497
Protozoal and metazoal infections 498
Toxoplasma gondii. 498
Acanthamoeba spp. 498
Toxocara canis. 499
Other parasites 499
Inflammation may occur without infection 499
Granulomatous inflammation 499
Reactions to endogenous materials 500
Reactions to exogenous non-biological materials 500
Non-granulomatous inflammation 500
Inflammation due to autoimmune disease 500
Sjögren syndrome 500
Rheumatoid eye disease 501
Other ocular surface disease 501
Lens-induced uveitis 501
Sympathetic ophthalmia 502
Vasculitis 503
Temporal (giant cell) arteritis. 503
Takayasu’s disease. 503
Polyarteritis nodosa. 503
Wegener’s granulomatosis. 503
Systemic lupus erythematosus 503
Metabolic disease 504
Diabetes 504
Thyroid eye disease 504
Disorders of amino acid metabolism 504
Homocystinuria 504
Cystinosis 505
Ageing, degeneration and dystrophies 505
Ageing 505
Degeneration 505
Composition/type of degeneration 505
Hyalinization. 505
Fatty degeneration. 506
Elastic fibre degeneration. 506
Pinguecula and pterygium. 507
Calcification. 507
Amyloid 507
Systemic amyloid deposition 507
Localized amyloid deposition 507
The exfoliation syndrome (pseudoexfoliation syndrome) 508
Degenerative vascular disease 508
Hyalinization. 508
Vaso-occlusive disease. 508
Microvascular occlusion. 509
Macrovascular occlusion. 510
Cataract 511
Cataract associated with ageing. 511
Secondary cataract. 512
Glaucoma 512
Primary open-angle glaucoma. 512
Primary closed-angle glaucoma. 512
Secondary glaucoma. 513
Age-related macular degeneration and disciform degeneration of the macula 513
Dystrophies 514
Retinal dystrophies 514
Retinitis pigmentosa. 514
Vitelliform dystrophy (Best disease). 515
Stargardt’s disease (fundus flavimaculatus). 515
Corneal dystrophies 515
Epithelial dystrophies. 516
Corneal dystrophies of Bowman’s layer. 516
Stromal dystrophies. 516
Lattice dystrophy. 516
Macular dystrophy. 516
Granular corneal dystrophy. 517
Combined granular–lattice dystrophy (Avellino dystrophy). 517
Endothelial dystrophies. 517
Congenital hereditary endothelial dystrophy. 518
Iridocorneal endothelial syndrome. 518
Posterior polymorphous dystrophy. 518
Fuchs’ endothelial dystrophy. 518
Neoplasia 518
Pathogenesis of neoplasia 519
Premalignancy 519
Carcinogenesis 519
Oncogenes and tumour suppressor genes 521
Tumour spread and metastases 521
Hamartomas 521
Haemangiomas 521
Naevi 521
Choristomas 522
Dermoid 522
Phakomatous choristoma 522
Teratoma 522
Benign epithelial tumours 523
Benign tumours of surface epithelium 523
Benign tumours of adnexal glands 523
Malignant epithelial tumours 523
Basal cell carcinoma 523
Squamous cell carcinoma 523
Sebaceous gland carcinoma 525
Malignant melanoma 525
Conjunctiva 525
Uveal melanoma 525
Iris melanomas. 526
Ciliary body and choroidal melanomas. 526
Neural tumours 526
Neurofibroma and schwannoma 526
Malignant peripheral nerve sheath tumours 529
Retinoblastoma 529
Astrocytic hamartoma 531
Glioma 531
Meningioma 533
Tumours derived from muscle 533
Leiomyoma/leiomyosarcoma 533
Rhabdomyoma/rhabdomyosarcoma 533
Vascular tumours 533
Haemangiomas 534
Epithelioid haemangioma 534
Kaposi sarcoma 534
Other connective tissue tumours 534
Lymphoid tumours 534
Lacrimal gland tumours 536
Pleomorphic adenoma (benign mixed tumour) 536
Adenoid cystic carcinoma 537
Other malignant epithelial tumours 537
Lacrimal sac tumours 537
Metastatic tumours 537
Disorders misdiagnosed as neoplasms 537
Cysts 537
Eyelid. 537
Conjunctiva. 537
Orbit. 537
Pseudoepitheliomatous hyperplasia 538
Idiopathic orbital inflammation 538
Further Reading 538
Further Reading 538.e1
Index 539
A 539
B 540
C 541
D 544
E 545
F 546
G 546
H 547
I 548
J 549
K 549
L 550
M 551
N 552
O 553
P 554
Q 555
R 555
S 556
T 558
U 559
V 559
W 560
X 560
Y 560
Z 560