Ocular Disease-a newly introduced companion volume to the classic Adler's Physiology of the Eye-correlates basic science and clinical management to describe the how and why of eye disease processes and the related best management protocols. Editors Leonard A. Levin and Daniel M. Albert-two of the world's leading ophthalmic clinician-scientists-have recruited as contributors the most expert and experienced authorities available in each of the major areas of ophthalmic disease specific to ophthalmology: retina, cornea, cataract, glaucoma, uveitis, and more. The concise chapter structure features liberal use of color-with 330 full-color line artworks, call-out boxes, summaries, and schematics for easy navigation and understanding. In print and online at expertconsult.com, this comprehensive resource provides you with a better and more practical understanding of the science behind eye disease and its relation to treatment. Includes access to the fully searchable text online at expertconsult.com, along with images and references. Covers all areas of disease in ophthalmology including retina, cornea, cataract, glaucoma, and uveitis for the comprehensive information you need for managing clinical cases. Presents a unique and pragmatic blend of necessary basic science and clinical application to serve as a clinical guide to understanding the cause and rational management of ocular disease. Features 330 full-color line artworks that translate difficult concepts and discussions into concise schematics for improved understanding and comprehension. Provides the expert advice of internationally recognized editors with over 40 years of experience together with a group of world class contributors in basic science and clinical ophthalmology. Your purchase entitles you to access the web site until the next edition is published, or until the current edition is no longer offered for sale by Elsevier, whichever occurs first. Elsevier reserves the right to offer a suitable replacement product (such as a downloadable or CD-ROM-based electronic version) should access to the web site be discontinued. Registration and use of the web site is subject to the terms of the non-transferable, limited license under which access to the site and its content is granted by Elsevier. Access to the site by individuals is limited to the first retail purchaser and may not be transferred to another party by resale, lending or other means.
Author(s): Leonard A Levin MD PhD, Daniel M. Albert MD MS
Edition: 1 Har/Psc
Year: 2010
Language: English
Pages: 701
Tags: Медицинские дисциплины;Офтальмология;
A......Page 2
Title page......Page 3
Copyright page......Page 4
List of Contributors......Page 5
Dedication......Page 12
Foreword......Page 13
Preface......Page 14
Overview......Page 15
Transparency loss from corneal edema......Page 16
Haze following photorefractive keratectomy......Page 18
Summary......Page 21
Key references......Page 22
Clinical manifestations of wound healing......Page 23
The importance of TGF-β......Page 25
Gene therapy......Page 26
In vitro wound-healing models and biomimetic corneas......Page 27
Acknowledgments......Page 28
Key references......Page 29
The normal wound-healing response......Page 30
Apoptosis and necrosis in initiation, modulation, and termination of wound healing (Box 3.2)......Page 31
Inflammatory cell influx (Box 3.3)......Page 32
Altered healing in corneas that develop haze (Box 3.5)......Page 33
Altered wound healing in femtosecond LASIK......Page 34
Key references......Page 35
Pathophysiology......Page 36
Clinical background......Page 37
Pathophysiology......Page 38
Pathophysiology......Page 39
Clinical background......Page 40
Clinical background......Page 41
Clinical background......Page 42
Pathology......Page 43
Clinical background......Page 44
Pathophysiology......Page 45
Key references......Page 47
The endothelium......Page 48
Descemet’s membrane in FECD......Page 50
Etiology......Page 51
Clinical diagnosis and evaluation of FECD......Page 52
Management......Page 53
Key references......Page 54
Treatment......Page 56
Prognosis and complications......Page 57
Enzyme activities in human corneas......Page 58
The biological basis of oxidative damage in keratoconus corneas......Page 59
The biological basis of corneal thinning in keratoconus......Page 60
Acknowledgments......Page 61
Key references......Page 62
Bacterial keratitis......Page 63
Fungal keratitis......Page 65
Immune response......Page 66
Role of hyphae in C. albicans keratitis......Page 67
Altered tissue physiology......Page 68
References......Page 69
Epidemiology......Page 70
Risk factors......Page 71
Etiology......Page 72
Alterations in the local microenvironment......Page 74
Conclusion......Page 76
Key references......Page 77
Clinical background......Page 78
Pathology......Page 79
Infancy to adulthood......Page 81
Barrier function......Page 83
Pump leak mechanism......Page 84
Pathophysiology of corneal edema......Page 85
Key references......Page 87
Pathology......Page 88
Etiology......Page 89
Multiple steps involved in corneal NV and lymphangiogenesis......Page 91
Corneal NV and lymphangiogenesis-related disorders......Page 92
Endostatin......Page 93
Examples......Page 94
Key references......Page 96
Diagnostic workup and differential diagnosis......Page 97
Prognosis and complications......Page 98
Environmental risk factors......Page 99
Pathophysiology......Page 101
Pathophysiology......Page 102
Conclusion......Page 103
Key references......Page 104
Clinical background......Page 105
Pathology......Page 106
Pathophysiology......Page 107
Initial phase of infection......Page 108
Key references......Page 110
Etiology......Page 112
Pathophysiology......Page 113
Clinical background......Page 114
Pathophysiology......Page 115
Pathophysiology......Page 116
Etiology/pathology/pathophysiology......Page 117
Key references......Page 118
Epidemiology......Page 119
Treatment......Page 120
Mechanisms of aqueous-deficiency dry eye......Page 121
Alteration in stimulation of secretion......Page 122
Conclusion......Page 125
Acknowledgment......Page 126
Key references......Page 127
Genetics and risk factors......Page 128
Conjunctiva and cornea......Page 129
Cytophysiological apparatus......Page 130
Constitutive exposure of autoantigens......Page 132
Maintaining homeostatic states......Page 133
Paracrine mediation of endocrine triggers......Page 134
Chronic disease processes......Page 135
Key references......Page 136
Tear film thickness and tear volumes on the ocular surface......Page 137
Tear film breakup mechanisms (Box 16.2)......Page 138
Dynamic tear system with regulation......Page 139
Delayed blinking......Page 140
Blinking with overloaded artificial tears......Page 141
Key references......Page 144
Normal anatomy and production......Page 145
Changes occurring with age......Page 146
The clinical characteristics of meibomian gland disease......Page 147
Therapeutic implications......Page 148
Future research and management......Page 150
Key references......Page 151
Mucins expressed by the ocular surface epithelium......Page 152
Membrane-associated mucins......Page 154
Detection of mucins in tear fluid......Page 155
Alteration of glycosylation of mucins......Page 156
Therapeutics for dry eye targeted toward mucin production......Page 157
Key references......Page 159
Treatment......Page 160
Endogenous glucocorticoids and glaucoma......Page 161
Effects of GCs on the trabecular meshwork (Box 19.3)......Page 162
GRE-dependent pathway......Page 163
GRß role in glucocorticoid-resistant diseases......Page 164
Differences in tissue/cell responses to GCs......Page 165
Key references......Page 166
Etiology......Page 167
Basic concepts in mechanics......Page 168
Scleral biomechanics......Page 169
Models of the optic nerve head......Page 170
Models of the lamina cribosa......Page 173
Other measures of acute intraocular pressure-related changes in the optic nerve head......Page 174
Alterations in connective tissue architecture, cellular activity, axoplasmic transport, and blood flow in early glaucoma......Page 175
Alterations in connective tissue architecture, cellular activity, axoplasmic transport, and blood flow in later stages of glaucomatous damage......Page 176
Key references......Page 177
Epidemiology......Page 179
Genetics......Page 180
Pathology......Page 181
Liberation of iris pigment......Page 182
Pigment-related insults to intraocular pressure......Page 183
Key references......Page 184
Trabecular meshwork and Schlemm’s canal cell profiles......Page 185
ECM composition, turnover, and modulation......Page 186
Cell adhesion......Page 189
Aging, oxidative stress, and other insults......Page 190
Key references......Page 191
Pathology......Page 192
Etiology......Page 193
Pathophysiology of glaucoma......Page 194
Ischemia factors......Page 195
RGC death......Page 196
Key references......Page 197
Epidemiology......Page 198
Treatment of exfoliative glaucoma......Page 200
Pathogenesis of exfoliation syndrome and exfoliative glaucoma......Page 201
Pathogenetic factors and key molecules......Page 202
Development of glaucoma......Page 203
Vacular abnormalities in XFS......Page 204
Key references......Page 206
Gonioscopy......Page 207
Acute primary angle closure......Page 208
Trabeculectomy......Page 209
Genetics......Page 210
Choroidal effusion......Page 211
Key references......Page 212
Etiology......Page 214
Transsynaptic degeneration of the lateral geniculate nucleus in glaucoma......Page 215
Central visual system changes in human glaucoma......Page 217
Clinical implications......Page 218
Acknowledgment......Page 219
Key references......Page 220
Etiology......Page 221
Wallerian degeneration versus die-back......Page 222
Intrinsic versus extrinsic apoptosis......Page 224
Cell shrinkage......Page 225
Future therapies/clinical management......Page 226
Key references......Page 227
Cytokines, chemokines, and growth factors......Page 228
Fibroblast proliferation and vascularization......Page 233
Matrix and cell-mediated contraction......Page 234
Acknowledgments......Page 235
Key references......Page 236
Pathology......Page 237
Vasospasticity and migraine......Page 239
Pathophysiology......Page 240
Pressure autoregulation......Page 241
Endothelial dysfunction......Page 242
Key references......Page 244
Pathology......Page 245
Etiology......Page 246
Sunlight, aging, and cortical cataracts......Page 248
Oxygen, the vitreous body and nuclear cataracts......Page 249
Key references......Page 251
Pathology......Page 252
Etiology......Page 253
Pathophysiology......Page 254
Key references......Page 256
Appearance of diabetic cataracts......Page 257
Pathophysiology......Page 258
Aldose reductase and sorbitol pathway activity......Page 259
Are localized osmotic changes possible in human lens?......Page 261
Antioxidants......Page 262
Key references......Page 263
Characteristics of steroid-induced cataract......Page 264
Steroids......Page 265
Receptor-mediated glucocorticoid action......Page 266
Glucocorticoid receptor-mediated signaling in lens epithelial cells......Page 268
Glucocorticoid-mediated alteration in lens hydration......Page 269
Conclusion......Page 270
Key references......Page 271
Epidemiology......Page 272
Introduction......Page 273
Accommodation......Page 274
The crystalline lens......Page 275
The development of presbyopia......Page 279
Key references......Page 280
Lens capsular changes in presbyopia......Page 281
Etiology......Page 282
Scleral expansion surgery......Page 283
Laser reduction of lens stiffness......Page 284
Accommodative intraocular lenses......Page 285
Key references......Page 287
Pharmacology......Page 288
Intraoperative measures......Page 289
Key references......Page 290
Prognosis......Page 292
Animal model......Page 293
ROS suppress oxidative phosphorylation......Page 294
Antioxidant gene therapy suppresses loss of OXPHOS in vitro......Page 295
Long-term antioxidant gene therapy suppresses optic neuritis......Page 296
Antioxidant gene therapy suppresses neuronal degeneration......Page 299
Additional approaches to suppress axonal loss......Page 300
Key references......Page 302
Treatment......Page 303
Brainstem paralysis of horizontal saccades......Page 304
Cerebral gaze paralysis......Page 305
Cerebral, cerebellar, and brainstem smooth pursuit circuits......Page 306
Unidirectional pursuit paresis......Page 307
Oculocephalic reflex......Page 308
Vertical gaze......Page 309
Key references......Page 310
Genetics......Page 312
Treatment......Page 313
Vitamin A connection......Page 314
Hypovitaminosis A......Page 315
Structure and function......Page 316
Increased cerebral venous sinus pressure......Page 318
Key references......Page 319
Clinical background......Page 320
Genetic associations......Page 323
Role for cytokines and chemokines in disease activity......Page 324
Conclusion......Page 325
Key references......Page 326
Neuroimaging......Page 327
Quantitative ocular imaging modalities......Page 328
Experimental ischemia of the optic nerve......Page 331
Amiodarone......Page 332
Nocturnal hypotension......Page 333
Treatment......Page 334
Key references......Page 335
Key symptoms and signs......Page 336
Pathology......Page 338
Effects on the retinal ganglion cell body......Page 339
Axonal degeneration is independent of soma degeneration......Page 341
Effects of axonal injury on nonneural cells......Page 342
Key references......Page 343
Differential diagnosis......Page 344
Pathology......Page 345
Genetic factors......Page 346
Pathophysiology......Page 347
Mitochondria and oxidative phosphorylation......Page 348
Proposed LHON pathogenesis that leads to RGC death......Page 349
Key references......Page 350
Mimics of optic atrophy......Page 351
Pathogenic mechanisms of optic atrophy......Page 352
Pathogenic mechanisms of optic disc pallor......Page 353
Timing and evolution of optic atrophy......Page 355
Key references......Page 356
Introduction......Page 358
Clinical background......Page 359
Pathophysiology......Page 360
Pathophysiology......Page 362
Spasmus nutans......Page 364
Nystagmus associated with retinal diseases and low vision......Page 366
Acquired nystagmus......Page 367
Vertical jerk nystagmus......Page 368
Acknowledgments......Page 369
Key references......Page 370
Epidemiology......Page 371
Treatment......Page 372
Nutrition......Page 373
Pathophysiology......Page 374
Key references......Page 375
Pathophysiology......Page 376
Proliferation independent of normal growth signals......Page 378
Recruitment of a tumor blood supply......Page 379
Metastasis......Page 380
Conclusions......Page 381
Key references......Page 382
Diagnostic workup......Page 383
Genetic testing for retinoblastoma......Page 384
Treatment (Box 48.1)......Page 385
Pathology......Page 386
Genetics......Page 387
Function of pRb......Page 388
Role of the pRb in the development of retinoblastoma......Page 389
Key references......Page 390
Genetic mechanisms of low-penetrance retinoblastoma......Page 391
Type 1 mutations that reduce the expression of normal retinoblastoma protein......Page 392
The pocket domain......Page 394
Conclusions......Page 395
Key references......Page 396
Overview and clinical context......Page 397
Are vasculogenic mimicry patterns a stromal response to the tumor (i.e., are these patterns fibrovascular septa)?......Page 398
Vasculogenic mimicry as a tumor biofilm: therapeutic implications......Page 399
Conclusion......Page 401
Key references......Page 402
Transpupillary thermotherapy (TTT)......Page 403
Plaque brachytherapy......Page 404
Brachytherapy versus enucleation......Page 405
External-beam radiation therapy (EBRT)......Page 406
Stereotactic radiotherapy......Page 407
Key references......Page 408
Clinical background......Page 410
Pathology......Page 411
Disease management......Page 412
The pilosebaceous gland, the bulge, and the role of hair follicle stem cells......Page 414
Genetic and molecular regulation of sebaceous cell carcinoma......Page 416
Summary......Page 420
Key references......Page 421
Plexiform neurofibromas (Figure 53.1C)......Page 422
Optic pathway gliomas......Page 423
Diagnostic evaluation of asymptomatic children with NF1......Page 424
Pathophysiology......Page 425
Small-animal models of NF1-associated OPG......Page 426
Key references......Page 428
Diagnostic workup......Page 429
Prognosis and complications......Page 430
Gross pathology of the external eye......Page 431
Histopathology......Page 432
Ocular hypotony and phthisis bulbi......Page 434
Ocular wound healing in phthisis bulbi......Page 435
Conclusion......Page 436
Key references......Page 437
Ocular morbidities associated with myopia......Page 438
Human emmetropization process......Page 439
Compensation for negative lenses......Page 440
The signaling cascade......Page 441
Visual response remodeling of the sclera......Page 442
Ocular refractive component genetics......Page 443
Molecular genetic studies of human high-grade myopia......Page 444
Mouse models of myopia......Page 445
Key references......Page 446
Pathology......Page 447
Radioiodine therapy for Graves’ disease......Page 448
TSHR autoantibodies......Page 449
Novel approaches to therapy......Page 450
Key references......Page 451
Etiology......Page 452
Imaging evidence of dysinnervation......Page 454
Duane syndrome with superimposed neuropathy......Page 456
Pathophysiology influences treatment of Duane syndrome......Page 457
Key references......Page 458
Treatment......Page 459
Psychophysics......Page 460
Models......Page 461
Critical periods......Page 463
Pathophysiology......Page 465
Key references......Page 466
Genetics......Page 468
Treatment......Page 469
Pathology......Page 470
Biological basis of the disease......Page 471
A trophic theory of strabismus......Page 472
Mutations......Page 473
Key references......Page 474
History......Page 475
Differential diagnosis......Page 477
Treatment......Page 480
Pathology......Page 481
OCA1 and OCA3......Page 482
Pathophysiology......Page 483
Key references......Page 484
Clinical background......Page 486
Etiology and distribution......Page 487
Prognosis, prevention, and treatment......Page 488
Etiology......Page 489
Pathophysiology......Page 490
Key references......Page 491
Historical development......Page 492
Inherited color vision defects......Page 493
Acquired color vision defects......Page 494
Inherited color vision defects......Page 495
Inherited color vision defects......Page 496
Pathophysiology......Page 497
Key references......Page 499
Arteritic CRAO......Page 500
Transient nonarteritic CRAO......Page 501
Clinical background......Page 502
Treatment......Page 503
CRVO and HCRVO......Page 504
CRVO and HCRVO......Page 505
CRVO and HCVO......Page 506
BRVO......Page 507
Nonischemic CRVO associated with cilioretinal artery occlusion......Page 508
Surgical or invasive treatments......Page 509
Photocoagulation......Page 510
Long-term complications of CRVO......Page 511
Key references......Page 512
Spectral characteristics of damaging light......Page 513
Genetic risk factors......Page 514
Dietary factors......Page 515
Antioxidants and oxidation......Page 516
Relationship between retinal light damage and macular degeneration......Page 517
Key references......Page 519
Current means of inhibiting development or progression of diabetic retinopathy......Page 520
Pathology......Page 522
Capillary cell death caused by metabolic abnormalities within capillary cells......Page 523
Vaso-occlusion by white blood cells or platelets......Page 524
Capillary permeability......Page 525
Key references......Page 526
Etiology......Page 528
Production of vasoactive factors......Page 529
Vascular endothelial growth factor......Page 530
Conclusions......Page 531
Key references......Page 532
Epidemiology (Box 67.1)......Page 533
Diagnostic workup (Box 67.2)......Page 535
Treatment (Table 67.2)......Page 536
Inner blood–retinal barrier dysfunction (Box 67.4)......Page 538
Role of systemic factors (Box 67.5)......Page 539
Key references......Page 540
Pathology......Page 541
Aging–AMD overlap......Page 543
Epidemiology......Page 544
Drusen, GA, and CNVs are associated with mutations in components of the complement pathway, which is part of the innate immune system92......Page 545
Oxidative damage can activate the complement system......Page 546
Mutations causing nonexudative versus exudative complications of AMD......Page 547
Conclusion......Page 548
Key references......Page 549
Historical development......Page 550
Diagnostic workup......Page 551
Differential diagnosis......Page 552
Pathophysiology......Page 553
Response to injury......Page 554
Neovascularization: angiogenesis and vasculogenesis......Page 555
Conclusion......Page 556
Key references......Page 557
Vascular endothelial growth factor......Page 558
Platelet-derived growth factor-B......Page 560
Notch......Page 561
Ephrins......Page 562
Integrins......Page 563
Ranibizumab......Page 564
Triamcinolone acetonide, dexamethasone, and fluocinolone......Page 565
Other therapeutic approaches based on modulating angiogenic factors......Page 566
Key references......Page 567
History......Page 568
Etiology......Page 570
Second- and third-order neurons......Page 571
Müller cells......Page 572
Microglia and the immune response......Page 574
Key references......Page 575
Historical development......Page 576
Genetics......Page 577
Differential diagnosis......Page 580
Environmental risk factors......Page 581
The role of supplemental oxygen......Page 582
HIF-1alpha......Page 583
Summary......Page 584
Key references......Page 585
Clinical background (Box 73.1)......Page 586
Supply of oxygen and glucose from the circulation (Box 73.2)......Page 587
Oxygen supply......Page 588
Oxidative metabolism (Box 73.3)......Page 589
Aerobic and anaerobic glycolysis (Box 73.4)......Page 590
Photoreceptors......Page 591
Key references......Page 592
Diagnostic workup......Page 593
Electroretinography......Page 594
Genetic testing......Page 595
Systemic evaluation......Page 596
Syndromic RP......Page 597
Defective signaling in photoreceptor cilia......Page 601
Defective photoreceptor cilia formation......Page 602
Key references......Page 603
Pathology......Page 604
More specific rationale for treatment of retinal blindness with a retinal prosthesis......Page 605
Sensory substitution......Page 606
Transplantation......Page 607
Comparison of different types of visual prosthetic devices......Page 608
Retinal and optic nerve prostheses......Page 609
Optobionics......Page 610
Optic nerve prostheses......Page 611
Key references......Page 612
Autoimmune retinopathy (AR)......Page 613
Bilateral diffuse uveal melanocytic proliferation (BDUMP)......Page 614
Historical development......Page 615
Diagnostic workup......Page 616
Etiology......Page 617
Pathophysiology......Page 618
Apoptosis of retinal cells......Page 619
Key references......Page 620
Etiology......Page 621
Retinal sheet transplantation......Page 622
Glial scar formation......Page 623
Key references......Page 625
Treatment......Page 626
Pathogenic cells......Page 627
Cell proliferation and apoptosis......Page 629
Key references......Page 630
Etiology......Page 632
Animal models of uveitis......Page 633
Immunogenetics and uveitis......Page 634
Cellular mediators of uveitis......Page 636
Cytokines......Page 637
The role of tolerance in uveitis......Page 638
Therapeutic advances in uveitis......Page 639
Key references......Page 640
Clinical background......Page 642
Diagnosis......Page 643
Etiology......Page 644
Role of the immune cells......Page 645
Key references......Page 647
Epidemiology......Page 649
Differential diagnosis......Page 650
Pathology......Page 651
Other risk factors......Page 653
Pathophysiology......Page 654
Key references......Page 655
Tests and investigations in scleritis......Page 656
Significance of antineutrophil cytoplasmic antibodies......Page 658
Other differentials of scleritis......Page 659
Treatment of scleritis......Page 660
Complications of scleritis......Page 661
Disease associations in scleritis......Page 662
Blood supply to the sclera and episclera......Page 664
Role of T cells in scleritis......Page 665
Conclusion......Page 666
Key references......Page 667
Diagnostic workup......Page 668
Key symptoms and signs......Page 669
Ocular manifestations......Page 670
Pathophysiology......Page 671
Historical development......Page 672
Ocular manifestations......Page 673
Etiology......Page 674
Differential diagnosis......Page 675
Etiology......Page 678
Key references......Page 679
Key symptoms and signs......Page 680
Diagnostic workup......Page 681
Pathology......Page 682
Etiology......Page 683
Key references......Page 684
A......Page 686
B......Page 687
C......Page 688
D......Page 689
E......Page 690
G......Page 691
I......Page 692
L......Page 693
M......Page 694
O......Page 695
P......Page 696
R......Page 697
S......Page 698
U......Page 700
Y......Page 701
