Books

Glaucoma (Portuguese)

qty17

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Foreword

1. Introduction
1.1 Purpose of the Book
1.2 What is Glaucoma?
1.3 What is Glaucomatous Damage?
1.4 What are the Consequences of Glaucomatous Damage?
1.5 How Common is Glaucoma?

2. Glaucomatous Damage
2.1 Phenomenology of Glaucomatous Damage

  • 2.1.1 Nerve Fiber Loss in Glaucoma
  • 2.1.2 Glaucomatous Tissue Loss
  • 2.1.3 Functional Loss in Glaucoma

2.2 How does Glaucomatous Damage Arise?

  • 2.2.1 The Problem of Causality
  • 2.2.2 The Significance of Intraocular Pressure
  • 2.2.3 The Significance of Ocular Perfusion

3. Classification of the Various Types of Glaucoma
3.1 Congenital Glaucoma
3.2 Infantile Glaucoma
3.3 Juvenile Glaucoma
3.4 Primary Chronic Open-Angle Glaucoma (POAG)

  • 3.4.1 POAG with Increased Intraocular Pressure
  • 3.4.2 POAG with Normal Intraocular Pressure
  • 3.4.3 POAG without Discernible Glaucomatous Damage

3.5 Primary Angle-Closure Glaucoma

  • 3.5.1 Acute Angle-Closure Glaucoma
    • 3.5.1.1 Pupillary Block Mechanism
    • 3.5.1.2 Plateau Iris Mechanism
  • 3.5.2 Intermittent Angle-Closure Glaucoma
  • 3.5.3 Chronic Angle-Closure Glaucoma
  • 3.5.4 Ciliary Block Glaucoma

3.6 Secondary Glaucoma

  • 3.6.1 Secondary Open-Angle Glaucoma
    • 3.6.1.1 Glaucoma Associated with Pseudoexfoliation Syndrome
    • 3.6.1.2 Glaucoma with Pigment Dispersion Syndrome
    • 3.6.1.3 Additional Causes
  • 3.6.2 Secondary Angle-Closure Glaucoma

4. Risk Factors
4. 1 General Risk factors for an Increase in IOP

  • 4.1.1 Age
  • 4.1.2 Family Background
  • 4.1.3 Race
  • 4.1.4 Gender
  • 4.1.5 Arteriosclerosis
  • 4.1.6 Near and Far-Sightedness

4.2 Risk Factors for Glaucomatous Damage

  • 4.2.1 Intraocular Pressure
  • 4.2.2. Age
  • 4.2.3 Family History
  • 4.2.4 Race
  • 4.2.5 Gender
  • 4.2.6 Near and Far-Sightedness
  • 4.2.7 Circulatory Problems
  • 4.2.8 Diabetes Mellitus
  • 4.2.9 The Appearance of the Optic disc
  • 4.2.10 Additional Factors

5. Pathogenesis of Glaucomatous Damage
5.1 Apoptosis, "Programmed Cell Death"

  • 5.1.1 Cells in Dialogue
  • 5.1.2 Causes of Apoptosis

5.2. The Importance of Ocular Perfusion

  • 5.2.1 The Role of Vascular Dysregulation
  • 5.2.2 The Role of Intraocular Pressure
  • 5.2.3 The Influence of Blood Pressure
  • 5.2.4 Additional Factors

5.3 Reperfusion Damage
5.4 Activation of Glial Cells
5.5 Altered Micro-Environment
5.6 The Pathogenetic Concept

6. Diagnosing Glaucoma
6.1 Which Symptoms are Noticed by the Patient?
6.2 When Should an Ophthalmologist be Consulted?
6.3 Examination by the Ophthalmologist

  • 6.3.1 Routine Eye Examination
  • 6.3.2 Measuring the Intraocular Pressure
  • 6.3.3 Examining the Anterior Chamber Angle
  • 6.3.4 Evaluating the Optic Disc

6.4 Documenting the Papilla and Nerve Fiber Layer

  • 6.4.1 Papillary Photography
  • 6.4.2 Laser Scanning Tomography
  • 6.4.3 Measuring the Thickness of the Nerve Fiber Layer

6.5 Testing the Visual Field
6.6 Assessing Ocular Perfusion

  • 6.6.1 Measuring Blood Pressure
  • 6.6.2 Capillary Microscopy
  • 6.6.3 Color Doppler Sonography
  • 6.6.4 Measuring Temperature

6.7 Special Examinations

  • 6.7.1 Dark Adaptation
  • 6.7.2 Color Vision
  • 6.7.3 Contrast Sensitivity
  • 6.7.4 Glare
  • 6.7.5 ERG
  • 6.7.6 VEP

6.8 Blood Chemistry

7. Therapy
7.1 General Remarks Regarding Treatment Options

  • 7.1.1 Avoiding Risk Factors
  • 7.1.2 The Therapy Spectrum
  • 7.1.3 Glaucoma Therapy and the Quality of Life
  • 7.1.4 Treatment Goals

7.2 IOP-Lowering Medication

  • 7.2.1 Parasympathomimetic Agents/Cholinergic Agents
    • 7.2.1.1 Pilocarpine
    • 7.2.1.2 Aceclidine
    • 7.2.1.3 Carbachol
  • 7.2.2 Sympathomimetic Agents
    • 7.2.2.1 Epinephrine (Adrenaline)
    • 7.2.2.2 Dipivefrin
    • 7.2.2.3 Clonidine
    • 7.2.2.4 Apraclonidine
    • 7.2.2.5 Brimonidine
  • 7.2.3 Sympatholytic Agents
    • 7.2.3.1 Timolol
    • 7.2.3.2 Betaxolol
    • 7.2.3.3 Levobunolol
    • 7.2.3.4 Carteolol
    • 7.2.3.5 Metipranolol
  • 7.2.4 Carbonic Anhydrase Inhibitors
    • 7.2.4.1 Acetazolamide
    • 7.2.4.2 Methazolamide
    • 7.2.4.3 Dichlorfenamide
    • 7.2.4.4 Dorzolamide
    • 7.2.4.5 Brinzolamide
  • 7.2.5 Prostaglandin Analogs
    • 7.2.5.1 Latanoprost
    • 7.2.5.2 Unoprostone
    • 7.2.5.3 Travoprost
    • 7.2.5.4 Bimatoprost
    • 7.2.6 Osmotic Agents
    • 7.2.7 Combination Therapies

7.3 IOP-reducing Laser Treatment

  • 7.3.1 Laser Iridotomy
  • 7.3.2 Laser Trabeculoplasty
  • 7.3.3 Transscleral Cyclophotocoagulation

7.4 IOP-Lowering Operations

  • 7.4.1 General Aspects
  • 7.4.2 Anesthesia
  • 7.4.3 Surgical Procedure
  • 7.4.4 Post-operative Treatment
  • 7.4.5 Other Pressure-reducing Operations
  • 7.4.6 Combined Cataract/Glaucoma Operation

7.5 Enhancing Ocular Perfusion

  • 7.5.1 Treating Low Blood Pressure
  • 7.5.2 Treating Vasospasms

7.6 Alternative Forms of Therapy

  • 7.6.1 Autogenic Training
  • 7.6.2 Acupuncture
  • 7.6.3 Homeopathy
  • 7.6.4 Anthroposophic Medicine
  • 7.6.5 Eye Training
  • 7.6.6 Dietary Treatment
  • 7.6.7 Phytotherapy

8. Living with Glaucoma
8.1 Lifestyle and Nutrition
8.2 Leisure and Sports
8.3 Contact Lenses
8.4 Pregnancy and Nursing

Supplementary Chapters
S 1 Anatomy and Physiology of the Visual System
S 2 The Development of the Eye
S 3 Genetics
S 4 Optics of the Eye
S 5 Cataracts
S 6 Arteriosclerosis
S 7 Diabetes Mellitus
S 8 Vascular Regulation and Dysregulation

  • S 8.1 Rgulation of blood flow
  • S 8.2 Vascular Dysregulation
    • S 8.2.1 The Primary Vascular Dysregulation (PVD)
    • S 8.2.2 The Secondary Vascular Dysregulation (SVD)
    • S 8.2.3 Additional Aspects of Vascular Dysregulation

S 9 Age-related Macular Degeneration (AMD)
S 10 Visual Field Examination / Perimetry
S 11 Measuring Perfusion
S 12 Ocular Pharmacotherapy (Eye Medications)
S 13 How do Lasers Function?

Appendices
A 1 Glossary
A 2 Catalogue of Medications
A 3 Additional Reading Material
A 4 Information for the Visually Impaired
A 5 Ophthalmology in Developing Countries
A 6 Acknowledgments

Index

CHF 20.00

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