DOCSLIB.ORG

Age-Related Macular Degeneration (2Nd Edition) TABLE of CONTENTS [-] Section 1

Total Page：16

File Type：pdf, Size：1020Kb

Download full-text PDF Read full-text
Age-Related Macular Degeneration (2Nd Edition) TABLE of CONTENTS [-] Section 1 Age-Related Macular Degeneration (2nd Edition) TABLE OF CONTENTS [-] Section 1 - Anatomy, Physiology, and Pathology of the Macula [+] 1 - Normal Anatomy of the Macula [+] 2 - Animal Models for Age-Related Macular Degeneration [+] 3 - Pathogenesis and Pathophysiology of Age-Related Macular Degeneration [+] 4 - Etiology of Late Age-Related Macular Disease [+] 5 - Histopathology of Age-Related Macular Degeneration [-] Section 2 - Classification of Age-Related Macular Degeneration [+] 6 - Classification of Exudative Age-Related Macular Degeneration [+] 7 - Polypoidal Choroidal Vasculopathy [+] 8 - Retinal Angiomatous Proliferation in Age-Related Macular Degeneration [+] 9 - Differential Diagnosis of Age-Related Macular Degeneration [-] Section 3 - Imaging [+] 10 - Fluorescein Angiography [+] 11 - Indocyanine Green Angiography in Age-Related Macular Degeneration [+] 12 - Fundus Autofluorescence Imaging in Age-Related Macular Degeneration [+] 13 - Optical Coherence Tomography [-] Section 4 - Nonexudative Age-Related Macular Degeneration [+] 14 - Antioxidants and Age-Related Macular Degeneration: Clinical Associations and Basic Mechanisms [-] Section 5 - Exudative Age-Related Macular Degeneration [+] 15 - Pre-Anti-VEGF Era [+] 16 - Macugen for Age-Related Macular Degeneration [+] 17 - Lucentis (Ranibizumab) [+] 18 - Bevacizumab for the Treatment of Exudative Age-Related Macular Degeneration [+] 19 - VEGF Trap-Eye for Neovascular Age-Related Macular Degeneration [+] 20 - Radiation for the Treatment of Wet Age-Related Macular Degeneration [+] 21 - Combination Therapy for Neovascular Age-Related Macular Degeneration [+] 22 - Fovista, A Pegylated Antipdgf Aptamer in Wet AMD [+] 23 - Complications of Intravitreal Injections [-] Section 6 - Frontiers of Therapy [+] 24 - Introduction to Gene Therapy and Related Techniques for Retinal Disorders and Age- Related Macular Degeneration [+] 25 - New Pharmacotherapies for Age-Related Macular Degeneration [+] 26 - Artificial Vision, Retinal Implants, and Implantable Telescope [+] 27 - Retinal Transplantation Atlas of Oculoplastic and Orbital Surgery (2nd Edition) TABLE OF CONTENTS [-] Part I - Eyelid Surgery - Introduction [+] Section A - Anesthesia [+] Section B - Surgical Anatomy of the Eyelid [+] Section C - Hordeolum and Chalazion [+] Section D - Trichiasis and Distichiasis [+] Section E - Cosmetic Blepharoplasty [+] Section F - Brow Ptosis [+] Section G - Blepharoptosis [+] Section H - Ectropion [+] Section I - Entropion [+] Section J - Correction of Eyelid Retraction [+] Section K - Repair of Superficial Nonmarginal Eyelid Defects [+] Section L - Upper Eyelid Reconstruction [+] Section M - Lower Eyelid Reconstruction [+] Section N - Medial and Lateral Canthal Reconstruction [+] Section O - Blepharospasm [+] Section P - Seventh Nerve Paralysis [-] Part II - Lacrimal Drainage System Surgery [+] Introduction [+] Section A - Surgical Anatomy of the Lacrimal Drainage System [+] Section B - Surgery on the Lacrimal Puncta and Canaliculi [+] Section C - Surgery on the Lacrimal Sac and Duct [-] Part III - Orbital Surgery [+] Introduction [+] Section A - Orbital Anatomy [+] Section B - Orbitotomy Procedures [+] Section C - Surgery on the Orbital Walls [+] Section D - Enucleation, Evisceration, and Exenteration Color Atlas & Synopsis of Clinical Ophthalmology: Cornea (3rd Edition) TABLE OF CONTENTS [-] Chapter 1 - Conjunctival Infections and Inflammations [+] BLEPHARITIS AND MEIBOMITIS [+] CHALAZION (INTERNAL HORDEOLUM, STYE) [+] BACTERIAL CONJUNCTIVITIS (NONGONOCOCCAL) [+] GONOCOCCAL BACTERIAL CONJUNCTIVITIS [+] VIRAL CONJUNCTIVITIS (TYPICALLY ADENOVIRUS) [+] CHLAMYDIAL CONJUNCTIVITIS (ADULT INCLUSION CONJUNCTIVITIS) [+] TRACHOMA [+] MOLLUSCUM CONTAGIOSUM [+] LIGNEOUS CONJUNCTIVITIS [+] PEDICULOSIS [+] PARINAUD OCULOGLANDULAR SYNDROME [+] OPHTHALMIA NEONATORUM [+] ALLERGIC CONJUNCTIVITIS [+] ATOPIC KERATOCONJUNCTIVITIS [+] VERNAL KERATOCONJUNCTIVITIS [+] SUPERIOR LIMBIC KERATOCONJUNCTIVITIS [+] FLOPPY EYELID SYNDROME [+] TOXIC AND FACTITIOUS KERATOCONJUNCTIVITIS (KERATITIS MEDICAMENTOSA) [+] OCULAR ROSACEA [+] Figures [-] Chapter 2 - Conjunctival Degenerations and Mass Lesions [+] PINGUECULA AND PTERYGIUM [+] OTHER CONJUNCTIVAL DEGENERATIONS [+] MELANOCYTIC CONJUNCTIVAL LESIONS [+] BENIGN AMELANOCYTIC CONJUNCTIVAL LESIONS [+] POTENTIALLY MALIGNANT AMELANOCYTIC CONJUNCTIVAL LESIONS [+] CYSTIC LESIONS [+] VASCULAR LESIONS [+] Figures [-] Chapter 3 - Anterior Segment Developmental Anomalies [+] ANOMALIES OF CORNEAL SIZE AND SHAPE [+] ANTERIOR SEGMENT DYSGENESES [+] Figures [+] Tables [-] Chapter 4 - Ectatic Conditions of the Cornea [+] KERATOCONUS [+] PELLUCID MARGINAL DEGENERATION [+] KERATOGLOBUS [+] Figures [-] Chapter 5 - Corneal Dystrophies [+] ANTERIOR CORNEAL DYSTROPHIES [+] STROMAL CORNEAL DYSTROPHIES [+] POSTERIOR CORNEAL DYSTROPHIES [+] Figures [-] Chapter 6 - Corneal Degenerations and Deposits [+] INVOLUTIONAL CHANGES [+] CORNEAL DEPOSITS—NONPIGMENTED [+] OTHER CORNEAL DEGENERATIONS [+] CORNEAL DEPOSITS—PIGMENTED [+] Figures [-] Chapter 7 - Corneal Infections, Inflammations, and Surface Disorders [+] BACTERIAL KERATITIS [+] FUNGAL KERATITIS [+] ACANTHAMOEBA KERATITIS [+] HERPES SIMPLEX KERATITIS [+] HERPES ZOSTER KERATITIS [+] INTERSTITIAL KERATITIS (SYPHILITIC, NONSYPHILITIC) [+] SUBEPITHELIAL INFILTRATES [+] SUPERFICIAL PUNCTATE KERATOPATHY (PUNCTATE EPITHELIAL EROSIONS) [+] THYGESON SUPERFICIAL PUNCTATE KERATOPATHY [+] DRY EYE SYNDROME (KERATOCONJUNCTIVITIS SICCA) [+] FILAMENTARY KERATOPATHY [+] EXPOSURE KERATOPATHY [+] NEUROTROPHIC KERATOPATHY [+] RECURRENT CORNEAL EROSION [+] BULLOUS KERATOPATHY [+] ACQUIRED IMMUNODEFICIENCY SYNDROME [+] CONTACT LENS COMPLICATIONS [+] Figures [-] Chapter 8 - Systemic and Immunologic Conditions Affecting the Cornea [+] WILSON DISEASE (HEPATOLENTICULAR DEGENERATION) [+] VITAMIN A DEFICIENCY [+] CYSTINOSIS [+] MUCOPOLYSACCHARIDOSES AND LIPIDOSES [+] COLLAGEN VASCULAR DISEASES [+] MUCOUS MEMBRANE PEMPHIGOID [+] STEVENS-JOHNSON SYNDROME (ERYTHEMA MULTIFORME MAJOR) [+] MOOREN ULCER [+] PHLYCTENULOSIS [+] STAPHYLOCOCCAL HYPERSENSITIVITY [+] CORNEAL GRAFT REJECTION [+] Figures [-] Chapter 9 - Anterior Sclera and Iris [+] EPISCLERITIS [+] ANTERIOR SCLERITIS [+] IRIS CYSTS [+] IRIS TUMORS [+] Figures [-] Chapter 10 - Surgery and Complications [+] CATARACT EXTRACTION AND INTRAOCULAR LENS IMPLANTATION [+] FULL-THICKNESS CORNEAL TRANSPLANTATION (PENETRATING KERATOPLASTY) [+] ENDOTHELIAL KERATOPLASTY [+] ANTERIOR LAMELLAR KERATOPLASTY [+] CORNEAL BIOPSY [+] SUPERFICIAL KERATECTOMY [+] EXCIMER LASER PHOTOTHERAPEUTIC KERATECTOMY [+] CONJUNCTIVAL FLAP [+] LIMBAL STEM CELL TRANSPLANTATION [+] AMNIOTIC MEMBRANE TRANSPLANTATION [+] CORNEAL PERFORATION [+] REFRACTIVE SURGERY [+] Figures [-] Chapter 11 - Trauma [+] CHEMICAL BURNS [+] THERMAL AND ELECTRICAL BURNS [+] ULTRAVIOLET KERATOPATHY (ARC WELDER FLASH) [+] CORNEAL ABRASION [+] CORNEAL AND CONJUNCTIVAL FOREIGN BODIES [+] SUBCONJUNCTIVAL HEMORRHAGE [+] CORNEOSCLERAL LACERATION AND WOUND DEHISCENCE [+] TRAUMATIC HYPHEMA [+] EPITHELIAL DOWNGROWTH [+] DESCEMET DETACHMENT [+] Figures Color Atlas & Synopsis of Clinical Ophthalmology: Glaucoma (3rd Edition) TABLE OF CONTENTS [-] Section I - Glaucoma Diagnosis [+] Chapter 1 - Introduction to Glaucoma Diagnosis [+] Chapter 2 - Basics of Aqueous Flow and the Optic Nerve [+] Chapter 3 - Tonometry [+] Chapter 4 - Gonioscopy [+] Chapter 5 - Anterior Segment Imaging [+] Chapter 6 - Optic Nerve Imaging [+] Chapter 7 - Glaucoma Imaging: Optic Nerve Head, Peripapillary, and Macular Regions [+] Chapter 8 - Psychophysical Testing [+] Chapter 9 - Blood Flow in Glaucoma [-] Section II - Clinical Syndromes - Chapter 10 - Introduction to Clinical Syndromes [+] Chapter 11 - Childhood Glaucomas (Congenital Glaucomas) [+] Chapter 12 - Primary Open-Angle Glaucoma [+] Chapter 13 - Secondary Open-Angle Glaucoma [+] Chapter 14 - Uveitic Glaucomas [+] Chapter 15 - Lens-Associated Open-Angle Glaucomas [+] Chapter 16 - Traumatic Glaucoma [+] Chapter 17 - Primary Acute Angle-Closure and Chronic Angle-Closure Glaucoma [+] Chapter 18 - Secondary Angle-Closure Glaucoma [+] Chapter 19 - Glaucoma Secondary to Elevated Venous Pressure [-] Section III - Glaucoma Management [+] Chapter 20 - Introduction to Glaucoma Management [+] Chapter 21 - Medical Management [+] Chapter 22 - Laser Trabeculoplasty [+] Chapter 23 - Deep Sclerectomy Surgery for Glaucoma [+] Chapter 24 - Trabeculectomy, the Ex-PRESS Mini Glaucoma Shunt, and the Xen Gel Stent [+] Chapter 25 - Glaucoma Drainage Devices [+] Chapter 26 - Schlemm Canal-Based Surgery [+] Chapter 27 - Cyclodestructive Procedures for Glaucoma [+] Chapter 28 - Late Complications of Glaucoma Surgery [+] Chapter 29 - Supraciliary Microstent Surgery Color Atlas & Synopsis of Clinical Ophthalmology Neuro-Ophthalmology (3rd Edition) TABLE OF CONTENTS [-] Chapter 1 - Examination of the Afferent Visual System - INTRODUCTION - VISUAL ACUITY - COLOR VISION [+] PUPILLARY TESTING - AMSLER GRID - CONTRAST SENSITIVITY - BRIGHTNESS COMPARISON - PHOTOSTRESS RECOVERY TEST - OPHTHALMOSCOPY [+] Figures [-] Chapter 2 - Visual Fields - INTRODUCTION [+] PRINCIPLES THAT CONTRIBUTE TO VISUAL FIELD INTERPRETATION - CONCLUSION [+] Figures [-] Chapter 3 - Magnetic Resonance Imaging for the Ophthalmologist - INTRODUCTION - FUNDAMENTALS OF MAGNETIC RESONANCE IMAGING [+] TERMINOLOGY AND MAGNETIC RESONANCE IMAGING PULSE SEQUENCES - RECOMMENDED IMAGING PROTOCOL [+] Figures [+] Tables [-] Chapter 4 - Transient Visual Loss/Retinal Artery Occlusion [+] TRANSIENT VISUAL LOSS [+] RETINAL ARTERY OCCLUSION
Load more

Recommended publications
  • Management of Microtropia
    Br J Ophthalmol: first published as 10.1136/bjo.58.3.281 on 1 March 1974. Downloaded from Brit. J. Ophthal. (I974) 58, 28 I Management of microtropia J. LANG Zirich, Switzerland Microtropia or microstrabismus may be briefly described as a manifest strabismus of less than 50 with harmonious anomalous correspondence. Three forms can be distinguished: primary constant, primary decompensating, and secondary. There are three situations in which the ophthalmologist may be confronted with micro- tropia: (i) Amblyopia without strabismus; (2) Hereditary and familial strabismus; (3) Residual strabismus after surgery. This may be called secondary microtropia, for everyone will admit that in most cases of convergent strabismus perfect parallelism and bifoveal fixation are not achieved even after expert treatment. Microtropia and similar conditions were not mentioned by such well-known early copyright. practitioners as Javal, Worth, Duane, and Bielschowsky. The views of Maddox (i898), that very small angles were extremely rare, and that the natural tendency to fusion was much too strong to allow small angles to exist, appear to be typical. The first to mention small residual angles was Pugh (I936), who wrote: "A patient with monocular squint who has been trained to have equal vision in each eye and full stereoscopic vision with good amplitude of fusion may in 3 months relapse into a slight deviation http://bjo.bmj.com/ in the weaker eye and the vision retrogresses". Similar observations of small residual angles have been made by Swan, Kirschberg, Jampolsky, Gittoes-Davis, Cashell, Lyle, Broadman, and Gortz. There has been much discussion in both the British Orthoptic Journal and the American Orthoptic journal on the cause of this condition and ways of avoiding it.
    [Show full text]
  • Cone Interaction with Progressive Macular Dysfunction
    Correspondence 823 Sir, occasionally in the context of ectodermal dysplasia Management of ankyloblepharon filiforme adnatum syndromes3 and popliteal pterygium syndrome.4 AFA has also been reported in association with Edward’s Ankyloblepharon filiforme adnatum (AFA) is a syndrome,5 and CHANDS6 (curly hair, ankyloblepharon, rare congenital malformation affecting the eyelids. nail dysplasia). Other associations include hydrocephalus, We report a case describing its management. meningomyelocoele, and imperforate anus,7 cardiac defects and syndactyly.4 Detailed systemic assessment by an experienced paediatrician is therefore imperative in Case report the management of AFA. Our report illustrates a simple surgical approach that A male neonate was referred for assessment of his left is modified from previously published cases.1,2,4 It is safe eyelids. He was born at term, to a primigravid mother, and well tolerated with the aid of topical anaesthesia. weighing 3150 g. Pregnancy and delivery were Surgical correction should be performed promptly to unremarkable. There was no family history of minimise any risk of occlusion amblyopia, and enable ophthalmic or systemic disease. A detailed systemic full examination of the eye. assessment by a paediatrician was clear. Ocular examination showed partial fusion of his left upper and lower eyelids by a central, narrow band Conflict of interest of tissue, arising from the grey lines (Figure 1). Full The authors declare no conflict of interest. eyelid opening was impaired and interpalpebral aperture was limited to 3.5 mm. Right eye examination was normal. The band of tissue was retracted anteriorly with References a squint hook, clamped for 10 s, and excised with Vannas 1 Scott MH, Richard JM, Farris BK.
    [Show full text]
  • Pupillary Disorders LAURA J
    13 Pupillary Disorders LAURA J. BALCER Pupillary disorders usually fall into one of three major cat- cortex generally do not affect pupillary size or reactivity. egories: (1) abnormally shaped pupils, (2) abnormal pupillary Efferent parasympathetic fibers, arising from the Edinger– reaction to light, or (3) unequally sized pupils (anisocoria). Westphal nucleus, exit the midbrain within the third nerve Occasionally pupillary abnormalities are isolated findings, (efferent arc). Within the subarachnoid portion of the third but in many cases they are manifestations of more serious nerve, pupillary fibers tend to run on the external surface, intracranial pathology. making them more vulnerable to compression or infiltration The pupillary examination is discussed in detail in and less susceptible to vascular insult. Within the anterior Chapter 2. Pupillary neuroanatomy and physiology are cavernous sinus, the third nerve divides into two portions. reviewed here, and then the various pupillary disorders, The pupillary fibers follow the inferior division into the orbit, grouped roughly into one of the three listed categories, are where they then synapse at the ciliary ganglion, which lies discussed. in the posterior part of the orbit between the optic nerve and lateral rectus muscle (Fig. 13.3). The ciliary ganglion issues postganglionic cholinergic short ciliary nerves, which Neuroanatomy and Physiology initially travel to the globe with the nerve to the inferior oblique muscle, then between the sclera and choroid, to The major functions of the pupil are to vary the quantity of innervate the ciliary body and iris sphincter muscle. Fibers light reaching the retina, to minimize the spherical aberra- to the ciliary body outnumber those to the iris sphincter tions of the peripheral cornea and lens, and to increase the muscle by 30 : 1.
    [Show full text]
  • Differentiate Red Eye Disorders
    Introduction DIFFERENTIATE RED EYE DISORDERS • Needs immediate treatment • Needs treatment within a few days • Does not require treatment Introduction SUBJECTIVE EYE COMPLAINTS • Decreased vision • Pain • Redness Characterize the complaint through history and exam. Introduction TYPES OF RED EYE DISORDERS • Mechanical trauma • Chemical trauma • Inflammation/infection Introduction ETIOLOGIES OF RED EYE 1. Chemical injury 2. Angle-closure glaucoma 3. Ocular foreign body 4. Corneal abrasion 5. Uveitis 6. Conjunctivitis 7. Ocular surface disease 8. Subconjunctival hemorrhage Evaluation RED EYE: POSSIBLE CAUSES • Trauma • Chemicals • Infection • Allergy • Systemic conditions Evaluation RED EYE: CAUSE AND EFFECT Symptom Cause Itching Allergy Burning Lid disorders, dry eye Foreign body sensation Foreign body, corneal abrasion Localized lid tenderness Hordeolum, chalazion Evaluation RED EYE: CAUSE AND EFFECT (Continued) Symptom Cause Deep, intense pain Corneal abrasions, scleritis, iritis, acute glaucoma, sinusitis, etc. Photophobia Corneal abrasions, iritis, acute glaucoma Halo vision Corneal edema (acute glaucoma, uveitis) Evaluation Equipment needed to evaluate red eye Evaluation Refer red eye with vision loss to ophthalmologist for evaluation Evaluation RED EYE DISORDERS: AN ANATOMIC APPROACH • Face • Adnexa – Orbital area – Lids – Ocular movements • Globe – Conjunctiva, sclera – Anterior chamber (using slit lamp if possible) – Intraocular pressure Disorders of the Ocular Adnexa Disorders of the Ocular Adnexa Hordeolum Disorders of the Ocular
    [Show full text]
  • Improved Preservation of Human Corneal Basement Membrane
    BritishJournal ofOphthalmology 1994; 78: 863-870 863 Improved preservation ofhuman corneal basement membrane following freezing of donor tissue for Br J Ophthalmol: first published as 10.1136/bjo.78.11.863 on 1 November 1994. Downloaded from epikeratophakia Robert D Young, W John Armitage, Paul Bowerman, Stuart D Cook, David L Easty Abstract States, good results continue to be achieved by Current methods for the production of the small number ofBritish surgeons performing lenticules for epikeratophakia involve rapid the technique.4 However, no comprehensive freezing, cryolathing, and slow warming of the account of its long term outcome has yet been donor cornea. We have found that this pro- published. cedure causes structural damage to the Several complications resulting in the failure epithelial basement membrane in the donor of epikeratophakia have been reported, includ- cornea which may subsequently contribute to ing infection, graft dehiscence, persistent inter- poor postoperative re-epithelialisation of the face haze or opacity, ulceration, and imperfect implant, leading to graft failure. Endeavouring re-epithelialisation. Among these, the failure of to overcome these problems, the effects of host epithelial cells to migrate over and re- cryoprotection of donor cornea were investi- surface the anterior face of the grafted tissue gated, using dimethyl sulphoxide, in conjunc- continues to be the major reason for the removal tion with different cooling and warming rates ofepikeratophakia lenticules.'-'0 as part of the protocol for cryolathing. The Epithelial healing is itselfa complex phenome- structural integrity of the epithelial basement non involving mitosis of host cells at the graft membrane zone (BMZ) was then assessed by periphery, centripetal migration, and attach- electron microscopy and by immunofluores- ment.
    [Show full text]
  • Taking the Mystery out of Abnormal Pupils
    Taking the mystery out of abnormal pupils No financial disclosures Course Title: Taking the mystery out [email protected] of abnormal pupils Lecturer: Brad Sutton, OD, FAAO Clinical Professor IU School of Optometry . •Review of Anatomy Iris anatomy Iris sphincter Iris dilator Parasympathetic pathway Sympathetic pathway Parasympathetic Pathway Parasympathetic Pathway Light stimulates the retina then impulse Four neuron arc travels with the ganglion cells through the Retina to the pretectal nucleus in the chiasm into the optic tracts. 80% go to the midbrain (1) LGN , 20% to the pretectal nuclei.They Pretectal nucleus to the EW nucleus (2) then hemidecussate and terminate at the EW nucleus EW nucleus to the ciliary ganglion (3) Ciliary ganglion to the iris sphincter with short ciliary nerves (4) 1 Points of Interest Sympathetic Pathway Within the second order neuron there are Three neuron arc 30 near response fibers for every light Posterior hypothalamus to ciliospinal response fiber. This allows for light - near center of Budge ( C8 - T2 ). (1) dissociation. Center of Budge to the superior cervical The third order neuron runs with cranial ganglion in the neck (2) nerve III from the brain stem to the ciliary Superior cervical ganglion to the dilator ganglion. Superficially located prior to the muscle (3) cavernous sinus. Points of Interest Second order neuron runs along the surface of the lung, can be affected by a Pancoast tumor Third order neuron runs with the carotid artery then with the ophthalmic division of cranial nerve V 2 APD Testing testing……………….AKA……… … APD / reverse APD Direct and consensual response Which is the abnormal pupil ? Very simple rule.
    [Show full text]
  • Whole Exome Sequencing Gene Package Vision Disorders, Version 6.1, 31-1-2020
    Whole Exome Sequencing Gene package Vision disorders, version 6.1, 31-1-2020 Technical information DNA was enriched using Agilent SureSelect DNA + SureSelect OneSeq 300kb CNV Backbone + Human All Exon V7 capture and paired-end sequenced on the Illumina platform (outsourced). The aim is to obtain 10 Giga base pairs per exome with a mapped fraction of 0.99. The average coverage of the exome is ~50x. Duplicate and non-unique reads are excluded. Data are demultiplexed with bcl2fastq Conversion Software from Illumina. Reads are mapped to the genome using the BWA-MEM algorithm (reference: http://bio-bwa.sourceforge.net/). Variant detection is performed by the Genome Analysis Toolkit HaplotypeCaller (reference: http://www.broadinstitute.org/gatk/). The detected variants are filtered and annotated with Cartagenia software and classified with Alamut Visual. It is not excluded that pathogenic mutations are being missed using this technology. At this moment, there is not enough information about the sensitivity of this technique with respect to the detection of deletions and duplications of more than 5 nucleotides and of somatic mosaic mutations (all types of sequence changes). HGNC approved Phenotype description including OMIM phenotype ID(s) OMIM median depth % covered % covered % covered gene symbol gene ID >10x >20x >30x ABCA4 Cone-rod dystrophy 3, 604116 601691 94 100 100 97 Fundus flavimaculatus, 248200 {Macular degeneration, age-related, 2}, 153800 Retinal dystrophy, early-onset severe, 248200 Retinitis pigmentosa 19, 601718 Stargardt disease
    [Show full text]
  • Pediatric Ophthalmology/Strabismus 2017-2019
    Academy MOC Essentials® Practicing Ophthalmologists Curriculum 2017–2019 Pediatric Ophthalmology/Strabismus *** Pediatric Ophthalmology/Strabismus 2 © AAO 2017-2019 Practicing Ophthalmologists Curriculum Disclaimer and Limitation of Liability As a service to its members and American Board of Ophthalmology (ABO) diplomates, the American Academy of Ophthalmology has developed the Practicing Ophthalmologists Curriculum (POC) as a tool for members to prepare for the Maintenance of Certification (MOC) -related examinations. The Academy provides this material for educational purposes only. The POC should not be deemed inclusive of all proper methods of care or exclusive of other methods of care reasonably directed at obtaining the best results. The physician must make the ultimate judgment about the propriety of the care of a particular patient in light of all the circumstances presented by that patient. The Academy specifically disclaims any and all liability for injury or other damages of any kind, from negligence or otherwise, for any and all claims that may arise out of the use of any information contained herein. References to certain drugs, instruments, and other products in the POC are made for illustrative purposes only and are not intended to constitute an endorsement of such. Such material may include information on applications that are not considered community standard, that reflect indications not included in approved FDA labeling, or that are approved for use only in restricted research settings. The FDA has stated that it is the responsibility of the physician to determine the FDA status of each drug or device he or she wishes to use, and to use them with appropriate patient consent in compliance with applicable law.
    [Show full text]
  • Photorefractive Keratectomy for Correction of Epikeratophakia
    CASE REPORTS AND SMALL CASE SERIES high myopia resulting from poste- results might be related to the pre- Photorefractive Keratectomy rior lenticonus. Postsurgical refrac- existing corneal stromal abnormali- for Correction of tion was stable for 8 years, then a ties in their patients, which were not Epikeratophakia Regression rapid myopic regression of the epi- observed in our group. Thus, PRK keratophakic lenses was observed can effectively be used to treat epi- Excimer laser photorefractive kera- the following year (Table). In- keratophakic regressed lenses in a se- tectomy (PRK) is widely used for the stead of removing the failed epikera- lected group of patients in whom correction of myopia, astigmatism, tophakic lenses, we performed PRK both the epikeratograft and the sur- and hyperopia.1,2 It has also been on the eyes. rounding cornea are clear. This used for correction of astigmatism method eliminates the need for re- after penetrating keratoplasty.3 Results. Two and a half years after moval of the epikeratograft and ex- Epikeratophakia has been used PRK, the refraction in all 4 eyes is posing the patient to the risks of suc- in the treatment of nontolerant con- stable and the epigrafts are clear. The cessive penetrating keratoplasty. tact lens keratoconous patients.4,5 Table presents the refraction and vi- The epigrafts were made from ma- sual acuity results for the eyes be- Hirsh Ami, MD chined corneal tissue that was found fore PRK and at 3 months, 1 year, Solberg Yoram, MD, PhD unsuitable for penetrating kerato- and 21⁄2 years after PRK. No haze has Cahana Michael, MD plasty.
    [Show full text]
  • Complete and Incomplete Forms of the Benign Disorder Characterised By
    Br J Ophthalmol: first published as 10.1136/bjo.16.8.449 on 1 August 1932. Downloaded from THE BRITISH JOURNAL OF OPHTHALMOLOGY AUGUST, 1932 COMMUNICATIONS COMPLETE AND INCOMPLETE FORMS OF THE BENIGN DISORDER CHARACTERISED BY TONIC PUPILS AND ABSENT copyright. TENDON REFLEXES BY W. J. ADIE, M.D., F.R.C.P. PHYSICIAN, CHARING CROSS HOSPITAL AND ROYAL LONDON OPHTHALMIC HOSPITAL. OUT-PATIENT PHYSICIAN, THE NATIONAL HOSPITAL FOR NERVOUS DISEASES, QUEEN SQUARE http://bjo.bmj.com/ IN earlier papers on this subject it has been suggested that certain apparently dissimilar abnormal pupillary reactions formerly described as occurring in unrelated conditions are manifestations of the same disorder. The abnormal reactions are, on the one hand, the tonic pupillary reaction (syn. pupillotonia, myotonic reaction, tonic convergence reaction of pupils apparently inactive to light, on September 30, 2021 by guest. Protected Marcus's peculiar pupil phenomenon, non-luetic Argyll Robertson pupil, pseudo-Argyll Robertson pupil) and, on the other hand what may be called atypical phases of the tonic pupil. In the atypical phases tonic reactions are absent or difficult to detect and the state of the pupil in cases that present them is usually desig- nated by the term fixed pupil, ophthalmoplegia interna, iridoplegia or partial iridoplegia, of unknown origin. The disorder referred to, if the views expressed here are correct, may manifest itself in the following clinical forms: A. The complete form characterized by the presence in one or both eyes of the tonic convergence reaction in a pupil apparently Br J Ophthalmol: first published as 10.1136/bjo.16.8.449 on 1 August 1932.
    [Show full text]
  • Genes in Eyecare Geneseyedoc 3 W.M
    Genes in Eyecare geneseyedoc 3 W.M. Lyle and T.D. Williams 15 Mar 04 This information has been gathered from several sources; however, the principal source is V. A. McKusick’s Mendelian Inheritance in Man on CD-ROM. Baltimore, Johns Hopkins University Press, 1998. Other sources include McKusick’s, Mendelian Inheritance in Man. Catalogs of Human Genes and Genetic Disorders. Baltimore. Johns Hopkins University Press 1998 (12th edition). http://www.ncbi.nlm.nih.gov/Omim See also S.P.Daiger, L.S. Sullivan, and B.J.F. Rossiter Ret Net http://www.sph.uth.tmc.edu/Retnet disease.htm/. Also E.I. Traboulsi’s, Genetic Diseases of the Eye, New York, Oxford University Press, 1998. And Genetics in Primary Eyecare and Clinical Medicine by M.R. Seashore and R.S.Wappner, Appleton and Lange 1996. M. Ridley’s book Genome published in 2000 by Perennial provides additional information. Ridley estimates that we have 60,000 to 80,000 genes. See also R.M. Henig’s book The Monk in the Garden: The Lost and Found Genius of Gregor Mendel, published by Houghton Mifflin in 2001 which tells about the Father of Genetics. The 3rd edition of F. H. Roy’s book Ocular Syndromes and Systemic Diseases published by Lippincott Williams & Wilkins in 2002 facilitates differential diagnosis. Additional information is provided in D. Pavan-Langston’s Manual of Ocular Diagnosis and Therapy (5th edition) published by Lippincott Williams & Wilkins in 2002. M.A. Foote wrote Basic Human Genetics for Medical Writers in the AMWA Journal 2002;17:7-17. A compilation such as this might suggest that one gene = one disease.
    [Show full text]
  • Upregulations of Clcn3 and P-Gp Provoked by Lens Osmotic Expansion in Rat Galactosemic Cataract
    Hindawi Journal of Diabetes Research Volume 2017, Article ID 3472735, 8 pages https://doi.org/10.1155/2017/3472735 Research Article Upregulations of Clcn3 and P-Gp Provoked by Lens Osmotic Expansion in Rat Galactosemic Cataract 1 2 1 Lixia Ji, Lixia Cheng, and Zhihong Yang 1Department of Pharmacology, School of Pharmacy, Qingdao University, Qingdao, China 2Department of Endocrinology, People’s Hospital of Weifang, Weifang, China Correspondence should be addressed to Lixia Ji; [email protected] Received 21 September 2017; Accepted 1 November 2017; Published 21 November 2017 Academic Editor: Hiroshi Okamoto Copyright © 2017 Lixia Ji et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Objective. Lens osmotic expansion, provoked by overactivated aldose reductase (AR), is the most essential event of sugar cataract. Chloride channel 3 (Clcn3) is a volume-sensitive channel, mainly participating in the regulation of cell fundamental volume, and P-glycoprotein (P-gp) acts as its modulator. We aim to study whether P-gp and Clcn3 are involved in lens osmotic expansion of galactosemic cataract. Methods and Results. In vitro, lens epithelial cells (LECs) were primarily cultured in gradient galactose medium (10–60 mM), more and more vacuoles appeared in LEC cytoplasm, and mRNA and protein levels of AR, P-gp, and Clcn3 were synchronously upregulated along with the increase of galactose concentration. In vivo, we focused on the early stage of rat galactosemic cataract, amount of vacuoles arose from equatorial area and scattered to the whole anterior capsule of lenses from the 3rd day to the 9th day, and mRNA and protein levels of P-gp and Clcn3 reached the peak around the 9th or 12th day.
    [Show full text]