Download Drug-Induced Ocular Side Effects: Clinical Ocular Toxicology by Frederick T. Fraunfelder MD, Frederick W. Fraunfelder Jr. MD PDF

By Frederick T. Fraunfelder MD, Frederick W. Fraunfelder Jr. MD M.B.A, Visit Amazon's Wiley A. Chambers Page, search results, Learn about Author Central, Wiley A. Chambers,

Ideal for ophthalmologists, optometrists and busy clinicians, Drug-Induced Ocular unwanted side effects provides the clinically suitable information you must diagnose and deal with chemical and drug-related ocular difficulties. An simply obtainable layout, meticulous revisions and comprehensive coverage of all medicines’ conventional and alternate names, basic makes use of, ocular and systemic negative effects, and scientific value make this best-selling source the correct reference for quick, on-the-spot consultation.

  • Manage any problem in ocular toxicology with broad assurance of ideas of treatment; ocular drug supply; easy methods to assessment drug-induced visible unintended effects; and the function of electrophysiology and psychophysics.
  • Benefit from the masterful advice and worldwide standpoint of world gurus within the box who offer need-to-know info on all facets of ocular toxicology―all in a single concise reference. 
  • Confer with the WHO type system to figure out no matter if a selected part impact is sure, possible, or prone to occur.
  • Zero in at the key details you must know with hugely templated, concise chapters.

  • Apply the newest wisdom and treatments for newly famous hostile Drug Reactions (ADR). establish which ADR’s are clinically appropriate and what to do approximately them.
  • Experience scientific scenarios with bright clarity via a wealth of latest and up to date medical pictures that supply unrivaled, visible diagnostic guidance.
  • Recognize and steer clear of drug-induced ocular facet effects with facts from the nationwide Registry of Drug precipitated Ocular Side-Effects (Casey Eye Institute, Portland, OR) and the realm health and wellbeing association (Uppsala, Sweden).
  • Stay brand new and supply state of the art care with the most recent info on authorized medications.
  • Access the total contents on-line at professional Consult.

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Extra info for Drug-Induced Ocular Side Effects: Clinical Ocular Toxicology

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2b). For example, chloroquine phosphate binds strongly to the RPE with a half-life of five years, 80 times more strongly than to the liver. This drug not only is used for malarial prophylaxis, but also plays an important role in the treatment of rheumatoid diseases (up to 4 mg/kg, or for hydroxychloroquine 6 mg/kg, of body weight per day). At these maximal rates, a critical cumulative dose can be reached within 3–6 months (Mavrikakis et al 2003). Signs of chloroquine phosphate retinopathy (typically following a cumulative dose of 100–300 g) are: • a relative paracentral scotoma, usually an annular perifoveal ring-shaped depression in visual fields • loss of blue/yellow color discrimination • RPE depigmentation often observed in a pattern matching the ring-shaped visual field depression (most easily seen during fluorescein angiography as window defects) • reduced light-evoked amplitude rise in the electrooculogram (EOG) • Functional alterations in photoreceptors Numerous substances can alter visual function by acting on the visual transduction process (lower part of Fig.

Amacrine cells (including interplexiform cells) Melatonin Photoreceptors Serotonin Amacrine cells, bipolar cells (in Basal K Photoreceptor (rod) Amacrine cells (in the INL and displaced in the GCL) Substance P Amacrine cells, ganglion cells Angiotensin II Amacrine cells Nitric oxide Amacrine cells Vasoactive intestinal Amacrine cells Apical Cl – HCO3 – nonmammalian vertebrates) Acetylcholine K+ Amacrine cells, bipolar cells, ganglion cells Taurine K+ K+ Choroidal vasculature Tight junction 2K+ Na+ + Cl – Na+ K+ Na+(K)+ Na+ nHCO3– Na+(K)+ 2Cl– 3Na+ H+ K+ HCO3 – Photoreceptor (cone) polypeptide (VIP) Somatostatin Amacrine cells, ganglion cells ATP Amacrine cells, ganglion cells Adenosine Amacrine cells, ganglion cells Brain-derived neurotrophic Amacrine cells, ganglion cells factor (BDNF) Kynurenic acid Amacrine cells Bruch’s membrane a – 6mV b + Fig.

Widespread damage to the pigment epithelial/photoreceptor complex results in a diminished light/dark ratio up to a complete loss of the light-induced potential increase. 2 – Origin of the Various Components of the Electrophysiological Recordings in Relation to Morphological Sites of the Retina (Modified after Apfelstedt and Zrenner 2007) Anatomic Structure Electrophysiological Potential Clinical Test Retinal pigment epithelium and photoreceptor outer Ocular resting potential Electrooculogram (EOG) Rod outer segments Rod a-wave Scotopic flash ERG Cone outer segments Cone a-wave Photopic flash ERG Rod ON-bipolar cells Rod b-wave Scotopic flash ERG Cone ON-bipolar cells Cone b-wave Photopic flash ERG Rod OFF-bipolar cells Rod off-effect Scotopic long duration flash ERG Cone OFF-bipolar cells Cone off-effect Photopic long duration flash ERG Müller glial cells Rod and cone b-wave Scotopic and photopic flash ERG Inner plexiform layer and especially amacrine cells Oscillatory potentials Scotopic flash ERG, with special filtering Ganglion cell layer N 95 potential Pattern ERG Posterior pole, cones, bipolar cells and amacrine cells Local retinal responses Multifocal ERG Retinocortical conduction time Latency/implicit time Visually evoked potentials (VEP): pattern-VEP Primary visual cortex and the cone dominated portion P100 amplitude, P2 amplitude Pattern-VEP, flash VEP, multifocal VEP segments OKAY FO The role of noninvasive electrophysiology in drug testing of the afferent pathway (central visual field) OD 60 RE 40 20 10 30 20 OKAY 40 FO 50 µV/deg 0 OS 60 LE 40 20 Light stimulus Fast oscillation Resting potential Dark trough Light peak Fig.

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