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Ocular Pathology
Myron Yanoff, Joseph W. Sassani
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eBook - ePub
Ocular Pathology
Myron Yanoff, Joseph W. Sassani
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Über dieses Buch
Bridge the gap between ophthalmology and pathology with the 8th Edition of this comprehensive, easy-to-understand reference from Drs. Myron Yanoff and Joseph W. Sassani. Designed to keep you up to date with every aspect of the field, from current imaging techniques to genetics and molecular biology to clinical pearls, Ocular Pathology provides the concise yet complete information you need for board exams and clinical practice.
- Includes new coverage of genetics and molecular biology, complications in diabetes mellitus, and the role of new drugs and other treatments for macular degeneration.
- Covers the latest imaging techniques, including optical coherence tomography (OCT), anterior segment OCT (AS-OCT) and OCT-angiography.
- Contains new images throughout that provide updated correlations between pathological and clinical aspects of each disorder. Clinicopathological correlations are presented with side-by-side image comparisons to make clinical pearl boxes even more useful.
- Features more than 1, 900 illustrations from the collections of internationally renowned leaders in ocular pathology.
- Presents information in a quick-reference outline format – ideal for today's busy physician.
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Information
1
Basic Principles of Pathology
The most important tool that the pathologist has at his/her disposal is meaningful communication with the patient's clinician regarding the suspected diagnosis so that the pathologist can choose the appropriate strategy for processing whatever tissue or other samples are received. As will be seen in the discussion under Modern Molecular Pathology Diagnostic Techniques, there is a dizzying array of techniques at the pathologist's disposal; however, it is only through communication with the clinician that the pathologist can determine which of these techniques to utilize to best serve the patient.
Inflammation
Definition
- I. Inflammation is the response of a tissue or tissues to a noxious stimulus.
- A. The tissue may be predominantly cellular (e.g., retina), composed mainly of extracellular materials (e.g., cornea), or a mixture of both (e.g., uvea).
- B. The response may be localized or generalized, and the noxious stimulus may be infectious or noninfectious.
- II. In a general way, inflammation is a response to a foreign stimulus that may involve specific (immunologic) or nonspecific reactions. Immune reactions arise in response to specific antigens, but they may involve other components (e.g., antibodies, T cells) or nonspecific components (e.g., natural killer [NK] cells, lymphokines).
- III. There is an interplay between components of the inflammatory process and blood clotting factors that shapes the inflammatory process.
Causes
- I. Noninfectious causes
- A. Exogenous causes: originate outside the eye and body, and include local ocular physical injury (e.g., perforating trauma), chemical injuries (e.g., alkali), or allergic reactions to external antigens (e.g., conjunctivitis secondary to pollen).
- B. Endogenous causes: sources originating in the eye and body, such as inflammation secondary to cellular immunity (phacoanaphylactic endophthalmitis [phacoantigenic uveitis]); spread from continuous structures (e.g., the sinuses); hematogenous spread (e.g., foreign particles); and conditions of unknown cause (e.g., sarcoidosis).
- II. Infectious causes include viral, rickettsial, bacterial, fungal, and parasitic agents.
Phases of Inflammation
(Table 1.1 lists the actions of the principal mediators of inflammation.)
TABLE 1.1
Mediator | Principal Sources | Actions |
---|---|---|
Cell-Derived | ||
Histamine | Mast cells, basophils, platelets | Vasodilation, increased vascular permeability, endothelial activation |
Serotonin | Platelets | Vasodilation, increased vascular permeability |
Prostaglandins | Mast cells, leukocytes | Vasodilation, pain, fever |
Leukotrienes | Mast cells, leukocytes | Increased vascular permeability, chemotaxis, leukocyte adhesion and activation |
Platelet-activating factor | Leukocytes, mast cells | Vasodilation, increased vascular permeability, leukocyte adhesion, chemotaxis, degranulation, oxidative burst |
Reactive oxygen species | Leukocytes | Killing of microbes, tissue damage |
Nitric oxide | Endothelium, macrophages | Vascular smooth muscle relaxation, killing of microbes |
Cytokines (TNF, IL-1) | Macrophages, endothelial cells, mast cells | Local endothelial activation (expression of adhesion molecules), fever/pain/anorexia/hypotension, decreased vascular resistance (shock) |
Chemokines | Leukocytes, activated macrophages | Chemotaxis, leukocyte activation |
Plasma Protein-Derived | ||
Complement products (C5a, C3a, C4a) | Plasma (produced in liver) | Leukocyte chemotaxis and activation, vasodilation (mast cell stimulation) |
Kinins | Plasma (produced in liver) | Increased vascular permeability, smooth muscle contraction, vasodilation, pain |
Proteases activated during coagulation | Plasma (produced in liver) | Endothelial activation, leukocyte recruitment |
IL-1, interleukin-1; MAC, membrane attack complex; TNF, tumor necrosis factor.
(Reproduced from Table 2.4, Kumar R, Abbas A, DeLancey A et al.: Robbins and Cotran Pathologic Basis of Disease, 8th edn. Philadelphia, Saunders. © 2010 by Saunders, an imprint of Elsevier Inc.)
- I. Acute (immediate or shock) phase (Fig. 1.1)
- A. Five cardinal signs: (1) redness (rubor) and (2) heat (calor)—both caused by increased rate and volume of blood flow; (3) mass (tumor)—caused by exudation of fluid (edema) and cells; (4) pain (dolor) and (5) loss of function (functio laesa)—both caused by outpouring of fluid and irritating chemicals. Table 1.2 lists the roles of various mediators in the different inflammatory reactions.TABLE 1.2
Role of Mediators in Different Reactions of Inflammation Role in Inflammation Mediators Vasodilation Prostaglandins Nitric oxide Histamine Increased vascular permeability Histamine and serotonin C3a and C5a (by liberating vasoactive amines from mast cells, other cells) Bradykinin Leukotrienes C4, D4, E4 PAF Substance P Chemotaxis, leukocyte recruitment and activation TNF, IL-1 Chemokines C3a, C5a Leukotriene B4 (Bacterial products; e....
- A. Five cardinal signs: (1) redness (rubor) and (2) heat (calor)—both caused by increased rate and volume of blood flow; (3) mass (tumor)—caused by exudation of fluid (edema) and cells; (4) pain (dolor) and (5) loss of function (functio laesa)—both caused by outpouring of fluid and irritating chemicals. Table 1.2 lists the roles of various mediators in the different inflammatory reactions.