By American Academy of Ophthalmology, Ramana S. Moorthy MD
Starts with an summary of immune-mediated eye illness, summarizing uncomplicated immunologic recommendations, ocular immune responses and distinctive themes in ocular immunology. Discusses the medical method of uveitis and experiences noninfectious (autoimmune) and infectious different types of uveitis, with an improved part on viral uveitis and new fabric on infectious and noninfectious scleritis.
Enhanced detection of infectious brokers through immunologic and genetic equipment and biologic therapeutics are distinctive. additionally covers endophthalmitis, masquerade syndromes, issues of uveitis and ocular facets of AIDS.
Upon final touch of part nine, readers will be capable to:
Identify common and particular pathophysiologic approaches that impact the constitution and serve as of the uvea, lens, intraocular cavities, retina, and different tissues in acute and protracted intraocular inflammation
Differentiate and establish infectious and noninfectious uveitic entities
Choose acceptable exam options and correct ancillary reports in response to even if an infectious or noninfectious reason is suspected
Read or Download 2014-2015 Basic and Clinical Science Course (BCSC): Section 9: Intraocular Inflammation and Uvetis PDF
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Extra resources for 2014-2015 Basic and Clinical Science Course (BCSC): Section 9: Intraocular Inflammation and Uvetis
Complement. Second of two parts. N Engl JMed. 2001 ;344(15):1140-1144. Fibrin and other plasma factors Fibrin is the fin al deposition product of another important plasma-derived enzyme system, and its deposition during inflammation promotes hemostasis, fibrosis, angiogenesis, and leukocyte adhesion. Fibrin is released from its circulating zymogen precursor,fibrinogen, upon cleavage by thrombin. In situ polymerization of smaller units gives rise to the characteristic fibrin plugs or clots. Fibrin dissolution is mediated by plasmin, which is activated from its zymogen precursor, plasminogen, by plasminogen activators such as tissue plasminogen activator.
These include hydrolytic enzymes, elastase, metalloproteinases, gelatinase, myeloperoxidase, vitamin B12-binding protein, cytochrome b558 , and others. Granule contents are considered to remain inert and membrane-bound when the granules are intact, but they become active and soluble when granules fuse to the phagocytic vesicles or plasma membrane. An example of the effect of neutrophil-derived granule products is collagenase; collagenases are thought to contribute to corneal injury and liquefaction during bacterial keratitis and scleritis, especially in Pseudomonas infections.
Components and fragments of the complement cascade, which account for approximately 5% of plasma protein and comprise more than 30 different proteins, represent important endogenous amplifiers of innate and adaptive immunity, as well as mediators of inflammatory responses. Both adaptive and innate immune responses can initiate complement activation pathways, which generate products that contribute to the inflammatory process (Fig 1-3). Adaptive immunity typically activates complement by the classic pathway with antigen-antibody (immune) complexes, especially those formed by IgM, IgGl, and IgG3.
2014-2015 Basic and Clinical Science Course (BCSC): Section 9: Intraocular Inflammation and Uvetis by American Academy of Ophthalmology, Ramana S. Moorthy MD