By American Academy of Ophthalmology, Ramana S. Moorthy MD
Starts off with an summary of immune-mediated eye ailment, summarizing easy immunologic recommendations, ocular immune responses and exact subject matters in ocular immunology. Discusses the scientific method of uveitis and studies noninfectious (autoimmune) and infectious types of uveitis, with an improved part on viral uveitis and new fabric on infectious and noninfectious scleritis.
Enhanced detection of infectious brokers via immunologic and genetic equipment and biologic therapeutics are distinctive. additionally covers endophthalmitis, masquerade syndromes, problems of uveitis and ocular elements of AIDS.
Upon finishing touch of part nine, readers could be capable to:
Identify basic and particular pathophysiologic methods that have an effect on the constitution and serve as of the uvea, lens, intraocular cavities, retina, and different tissues in acute and persistent intraocular inflammation
Differentiate and determine infectious and noninfectious uveitic entities
Choose acceptable exam concepts and appropriate ancillary reviews according 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
These cells carry antigenic information via the afferent lymphatic channels to the lymph node. There, processing of the antigenic signal occurs, resulting in the release of immune messengers (antibodies, B lym phocytes, and T lymphocytes) into efferent lymphatic channels and venous circulation. These molecules and cells are conveyed back to the original site, where an effector response 33 34 • lntraocular Inflammation and Uveitis CLINICAL EXAMPLES 2-1 • Primary response to poison ivy toxin The first contact between the poison ivy resin urushiol and the epidermis triggers the immunologic mechanisms of poison ivy dermatitis.
The secondary effector phase commences when these reactivated memory T lymphocytes recirculate and home back into the dermis and encounter additional antigen and macrophages at the site, causing the T lymphocytes to become fully activated and release cytokines. Within 24-72 hours, these cytokines induce infiltration of additional lymphocytes and monocytes as well as fibrin clotting. This process produces the typical indurated dermal lesion of the tuberculosis skin test, called the tuberculin form of DH.
CHAPTER 2 • Immunization and Adaptive Immunity: The Immune Response Arc and Immune Effectors Unlike the innate immune response discussed in the previous chapter, the adaptive immune response is a "learned" response to specific antigens. To understand the clinically relevant features of the adaptive immune response, the reader can consider the sequence of events that follows immunization with antigen using the skin, which is the classic experimental method of introducing antigen to the adaptive immune response (see Clinical Examples 2-1).