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lecture 4 - Pathophysiology JP Advis DVM Ph.D Bartlett Hall...

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Page 1 Pathophysiology 04 JP Advis DVM, Ph.D. Bartlett Hall, Animal Sciences, Cook, 932 - 9240, [email protected] Course website: rci.rutgers.edu/~advis Lectures, tests, grades, office hours, textbook, Material to be covered: About lecture slides: There are not intended to be the sole source for studying the course material !!!!!!!!!!!!!!!! Slides are good to review the course material after you have study your course textbook Slides are a good indicator of the relative importance of lecture topics (see slide # per topic Group slides by titles when using them to review course material. Match lectures and text. Lectures 1-2: Introduction to Pathophysiology (2) Lectures 3-4: Mechanisms of Self-Defense and Stress (2) Lectures 5-8: Endocrine and Nervous System Dysfunctions (4) Lecture 9: Alterations of Skeletal Muscle Function (1) REVIEW AND TEST #1 Lectures 12-18: Cardiovascular, Respiratory and Renal Dysfunctions (7) REVIEW AND TEST #2 Lectures 21-24: Alterations of Digestive Function and Intermediary Metabolism (4) Lectures 25-26: Alterations of the Reproductive System (2) REVIEW AND TEST #3 Hypersensitivities HYPERSENSITIVITIES (autoimmunity, alloimmunity, allergy): Hypersensitivity is an inappropriate immune response mis- directed against the host’s own tissues (autoimmunity), or directed against beneficial foreign tissues such as transfu- sions or transplants (alloimmunity), or it can be exagerated responses against enviromental agents (allergy). They are classified as: type I (IgG mediated); type II (tissue specific); type III (immune complex mediated) & type IV (cell mediated) reactions (immediate, min / hrs, or delayed, hrs / days). The most rapid immediate hypersensitivity reaction, anaphylaxis, occurs within minutes of reexposure (can lead to CV shock). Type I, Ag reacts with mast cell’s IgE & elicits degranulation. Type II, caused by complement mediated lysis, opsonization and phagocytosis, Ab-dependent cell-mediated cytotoxity, & modulation of cellular function. Type III, caused by formation of immune complexes deposited in target tissues where they activate complement cascade, generating chemotactic frag- ments that attract neutrophils. Type IV, caused by specifical- ly sensitized T-cells to kill target cells directly or to release chemokines that activate other cells, such as macrophages. Hypersensitivities mechanisms antigenic targets Infection infectious microorganim defense mechanisms infection and injury clinical manifestations countermeasures Immune Deficiency clinical presentation primary deficiency secondary deficiency evaluation and care replacement therapy Stress Response general adaptation synd. neuroendocrine control role of immune system Aging in general, and its effect on specific endocrine organss, as an example Hypersensitivity is an inappropriate immune response
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