Week 2- Chapter 5 Innate Immunity Note Outline
Week 2- Chapter 5 Innate Immunity Note Outline Nursing 240
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This 5 page Class Notes was uploaded by Jordan Smith on Wednesday April 6, 2016. The Class Notes belongs to Nursing 240 at Southern Illinois University Edwardsville taught by Dr. Jo Anne Pritchett in Spring 2016. Since its upload, it has received 22 views. For similar materials see Pathophysiology N240 in Nursing and Health Sciences at Southern Illinois University Edwardsville.
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Date Created: 04/06/16
Chapter 5 Innate Immunity: Inflammation and Wound Healing Innate Immunity: First Line of Defense Physical barriers—epithelial cells of skin, GI, GU & respiratory tracts remove pathogens by sloughing off dead skin, cilia—mediated coughing, sneezing, vomiting, & urination Epithelial—derived chemicals that protect against infections—mucus, perspiration, saliva, tears, and earwax which create an acidic environment Normal flora—nonpathogenic microorganisms such as bacteria and some fungi unique to skin and mucus membranes Innate Immunity: Second Line of Defense Inflammation—programmed response to damage to the body through a response that initiates an interactive system of humoral (soluble in the blood) & cellular systems. First response to injury that occurs within seconds after damage occurs in tissues with a blood supply Depends on activity of cellular and chemical components Nonspecific in that it takes place in the same way regardless of stimulus and whether exposure to the same stimulus has occurred in the past Inflammatory Process Vasodilation slows velocity and increases blood flow to injured site Increase vascular permeability with leakage of fluid (exudate) out of a vessel causing swelling at site As plasma fluid moves outward, blood in the microcirculation becomes more viscous and slow flow Increased concentration of RBCs causes localized erythema and warmth WBCs migrate through junctions between endothelial cells lining the vessels Inflammation Goals: o Limit and control the inflammatory process o Prevent and limit infection and further damage o Initiate adaptive immune response o Initiate healing Mast Cells Most important cellular activator inflammatory response Filled with granules and are located in loose connective tissue close to blood vessels in skin, GI & respiratory tracts Release potent inducers of inflammation by the process of degranulation that dumps the content of the mast cell into bloodstream within seconds and exert effect immediately Mast Cell Degranulation Histamine o Vasoactive amine that causes temporary, rapid constriction of the large blood vessels and the dilation of the postcapillary venules o Retraction of endothelial cells lining the capillaries o Receptors H1 receptor (proinflammatory) H2 receptor (antiinflammatory) Classic Symptoms of Acute Inflammation Redness (erythema), heat, swelling, pain, and loss of function Microscopic changes in microcirculation (arterioles, capillaries, & venules) near the site of injury Complement System Consists of a large number of proteins called complement factors that make up about 10% of the total circulating protein Activation of system produces factors that can destroy pathogens directly or can activate/ increase the activity of other cells of the inflammatory and immune response Factors produced during activation of the complement system are among the most potent defense against bacterial infection Complement System/ Activation of C3 & C5 Opsonins (C3b) coat the surface of bacteria and increase their susceptibility to being phagocytized & killed by neutrophils & macrophages Chemotactic factors (C5a) diffuse from inflammatory site & attract phagocytic cells to that site Anaphylatoxin (C3a, C5a) induces rapid degranulation of mast cells that release histamine inducing vasodilation and increased capillary permeability which is a major component of inflammation Membrane attack complex (MAC) from C5b – C9 results in a complex that creates pores in outer membranes of bacterial cells that allow water to enter causing the cell to burst/die or at least prevent its reproduction Three Major Pathways for Complement Activation Classical—primarily activated by antibodies which are proteins of the acquired immune system Antibodies must first bind to their targets/antigens that are molecules that stimulate production of antibodies Antibodies activate C1 which then lead to activation of C3 and C5 Antibodies of the acquired immune response use the complement system to kill bacteria and activate inflammation Coagulation/ Clotting System Coagulation system o Forms a fibrinous meshwork at an injured or inflamed site Prevents the spread of infection Keeps microorganisms and foreign bodies at the site of greatest inflammatory cell activity Forms a clot that stops bleeding Provides a framework for repair and healing o Man substance is an insoluble protein called fibrin Coagulation System (extrinsic) Group of plasma proteins, that when activated sequentially, form a blood clot Tissue factor (extrinsic) pathway activates when there is tissue damage and TF is released from damaged endothelial cells in blood vessels and reacts with factor VII Contact activation (intrinsic) pathway activates when there is an abnormal vessel wall & Factor XII is activated by contact with subendothelial substances Clotting System (Con’t) Activation of Factor X begins a common pathway leading to activation of fibrin which is framework for clot formation Kinin System Acts at site of injury to induce vasodilation and smooth muscle contraction, vascular permeability Functions to activate, attract (chemotaxis), & assist inflammatory cells such as leukocytes Primary kinin is bradkinin which acts with prostaglandins to produce PAIN Cytokines Small proteins released by cells that have a specific effect on the interactions between cells, on communication between cells, or on the behavior of cells Cytokines include the interleukins, lymphokines and cell signal molecules, such as tumor necrosis factor and the interferons, which trigger inflammation and respond to infections Interleukins (IL) o Produced primarily by macrophages and lymphocytes in response to a pathogen or stimulation by other products of inflammation o Many types/selected examples: IL1 is a proinflammatory cytokine – produced primarily by macrophages, enhances innate & acquired immunity, & acts as a growth factor for many cells; causes fever which helps to kill off infections IL10 is an antiinflammatory cytokine – produced primarily by lymphocytes, suppresses lymphocyte growth & production of pro inflammatory cytokines leading to downregulation of both inflammatory & acquired immune responses Interferon (IFN) o Protects against viral infections o Produced and released by virally infected host cells in response to viral double stranded RNA o Types: IFNalpha and IFNbeta—induce production of antiviral proteins IFNgamma—increases microbiocidal activity of macrophages Tumor necrosis factoralpha (TNFa) o Secrete by macrophages in response to receptor recognition Induces fever by acting as an endogenous pyrogen Increases synthesis of inflammatory serum proteins Causes muscle wasting (cachexia) and intravascular thrombosis Very high levels of TNFa can be lethal and are probably responsible for fatalities from shock caused by gram negative bacterial infections Chemokines o Attract leukocytes to site of inflammation o Synthesized by many cells (macrophages, fibroblasts, endothelial cells) Endothelium Endothelial cells adhere to underlying connective tissue matrix o Interact with circulating cells, platelets, plasma proteins o Regulate circulating inflammatory components o Damage to endothelial cells initiates platelet adherence due to exposure of the underlying connective tissue which is prothrombogenic &initiates clot formation through the intrinsic clotting pathway Platelets Circulate in bloodstream until vascular injury occurs Activated by tissue destruction and inflammation Activation leads to interaction with coagulation cascade o Degranulation activity with serotonin release (acts like histamine) Phagocytes Neutrophils o Also referred to as polymopphonuclear neutrophils (PMNs) o Predominate in early inflammatory responses o Ingest bacteria, dead cells, and cellular debris o Cells are short lived and become a component of the purulent exudate Monocytes and macrophages o Monocytes are produced in the bone marrow, enter the circulation, and migrate to the inflammatory site, where they develop into macrophages o Macrophages typically arrive at the inflammatory site 24 hours or later after neutrophils Eosinophils o Mildly phagocytic o Defense against parasites and regulation of vascular mediators Dendritic cells o In peripheral organs and skin o Migrate through lymph vessels to lymph tissue and interact with T lymphocytes to generate an acquired immune response T lymphocytes o Active during wound healing Phagocytosis Process by which a cell ingests and disposes of foreign material Production of adhesion molecules Margination (pavementing)—leukocytes “fall out of blood flow in the middle of the vessel & stick/adhere to the endothelial cells Diapedesis—movement of leukocytes out of circulatory system through the endothelial junctions to the site of injury Acute Inflammation Acute o Self limiting o Local manifestations—result from vascular changes and corresponding leakge of circulating components into the tissue Heat, swelling, redness, pain Edudative fluids Exudative Fluids Serous exudate o Wastery exudate: indicated early inflammation Fibrinous exudate: thick, clotted exudate: indicates more advanced inflammation Purulent exudate (suppurative) o Pus: indicates a bacterial infection Hemorrhagic exudate o Exudate contains blood: indicates bleeding o Serosanguious—thin, clear, pinkish o Sanguinous—bloody Systemic Manifestations of Acute Inflammation Fever caused by exogenous and endogenous pyrogens and act directly on the hypothalamus Leukocytosis—increased number of circulating leukocytes Increased plasma protein synthesis/ acutephase reactants: o Creactive protein o Fibrinogen o Haptoglobin o Amyloid Chronic Inflammation Inflammation lasting two weeks or longer Often related to an unsuccessful acute inflammatory response Other causes of chronic inflammation: o High lipid and wax content of a microorganism o Ability to survive inside of the macrophage o Toxins o Chemicals, particulate matter, or physical irritants Wound Healing Primary intention—wounds that heal under conditions of minimal tissue loss Secondary intention—wounds that require a great deal more tissue replacement/ open wound Dysfunctional wound healing—dysfunction during inflammatory response Dysfunction during Reconstruction Phase Impaired collagen matrix assembly o Keloid scar – raised scar that extends beyond the original boundaries of the wound, invades surrounding tissue, & may recur after surgical removal o Hypertrophic scar – raised, but remains within original boundaries of the wound & tends to regress over time Impaired epithelialization o Antiinflammatory steroids, hypoxemia, and nutritional deficiencies Wound disruption o Dehiscence (increases risk of infection) – wound pulls apart at suture line o Evisceration extrusion of viscera outside the body, especially through a surgical incision. Impaired contraction – contracture a condition of shortening and hardening of muscles, tendons, or other tissue, often leading to deformity and rigidity of joints Older Adults Impaired function of innate immune cells (phagocytes) Impaired inflammation is likely a result of chronic illness – diabetes, CV disease, COPD Chronic medication intake decreases the inflammatory response Healing response is diminished because of skin’s loss of regenerative ability Infections and chronic inflammation are more common in older adults
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