Jan 20 - inflammation

Jan 20 - inflammation - Inflammation and Repair...

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Unformatted text preview: Inflammation and Repair Inflammation NURS 216 Spring 2010 Sabra Smith, MS, RN Objectives Review different types of blood cells s Understand the functions and s/sx of inflammation s Explain vascular and cellular stages of inflammation s Discuss chemical mediators of inflammation s Discuss normal and abnormal wound healing s Components of the Blood Components Plasma (water and solutes) – 50-55% s Cells and proteins - 45-50% s 5.5 L total volume s Plasma Plasma Proteins – albumins, globulins, clotting Proteins factors factors s Electrolytes dissolved in the plasma s Gases s Glucose, lipids, cholesterol s Waste products s Cells of the Blood Cells s Erythrocytes (RBCs) – most abundant Erythrocytes blood cell, contain hemoglobin, transport O2, 42-48% of blood volume Leukocytes (WBCs) – tissue repair and Leukocytes defense against infection, divided by structure and function s Platelets – fragments of cytoplasm, no Platelets nucleus, are activated by vessel injury to form a clot form s This is an actual picture of White Blood Cells, in with some red blood cells. The platelets are stained purple, a T-Lymphocyte white cell is stained green, and a Monocyte white cell is stained gold as seen through a scanning electron microscope. Leukocytes Leukocytes Granulocytes: neutrophils, basophils, Granulocytes: eosinophils – all phagocytes eosinophils s Agranulocytes: monocytes/macrophages Agranulocytes: (phagocytes) and lymphocytes (immunocytes) (immunocytes) s Granulocytes Granulocytes So called because of granules in cytoplasm, So which contain enzymes for phagocytosis which s Capable of ameboid movement to get Capable through vessel walls through s Agranulocytes Agranulocytes Do not contain enzyme-filled granules, are Do phagocytes and immune cells phagocytes s Monocytes/macrophages – monocytes Monocytes/macrophages circulate in the blood, mature into macrophages which settle in tissue, digest injured tissue, breakdown RBCs injured s Lymphocytes – control the immune Lymphocytes response response s The Lymphatic System The -A second circulatory system that absorbs excess fluid from tissues and returns it to the veins -Lymph vessels run alongside blood vessels and capillaries -Once fluid is absorbed from tissue into the lymphatic vessels, it is called lymph -Lymph nodes along the route back to the bloodstream contain phagocytes which digest foreign material Inflammation Inflammation is the process in which healthy tissue responds to an injury s A general/nonspecific response s Purposes of inflammation s – – – Prevent infection, limit tissue damage Prepare the immune response To prepare any damaged tissue for repair I’ve got ____itis! s -itis is added to the affected body part to indicate an inflammatory disease – appendicitis – tonsilitis – conjunctivitis Classic Signs of Inflammation Classic Rubor -- erythema due to capillary dilation s Calor -- warmth due to increased blood flow s Tumor -- edema from exudate accumulation s Dolor -- pain due to local pressure, stimulation of nerve endings and chemicals (i.e. prostagladins) prostagladins) s Functio laesa -- alteration in function s Two types of Inflammation: Acute & Chronic s Acute: short term inflammatory process that Acute: completely resolves (minutes to days) completely – mostly Neutrophils respond mostly s Chronic: long term inflammation that may Chronic: or may not completely resolve (weeks to years) years) – mostly macrophages responding after acute mostly period period 3 parts of Inflammation parts Vascular Phase which sets the stage for the s Cellular Phase Vascular phase changes bring blood to the Vascular area and allow the WBCs and plasma proteins to act on the offending agent proteins s Inflammatory Mediators s chemical substances released by tissue injury chemical that coordinate the inflammatory response Vascular Response Vascular s s s s s Momentary vasoconstriction which decreases blood Momentary flow flow Followed by vasodilation of the arterioles and venules Followed which increases blood flow (hyperemia) which Increased vascular permeability occurs d/t plasma Increased proteins and vasodilation (capillary cells are farther apart and allow fluids to leak out) apart Fluid and phagocytes move into extravascular space Results? Vascular Response Vascular Histamine: potent mediator of fluid leakage s Bradykinin is formed s – stimulates capillary and venule endothelial cells stimulates to retract (body’s own chemical for vasodilation) vasodilation) s End Result – creates spaces between the junctions of the cells – allows leukocytes to squeeze out of the allows capillaries into tissue capillaries Capillary Beds – Vascular Phase Capillary Increased Capillary Permeability Increased Overview of cellular response Overview High concentration of leukocytes end up in High the vessel near injury site d/t increased blood flow s Leukocytes migrate to the site of injury, Leukocytes leak out of capillaries into tissue leak s Once there, phagocytosis occurs s Initiation of Cellular Response Initiation Mast cells cause the initial reaction s When they are damaged, they release three When important chemicals: “degranulation” important - Histamine - Neutrophil chemotactic factor - Eosinophil chemotactic factor Basophils function same way in the blood s Cellular Response - Phagocytosis Cellular Process in which macrophages and Process neutrophils ingest particles neutrophils s Once engulfed, lysosomes release Once chemicals which digest the foreign particle chemicals s The phagocyte often dies s Cellular debris is removed by monocytes Cellular and macrophages and s Phagocytosis Phagocytosis Cellular Response Cellular s Neutrophils – – – – main cell of acute inflammation circulates in blood first to arrive at the injury Conduct phagocytosis and secrete powerful Conduct chemotactic chemicals chemotactic Monocytes Monocytes Attracted to the area by neutrophils s Blood: Monocytes s Exudate : Macrophages s usually respond later than neutrophils s With chronic inflammation they wall off the With area that can’t be repaired area s Macrophages Macrophages any large cell that can surround and digest foreign substances in the body, as protozoa or bacteria s found in the liver, spleen, and in the loose connective tissue s Cellular Response - Chemotaxis Cellular Chemotaxis is the directional and Chemotaxis purposeful movement of cells by ameboid movement toward an area of injury in response to a chemical mediator response s Chemotactic factors are released by are damaged mast cells, attract neutrophils and eosinophils eosinophils s Inflammatory Mediators Inflammatory s Plasma-derived: kinins (bradykinin), Plasma-derived: coagulation proteins, complement proteins coagulation s Cell-derived: histamine, serotonin, Cell-derived: arachidonic acid metabolites, PAFs, cytokines, NO cytokines, Histamine Histamine Histamine is one of the two major Histamine substances responsible for increased blood flow and increased vascular permeability flow s Released from mast cells, basophils and Released platelets platelets s Also involved in allergic reactions s Serotonin very similar, in platelets s Arachidonic Acid Metabolites Arachidonic Arachidonic Acid is released from injured Arachidonic cell membranes, then metabolized by two pathways: pathways: s Leukotrienes s – increased vascular permeability – neutrophil and eosinophil chemotaxis s Prostaglandins Prostaglandins – increased vascular permeability – neutrophil chemotaxis Clotting System Clotting s Forms a fibrinous meshwork at the Forms inflamed site to trap exudate, microorganisms, and foreign bodies. microorganisms, – Fibrinogen converted to fibrin – prevents spread of infection – keeps microorganisms at site of greatest keeps phagocytosis phagocytosis – forms clot that stops bleeding Steps of Inflammation Steps Tissue injury damages blood vessels and connective tissue Mast cells in connective tissue, basophils in blood degranulate/ release histamine Capillary dilation and increased vessel permeability WBCs & platelets leak into damaged tissue Macrophages arrive later, continue process Neutrophils arrive first, start phagocytosis and call other WBCs Resolution, regeneration, scar formation, or chronic inflammation Clotting cascade is activated, blood clot begins to form Systemic Manifestations Systemic s Leukocytosis – elevation of white blood cell count s Fever “pyrexia” – endogenous pyrogens are produced by the endogenous macrophages and possibly by the eosinophils macrophages – Results in tachycardia 1º F = 10bpm s Lymphadenopathy – enlarged lymph nodes due to filtering, trapping enlarged of WBCs and fluid of Resolution of Acute Inflammation Inflammation Complete restoration of normal tissue s Factors favoring complete resolution: s – – – – min. cell death/damage tissue capacity for regeneration destruction of causal agent removal of debris and fluid Cell Types and Ability to Regenerate Regenerate Labile cells undergo complete regeneration Labile (epithelium, bone marrow cells) (epithelium, s Stable cells regenerate if they are stimulated Stable to do so (hepatocytes, endothelial cells) to s Permanent cells do not regenerate, but are Permanent replaced by scar tissue (cardiac, neurons) replaced s Wound Healing Wound s First intention: simple, rapid healing process -epidermis regenerates, minimal scar (ex: clean -epidermis surgical wound) surgical s Second intention: slower process, development of scar Second tissue (larger wounds, burns) tissue Wound Healing s s Inflammatory phase: first day or two Proliferative phase: 2-3 days post-injury to 3 Proliferative weeks weeks -new tissue created, collagen synthesis, -new epithelialization epithelialization Remodeling phase: 3 weeks post-injury to 6 Remodeling months months -collagen formation, wound strength increases s Aberrant Healing Aberrant s Exuberant granulation (proud flesh) – excessive scar tissue – block epitheliazation of the wound – do not return when removed s Keloids – bulging, tumorous scars that result from bulging, abnormalities in collagen synthesis and breakdown breakdown – tend to return when removed Aberrant Healing Aberrant s Contracture – migration of wound margins toward the center migration s Dehiscence – bursting open of a previously closed wound – collagen framework not strong enough Aberrant Healing Aberrant s Evisceration – the protrusion of abdominal organs through a the dehiscence dehiscence s Stenosis – the narrowing or obstruction of an opening by the the formation of scar tissue around a tubular area area Aberrant Healing Aberrant s Adhesions – Inflamed membranes – Scar tissue binds or adheres to adjacent surfaces surfaces » loops of bowel » abdominal viscera » labial – Partial or complete obstruction may occur Chronic Inflammation Occurs when an injury or infection can’t be resolved s Macrophages heavily involved s Nonspecific s Granulomatous -examples? s ...
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This note was uploaded on 02/15/2011 for the course NURS 216 taught by Professor Smith during the Spring '10 term at South Carolina.

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