{"id":477,"date":"2023-08-22T16:45:06","date_gmt":"2023-08-22T20:45:06","guid":{"rendered":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/?post_type=chapter&#038;p=477"},"modified":"2026-01-03T16:16:56","modified_gmt":"2026-01-03T21:16:56","slug":"inflammation-fever-healing-cell-proliferation-tissue-regeneration-and-repair","status":"web-only","type":"chapter","link":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/chapter\/inflammation-fever-healing-cell-proliferation-tissue-regeneration-and-repair\/","title":{"raw":"The Inflammatory Response, Fever, Healing, Cell Proliferation, Tissue Regeneration and Repair - Learning Objectives","rendered":"The Inflammatory Response, Fever, Healing, Cell Proliferation, Tissue Regeneration and Repair &#8211; Learning Objectives"},"content":{"raw":"<div class=\"textbox textbox--learning-objectives\"><header class=\"textbox__header\">\r\n<p class=\"textbox__title\">Learning Outcomes and Specific Learning Objectives Study Guide<\/p>\r\n\r\n<\/header>\r\n<div class=\"textbox__content\">\r\n\r\n<strong>Learning Outcomes:<\/strong>\r\n\r\nBy the end of this section you will be able to:\r\n\r\n<strong>Describe common cellular adaptations and understand why each occurs, including:<\/strong>\r\n<ol>\r\n \t<li>Use of pathophysiology terminology<\/li>\r\n \t<li>Listing of\u00a0 common causes of cellular damage and types of cellular necrosis.<\/li>\r\n \t<li>Familiarization with the steps of inflammation and its role in cell injury and healing<\/li>\r\n \t<li><span style=\"font-size: 1em\">Exemplars include: Cuts, Pap smears, Fire Burn Injury, Electrical Burn, Frost bite, Mercury poisoning, Alzheimer\u2019s, Radiation poisoning, Liquefaction of Brain, Liquefaction of infection, Pancreas\/Breast trauma; Myocardial &amp; Kidney Infarction, Tuberculosis, Hypercalcemia, Diabetes circulation<\/span><\/li>\r\n<\/ol>\r\n\r\n<hr \/>\r\n\r\n<strong>Specific Learning Objectives Study Guide:<\/strong>\r\n\r\nBy the end of this section you will be able to:\r\n\r\n<strong>Describe Normal Defenses of the Body:<\/strong>\r\n<ul>\r\n \t<li><strong><span style=\"font-size: 1em\">Innate (non-specific) Defenses:<\/span><\/strong>\r\n<ul>\r\n \t<li><span style=\"font-size: 1em\"><strong>Mechanical\/Physical<\/strong>\u00a0- skin, hair, mucus, sebum, urination, cilia, cell shedding<\/span><\/li>\r\n \t<li><span style=\"font-size: 1em\"><span style=\"font-size: 1em\"><strong>Biochemical<\/strong> - <\/span><\/span>sweat, tears &amp; saliva (lysozymes), bile, stomach pH, cerumen, mucus, vaginal secretions, prostatic and testicular secretions,<\/li>\r\n \t<li><strong><span style=\"font-size: 1em\">Normal Flora<\/span><\/strong><\/li>\r\n \t<li>\r\n<div><strong>Phagocytes:<\/strong> (WBCs such as monocytes, fixed and free macrophages, microglia, neutrophils, eosinophils, dendritic cells) capable of diapedesis\/emigration\/transmigration.<\/div><\/li>\r\n \t<li><strong>Complement System<\/strong> (Classical Pathway with antibody, Lectin Pathway, and Alternative Pathway) - involving 30+ complement plasma protein cascade of activation - resulting in opsonization, MAC (Membrane Attack Complexes), stimulation of mast cells &amp; basophils<\/li>\r\n \t<li><strong>Cytokine family:<\/strong>\u00a0 Glycoproteins produced by WBCs, fibroblasts, endothelial cells, stromal (connect tissue) cells\r\n<ul>\r\n \t<li>\r\n<div><strong>Interferons:<\/strong> (chemical messages that stimulate defense)<\/div>\r\n<ul>\r\n \t<li><strong>Alpha Interferons<\/strong> - produced by virally infected host cells to attract &amp; stimulate NK cells and stimulate AVP production in neighbouring cells.<\/li>\r\n \t<li><strong>Beta Interferons<\/strong> - produced by fibroblasts to slow inflammation, and promote healing<\/li>\r\n \t<li><strong>Gamma Interferons<\/strong> - produced by T\u00a0 &amp; NK cells to stimulate macrophage activity<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li>\r\n<div><strong>Chemokines:<\/strong> induce chemotaxis<\/div><\/li>\r\n \t<li>\r\n<div><strong>Lymphokines:<\/strong> produced by T lymphocytes to: 1) attract macrophages &amp; 2) stimulate B lymphocytes to produce antibodies<\/div><\/li>\r\n \t<li>\r\n<div><strong>Interleukins:<\/strong> produced by helper T cells to:<\/div>\r\n<div>1. activate macrophages and stimulate fever (act as endogenous pyrogens)<\/div>\r\n<div>2. stimulate T &amp; B cell differentiation<\/div>\r\n<div>3. Stimulate hemopoietic cells to proliferate \u2192 producing more WBCs<\/div><\/li>\r\n \t<li>\r\n<div>Natural Killer cells (NK Lymphocytes) - type of WBC (White Blood Cell\/Leukocyte)<\/div><\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong>Inflammatory Response<\/strong><\/li>\r\n \t<li><strong>Fever<\/strong> - speeds up WBC activity and repairs, inhibits pathogen activity<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<ul>\r\n \t<li><strong>Describe plasma components &amp; define vocabulary words:<\/strong>\r\n<ul>\r\n \t<li><strong>Plasma<\/strong> - liquid matrix containing water, electrolytes, and plasma proteins<\/li>\r\n \t<li><strong>Plasma proteins<\/strong> - antibodies, complement proteins, clotting factors, albumen and transporter proteins<\/li>\r\n \t<li><strong>Platelets\/Thrombocytes<\/strong> - a nuclear cell fragments formed from large megakaryocytes;\u00a0 involved in clotting (hemostasis)<\/li>\r\n \t<li><strong>Leukocytes<\/strong> - WBCs<\/li>\r\n \t<li><strong>Lymphocytes:<\/strong> type of WBC involved in antibody production (B lymphocytes), targeted immune response (T lymphocytes), and surveillance (NK lymphocytes)<\/li>\r\n \t<li><strong>Neutrophils:<\/strong> The most abundant phagocyte in the blood; contain extensive lysosomes<\/li>\r\n \t<li><strong>Eosinophils:<\/strong> Destroy parasitic worms &amp; immune complexes<\/li>\r\n \t<li><strong>Basophils<\/strong> &amp; <strong>Mast cells<\/strong>: Release histamine, heparin, prostaglandins, and leukotrienes in process known as degranulation<\/li>\r\n \t<li><strong>Erythrocytes<\/strong> - RBCs; transport oxygen &amp; carbon dioxide<\/li>\r\n \t<li><strong>Hematocrit<\/strong> -\u00a0 % by volume of blood that is \u00a0 formed elements<\/li>\r\n \t<li><span style=\"font-size: 1em\"><strong>Anemia:<\/strong> reduced oxygen-carrying capacity of blood due to low levels of functional RBCs or hemoglobin.<\/span><\/li>\r\n \t<li><strong>Polycythemia;<\/strong> greater than normal # of RBCs<\/li>\r\n \t<li><strong>EPO, erythropoietin<\/strong>: hormone that stimulates production of RBCs<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<ul>\r\n \t<li><strong>Describe 3 stages of hemostasis:<\/strong>\u00a0 vascular spasm (role of endothelin and tunica media), platelet plug formation (extrinsic and intrinsic pathways, roles of Factor X, thrombin, clotting factors, and Ca++) and coagulation (role of fibrin)<\/li>\r\n<\/ul>\r\n<ul>\r\n \t<li><strong>Describe stages of healing:<\/strong> fibrinolysis (role of tPA, and plasmin) and regeneration (role of PDGF)<\/li>\r\n<\/ul>\r\n<ul>\r\n \t<li><strong>Describe components of the Lymphatic System:<\/strong>\r\n<ul>\r\n \t<li>Lymph Vessels<\/li>\r\n \t<li>Lymph Nodes<\/li>\r\n \t<li>Lymphocytes (Helper T, Cytotoxic T, Memory T, Suppressor\/Regulator T, B, Memory B, plasma cells), Cell-mediated and Humoral Immunity<\/li>\r\n \t<li>Macrophages, Dendritic Cells<\/li>\r\n \t<li>Primary and Secondary Response, Vaccination<\/li>\r\n \t<li>Antibody Roles - Neutralization, Agglutination, Precipitation, Opsonization<\/li>\r\n \t<li>Cytotoxic T cell activity - perforin, lymphotoxin, apoptosis<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<ul>\r\n \t<li style=\"list-style-type: none\">\r\n<ul>\r\n \t<li><strong>Explain cause of Inflammation<\/strong> - innate (non-specific) response to tissue injury; caused by: tissue damage from cuts, sprains, chemicals, ischemia, heat, cold, infections, or foreign objects\r\n<ul>\r\n \t<li>Stimulated by vasoactive chemicals released by mast cells: histamine, prostaglandin, leukotrienes - all induce: vasodilation, increased capillary permeability, bronchoconstriction, mucous production (stim. gland secretion), and chemotaxis of WBCs<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong>Explain 5 signs of Inflammation:<\/strong>\r\n<ul>\r\n \t<li>\r\n<div><strong>Redness<\/strong> &amp; <strong>warmth:<\/strong> due to \u2191 blood flow (hyperemia) to damaged area<\/div><\/li>\r\n \t<li>\r\n<div><strong>Swelling<\/strong> (edema): protein &amp; fluid into interstitial space<\/div><\/li>\r\n \t<li>\r\n<div><strong>Pain:<\/strong> increased pressure of fluid on nerves; release of chemical mediators \u2013 i.e., bradykinins, histamine (itch), prostaglandins<\/div><\/li>\r\n \t<li>\r\n<div><strong>Loss of function<\/strong>: may develop if cells lack nutrients; edema may interfere with movement<\/div><\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<strong>Explain 2 phases of inflammation:<\/strong>\r\n<ul>\r\n \t<li>1. Vascular:\u00a0 vasodilation &amp; increased cap perm \u2192 exudate (fluid); stagnation of flow &amp; clotting of blood occurs which aids in localizing the spread of infectious microorganisms.\r\n<ul>\r\n \t<li style=\"list-style-type: none\">\r\n<ul>\r\n \t<li><strong>Histamine, Leukotrienes, Bradykinin, Prostaglandins:<\/strong> induces vasodilation, increased capillary permeability<\/li>\r\n \t<li><strong>Histamine:<\/strong> additionally induces itch<\/li>\r\n \t<li><strong>Prostaglandins:<\/strong> additionally induce pain, fever<\/li>\r\n \t<li><strong>Bradykinogen<\/strong> (plasma protein): additionally induce pain when in active bradykinin form<\/li>\r\n \t<li><strong>Histamine receptors<\/strong> found on nerve endings and on blood vessel walls<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><span style=\"font-size: 1em\">2. <\/span><strong style=\"font-size: 1em\">Cellular:<\/strong><span style=\"font-size: 1em\"> \u2013 emigration (diapedesis) of WBCs;\u00a0 <\/span><span style=\"font-size: 1em\">Production of more WBCS (e.g. neutrophils, shift to the left)<\/span><\/li>\r\n<\/ul>\r\n<\/div>\r\n<ul>\r\n \t<li><span style=\"text-align: initial;font-size: 1em\">Four types of Exudate:<\/span><\/li>\r\n \t<li>\r\n<div>1. <strong>Serous:<\/strong> watery, consists primarily of fluid, some proteins, &amp; WBCs (e.g. allergic rxns &amp; burns);<\/div>\r\n<div>2. <strong>Fibrinous:<\/strong> thick, sticky, high cell &amp; fibrin content;\u00a0 Increased risk of scar tissue (e.g. severe injuries, rheumatic heart disease, bacterial pneumonia)<\/div>\r\n<div>3. <strong>Purulent<\/strong> (\u201cpus\u201d): thick, yellow-green, contains more WBCs, cell debris, &amp; microorganisms; Bacterial infection \u00a0 \u00a0*An abscess contains purulent exudate<\/div>\r\n<div>4. <strong>Hemorrhagic:<\/strong> blood from damaged blood vessels<\/div>\r\n<ul>\r\n \t<li><\/li>\r\n \t<li>\r\n<div>Mild fever <strong>(pyrexia)<\/strong> \u2013 oral temp above 38\u00baC;\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 (Side note:\u00a0 <strong>Heatstroke<\/strong> = 40\u00baC or higher)<\/div>\r\n<ul>\r\n \t<li>\r\n<div>Common if inflammation is extensive (can occur with heart attack, stroke, trauma, cancer)<\/div><\/li>\r\n \t<li>\r\n<div>Due to WBC release of endogenous pyrogens (interferons, interleukins) or (LPS= <strong>LipoPolySaccharide<\/strong> = slimy coat of bacteria = exogenous pyrogen)<\/div>\r\n<div>\u00a4What is the most accurate way to take someone\u2019s temperature?\u00a0\u00a0\u00a0 Rectal<\/div>\r\n<div>\u00a4What is preferred method?\u00a0 Tympanic for elderly and Axillary for babies<\/div>\r\n<div>\u00a4What is <strong>FUO?<\/strong> Fever of Unknown Origin\u00a0 (unknown drug rxn; undetectable infection\/trauma\/injury\/cancer\/heart attack\/blood clots\/inflammatory disease)<\/div>\r\n<div>\u00a4What is a <strong>blunted\/absent febrile response<\/strong> to infection?\u00a0 Indicates poorer immune response<\/div><\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li>\r\n<div>What is <strong>Systemic Inflammatory Response Syndrome<\/strong>?\u00a0\u00a0\u00a0 Can be in response to burn or infection and is as follows:\u00a0 Enormous release of inflammatory cytokines \u2192 systemic vasodil. &amp; cap perm \u2192 low BP \u2192 Circulatory\/Septic shock (can be fatal)<\/div>\r\n<ul>\r\n \t<li>\r\n<div>Malaise (Feeling unwell), Fatigue, Headache, Anorexia<\/div><\/li>\r\n \t<li>\r\n<div>Decreased mental function (in elderly) due to cerebral hypoxia<\/div>\r\n&nbsp;<\/li>\r\n<\/ul>\r\n<\/li>\r\n<\/ul>\r\n<ul>\r\n \t<li><strong>Describe the 4 stages of Fever<\/strong>\r\n<ul>\r\n \t<li><span style=\"font-size: 1em\">Prodromal<\/span><\/li>\r\n \t<li><span style=\"font-size: 1em\">Chills<\/span><\/li>\r\n \t<li><span style=\"font-size: 1em\">Flush<\/span><\/li>\r\n \t<li><span style=\"font-size: 1em\">Defervescence (Sweating)<\/span><\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong><span style=\"font-size: 1em\">Define and explain the significance of:<\/span><\/strong>\r\n<ul>\r\n \t<li><span style=\"font-size: 1em\">Leukocytosis<\/span><\/li>\r\n \t<li>Differential Count<\/li>\r\n \t<li>Plasma<\/li>\r\n \t<li><span style=\"font-size: 1em\">Erythrocyte Sedimentation Rate<\/span><\/li>\r\n \t<li><span style=\"font-size: 1em\">C-reactive protein<\/span><\/li>\r\n \t<li>Neutrophilia<\/li>\r\n \t<li>Neutropenia<\/li>\r\n \t<li>Lymphocytosis<\/li>\r\n \t<li>Lymphocytopenia<\/li>\r\n \t<li>Thrombocytopenia<\/li>\r\n \t<li>Eosinophilia<\/li>\r\n \t<li>Scar Tissue<\/li>\r\n \t<li>Cellular Regeneration<\/li>\r\n \t<li>Cellular Resolution<\/li>\r\n \t<li>Cellular Replacement<\/li>\r\n \t<li>Granuloma; Granulation tissue<\/li>\r\n \t<li>Healing by 1st Intention<\/li>\r\n \t<li>Healing by 2nd Intention<\/li>\r\n \t<li>Angiogenesis<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong><span style=\"font-size: 1em\">Explain the presence of liver\/heart proteins in blood<\/span><\/strong><\/li>\r\n \t<li><strong>Explain possible complications of inflammation<\/strong>\r\n<ul>\r\n \t<li>Infection<\/li>\r\n \t<li>Deep ulcers<\/li>\r\n \t<li>Skeletal Muscle Spasms<\/li>\r\n \t<li>Chronic inflammation<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li><strong>Explain the difference between<\/strong>\r\n<ul>\r\n \t<li>ASA<\/li>\r\n \t<li>Acetaminophen<\/li>\r\n \t<li>NSAIDs<\/li>\r\n \t<li>Glucocorticoids<\/li>\r\n<\/ul>\r\n<\/li>\r\n \t<li>Explain <strong>RICE<\/strong> (Rest, Ice, Compression, Elevation)<\/li>\r\n \t<li>Explain stenosis, strictures, contractures, adhesions, keloids<\/li>\r\n \t<li><strong>Distinguish between 1st, 2nd, and 3rd degree burns and basic treatment strategies<\/strong><\/li>\r\n \t<li>Define <strong>eschar<\/strong><\/li>\r\n \t<li>Define <strong>Hypovolemic shock<\/strong><\/li>\r\n<\/ul>\r\n&nbsp;<\/li>\r\n<\/ul>\r\n<\/div>\r\n&nbsp;","rendered":"<div class=\"textbox textbox--learning-objectives\">\n<header class=\"textbox__header\">\n<p class=\"textbox__title\">Learning Outcomes and Specific Learning Objectives Study Guide<\/p>\n<\/header>\n<div class=\"textbox__content\">\n<p><strong>Learning Outcomes:<\/strong><\/p>\n<p>By the end of this section you will be able to:<\/p>\n<p><strong>Describe common cellular adaptations and understand why each occurs, including:<\/strong><\/p>\n<ol>\n<li>Use of pathophysiology terminology<\/li>\n<li>Listing of\u00a0 common causes of cellular damage and types of cellular necrosis.<\/li>\n<li>Familiarization with the steps of inflammation and its role in cell injury and healing<\/li>\n<li><span style=\"font-size: 1em\">Exemplars include: Cuts, Pap smears, Fire Burn Injury, Electrical Burn, Frost bite, Mercury poisoning, Alzheimer\u2019s, Radiation poisoning, Liquefaction of Brain, Liquefaction of infection, Pancreas\/Breast trauma; Myocardial &amp; Kidney Infarction, Tuberculosis, Hypercalcemia, Diabetes circulation<\/span><\/li>\n<\/ol>\n<hr \/>\n<p><strong>Specific Learning Objectives Study Guide:<\/strong><\/p>\n<p>By the end of this section you will be able to:<\/p>\n<p><strong>Describe Normal Defenses of the Body:<\/strong><\/p>\n<ul>\n<li><strong><span style=\"font-size: 1em\">Innate (non-specific) Defenses:<\/span><\/strong>\n<ul>\n<li><span style=\"font-size: 1em\"><strong>Mechanical\/Physical<\/strong>\u00a0&#8211; skin, hair, mucus, sebum, urination, cilia, cell shedding<\/span><\/li>\n<li><span style=\"font-size: 1em\"><span style=\"font-size: 1em\"><strong>Biochemical<\/strong> &#8211; <\/span><\/span>sweat, tears &amp; saliva (lysozymes), bile, stomach pH, cerumen, mucus, vaginal secretions, prostatic and testicular secretions,<\/li>\n<li><strong><span style=\"font-size: 1em\">Normal Flora<\/span><\/strong><\/li>\n<li>\n<div><strong>Phagocytes:<\/strong> (WBCs such as monocytes, fixed and free macrophages, microglia, neutrophils, eosinophils, dendritic cells) capable of diapedesis\/emigration\/transmigration.<\/div>\n<\/li>\n<li><strong>Complement System<\/strong> (Classical Pathway with antibody, Lectin Pathway, and Alternative Pathway) &#8211; involving 30+ complement plasma protein cascade of activation &#8211; resulting in opsonization, MAC (Membrane Attack Complexes), stimulation of mast cells &amp; basophils<\/li>\n<li><strong>Cytokine family:<\/strong>\u00a0 Glycoproteins produced by WBCs, fibroblasts, endothelial cells, stromal (connect tissue) cells\n<ul>\n<li>\n<div><strong>Interferons:<\/strong> (chemical messages that stimulate defense)<\/div>\n<ul>\n<li><strong>Alpha Interferons<\/strong> &#8211; produced by virally infected host cells to attract &amp; stimulate NK cells and stimulate AVP production in neighbouring cells.<\/li>\n<li><strong>Beta Interferons<\/strong> &#8211; produced by fibroblasts to slow inflammation, and promote healing<\/li>\n<li><strong>Gamma Interferons<\/strong> &#8211; produced by T\u00a0 &amp; NK cells to stimulate macrophage activity<\/li>\n<\/ul>\n<\/li>\n<li>\n<div><strong>Chemokines:<\/strong> induce chemotaxis<\/div>\n<\/li>\n<li>\n<div><strong>Lymphokines:<\/strong> produced by T lymphocytes to: 1) attract macrophages &amp; 2) stimulate B lymphocytes to produce antibodies<\/div>\n<\/li>\n<li>\n<div><strong>Interleukins:<\/strong> produced by helper T cells to:<\/div>\n<div>1. activate macrophages and stimulate fever (act as endogenous pyrogens)<\/div>\n<div>2. stimulate T &amp; B cell differentiation<\/div>\n<div>3. Stimulate hemopoietic cells to proliferate \u2192 producing more WBCs<\/div>\n<\/li>\n<li>\n<div>Natural Killer cells (NK Lymphocytes) &#8211; type of WBC (White Blood Cell\/Leukocyte)<\/div>\n<\/li>\n<\/ul>\n<\/li>\n<li><strong>Inflammatory Response<\/strong><\/li>\n<li><strong>Fever<\/strong> &#8211; speeds up WBC activity and repairs, inhibits pathogen activity<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<ul>\n<li><strong>Describe plasma components &amp; define vocabulary words:<\/strong>\n<ul>\n<li><strong>Plasma<\/strong> &#8211; liquid matrix containing water, electrolytes, and plasma proteins<\/li>\n<li><strong>Plasma proteins<\/strong> &#8211; antibodies, complement proteins, clotting factors, albumen and transporter proteins<\/li>\n<li><strong>Platelets\/Thrombocytes<\/strong> &#8211; a nuclear cell fragments formed from large megakaryocytes;\u00a0 involved in clotting (hemostasis)<\/li>\n<li><strong>Leukocytes<\/strong> &#8211; WBCs<\/li>\n<li><strong>Lymphocytes:<\/strong> type of WBC involved in antibody production (B lymphocytes), targeted immune response (T lymphocytes), and surveillance (NK lymphocytes)<\/li>\n<li><strong>Neutrophils:<\/strong> The most abundant phagocyte in the blood; contain extensive lysosomes<\/li>\n<li><strong>Eosinophils:<\/strong> Destroy parasitic worms &amp; immune complexes<\/li>\n<li><strong>Basophils<\/strong> &amp; <strong>Mast cells<\/strong>: Release histamine, heparin, prostaglandins, and leukotrienes in process known as degranulation<\/li>\n<li><strong>Erythrocytes<\/strong> &#8211; RBCs; transport oxygen &amp; carbon dioxide<\/li>\n<li><strong>Hematocrit<\/strong> &#8211;\u00a0 % by volume of blood that is \u00a0 formed elements<\/li>\n<li><span style=\"font-size: 1em\"><strong>Anemia:<\/strong> reduced oxygen-carrying capacity of blood due to low levels of functional RBCs or hemoglobin.<\/span><\/li>\n<li><strong>Polycythemia;<\/strong> greater than normal # of RBCs<\/li>\n<li><strong>EPO, erythropoietin<\/strong>: hormone that stimulates production of RBCs<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<ul>\n<li><strong>Describe 3 stages of hemostasis:<\/strong>\u00a0 vascular spasm (role of endothelin and tunica media), platelet plug formation (extrinsic and intrinsic pathways, roles of Factor X, thrombin, clotting factors, and Ca++) and coagulation (role of fibrin)<\/li>\n<\/ul>\n<ul>\n<li><strong>Describe stages of healing:<\/strong> fibrinolysis (role of tPA, and plasmin) and regeneration (role of PDGF)<\/li>\n<\/ul>\n<ul>\n<li><strong>Describe components of the Lymphatic System:<\/strong>\n<ul>\n<li>Lymph Vessels<\/li>\n<li>Lymph Nodes<\/li>\n<li>Lymphocytes (Helper T, Cytotoxic T, Memory T, Suppressor\/Regulator T, B, Memory B, plasma cells), Cell-mediated and Humoral Immunity<\/li>\n<li>Macrophages, Dendritic Cells<\/li>\n<li>Primary and Secondary Response, Vaccination<\/li>\n<li>Antibody Roles &#8211; Neutralization, Agglutination, Precipitation, Opsonization<\/li>\n<li>Cytotoxic T cell activity &#8211; perforin, lymphotoxin, apoptosis<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<ul>\n<li style=\"list-style-type: none\">\n<ul>\n<li><strong>Explain cause of Inflammation<\/strong> &#8211; innate (non-specific) response to tissue injury; caused by: tissue damage from cuts, sprains, chemicals, ischemia, heat, cold, infections, or foreign objects\n<ul>\n<li>Stimulated by vasoactive chemicals released by mast cells: histamine, prostaglandin, leukotrienes &#8211; all induce: vasodilation, increased capillary permeability, bronchoconstriction, mucous production (stim. gland secretion), and chemotaxis of WBCs<\/li>\n<\/ul>\n<\/li>\n<li><strong>Explain 5 signs of Inflammation:<\/strong>\n<ul>\n<li>\n<div><strong>Redness<\/strong> &amp; <strong>warmth:<\/strong> due to \u2191 blood flow (hyperemia) to damaged area<\/div>\n<\/li>\n<li>\n<div><strong>Swelling<\/strong> (edema): protein &amp; fluid into interstitial space<\/div>\n<\/li>\n<li>\n<div><strong>Pain:<\/strong> increased pressure of fluid on nerves; release of chemical mediators \u2013 i.e., bradykinins, histamine (itch), prostaglandins<\/div>\n<\/li>\n<li>\n<div><strong>Loss of function<\/strong>: may develop if cells lack nutrients; edema may interfere with movement<\/div>\n<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<p><strong>Explain 2 phases of inflammation:<\/strong><\/p>\n<ul>\n<li>1. Vascular:\u00a0 vasodilation &amp; increased cap perm \u2192 exudate (fluid); stagnation of flow &amp; clotting of blood occurs which aids in localizing the spread of infectious microorganisms.\n<ul>\n<li style=\"list-style-type: none\">\n<ul>\n<li><strong>Histamine, Leukotrienes, Bradykinin, Prostaglandins:<\/strong> induces vasodilation, increased capillary permeability<\/li>\n<li><strong>Histamine:<\/strong> additionally induces itch<\/li>\n<li><strong>Prostaglandins:<\/strong> additionally induce pain, fever<\/li>\n<li><strong>Bradykinogen<\/strong> (plasma protein): additionally induce pain when in active bradykinin form<\/li>\n<li><strong>Histamine receptors<\/strong> found on nerve endings and on blood vessel walls<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<\/li>\n<li><span style=\"font-size: 1em\">2. <\/span><strong style=\"font-size: 1em\">Cellular:<\/strong><span style=\"font-size: 1em\"> \u2013 emigration (diapedesis) of WBCs;\u00a0 <\/span><span style=\"font-size: 1em\">Production of more WBCS (e.g. neutrophils, shift to the left)<\/span><\/li>\n<\/ul>\n<\/div>\n<ul>\n<li><span style=\"text-align: initial;font-size: 1em\">Four types of Exudate:<\/span><\/li>\n<li>\n<div>1. <strong>Serous:<\/strong> watery, consists primarily of fluid, some proteins, &amp; WBCs (e.g. allergic rxns &amp; burns);<\/div>\n<div>2. <strong>Fibrinous:<\/strong> thick, sticky, high cell &amp; fibrin content;\u00a0 Increased risk of scar tissue (e.g. severe injuries, rheumatic heart disease, bacterial pneumonia)<\/div>\n<div>3. <strong>Purulent<\/strong> (\u201cpus\u201d): thick, yellow-green, contains more WBCs, cell debris, &amp; microorganisms; Bacterial infection \u00a0 \u00a0*An abscess contains purulent exudate<\/div>\n<div>4. <strong>Hemorrhagic:<\/strong> blood from damaged blood vessels<\/div>\n<ul>\n<li><\/li>\n<li>\n<div>Mild fever <strong>(pyrexia)<\/strong> \u2013 oral temp above 38\u00baC;\u00a0\u00a0\u00a0\u00a0\u00a0\u00a0 (Side note:\u00a0 <strong>Heatstroke<\/strong> = 40\u00baC or higher)<\/div>\n<ul>\n<li>\n<div>Common if inflammation is extensive (can occur with heart attack, stroke, trauma, cancer)<\/div>\n<\/li>\n<li>\n<div>Due to WBC release of endogenous pyrogens (interferons, interleukins) or (LPS= <strong>LipoPolySaccharide<\/strong> = slimy coat of bacteria = exogenous pyrogen)<\/div>\n<div>\u00a4What is the most accurate way to take someone\u2019s temperature?\u00a0\u00a0\u00a0 Rectal<\/div>\n<div>\u00a4What is preferred method?\u00a0 Tympanic for elderly and Axillary for babies<\/div>\n<div>\u00a4What is <strong>FUO?<\/strong> Fever of Unknown Origin\u00a0 (unknown drug rxn; undetectable infection\/trauma\/injury\/cancer\/heart attack\/blood clots\/inflammatory disease)<\/div>\n<div>\u00a4What is a <strong>blunted\/absent febrile response<\/strong> to infection?\u00a0 Indicates poorer immune response<\/div>\n<\/li>\n<\/ul>\n<\/li>\n<li>\n<div>What is <strong>Systemic Inflammatory Response Syndrome<\/strong>?\u00a0\u00a0\u00a0 Can be in response to burn or infection and is as follows:\u00a0 Enormous release of inflammatory cytokines \u2192 systemic vasodil. &amp; cap perm \u2192 low BP \u2192 Circulatory\/Septic shock (can be fatal)<\/div>\n<ul>\n<li>\n<div>Malaise (Feeling unwell), Fatigue, Headache, Anorexia<\/div>\n<\/li>\n<li>\n<div>Decreased mental function (in elderly) due to cerebral hypoxia<\/div>\n<p>&nbsp;<\/li>\n<\/ul>\n<\/li>\n<\/ul>\n<ul>\n<li><strong>Describe the 4 stages of Fever<\/strong>\n<ul>\n<li><span style=\"font-size: 1em\">Prodromal<\/span><\/li>\n<li><span style=\"font-size: 1em\">Chills<\/span><\/li>\n<li><span style=\"font-size: 1em\">Flush<\/span><\/li>\n<li><span style=\"font-size: 1em\">Defervescence (Sweating)<\/span><\/li>\n<\/ul>\n<\/li>\n<li><strong><span style=\"font-size: 1em\">Define and explain the significance of:<\/span><\/strong>\n<ul>\n<li><span style=\"font-size: 1em\">Leukocytosis<\/span><\/li>\n<li>Differential Count<\/li>\n<li>Plasma<\/li>\n<li><span style=\"font-size: 1em\">Erythrocyte Sedimentation Rate<\/span><\/li>\n<li><span style=\"font-size: 1em\">C-reactive protein<\/span><\/li>\n<li>Neutrophilia<\/li>\n<li>Neutropenia<\/li>\n<li>Lymphocytosis<\/li>\n<li>Lymphocytopenia<\/li>\n<li>Thrombocytopenia<\/li>\n<li>Eosinophilia<\/li>\n<li>Scar Tissue<\/li>\n<li>Cellular Regeneration<\/li>\n<li>Cellular Resolution<\/li>\n<li>Cellular Replacement<\/li>\n<li>Granuloma; Granulation tissue<\/li>\n<li>Healing by 1st Intention<\/li>\n<li>Healing by 2nd Intention<\/li>\n<li>Angiogenesis<\/li>\n<\/ul>\n<\/li>\n<li><strong><span style=\"font-size: 1em\">Explain the presence of liver\/heart proteins in blood<\/span><\/strong><\/li>\n<li><strong>Explain possible complications of inflammation<\/strong>\n<ul>\n<li>Infection<\/li>\n<li>Deep ulcers<\/li>\n<li>Skeletal Muscle Spasms<\/li>\n<li>Chronic inflammation<\/li>\n<\/ul>\n<\/li>\n<li><strong>Explain the difference between<\/strong>\n<ul>\n<li>ASA<\/li>\n<li>Acetaminophen<\/li>\n<li>NSAIDs<\/li>\n<li>Glucocorticoids<\/li>\n<\/ul>\n<\/li>\n<li>Explain <strong>RICE<\/strong> (Rest, Ice, Compression, Elevation)<\/li>\n<li>Explain stenosis, strictures, contractures, adhesions, keloids<\/li>\n<li><strong>Distinguish between 1st, 2nd, and 3rd degree burns and basic treatment strategies<\/strong><\/li>\n<li>Define <strong>eschar<\/strong><\/li>\n<li>Define <strong>Hypovolemic shock<\/strong><\/li>\n<\/ul>\n<p>&nbsp;<\/li>\n<\/ul>\n<\/div>\n<p>&nbsp;<\/p>\n","protected":false},"author":1370,"menu_order":1,"template":"","meta":{"pb_show_title":"on","pb_short_title":"","pb_subtitle":"","pb_authors":["zoe-soon"],"pb_section_license":"cc-by-nc-sa"},"chapter-type":[],"contributor":[60],"license":[57],"class_list":["post-477","chapter","type-chapter","status-web-only","hentry","contributor-zoe-soon","license-cc-by-nc-sa"],"part":25,"_links":{"self":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/477","targetHints":{"allow":["GET"]}}],"collection":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters"}],"about":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/types\/chapter"}],"author":[{"embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/users\/1370"}],"version-history":[{"count":22,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/477\/revisions"}],"predecessor-version":[{"id":4381,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/477\/revisions\/4381"}],"part":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/parts\/25"}],"metadata":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapters\/477\/metadata\/"}],"wp:attachment":[{"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/media?parent=477"}],"wp:term":[{"taxonomy":"chapter-type","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/pressbooks\/v2\/chapter-type?post=477"},{"taxonomy":"contributor","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/contributor?post=477"},{"taxonomy":"license","embeddable":true,"href":"https:\/\/pressbooks.bccampus.ca\/pathophysiology\/wp-json\/wp\/v2\/license?post=477"}],"curies":[{"name":"wp","href":"https:\/\/api.w.org\/{rel}","templated":true}]}}