Mechanisms of Self-Defense PDF

‭Innate Immunity: Inflammation and Wound Healing‬ ‭Adaptive Immunity‬ ‭‬ ‭Immunity‬ ‭○‬ ‭First line of defense‬ ‭‬ ‭Innate‬‭(natural) (native) immunity‬ ‭‬ ‭Physical barriers‬...

‭Innate Immunity: Inflammation and Wound Healing‬ ‭Adaptive Immunity‬ ‭‬ ‭Immunity‬ ‭○‬ ‭First line of defense‬ ‭‬ ‭Innate‬‭(natural) (native) immunity‬ ‭‬ ‭Physical barriers‬ ‭○‬ ‭Skin‬ ‭○‬ ‭Linings of GI tract‬ ‭○‬ ‭Mucus membranes‬ ‭‬ ‭Epithelia cell-derived chemical barriers‬ ‭○‬ ‭Secrete saliva, tears‬ ‭○‬ ‭Antimicrobial peptides‬ ‭‬ ‭Normal microbiome‬ ‭○‬ ‭○‬ ‭Second line of defense‬ ‭‬ ‭Inflammatory response (first immune repsone to injury)‬ ‭‬ ‭Nonspecific‬ ‭‬ ‭Local manifestation‬ ‭‬ ‭Redness, heat, swellng, pain, loss of function‬ ‭‬ ‭Vascular responses‬ ‭‬ ‭Blood vessel dilation‬ ‭‬ ‭Increased vascular permeability and leakabge‬ ‭‬ ‭White blood cell adherence to the inner walls of the vessels and‬ ‭miration thorugh the vessels‬ ‭‬ ‭Immune system‬ ‭○‬ ‭Innate‬ ‭‬ ‭Surface barriers‬ ‭‬ ‭Internal defenses‬ ‭‬ ‭*inflamation*‬ ‭○‬ ‭Adative‬ ‭‬ ‭Humeral immunity‬‭B-cells‬‭(white bloodcells)‬ ‭‬ ‭Cell-media immunity‬‭T-cells‬‭(white bloodcells)‬ ‭‬ ‭Have cytotoxins within to create another level of protection, attack‬ ‭bacteria‬ ‭‬ ‭Someone with cancer, does not have enough T cells.‬ ‭‬ ‭When someone is sick, more WB are produces - lymphocytes‬ ‭‬ ‭Lymph noodles‬ ‭○‬ ‭Where lots of whiteblood cells are stored‬ ‭○‬ ‭Filter pathogens in the body‬ ‭○‬ ‭When we get sick lymph noodles release more white blood cells - they will get‬ ‭swollen‬ ‭‬ ‭Hypersensitivity reactions‬ ‭○‬ ‭Type I‬  ‭ ‬ ‭Allergic reactions‬ ‭‬ ‭Antigens are getting released‬ ‭‬ ‭IgE antibody antigens are relasred too much‬ ‭‬ ‭Body produces too much histamine creates hives‬ ‭‬ ‭Anaphylaxis‬ ‭○‬ ‭Most rapid and severe immediate hypersensitivity‬ ‭○‬ ‭Occurs within minutes of exposure to antigen‬ ‭○‬ ‭Systemic, affecting whole body‬ ‭‬ ‭Inflammation‬ ‭○‬ ‭Goals‬ ‭‬ ‭Limit and control the inflammatory process‬ ‭‬ ‭Prevent and limit infection and further damage‬ ‭‬ ‭The white blood cells accumilate, anything with white blood cells will hurt‬ ‭when they go to an area that they are not normally acumulating in.‬ ‭‬ ‭Plama protein systems‬ ‭○‬ ‭Complement system‬ ‭‬ ‭Stopping the spead of the inflammation‬ ‭‬ ‭Migration of white bloodcells‬ ‭○‬ ‭Clotting system (coagulation)‬ ‭‬ ‭Can continue for few days‬ ‭‬ ‭Occurs after cleanup (phagocytosis)‬ ‭‬ ‭Healing of the injured vessles‬ ‭‬ ‭Thrombin is sticky kind of like to ‘glue’ injury‬ ‭○‬ ‭Kinnin system‬ ‭‬ ‭Cytokines‬ ‭○‬ ‭Small signaling protiens secreted by a variety of cell types‬ ‭○‬ ‭Responsible for activating other cells and regulating other cells‬ ‭‬ ‭Mast cells and Basophils‬ ‭○‬ ‭Mast cells are cellular bags of granules located in the loose connective tissues‬ ‭close to blood vessels‬ ‭○‬ ‭Basophils are found in the blood and probably function in same way as mast‬ ‭cells‬ ‭○‬ ‭Chemical release in two ways‬ ‭‬ ‭Degranulation‬ ‭‬ ‭Histamine‬ ‭‬ ‭Vasiactive amine that causes temporary, rapid constriction of the‬ ‭large blood vessels and the dilation of the postcapillary venules‬ ‭‬ ‭Synthesis‬ ‭‬ ‭Endothelium‬ ‭○‬ ‭Endothelial cells adhere to underlying connective tissue mateix‬ ‭○‬ ‭Regulating circulating inflammatory components‬ ‭‬ ‭Platelets‬ ‭○‬ ‭Part of clotting system‬ ‭○‬ ‭Activated by tissue destruction and inflammation‬ ‭‬ ‭Phagocytosis‬ ‭○‬ ‭Innaiated by white blood cells‬ ‭○‬ ‭A cell ingests and siposes of foreign material‬ ‭‬ ‭Inflamatory process (*slide 43)‬ ‭‬ ‭Acute inflammation‬ ‭○‬ ‭Self-limiting‬ ‭○‬ ‭Local manifestations - result from vascular changes and corresponding leakage‬ ‭of circulating compinets,‬‭whats going on to the damage‬‭of the blood vessels‬‭.‬ ‭○‬ ‭White blood cells cause pain‬ ‭○‬ ‭Red blood cells cause heat, too much oxygen in an area‬ ‭○‬ ‭If we dont reverse the inflamation, it can turn to inflammation‬ ‭○‬ ‭Systemic manifestations of acute inflammation‬ ‭‬ ‭Fever‬ ‭‬ ‭Casued by exogenous and endogenous pyrogens, acts directly on‬ ‭the hypothalamus‬ ‭‬ ‭Lecukocytosis‬ ‭‬ ‭Increased number of curculatting leukocytes (white blood cells)‬ ‭‬ ‭Shown on labwork, white count‬ ‭‬ ‭Increaed plasma protien syntheisis‬ ‭‬ ‭Exudative fluids‬ ‭‬ ‭Exudate means drangage‬ ‭○‬ ‭Serous exudate‬ ‭‬ ‭Watery, indicates early inflammation‬ ‭○‬ ‭Fibrinous exudate‬ ‭‬ ‭Thick, clotted exudate: indicates more advance inflammation‬ ‭○‬ ‭Purulent exudate (suppurative)‬ ‭‬ ‭Pus: indicates an advance bacterial infection‬ ‭○‬ ‭Hemorrhagic exudate‬ ‭‬ ‭Contain blood, indicates bleeding‬ ‭‬ ‭Chronic inflamation‬ ‭○‬ ‭Inflamatiton lasting 2 weeks or longer‬ ‭○‬ ‭Harder to reverse‬ ‭○‬ ‭Can casue increase in certain desises, ie COPD‬ ‭‬ ‭Would healing‬ ‭○‬ ‭Regeneration‬ ‭○‬ ‭Resolution‬ ‭‬ ‭Returing injured tissue w scar tissue‬ ‭○‬ ‭Repair‬ ‭○‬ ‭Healing‬ ‭‬ ‭Phases of wound healing‬ ‭○‬ ‭1. Inflamation phase‬ ‭‬ ‭Angiogensis‬  ‭‬ C ‭ reates new netoworks of blood vessles to come into injured area‬ ‭and help the healing. Lets the good oxygenated blood get to the‬ ‭affected area‬ ‭○‬ ‭2. Proliferative phase‬ ‭‬ ‭Granulation‬ ‭‬ ‭Epithelialization‬ ‭‬ ‭Need to close wound with fibroblast proliferation. Collagen formation.‬ ‭Wound contraction‬ ‭○‬ ‭3. Remodeling and maturation phase‬ ‭‬ ‭Creates scab/scare tissue‬ ‭‬ ‭Primary intention‬ ‭○‬ ‭When wound margins are neatly approximated such as with some surgical‬ ‭incisions or paper cuts‬ ‭○‬ ‭Suture‬ ‭‬ ‭Secondary intention‬ ‭○‬ ‭Wounds due to trama‬ ‭○‬ ‭Edges cannot be approximated‬ ‭○‬ ‭Wont close with suture becasue could cause infection‬ ‭○‬ ‭Body has to heal from inside out‬ ‭○‬ ‭Results in more granulation tissue with larger scar‬ ‭‬ ‭Tertiary intention‬ ‭○‬ ‭Occurs due to delayed suturing of a wound where two layers of granulation‬ ‭tissue are sutured together‬ ‭○‬ ‭Use wound vac‬ ‭‬ ‭Problems with wound healing‬ ‭○‬ ‭Diabetes too much glucose, unable to heal wound‬ ‭○‬ ‭Smooking - vessels too constricted so cannot heal‬ ‭‬ ‭Keloid scar‬ ‭○‬ ‭Dysfunctional collagen synthesis‬  ‭Infection‬ ‭ ‬ I‭f inflammation is not treated, can turn into infection‬ ‭‬ ‭When mircobe or parasite is able to survive and reproduce in or on the body’s tissues, it‬ ‭creates an optimal environment for infection to occur‬ ‭‬ ‭Bateria‬ ‭‬ ‭Process of infection‬ ‭○‬ ‭Encounter‬ ‭○‬ ‭Transmission‬ ‭○‬ ‭Colonization‬ ‭○‬ ‭Invasion or penetration‬ ‭○‬ ‭Dissemination‬ ‭○‬ ‭Cellular or tissue damage‬ ‭‬ ‭Factors of infection‬ ‭○‬ ‭Communicability‬ ‭○‬ ‭Immunogenicty‬ ‭○‬ ‭Infectivity‬ ‭○‬ ‭Pathogenicity‬ ‭‬ ‭Ability of an agent to produce disease‬ ‭○‬ ‭Portal of entery‬ ‭○‬ ‭Mechanism of action‬ ‭‬ ‭How it damages tissues‬ ‭○‬ ‭Toxigenicity‬ ‭‬ ‭Ability to produce soluble toxins or endotoxins‬ ‭○‬ ‭Virulence‬ ‭‬ ‭Stages of infection‬ ‭○‬ ‭1. Incubation period‬ ‭‬ ‭From initial exposure to onset of first symptoms‬ ‭‬ ‭Pathogens undergoing inital colonization‬ ‭○‬ ‭2. Prodromal stage‬ ‭‬ ‭Occurrence of inital symptoms (often mild)‬ ‭‬ ‭Pathogens continue to multiply‬ ‭○‬ ‭3. Invasion or acute illness period‬ ‭‬ ‭Immune and inflammatory responses triggered‬ ‭‬ ‭Pathogens multiplying rapidly and invading father‬ ‭○‬ ‭4. Convalescence‬ ‭‬ ‭Usually immune and inflammation systems remove pathogens and‬ ‭symptoms decline‬ ‭‬ ‭Alternately - desase is fatal‬ ‭‬ ‭Bacterial disease‬ ‭○‬ ‭Can use antibotics‬ ‭○‬ ‭Prokaryocytes‬ ‭○‬ ‭Areobic or anareobic‬ ‭○‬ ‭Staphylococcus - staff infection‬  ‭‬ ‭Bacteremia‬ ‭‬ ‭Presence of bacteria in blood, going to travel, becoming‬ ‭systemicly infected‬ ‭‬ ‭Septicemia‬ ‭‬ ‭Large amounts of toxins that comes from gram-negative bacteria‬ ‭‬ ‭Viral diases‬ ‭○‬ ‭Do not have a treatment‬ ‭○‬ ‭Antiviral drugs will not cure, but will help manage symptoms‬ ‭○‬ ‭Replication depends on abiliby to infect host cell‬ ‭‬ ‭Not cabable of independent reproduction‬ ‭○‬ ‭Viruses have the ability to change our own cells‬ ‭ ‬ ‭Fungal infection‬ ‭○‬ ‭Very hard to cure‬ ‭○‬ ‭Usally lingers within the epidermis‬ ‭○‬ ‭Candida - most common infections‬ ‭‬ ‭Antibiotics‬ ‭○‬ ‭Bacteriacdal - kill the microrganism‬ ‭○‬ ‭Bacteriostatic - inhibit growth‬ ‭Stress and Disease‬