Immunity/Inflammation/Infection
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94 terms
Terms | Definitions |
|---|---|
 Purpose of Immune Response | To prevent infection of the injured tissue |
| First line of defense | Innate resistance natural or native immunity natural barriers (physical, mechanical, and biochemical) Inflammation |
| Second line of defense | Inflammation activated to protect the body from further injury, prevent infection of the injured tissue, and promote healing |
| Third line of defense | Adaptive (acquired) immunity acquired or specific immunity induced in a relatively slower and more specific process involves memory, creating a more rapid response for next exposure to the same microorganism |
| Innate Immunity | Includes Physical barriers Mechanical barriers Biochemical barriers Inflammation |
| Physical barriers | Skin Lining of hollow organs (eg: stomach) Membrane sheets (genitourinary tract) protection from pathogens epithelial cells and other linings sloughed off with dead skin trapped and moved by cilia (coughing, sneezing) |
| Biochemical barriers | substances secreted to trap/ destroy pathogens Mucus Perspiration: lysozyme attack the cell walls of gm.pos. bacteria Saliva (lysozyme) Tears (lysozyme) Ear wax (cerumen) Glands in skin secrete antibacterial/antifungal lactic acid/fatty acids |
| sebaceous glands | in skin secrete fatty acids and lactic acid kill bacteria and fungi |
| antimicrobial peptides | toxic to certain bacteria, fungi, and viruses |
| Normal Bacterial Flora | NON PATHOGENIC Do not cause disease Help digest food in GI tract Intestine helps digest fatty acids and other substances while preventing colonization with disease causers |
| Antibiotic | treatment can disturb the natural flora, leading to an overgrowth of: Candida (yeast): yeast vaginitis common in women Clostridium Difficile (bacteria) |
| Inflammation | Caused by a variety of materials, including infection, mechanical damage, ischemia, nutrient deprivation, temperature extremes, radiation, etc. blood vessels dilate, increasing blood flow to the area vascular permeability increases Usually has local manifestations - Redness - Heat - Swelling - Pain - Loss of Function |
| Inflammatory process | 1) Bacteria and other pathogens enter wound 2) Platelets from blood release blood clotting proteins at would site 3) Mast cells secrete factors that mediate VASODILATION, vascular constriction, 4) Delivery of blood, plasma, & cells to injured area increases 5) Neutrophils secrete factors that kill and degrade pathogens 6) Neutrophils and macrophages remove pathogens by phagocytosis 7) Macrophages secrete hormones called cytokines that attract immune system cells to the site and activate cells involved in tissue repair 8) Inflammatory response continues until the foreign material is eliminated and the wound is repaired |
| Vascular response | Blood vessel dilation, increased vascular permeability and leakage, white blood cell adherence to the inner walls of the vessels and migration through the vessels Occurs at site of tissue injury (localized reaction to contrast with immune response which is generalized) Depends on activity of cellular and chemical components Nonspecific: tissues respond the same way regardless of cause of injury - hypoxia, cut, infection etc. |
| Redness and Heat | occurs due to blood vessel dilation (increased circulation) |
| Swelling | occurs due to increased vascular permeability and leakage of fluid out of the vessel |
| Serous Fluid and Pus | occurs due to white blood cell migration through vessel to injury. WBCs (leukocytes) instructed to do so by CHEMOTACTIC FACTOR |
| Mast Cell | important to inflammatory process Bags of cellular granules outside blood vessels Activated by stimuli: tissue injury, chemical toxins, immunologic disturbances, after activation of toll-like receptors by viruses or bacteria Granules break down and their chemical components are released and become active immediately release histmaine, chemotactic factors (neurtrophils, eosinophils) & prostagladins |
| Mast cell degranulation | chemotactic factors are released - neutrophils & eosinophils histamine is released prostaglandins are released |
| Histamine | Released post mast cell activation Causes temporary, rapid vasoconstriction in large vessels and dilation in small vessels Enhances vascular permeability Two types of histamine receptors: H1 and H2. Activation of H1's promotes inflammation, while activation of H2 receptors discourages inflammation |
| prostaglandins | platelet-activating factor increase vasopermeability, vasodilation, platelet aggregation, neutrophil chemotaxis, and pain |
| Plasma protein systems | contain inactive enzymes (proenzymes) responsible for: Protein systems Complement system Coagulation system Kinin system |
| Complement system | Can destroy pathogens directly Activates or collaborates with every other component of the inflammatory response 1) opsonization of bacteria 2) chemo-attraction of leukocytes 3) induction of mast cell degranulation (anaphylatoxins) 4) formation of an attack complex that lyses cells by disrupting their outer membranes |
| Coagulation (clotting) system | 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 contains fibrin (an insoluble protein) |
| Kinin system | Functions to activate and assist inflammatory cells Primary kinin is bradykinin Causes dilation of blood vessels, pain, smooth muscle contraction, vascular permeability, and leukocyte chemotaxis |
| Phagocytosis | A cell ingests and disposes of foreign material, including bacteria, through phagocytosis 1) Phagocyte recognizes and binds to the target 2) Engulphment (endocytosis) of the target 3) Fusion of the phagocytic vacuole (phagosome) with the lysosome of the phagocyte 4) Destruction of the target by lysosomal enzymes |
| Phagocytes | live in the blood stream, and must exit into the tissues once inflammatory response has been activated ingest bacteria, dead cells, and cellular debris remove them from the area |
| Steps of phagocytosis | Margination: become more sticky, adhere Diapedesis: emigration through to tissues Opsonization: adherence to target Engulfment : ingestion or endocytosis Phagosome formation Fusion with lysosomal granules Destruction of the target |
| Neutrophils | Polymorphonuclear neutrophils (PMNs) Predominate in early inflammatory responses Ingest bacteria, dead cells, and cellular debris Cells are short lived and become a component of the purulent exudate first at site of injury |
| Monocytes | produced in the bone marrow, enter the circulation, and migrate to the inflammatory site, where they develop into macrophages |
| Macrophages | typically arrive at the inflammatory site 24 hours or later after neutrophils release mediators and cytokines, allowing for prolonged inflammation |
| cytokines | intracellular chemical messengers produced by macrophages released during inflammation increase adhesion molecules on endothelial cell membranes cause chemotaxis and activation of neutrophils, macrophages, and eosinophils |
| Eosinophils | Mildly phagocytic Defense against parasites and regulation of vascular mediators contains granules with basic proteins |
| Natural killer (NK) cells | recognize and eliminate cells infected with viruses and some function in eliminating cancer cells |
| Platelets | Activation results in degranulation and interaction with components of the coagulation system |
| Opsonins | Fragments generated during complement activation Adhere to surface of pathogenic microorganisms Give phagocytes signal to destroy microorganism usually instruct neutrophils and macrophages to destroy via phagocytosis |
| Interleukins | Cytokines produced primarily by macrophages and lymphocytes in response to a pathogen or stimulation by other products of inflammation |
| Interferon | Protects against viral infections Produced and released by virally infected host cells in response to viral double-stranded RNA |
| Tumor necrosis factor-alpha | Secreted by macrophages Induces fever by acting as an endogenous pyrogen Increases synthesis of inflammatory serum proteins Causes muscle wasting (cachexia) and intravascular thrombosis |
| chronic inflammation | Two weeks or longer Sometimes preceded by an unsuccessful acute response Large amounts of neutrophils degranulation and die Leads to pus formation, purulent discharge and sometimes incomplete wound healing Dense infiltration of lymphocytes and macrophages If macrophages can't ward off infection, then a granuloma may form (encapsulated mass) |
| Systemic response to inflammation | Fever, Leukocytosis & pain |
| Fever | Induced by cytokines Induced by endogenous pyrogens Both act on the hypothalamus - raise temperature |
| Leukocytosis | Circulating leukocytes increase (mostly neutrophils). Causes a "left shift" - more immature leuks than mature |
| Pain | Caused by kinins (eg: bradykinin) and prostaglandins at the site of injury (active in the inflammatory process) |
| Dysfunctional wound healing | Some part of the process was abnormal Abnormalities in the inflammatory process, insufficient or excessive repair or re-infection physiologic states : eg: diabetes, hypoxia |
| Keloid scar | Raised and extends beyond original wound boundaries. Often after surgery/piercing |
| Hypertrophic Scar | Remains within original boundaries but excessive tissue build up. Tends to regress over time. |
| Contracture | Results in deformity. Eg: scar tissue over a joint. Commonly seen with serious burns. |
| Dehiscense | Wound pulls apart at the suture line. Usually 5-12 days after suturing. |
| Innate (natural) Immunity | Inflammation |
| Active Immunity | Produced by an individual in response to an antigen or after immunization |
| Adaptive (Acquired) Immunity | Affords long-term protection Also called "immune response" Slow acting, specific and long lived. |
| Passive Acquired Immuity | Does not involve the host's immune response at all Occurs when antibodies or T lymphocytes are transferred from a donor to recipient (eg: mother to child in utero or clinical immunotherapy) temporary - last as long as the donated immune cells do |
| Immune response | involves antibodies (Humoral) and T-Cells (Cellular) |
| Antibody | protect individuals from infection circulates in the blood and binds to antigens on infectious agent cells (bacteria/viruses) Kills or triggers a response within the vicinity that leads to death of the bacteria/virus |
| T cells | triggered by an immune response Develop into a variety of types of cells that react directly with antigen on surface of bacteria/viruses Some of the resulting cells instruct other cells to secrete cytokines to kill the bacteria/viruses Cytotoxic T Cells (Tc cells) attack and kill targets directly |
| Immune globulins | Prepared from individuals who've had the infection (eg: rabies) |
| Antigens | Molecules that react with antibodies or antigen receptors on B and T cells. Can also be immunogens. often combined with "adjuvants" in vaccines also present in allergens, and lead to the responses we call allergic reactions |
| Immunogenic antigens | immunogens INDUCE an immune response produce antibodies and T cells |
| Epitope | precise area of the molecule recognized matches with the paratope (antigen binding site) on the antibody |
| Adjuvants | substances that boost the immune response producing activity |
| Immunogens | produce an immune response leading to activation of T cells |
| antibody titer | used to check a person's immunity to certain viruses. Since some antibodies don't circulate in blood, this assessment cannot always be done. |
| Cytotoxic T Lymphocytes | Instruct cells to self destroy (apoptosis) (tumour cells, viruses) |
| T lymphocytes | T cells that produce cytokines that activate macrophages (phagocytosis) |
| Regulatory T Lymphocytes | (Treg Cells): Produced in response to antigen recognition. Control/limit the immune response to protect the host's healthy cells. |
| Allergy | Deleterious effects of hypersensitivity to environmental (exogenous) antigens |
| Autoimmunity | Disturbance in the immunologic tolerance of self-antigens (antigen in the body that does not elicit an immune response) |
| Alloimmunity | Immune reaction to tissues of ANOTHER INDIVIDUAL Disturbance in the immunologic tolerance of self - antigens (body usually controls and limits these). Antibodies against their own antigens. Damages host tissues. Basis for many clinical disorders (lupus, rheumatoid arthritis) |
| Systemic lupus erythematosus (SLE) | Chronic multisystem inflammatory disease Autoantibodies against: Nucleic acids, erythrocytes, coagulation proteins, phospholipids, lymphocytes, platelets, etc. |
| type 1 hypersensitivity reaction | IgE-mediated reaction Principally involves mast cells Caused by foods, drugs, pollens, dust, molds, bees, etc. S&S include itching, edema, hypotension, bronchospasms (esp. with asthma) conjunctivitis, rhinitis, urticaria (hives) & dysrhythmias Ex: allergic rhinitis |
| allergic rhinitis | Type 1 IgE mediated reaction allergic reaction that occurs when the immune system overreacts to substances that have been inhaled seasonally caused by an allergic reaction to pollen spores caused by ragweed, fungus, grass, tree pollen, pet danders, etc. |
| type 2 hypersensitivity reaction | Tissue-specific reaction Mediated by IgG and IgM Principally involves macrophages in tissues Generally reactions against a specific cell or tissue Occurs with graves disease, autoimmune hemolytic anemia, etc. Often caused by drugs |
| HIV | infects and destroys helper T cells necessary for the development of plasma cells and cytotoxic T cells suppress the immune response against itself & creates a generalized immune deficiency by suppressing the development of immune responses against other pathogens and microorganisms. LEADS TO AIDS!!! a blood-borne pathogen. Most common route of transmission is through heterosexual activity. It is also a retrovirus, containing genetic information in the form of RNA rather than DNA The presence of circulating antibody against the HIV indicates infection by the virus, although most people asymptomatic Although the person may appear asymptomatic, the virus is actively proliferating in lymph nodes |
| coagulation cascade | intrinsic pathway: Hageman factor circulates in its inactive form in the blood. the intrinsic clotting pathway is activated when it contains injured endothelium extrinsic pathway: endothelial cells and macrophages are damaged, releasing tissue thromboplastin |
| tissue regeneration | Restoration of the original structure and physiologic function Occurs with healthy cells that remain after tissue has been destroyed Begin to proliferate by mitosis to replace the lost cells |
| tissue repair | Takes place if fibrin persists in the wound Regeneration is not possible Replacement of destroyed tissue with scar tissue Scar tissue is not able to perform the physiologic functions of the destroyed tissue |
| primary intention | wounds heal after there has been minimal tissue loss, such as after a clean surgical incision process of collagen synthesis |
| secondary intention | occurs in wounds with significant tissue loss left open and closes naturally |
| fibroblasts | migrate to the site of inflammation to begin the process of tissue repair synthesize collagen and fibrin form a matrix for replacement of tissue cells or scar tissue |
| B lymphocytes | B cells produce antibodies that enter blood and react with antigens |
| T lymphocytes | T cells attack the antigen directly |
| allergens | antigens that induce an allergic response |
| immunoglobulin | Molecules known to have specificity for several antigens Characterized by antigenic, structural, and functional differences IgG, IgM, IgA, IgD, IgE |
| IgM | largest of immunoglobulins |
| IgE | spacial class of antibody that protects the individual from infection with large parasites produced against relatively harmless environmental antigens causes allergies such as allergic rhinitis designed to initiate an inflammatory response attracts eosinophils to the site of a parasitic infection |
| hypersensitivity | an altered immunologic response to an antigen results in disease or damage to the individual cell immediate: within minutes to hours delayed: several hours. reaches max. severity days later |
| anaphylaxis | most rapid and sever immediate hypersensitivity reaction |
| non immunologic urticaria | hives that occur as a result of exposure to cold temperatures, emotional stress, meds, etc. |
| atopic | individual genetically predisposed to developing allergies |
| tolerance | State of immunologic control of that the individual does not make a detrimental immune response against their own cells and tissues |
| blood group antigens | RBC surface antigens which can be target of alloimmune reactions |
| type 3 | immune complex mediated hypersensitivity reaction no organ specific reactions |
| type 4 | cell-mediated hypersensitivity reactions |
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