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BIO170 - Obj 6
BIO170 - Obj 6 - Fever as a homeostatic mechanism
| Question | Answer |
|---|---|
| What are the 3 lines of defense in immunity? | 1st line of defense: innate resistance; 2nd line of defense: inflammation; 3rd line of defense - adaptive (acquired immunity) |
| What is the inflammation process? | the body response to cellular injury |
| What are types of injury that will lead to inflammation? | mechanical damage, chemical damage, ischemia, nutrient deprivation, temperature extremes, radiation, microbes, etc |
| Where are manifestations of inflammation found? | Locally, around the site of injury/infection |
| What is the vascular response in inflammation? (4) | 1) blood vessel dilation; 2) increased vascular permeability and leakage (to allow WBCs in and out); 3) WBC adherence to the inner walls of the vessels and 4) WBC migration through the vessels |
| What are the goals of inflammation? (4) | 1) limit/control the inflammatory process; 2) prevent/limit the infection and further damage; 3) interact with components of the adaptive immune system; 4) prepare the area of injury for healing |
| What are the 3 protein systems involved in inflammation? What do they have in common? | 1) coagulation system; 2) complement system; 3) kinin system; all systems contain inactive enzymes (proenzymes) that are sequentially activated in a cascade; these proteins are freely floating through the body until needed |
| What is the cogulation system: What does it do? | the coagulation system is the clotting system; it forms a fibrin (insoluble protein) meshwork at an injured or inflamed site |
| What are the 4 mechanisms of the coagulation system? | 1) forms a clot that stops bleeding; 2) keeps microorganisms and foreign bodies close to large # of inflammatory/phagocytic cells; 3) prevents the spread of infection; 4) provides a framework for repair and healing |
| Describe the plasma protein complement system: | very potent; it can destroy pathogens directly and it activates and collaborates with other components of the inflammatory response |
| What are the 3 different ways the complement system can be activated (i.e. the different pathways)? | 1) classical, 2) lectin; 3) alternative |
| Describe the classical complement pathway: | antigen + antibody + bacterium (antigen/antibody complex) |
| Describe the lectin complement pathway: | carbohydrates from bacterium |
| Describe the alternative complement pathway: | activated by G- (gram negative) bacterial and fungal cell wall polysaccharides |
| What is one of the main methods used by the complement system in the inflammation response? | It tags cells to be destroyed so that they may be recognized by other proteins |
| Describe the kinin plasma protein system and identify the primary kinin: | it activates and assists inflammatory cells; the primary kinin is bradykinin |
| What are the effects of the kinin system? (4) | 1) dilation of blood vessels; 2) *pain*; 3) smooth muscle contraction; 4) vascular permeability; 4) leukocyte chemotaxis (note - think of kinin -> kinetics -> moving) |
| What are the 2 types of cellular mediators of inflammation? | Cellular components and cell surface receptors |
| What are the 4 types of celullar components mediators? | granulocytes (neutrophils, basophils, eosinophils), platelets, monocytes, and lymphocytes |
| What are the 5 types of cell surface receptors? | 1) pattern recognition receptors (PRRs); 2) pathogen-associated molecular patterns (PAMPs); 3) toll-like receptors; 4) complement receptors (found on many cells); 5) scavenger receptors (found on macrophages) |
| How do pattern recognition receptors work? | they recognize molecular patterns on the infectious agents or their products |
| How do pathogen-associated molecular patterns (PAMPs) work? | They recognize products from infectious agents |
| What types of cells have toll-like receptors? What is their significance? | toll-like receptors are found on many cells (mucosal epithelial, mast, macrophils, neutrophils, etc); they have very early contact with pathogens (i.e. mouth, lungs, genital area, etc) |
| What types of WBCs are first activated in an acute infection? | neutrophils |
| What are mast cells? What do they contain? | central cells in inflammation; located in the loose connective tissues close to the blood vessels (skin, digestive lining, and respiractory tract); they contain bags of granules: histamine, kinins, chemotactic factors, and prostaglandins |
| How are mast cells activated? | by physical injury, chemical agents, immunologic processes, and toll-like receptors |
| What are the 2 ways mast cells are activated to release chemicals? | 1) degranulation (immediate response)(by exocytosis) and 2) synthesis of lipid-derived chemical mediators |
| What is the function of histamine, which is release from the mast cells? | histamine is a vasoactive amine; causes constriction of large blood vessels and dilation of postcapillary venules (increases microcirculation blood flow); provides for retraction of endothelial cells lining the capillaries (increasing permeability) |
| What are the main 2 histamine receptors, where are they located, and what is their function? | 1) H1 receptors are proinflammatory; present in the smooth cells of the bronchi; 2) H2 receptors are anti-inflammatory; found in the parietal cells of the stomach mucosa; decrease WBCs response to inflammation/infection and induce gastric acid secretion |
| What are the 2 chemotactic factor products of mast cells? | neutrophil chemotactic factor which attracts neutrophils and eosinophil chemotactic factor of anaphylaxis (ECF-A) which attracts eosinophils |
| What are the 3 types of lipid-derived products synthesized during mast cell activation? | leukotrienes, prostaglandings, and platelet-activating factor |
| What are leukotrienes? | products of arachidonic acid from mast cell membranes; their effect are similar to histamine in later stages |
| What are prostaglandins? | their effects are similar to leukotrienes; they also induce pain |
| What is platelet-activating factor? | effects are similar to leukotrienes and platelet activation |
| What is the vascular phase of inflammation caused by? What are the 3 effects? | vascular phase of inflammation is caused by release of tissue chemicals; the 3 effects are vasoconstriction, vasodilation, and increased capillary permeability |
| Describe the vasoconstriction of the vascular phase: | within seconds after injury, arterioles (small arteries), near the site of the injury will constrict |
| Which chemicals cause the vasoconstriction of the vascular phase? Vasodilation? | first, histamine from the mast cells and serotonin from platelets cause vasoconstriction; later these same chemicals cause vasoconstriction |
| Describe the vasodilation of the vascular phase: | aka hyperemia; additional blood flows into the inflamed area, bringing additional leukocytes to the damaged area |
| Describe the increased capillary permeabilty: | leaky capillaries will allow tissue fluid, leukocytes and clotting factors to escape into the damaged tissue spaces |
| Which chemicals are responsible for increased capillary permeability? | histamine (from mast cells), serotonin (from platelets), and kinins (specifically, leukotrienes (from mast cells) increase capillary permeability |
| What is edema? | the tissue fluid that escape into the damaged tissue as a result of the inflammation response |
| What is the purpose of edema and clot formation? | it helps to "wall off" the inflammation and protect surrounding healthy tissue |
| What is the function of the leukocytes which are released from the leaky capillaries? | they can destroy invading microbes and damaged tissue cells by phagocytosis |
| What occurs after the capillaries leak? | new tissue growth and healing occurs |
| What are the 5 cardinal signs of inflammation (in order!)? | 1) rubor (rednessed); 2) turgor (swelling of the inflamed area); 3) calor (heat); 4) dolor (pain); 5) loss of function |
| What causes rubor, turgor, and calor? | vasodilation and hyperemia cause the rubor and turgor; turgor is also a result of edema; active phagocytosis and hyperemia cause calor |
| Why is pain a symptom of inflammation? | pain is a protective mechanism; chemical mediators (prostaglandins, bradykinin), bacterial products, toxins cause inflammation & stimulate pain nerve endings; also, swelling from inflammation (exudate/pus/fibrous material) impinges on pain nerve endings |
| What are the pain nerve endings? | bare dendritic endings of pain neurons |
| Why does loss of function result from inflammation? | swelling and pain will cause loss of function, especially at a joint; losing function may force resting and healing |
| What are the 5 steps of the cellular phase of inflammation (in order)? | 1) chemotaxis; 2) margination; 3) pavementing; 4) diapedesis or emigrimation; 5) phagocytosis |
| Describe the chemotaxis that occurs in the cellular phase: | the mast cell releases its tissue chemicals, leukocytes are drawn to the inflamed area |
| What is margination? | the movement of the leukocytes out of the blood flow and toward the "margins" or the walls of the blood vessel |
| What is pavementing? | the flattening of the leukocytes against the wall of the capillary |
| What is diapedesis or emigration? | the movement of the leukocyte out of the capillary and into the tissue space of the inflamed area; leukocytes can move by "amoeboid" motion, oozing through the pores found in a capillary wall |
| What are the steps of phagocytosis? (6) | 1) opsonization, recognition, and adherence; 2) engulfment; 3) phagosome formation; 4) fusion w/lysosomal granules; 5) destruction of the target; 6) exocytosis |
| Describe the opsonization, recognition, and adherence phase of phagocytosis: | opsonins are molecules that tag pathogens (ex: in the complement system); opsonization causes the pathogen to be easily recognized by phagocytic/inflammatory cells and adhere to them |
| What are the 5 types of phagocytes? | 1) neutrophils; 2) monocytes and macrophages; 3) eosinophils; 4) natural killer (NK) cells; 5) platelets |
| Describe the phagocytic role of neutrophils: | particularly polymorphonuclear neutrophils (PMNs); the predominate in *early inflammatory responses*; they ingest bacteria, dead cells, and cellular debris; the cells are short-lived and become a component of the purulent exudate |
| Describe the role of monocytes and macrophages: | monocytes are produced in bone marrow, enter circulation, migrate to inflammatory site (3-7 days after neutrophils) & develop into macrophages; macrophage activation results in increased size: # of lysosomes, secretory products, glucose metabolism |
| Describe the phagocytic role of eosinophils: | only mildly phagocytic; their function is defense against parasites and regulation of vascular mediators |
| Describe the role of natural killer cells: | aka NK cells; they recognize/eliminate cells infected with viruses and some function in eliminating cancer cells |
| Describe the role of platelets: | their activation results in degranulation and interaction with components of the coagulation system |
| What are the 3 most important types of cytokines? | 1) interleukins; 2) interferon; 3) tumor necrosis factor - alpha (TNF-alpha) |
| What types of cells produce interleukins? Which type is proinflammatiory? anti-inflammatory? | macrophages and lymphocytes; IL-1 is proinflammatory; IL-10 is anti-inflammatory |
| What types of cells produce interferon? What is the purpose of interferon? | virally infected host cells; protects against viral infections by inducting production of antiviral proteins or by increasing microbiocidal activity of macrophages |
| What type of cells produces tumor necrosis factor alpha? What is its function? | TNF-alpha is secreted by macrophages; it induces fever by acting as an endogenous pyrogen and *causes muscle wasting* and intravascular thrombosis, in case of chronic conditions |
| What is cachexia? | muscle-wasting |
| What are the 4 types of exudative fluids? | 1) serous (water-indicates early inflammation); 2) fibrinous: thick, clotted (indicates more advanced inflammation); 3) purulent: pus (indicates bacterial infection); 4) hemorrhagic: contains blood (indicates bleeding) |
| What are the 3 systemic manifestations of inflammation in the acute phase? | 1) fever: caused by exogenous (ex: bacteria) and endogenous pyrogens which act directly on the hypothalamus; 2) leukocytosis: increased # of circulating leukocytes; 3) increased plasma protein synthesis |
| What is chronic inflammation: | inflammation lasting 2 weeks or more |
| What are the causes of chronic inflammation? (6) | 1) unsuccessful acute inflammatory response; 2) very large injury; 3) high lipid/wax content of microorganism; 4) ability to survive inside the macrophage; 5) toxins; 6) chemicals or particulate matter in the wound, or physical irritants |
| What are the 4 characteristics of chronic inflammation? | * 1) Dense infilitration of lymphocytes & macrophages * *2) granuloma formation*; 3) epithelioid cell formation; 4) giant cell formation |
| What is granuloma formation? | nodular inflammatory lesions, firm and consistent; means that neutrophils/macrophages are unable to destroy microorganisms |
| What is epithelioid cell formation? | macrophages and other phagocytic cells differentiate into cells with certain characteristics of epithelial cells |
| What is giant cell formation? | activated macrophages fuse together to engulf large microorganisms |
| What is regeneration? | the returning of injured tissues to an approximation of their original structure; may occur if damage was minor and no complications |
| What is resolution? | the restoration of tissue to the original structure and function |
| What is repair? | this occurs if resolution is not possible; destroyed tissue is replaced with scar tissue |
| What is scar tissue? | it is composed primarily of collagen to restore the tensile strength of the tissue |
| What is debridement? | excision/clean up of dissolved clots, microorganism, erythrocytes, and dead tissues cells (by phagocytosis & fibrinolytic enzymes) |
| What are the 3 steps of the healing process? | 1) filling in the wound; 2) sealing the wound (epithelialization); 3) shrinking thw ound (contraction) |
Created by:
debmurph