Patho Chp. 3

PlateletsAKA thrombocytes; play role in blood clotting; release chemicalsTypes of Granulocytes-Neutrophils -Esoinophils -Basophils -Mast cellsNeutrophils-most numerous leukocytes: 60-70% of WBC's -important- fasted b.c pseduopods -within 90 mins of injury -manage inflammation -O2 dependent -produce hydrogen peroxide & nitrate oxideEosinophils-2-3% -come 2-3 hours after neutrophils -slower mobility & slower reaction -play role in parasites (like bigger worms that cannot be phagocytize) & allergies -hay fever, bronchial asthmaBasophils<1%; bind IgE; important for allergic response most prominent but does help with inflammation -release of histamineMast Cells-located in lung, GI, & skin -activation releases contents of preformed granules (histamine, proteases, cytokines) produce hormones to make neutrophilsMonocytes-3-8% -largest of circulating leukocytes -half life=day (short) before turning into macrophages -mature into macrophages -work in phagocytosisMacrophagesengulf larger quanities of foreign materials than neutrophils -circulating lifespan is 3-4 times longer than any granulocytes -esp. important in maintaining chronic inflammation2 granules that work in chronic inflammation-lymphocytes -macrophagesCellular stageLeukocytes line the vessel wall in preparation for moving into surrounding tissue While this is happening, endothelial cells in vessel wall react to chemicals that cause vessels to retract This gives the space for leukocytes to squeeze out to interstitial space Go toward the damage by chemotaxis Here they clean up: phagocytosis, engulfing & digesting debrisCellular stage with Leukocyte Activation & PhagocytosisWBC's enter the injured tissue: -destroying infective organisms -removing damaged cells -releasing more inflammatory mediators to control further inflammation and healingKilling of Pathogens: intracellular killing of pathogens trough several means..-toxic oxygen & nitrogen products (nitric oxide & hydrogen oxide) these pathways require oxygen & metabolic enzymes to work -lysozomes -proteases- digest proteins -defensins- antimicrobial peptides (little proteins that fight germs-microbes)Fibrin-fibrin will be used as a "patch" to wall off the injured area so foreign matter is contained -a meshwork of cells forms to be used in healing -blood clotting begins if blood vessels have been damaged -prevents loss of bloodLeukocytes releasemany inflammatory mediators at the injured area -colony- stimulating factors -interleukins -interferons -tumor necrosis factorCell-derived mediators include:Histamine & serotonin- in mast cells -produce vasodilation & > permeability Platelet-activating factor Cytokines- hormone-like -role in acute & chronic inflammationinterleukinsare not stored within cells but are instead secreted rapidly, and briefly, in response to a stimulus, such as an infectious agent.interferonsa group of signaling proteins made & released by host cells in response to the presence of pathogens, such as viruses, bacteria, parasites, or tumor cells.tumor necrosis factora cell signaling protein involved in systemic inflammation and is one of the cytokines that make up the acute phase reaction.Inflammatory Mediators: Plasma-derived mediators-kinins -coagulation and fibrinolysis proteins: promote clot -complementary system -C-reactive proteinkininslike bradykinin cause increased capillary permeability & paincomplementary system-vasodilation -increase vascular permeability -promote leukocyte activation, adhesion, & chemotaxis -augment phagocytosisC-reactive proteincan target microorganisms for destructionInflammatory Mediators: Cell Deprived-released from cells at site of inflammation -histamine & serotonin -Arachidonic Acid Metabolites -Omega-3 Polyunsaturated Fatty Acids -Platelet-Activating Factor -Cytokines & Chemokines -Oxygen-derived free radicalsHistamine & serotoninsome of first released -dilation of arterioles & >permeabilityArachidonic Acid Metabolitesproduction of prostaglandins & leukotrienesOmega-3 Polyunsaturated Fatty Acidsconsidered antithrombic & antinflammatoryNitric OxidePlays multiple roles in inflammation Relaxes vascular smooth muscle Antagonism of platelet adhesion, aggregation, and degranulation Regulates leukocyte recruitment Reduces the cellular phase of inflammationSerous Exudatewatery fluids low in protein that result from plasma entering site -sticky: after fall & rip skin offHERMORRHAGIC Exudatesevere tissue injury causes damage to blood vessels or significant leakage of RBC's from capillariesFIBRINOUS ExudateLarge amts. of fibrinogen -form thick, sticky meshwork-like fibers of blood clotMEMBRANOUS Exudatedevelop on mucous mem. -like a sore in your mouthPURULENT Exudatecontains pus; degraded WBC's, proteins, tissue debrisPYOGENIC Exudate"pus forming"ABSCESS Exudatelocalized area of inflammation containing purulent exudateSystemic Manifestation of Inflammation: Acute Phase ResponseLeukocytes release interleukins, tumor necrosis factor -affect thermoregulatory center---fever -affect CNS----lethargy -skeletal muscle breakdown---weakness -increased HRFibrinogen and C-reaction protein-facilitate clotting -bind to pathogens -fibrinogen causes RBC's to stack; cause increased erythrocyte sedimentation rateWBC countnormal- 4,000-10,000 when inflammatory mediators cause WBC count to rise it hits 15,000-20,000bacterial infectionsneutrophilsparasite & allergieseosinophilsvirusesneutrophils & lymphocytesbody temp is regulated by?thermoregulatory center in the hypothalamus; it also initiates shiveringintermittent fevernormal at least once every 24 hours ex: sepsisremittent feverdoes not return to normal and varies by few degrees in either directionsustained fever (continuous)above normal with minimal variationsrecurrent or relapsing feverone or more episodes of fever up to several days with normal days betweenFever in elderly-slight elevations may indicate serious infection -elderly often have lower baseline temp -fever is usually bacterial infection -look for unexplained changes in functioning: mental status, weakness, fatigue, weight lossfever and negative feedback-vasodilation and sweating with increased temps -vasoconstriction and shivering with decreased tempsmanifestations of fever (4 stages)-Prodrome (1st stage)- mild HA, fatigue, aches, pains, malaise -Chill (2nd stage)- uncomfortable chilled feeling; temp up, shivering, pale, "goose flesh", feel cold, urge to put on more cover -Flush (3rd stage)- vasodilation, skin warm, reddened -Defervescence (4th stage)- imitation of sweating