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37 Cards in this Set

  • Front
  • Back

innate immunity

chemical and physical barriers


non-specific mechanisms


non-adaptive mechanisms

adaptive (aquired) immunity

both specific and adaptive

first line of defense

physical barriers


biochemical barriers

second line of defense

inflammation and phagocytosis

third line of denfense

adpative, specific immunity


cell-mediated


antibody-mediated

protect uninfected host cells from viral infection

interferons IFNs

causes bursting of microbes, promotes phagocytosis, contributes to inflammation

complete system

kill infected target cells by releasing granutes that contain perforin. Phagocytes then kill the released microbes

natural killer cells

inflammation

non-specific


non-adaptive


immediate

inflammation mediated by

chemicals found in ciruculation

steps of inflammation

1. blood vessels dilate bringing increased blood flow to the injured area


2. fluid and phagocytic white blood cells pass out of capillaries


3. lymphatic drainage removes dissolved poisonous substances


4. phagocytes migrate to the injury site and ingest microbes and other foreign substances

local manifestations of inflammation

changes in microcirculation


-vasodilation, increased capillary permeability, white cell migration from capillaries to the site of inflammation, inflammatory chemicals stimulate nociceptors


-observable characteristics

fever

exogenous and endogenous chemical mediators act to reset the hypothalamic thermostat

systemic manifestations of inflammation

fever


increase in both-or inflammatory and anti-inflammatory plasma proteins produced by liver




leukocytosis

leukocytosis

increases circulating neutrophils


-increase in immature granulocytes because of mature neutrophil depletion

increase in both pro-inflammatory and anti-inflammatory plasma proteins producted by the liver causes

levated acute-phase preactions


-erythrocyte sedimentation rate


-blood levels of c-reactive protein

erythrocyte sedimentation rate

rate at which RBCs fall through plasma


relfects level of fibrnogen and adhesion of RBCs

events of acute inflammation


activation of three plasma protein systems:

complement system


-direct or indirect destruction of cells


coagulation system


-isolates infections by trapping pathogens and prevents hemorrhage


kinin system


-interacts with coagulation system


-pro-inflammatory

plasma protein system


-complement system

a group of plasma proteins




participate at all levels of inflammation




three pathways


-classical


-alternative and lectin


c1 activates a cascade of c2-c5a which enhances inflammation

c1 activates a cascade of c2-c5a which enhances inflmmation by

opsonizing bacteria (end product c3b)




inducing mast cell degranulation (c3a/c5a)



inducing mast cell degranulaiton in turn

encourages neutrophil chemotaxis




complement progeins c5b-c9 form a membrane attack complex (mac)




cells are lysed through the influx of entracellular fluids

coagulation system does what

stops bleeding




localized microorganisms




provides a meshwork for healing

the kinin system

activated by coagulation system





primary kinin is

brady kinin

augments inflammation (pro inflammatory)

vascular permeability, vasodilation, smooth muscle contraction

cytokines

more than 100 different kinds




chemical sigmal from one cell that affects another




its how cells talk




can be pro/antiinflammitory

examples of cytokines

interleukins, interferons, chemokines

interleukins

cytokines produced primarily by macrophages and lymphocites in repsonse to microorganisms and products of inflammation

interleukins does what

emcourages cell adhesion molecule expression




chmotaxis




proliferation and maturation of wbc




both pro and anti inflammatory

interferons

proteins produced to protect agains viral infections and encourage the immune system

interferons does what

defense against viral infections




made by leukocytes to help other cells defend against viruses

mast cells

a critical cell in inflammatory response




mast cells are large, granular cells in loose connective tissue, adgacent to blood vessels




early initial activators of inflammatory response

degranulation

quick release of preformed mediators




histame and cemotactic factors




syntheiss of inflammatory medators

mast cell degranulation

released from granules:


-histamine


-mast cell proteases-tryptase


-proteoglycans

effects of histamine

related to type of histamine receptors in cell


-inflammation


-contracts smooth muscle in bronchi, gi tract, and uterus


-increases broncial, intestinal, salivary secretions


-dilation of cerebral blood vessels


-stimulates secretion of gastric juices


-stimulates nerve endings to cause pain and intching

mast cell mediator synthesis made by

these are made by mast cell when it is stimulated

lipid mediators

protaglandins




leukotrienes




platelet-activating factor