Exam 2 Flashcards
(170 cards)
Inflammation
reaction to living tissue to injury
innate defensive mechanism. stereotyped response, blood derived components, may be more harmful than inciting injury
important to control inflammation through drugs NSAID or steroids
most things that can injure tissues, living or inanimate, endogenous or exogenous
it is a steotypical and defensive response to rid tissue of injury, reove damaged tissue, initiate healing and repair
What are the cardinal signs of inflammation?
Hemodynamic changes, increase in vascular permeability, and efflux of WBC
Arteriolar constriction
a hemodynamic event of inflammation that is a direct action of injurious stimulation on vessel wall and local neurogenic reflex with epinephrine release
Hemodynamic events of inflammation
arteriolar constriction, vasodilation and opening of capillary beds, increased hydrostatic pressure, and slowing/stasis of blood flow
Vasodilation in inflammation
a hemodynamic event where arterioles, pre-capillaries, and effluent veins dilute
histamine acts on venules
bradykinin and some prostaglandins relax vascular smooth muscle
Edema with inflammation
hyperemia and venous engorgement lead to increased hydrostatic pressure
increased hydrostatic pressure favors fluid efflux. from the vessel (edema) this fluid loss from vasculature leads to hemo-concentration and decreases blood flow
permeability changes with inflammation
primarily venular leakage but arterioles and capillaries leak in more severe injuries
increased vascular permeability- low protein with mild injurt
with further damage, protein rich exudate, leakage of proteins enhances osmotic pull of fluid into interstitium
Chemical mediators of vascular permeability
vasoactive amines (esp released by mast cells), kinins, complement fragments, arachidonic acid mediators, cytokines, platelet activating factor
serous inflammation
exudation of thin watery fluid
most apparent on body or organ surfaces
may be perceived in tissue as edema
functions to dilute or wash away injurious agent
common causes are environmental, irritants, trauma, early infectious process
Catarrhal inflammation
can only occur in tissues containing goblet cells, appears as shiny mucoid material coating mucosal surfaces
serves to dilute, wash away injurious agent (provide a barrier)
caused by irritants, infectious processes affecting mucus membrane
called an exudate but is a glandular secretory product, not a product of increased vascular permeability.
fibrinous inflammation
the increased vascular permeability results in exudation of fibrinogen from the blood which polymerizes into fibrin polymer.
visible exudate which polymerized fibrin is present
fibrin forms adherent strands and sheet which can be stripped off surfaces
most visible on serosal surfaces and in response to infectious disease
functions to wall off the agent and serves as a matrix for migration of WBC, endothelial cells and fibroblasts into the injured area
Neutrophils
first line of defense in response to any injury but often associated with foci of bacterial infection
circulating and marginated pools
short lived
actively phagocytic
glycolytic metabolism
produce oxidative species in response to phagocytic stimulus
release enzymes, antimicrobial molecules and secrete pro-inflammatory mediators
granule contents expelled by degranulation
Suppurative/Purulent Inflammation
dominated by neutrophils, marked by vascular exudation
tissue at site is typically liquified with thick creamy to yellow exudate
usually in response to infectious agent
immediate defensive reaction
acute Stimulus
WBC emigration
neutrophils emigrate within 1 hour, short lifespan in the tissue
macrophages enter after 12-48 hours, capable of long life in tissue, may undergo mitosis
lymphocytes slow to enter tissue, capable of mitosis in tissue
How do neutrophils cross endothelial cells with activation?
Neutrophils in the blood roll, adhesion, and transmigrate across endothelial cells
selectins allow neutrohpils to roll and slow across the surface and integrins
stimulus: endothelial activation, leukocyte activation and chemotaxis activation
Chemotaxis
a direct motion up concentration gradient
surface receptors sense gradient
cell rearranges its cytoplasm
molecules: C5a, bacterial products, leukotrienes, fibrin degradation products, WBC products (IL-8, MCP-1, PAF)
Phagocytosis
uptake and destruction of particulate matter
macrophages and neutrophils most important
purpose:
1) destroy injurious agent
2) clean up tissue debris
Opsonization
surface of particle coated with material that aids recognition by phagocytes and needed for phagocytosis–> allows binding
C3b and C3bi, immunoglobin, lysozyme, fibronectin
What happens once bacteria is opsonized?
It gets engulfed, a phagocytic vacuole is formed which fuses with the lysosome (phagolysosome) , this kills the bacteria and it is digested to later have debris extruded
Oxygen-dependent killing
tremendous oxygen uptake by neutrophils
NADPH oxidase reduces oxygen to super-oxide and subsequent reactions form to produce hydrogen peroxide, hydroxyl radical, singlet oxygen, secondary reactive nitrogen oxides, hydroxyl radical, singlet oxygen, secondary reactive nitrogen oxides, hypohalous species
How can neutrophils damage tissues?
destructive enzymes can be released into the tissue upon cell death and membrane rupture
Cellulitis
purulent inflammation of connective tissues
(suppurative inflammation)
contained to the skin
Phlegmon
suppurative inflammation where there is a fluctuant pocket of pus in the subcutis
Fasciitis
purulent inflammation of fascia (suppurative inflammation)