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principle leukocyte (chief phagocytic cell) in acute inflammation; aka PMN; granulocyte in which granules do not stain
leukocytes with granules that contain a protein toxic to parasitic worms; pink-staining granules
what are endothelial cells?
cells that make up the lining of blood vessels and are connected to the basement membrane
what are basophils? what is their prevalence in the blood?
leukocytes with granules that stain blue; < 1% of circulating leukocytes; important in allergic reactions mediated by IgE
first cells to appear at the site of acute inflammation
60-70% of circulating leukocytes
derived from same stem cells as basophils, but only activated when lodged in tissue sites; release histamine, cytokines, chemotactic facotrs, leukotrienes, prostaglandins when activated
the most phagocytic leukocyte; life span 3-4 times longer than granulocytes; produce prostaglandins, leukotrines, PAF, inflammatory cytokines, and growth factor to promote regeneration of tissue
participate in immune-mediated inflammation caused by infectious agents; participate in non-immune-mediated inflammation associated with cell injury and death
5 cardinal signs of inflammation
redness, pain, swelling, heat, loss of function
lymphadenitis can also occur as nodes filter all the harmful substances from the injury site
events in the vascular stage of acute inflammation
quick vasoconstriction-->vasodilation-->increased vascular permeability with outpouring of exudate causing increased concentration of RBC, WBC, platelets and clotting factors
vasodilation (mediated by histamine, leukotrienes, prostaglandins) causes which of the clinical manifestations of inflammation?
redness and warmth
vascular permeability causes which of the clinical manifestations of inflammation?
swelling, pain, and impaired function
what is margination and adhesion?
leukocytes slow migration, adhere to endothelium and move along periphery of vessel
what happens in chemotaxis?
leukocytes guided by a gradient of chemoattractants and cellular debris
what happens in phagocytosis?
neutrophils, monocytes and macrophages activated to engulf and degrade bacteria and cellular debris
these mediators need to be activated when in pre-cursor form to work; mediators that include acute-phase proteins, coagulation factors and complement proteins
mediators that come in the form of granules that need to be secreted from the plasma-membrane.
cytokines, histamine, chemotactic factors, leukotrienes, prostaglandins, phospholipids/fatty acids (converted to mediators) like arachidonic acid.
what do kinins, products of the coagulation/fibrinolysis system & complement proteins have in common?
3 major plasma-derived inflammatory mediators
What does the complement system do?
1) vasodilation and increased vascular permeability
2) promotes leukocyte activation, adhesion and chemotaxis
3) augments phagocytosis
cell-derived mediators are produced by (4 cell types)
macrophages, mast cells, endothelial cells, platelets, leukocytes
histamine and serotonin
first mediators to be released in an acute inflammatory response; cell-derived; cause dilation of arterioles and increase venule permeability
systemic responses to inflammation include:___
fever (pyrexia), leukocytosis, high plasma proteins
when inflammation lasts several weeks or longer. happens because acute inflammation & immune responses are unsuccessful.
develops from unrelenting injury, persistent infectious process, or autoimmune condition.
causes of chronic inflammation
persistent infections, foreign bodies, viral/bacterial infection, obesity
How does obesity relate to chronic inflammation?
adipose tissue is a source of TNF which is correlated to insulin resistance
this protein binds to the surface of invading microorganisms and marks them for destruction
body's 3 major lines of defense
1. skin/mucous membranes
2. inflammatory response
3. immune response
T/F: the inflammatory response is specific
false; does the same thing regardless of the invader, unlike the immune response.
any form of damage, harm or loss to the cell, tissue, organ or organ system. what triggers inflammation.
ex: microorg invasion, cell mutations, anoxia, phys/chem damage
3 goals of inflammation
1. increase blood flow to injury (VASCULAR RESPONSE)
2. alert products of healing to get to the site (CELLULAR RESPONSE)
3. remove injured tissue to prep for healing
what do vasoactive chemical mediators do?
facilitate the widening/loosening of blood vessels at site of injury. this is the VASCULAR response of inflammation
where can chemical mediators be found? what phases of inflammation are they active in?
plasma and many cells:
primary intention vs. secondary intention
wound is basically closed with all areas connecting/healing simultaneously
wound heals from the bottom up.
nodular inflammatory lesions that encase harmful substances. form when injury can't be controlled w/ usual inflammatory/immune mechanisms (ex - foreign bodies, some microorganisms) regulated by macrophages
what do monocytes produce as they mature into macrophages?
fibroblasts and protinases, which break down elastin & other cell components
is there scarring after restoration from acute inflammation?
no, it's minimal. in chronic, however, there is fibrosis, scarring & granuloma formation.
macrophages adapt into these; gather small substances & form a fibrous wall surrounding them
perform specific body functions (neuronal, epithelial, cardiac myocytes, hepatocyes)
3 processes for restoring functioning integrity (the main goal of healing)
1. resolution - mild disruption to cells; rapid recovery
how can you accomplish regeneration or replacement of parenchymal tissue?
proliferation (growth & reproduction)
cells that stop regenerating when growth is complete, but can resume regeneration if injured (ex - heaptocytes)
what component of the inflammatory response is responsible for many of the clinical manifestations?
where are cell-derived chemical mediators found
plasma membrane or they are proteins within the cell
what are the 5 types of leukocytes?
basophils, neutrophils, eosinophil (granulocytes) [mast cell?]
hormone-like cell protein that oversees the chemical mediators. triggers, enhances, and discontinues the inflammatory response.
ex - interleukins, growth factors, interferons, chemokines
group of anti-inflammatory drugs that block the production of arachidonic acid, thus reducing these chem mediators: prostaglandins, lipoxins, leukotienes, thromboxane.
what activates complement? what 4 things does complement induce?
the presence of microorganisms
3. release of chemical mediators from mast cells & basophils
4. cell lysis
what is MAC?
membrane attack complex. the goal of the complement reaction is to form this. it enables complement to recognize, attack & destroy microogs with minimal damage to surrounding cells.
3 plasma protein systems
2. clotting system
3. kinin system
ALL INTER-RELATED. can either activate or inhibit chemical mediators
"acute phase reactants"... measured in lab tests like C-reactive protein
why are blood & fluid needed at the site of injury?
blood has cells active in phagocytosis & healing
fluid dilutes harmful substances at the site of injury
3 steps to a successful cellular response
1. chemotaxis - moving cells to the site of injury
2. cellular adherence - attraction & binding
3. cellular migration - leukocytes moving across endothelial cells (diapedesis)
what minimizes tissue destruction?
inhibitor proteins in the plasma-derived complement, clotting & kinnin systems
what is clotting needed for?
1. trap harmful substances to prevent their spread to other areas
2. stop bleeding
3. form structural origins of repair
3 ways to treat inflammation
reduce blood flow to the area
block action of chemical mediators
non-pharm treatments: rest, ice, compression, elevation (RICE)
3 goals of tissue healing/repair, and the 3 phases
1. COVER the wound
2. CLEAR the debris
3. RESTORE struct/funct integrity
"construction workers" of tissue healing/repair
1. clotting factors
2. chem mediators
4. matrix/structural proteins
5. molecule receptors
6. adhesion molecules
7. growth factors
protective clot & subsequent scab formed on a wound. physical barrier to keep harmful substances out.
what is granulation tissue? what is it most noted for?
connective tissue characterized by extensive macrophages/fibroblasts & the promotion of angiogenesis.
most noted for extensive network of capillaries.
deficient scar formation; wound spits/burst open, along suture line. caused by poor development of extracellular matrix &/or inadequate collagen.
what are agents that cause cell injury (& thus trigger inflammation?
microbiologic (virus, bacterium)
what are the 2 things the vascular response induces?
2. increased capillary permeability
what is the first step in the cellular stage of inflammation?
white blood cells enter the injured tissue
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