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103 terms

Chap 3

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neutrophil
principle leukocyte (chief phagocytic cell) in acute inflammation; aka PMN; granulocyte in which granules do not stain
eosinophils
leukocytes with granules that contain a protein toxic to parasitic worms; pink-staining granules
what do neutrophils,eosinophils, basophils have in common?
leukocytes with multi-lobed nuclei
3 cells associated with CHRONIC inflammation
monocytes/macrophages, lymphocytes
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
monocytes
has a single nucleus with no lobes
lymphocytes
smallest leukocyte with deeply staining nucleus
neutrophils
first cells to appear at the site of acute inflammation
60-70% of circulating leukocytes
what do basophils, eosinophils, neutrophils have in common?
have granules
2 cells without granules
lymphocytes, monocytes/macrophages
mast cells
derived from same stem cells as basophils, but only activated when lodged in tissue sites; release histamine, cytokines, chemotactic facotrs, leukotrienes, prostaglandins when activated
eosinophils
2-3% of circulating leukocytes
monocytes
3-8% of circulating leukocytes
macrophages
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
what are circulating, immature macrocytes?
monocytes
lymphocytes
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 is transmigration?
leukocytes extend pseudopodia and "crawl" through the vessel wall
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
plasma-derived mediators are produced where?
liver
plasma-derived mediators
these mediators need to be activated when in pre-cursor form to work; mediators that include acute-phase proteins, coagulation factors and complement proteins
cell-derived mediators
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
bradykinin
this is an inflammatory mediator that causes increased capillary permeability and pain
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
antihistamines
drugs that antagonize the immediate inflammatory response
prostaglandins
this mediator induces inflammation and enhances other mediators
thromboxane A
promotes platelet aggregation and vasoconstriction
aspirin and NSAIDS
drugs that reduce inflammation
leukotrines
this mediator is slower to action, but similar in function to histamine
nitric oxide
this mediator relaxes vascular muscle and antagonizes platelet adhesion/aggregation
systemic responses to inflammation include:___
fever (pyrexia), leukocytosis, high plasma proteins
nitric oxide
this mediator helps to REDUCE inflammation
serous exudate
watery exudate; one of most common types
hemorrhagic exudate
bloody exudate
fibrinous exudate
exudate with large amounts of fibrinogen
membranous/pseudomembranous
exudate that on mucous membrane surface that traps necrotic cells
purulent exudate
exudate that contain pus; one of most common types
chronic inflammation
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.
characteristics of chronic inflammation
proliferation of blood vessels, necrosis, fibrosis
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
C-reactive protein
this protein binds to the surface of invading microorganisms and marks them for destruction
10 hours
life span of a neutrophil
leukocytosis
increase in WBC
leukopenia
decrease in WBC
immature neutrophils are called ________
bands
normal WBC count
5,000 -- 10, 000 cells/ml
"shift to the left" means...
increase in bands
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.
injury; examples
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:
platelets
mast cells
basophils
neutrophils
endothelial cells
monocytes
macrophages
primary intention vs. secondary intention
wound is basically closed with all areas connecting/healing simultaneously

wound heals from the bottom up.
granuloma
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
giant cells
macrophages adapt into these; capable of engulfing particles much larger than usual.
is there scarring after restoration from acute inflammation?
no, it's minimal. in chronic, however, there is fibrosis, scarring & granuloma formation.
epitheloid cells
macrophages adapt into these; gather small substances & form a fibrous wall surrounding them
parenchymal tissues
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
2. regeneration
3. replacement
how can you accomplish regeneration or replacement of parenchymal tissue?
proliferation (growth & reproduction)
differentiation (specialization
diapedesis (migration)
labile cells
cells that constantly regenerate through mitosis (ex: skin)
stable cells
cells that stop regenerating when growth is complete, but can resume regeneration if injured (ex - heaptocytes)
permanent cells
don't undergo mitosis and can't regenerate (ex - neurons)
what component of the inflammatory response is responsible for many of the clinical manifestations?
chemical mediators
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?]
monocyte/macrophage
lymphocyte
degranulation
release of chemical mediators in the form of extracellular granules
cytokines
"workaholic"
hormone-like cell protein that oversees the chemical mediators. triggers, enhances, and discontinues the inflammatory response.

ex - interleukins, growth factors, interferons, chemokines
corticosteroids
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

1. opsonization
2. chemotaxis
3. release of chemical mediators from mast cells & basophils
4. cell lysis
opsonization
complement induces this process, which makes bacterial vulnerable to phagocytosis.
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
1. complement
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
exudate
fluid mixture of protein, leukocytes & tissue debris; accumulates 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
what % of the blood is erythrocytes?
42-48%
3 ways to treat inflammation
reduce blood flow to the area
decrease swelling
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

1. inflammatory
2. proliferative
3. remodeling
"construction workers" of tissue healing/repair
1. clotting factors
2. chem mediators
3. proteinases
4. matrix/structural proteins
5. molecule receptors
6. adhesion molecules
7. growth factors
thrombus
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.
dehiscence
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?
physical (heat/cold)
chemical (acid)
microbiologic (virus, bacterium)
what are the 2 things the vascular response induces?
1. vasodilation
2. increased capillary permeability
what is the first step in the cellular stage of inflammation?
white blood cells enter the injured tissue
margination
leukocytes slow movement & accumulate/adhere to endothelium
emigration
leukocytes changes shape & squeeze thru enter-endothelial junctions
5 complications of healing
infection
ulceration
dehiscence
keloids
adhesions