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38 Cards in this Set

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2 main components of inflammation
vascular reaction + cellular reaction
2 distinct phases of inflammation
Acute --> minutes to days --> leukocyte emigration (neutrophils) + edema
Chronic --> months to decades --> lymphocytes + macrophages
3 main components of acute inflammation
1. Increased blood flow
2. Increased vascular permeability - allow protein extravasation, leukocyte movement to interstitium
3. Emigration of leukocytes - accumulation at site of injury, activation to eliminate agent
Exudate
inflammatory extravascular fluid that has high protein concentration, usually due to increased permeability
Transudate
a fluid with low protein concentration (most albumin), permeability not increased
Edema
excess interstitial fluid, can be either exudate or transudate
Pus
Purulent exudate, leukocytes (neutrophils), debris of dead cells and microbes
Stimuli for acute inflammation
-Infections (bacteria, viral, parasitic) + microbial toxins
-Trauma
-Physical and chemical (burns, frostbite, radiation)
-tissue necrosis
-foreign body
-immune reactions - hypersensitivity
Vascular changes of inflammation
Responsible for delivering cellular components (neutrophils, Ab's ) to the site of infection
Blood vessels change to allow movement of plasma proteins from circulation to site of injury
Vasodilation
one of earliest changes of acute inflammation
occasionally follows a transient vasoconstriction of arterioles - lasts only seconds
dilates arterioles first
As a result blood flow increases
Increased permeability
quickly follows vasodilation --> increases protein movement into interstitium
Stasis
With fluid movement as result of permeability changes, RBC concentrate in vasculature causing stasis
Which leukocytes are present in acute inflammation
Neutrophils
What is a landmark of acute inflammation
Increased vascular permebaility - exudate extravasation, decreases plasma oncotic pressure, increases tissue oncotic pressure --> edema formation
What is the mechanism for endothelial cells to become "leaky" - increasing permeability
ENDOTHELIAL GAPS IN VENULES - mediated via histamine, bradykinin, leukotrienes
-occurs rapidly, reversible and short lived
-capillaries and arterioles are not affected
How does histamine affects permeability
Causes contraction of venular endothelial cells - causes separation of intercellular junctions - increased permeability
Direct endothelial cell injury
Usually associated with platelet cell attachment
-necrotizing injuries
-such as severe burns
-"immediate sustained response"
-all levels of microcrculation are affected - arterioles, venules and capillaries
Delayed prolonged leakage
Begins after delay (2-12 hrs)
-venules and capillaries
-late appearing sunburn
4 steps of journey of leukocytes from vessel lumen to interstitium
Margination
Rolling
Adhesion
Transmigration (diapedesis)
Describe normal blood flow through venules
Axial streaming- RBC at center, plasma and leukocytes toward vessel wall
Margination of leukocytes
inflammation induces stasis - causing more leukocytes to gather at blood vessel wall
Rolling of leukocytes
Lwukocytes tumble slowly along endothelium and adhere transiently
Adhesion of leukocytes
Leukocytes come to rest and adhere to the wall
Transmigration = diapedesis
Leukocytes are regulated by adhesion molecules and chemical mediators
4 types of adhesion receptors
1. Selectins
2. Ig super family - ICAM + PCAM
3. Integrins - expressed on many cell types, bind to ligands
4. Mucin line glycoproteins - heparan sulfate
Leukocyte effects
-Increase arachidonic acid metabolites
-Increase lysosomal enzymes and activation of O2 burst
-Increase cytokines
-Leukocyte adhesion modulation
Leukocyte receptors
Toll like receptors - activated by microbes
Seven transmembrane
Cytokine receptors - on phagocytes
3 steps of phagocytosis
Recognition and attachment
Engulfment
Killing and degradation
What converts H2O2 to HOCl
Myeloperoxidase
Most frequent cause of leukocyte dysfunction
Bone marrow suppression
Histamine comes from
mast cells
Histamine causes
vasodilation
increase vascular permeability
immediate transient phase of inflammation
Serotonin comes from
Platelets
Complement mostly located in
Plasma
Name anaphylotoxins
C3a and C5a --> histamine
C5a
Chemotaxis
C3b
opsonin
Activated Hageman factor initiates
Clotting
Kinin
Fibrinolytic
COmplement