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88 Cards in this Set

  • Front
  • Back
What is acute inflammation?
a RAPID response to injury
What are the main players in acute inflammation?
Leukocytes + Plasma proteins
What are the 3 major components of acute inflammation?
1. Vessel caliber alteration
2. Vessel structure changes
3. Chemotaxis of WBCs
What is an exudate?
Fluid that has escaped from the vascular system as a result of significantly altered permeability of small blood vessels.
3 characteristic findings that identify an exudate:
-High protein
-Cell debris
-Sp gravity >1.020
What is a Transudate?
An ultrafiltrate fluid that escaped from the vessel wall due to an osmotic or hydrostatic imbalance; not increased vascular permeability.
What are the characteristic findings in a Transudate?
-Low protein (mostly albumin)
-Low sp grav <1.012
What are 6 stimuli for acute inflammation?
Physical/chemical fx
Tissue necrosis
Foreign bodies
Immune reactions
What are the 4 steps in changing the vascular in acute inflammation?
1. Vasodilation
2. Increased permeability of microvasculature (outpouring)
3. Stasis
4. Leukocyte emigration
What 2 factors cause vasodilation of vessels?
-Nitric oxide
What are two consequences of increased vascular permeability?
-Edema (outflow of fluid)
-Lower colloid osmotic pressure in the capillary
Normally how does fluid change in capillary beds as it flows through?
-Net flow out at afferent end
-Net flow in at efferent end due to increased colloid osmotic pressure
How does edema affect the fluid change as blood flows through capillary beds?
Because protein is lost, the lower colloid osmotic pressure means fluid fails to be taken back up at the efferent end. EDEMA
What is pus?
A purulent exudate rich in leukocytes
What is the first thing that causes increased microvascular permeability? How long does it last?
Gaps in venular endothelium due to endothelial cell contractions; FAST and short-lived.
What factors cause the fast and transient venular EC contraction?
-Substance P
What causes fast and LONG lived increased microvascular permeability?
Direct injury
What are 3 physical factors that can cause prolonged leakage?
-Thermal injury
-UV light injury
-Bacterial injury
What causes a late-response and long-lived increase in microvascular permeability?
LEUKOCYTES injury to EC's
What is the result of increased microvascular permeability again?
Edema and increased transcytosis
What other vessels are subject to leakiness?
New vessels from angiogenesis
What happens after microvascular permeability increases and stasis?
What are the 4 steps in extravasation?
1. Margination
2. Rolling
3. Adhesion
4. Diapedesis
What is diapedesis?
Transmigration across the endothelium
What is the stimulus for leukocyte migration through interstitial tissue?
A chemotactic trail of factors
What molecules are responsible for leukocyte rolling?
-on ECs
-on WBCs
EC: P-selectin, E-selectin

WBC: Sialyl-lewis X, PSGL-1
What molecules are responsible for leukocyte adhesion?
-on ECs
-on WBCs

WBC: LFA-1, VLA-4 (integrins)
What molecule is responsible for lymphocyte specific extravasation? Where does this occur?
EC: GlyCam-1

Lymph: L-selectin

(at peripheral lymphatic tissues)
What is the important molecule for leukocyte migration?

What two cytokines induce endothelial adhesion molecules?
What is chemotaxis?
The emigration of leukocytes toward an injury site
What is one exogenous and three endogenous chemokines?
-Bacterial products (exogenous)
-C5a, Leukotriene B4, Cytokines
What happens to leukocytes upon arrival at the injury site?
What allows for leukocyte activation?
Surface receptors
What are 4 classes of receptors on leukocytes that serve as activation signals?
-7-transmemb GPC receptors
-Cytokine receptors
-Opsonin receptors
What is the cellular response of a WBC when a microbe's LPS binds to a TLR receptor?
-Production of cytokines
-Respiratory burst, ROIs
-Killing of microbes
What is the cellular response of a WBC when a microbe binds the MANNOSE receptor?
Activation of the complement cascade, respiratory burst, and killing of the microbe
What is the cellular response of a WBC when chemokines and other mediators bind 7-transmemb GPC receptors?
-Increased integrin avidity
-Cytoskeletal changes
-Chemotaxis and migration to tissues
There are 3 distinct steps in phagocytosis; what are they?
1. Recognition/attachment of the particle to the cyte
2. Engulfment and vacuole formation
3. Killing/degradation
How do lysosomal enzymes get into the phagocytic vacuole?
By fusion to form a phagolysosome
What enzymes are required for generating NO, ROIs, and HOCl?
-PHagocyte oxidase (NADPH)
-Nitric oxide synthase (inducible)
What does oxygen get converted to?
What does superoxide get converted to?
Hydrogen peroxide
What does H2O2 get converted to?
Hypochlorite + Hydroxyl radical
What happens AFTER normal phagocytosis to neutrophils?
They undergo apoptotic cell death
What disease is associated with defects in phagolysosome function?
Chediak Higashi
What disease is associated with defective microbicidal activity?
Chronic granulomatous disease
There are two sources of chemical mediators of inflammation; what are they?
1. Cellular
2. Plasma
What are two forms of chemical mediators from cells?
-Preformed in secretory granules
-Newly synthesized
What are 3 preformed mediators of inflammation in cells?
1. Histamine
2. Serotonin
3. Lysosomal enzymes
Which cell type is serotonin specific to?
What cells have Histamine?
Mast cells
What cellular mediators of inflammation are synthesized upon activation?
-ROI's, NO, cytokines
What cells produce nitric oxide?
What is the major source of plasma chemical mediators of inflammation?
The liver
What are the important chemical mediators of inflammation in the plasma? What 3 systems are involved?
-Factor 12 (hageman) - Kinin system and Clotting system
-Complement System proteins
Which complement proteins are anaphylatoxins?
C5a and C3a
What are the Vasoactive amines?
What are the major effects of the vasoactive amines?
-Arteriole dilation
-Venule permeability increase
How many proteins are in the complement system?
What are 3 effects that complement proteins have on inflammation?
-Increased vascular permeability (C3a, C5a)
-Opsonization (C3b)
What triggers the kinin system?
Hagemen factor 12
What is the result of Kinin system activation?
kallikreins generate kininogens
What are Kallikreins?
Specific proteases
What are Kininogens?
Vasoactive peptides
What is the most important kininogen generated in the Kinin system?
What are 4 effects of Bradykinin release?
-Increased vascular permeability
-Smooth muscle contraction
-Blood vessel dilation
What else does Hageman factor XII trigger?
The clotting cascade
What is the ultimate factor activated by the clotting cascade?
Thrombin causes what to form?
Fibrin clots
What factor provides the main link between coagulation and inflammation?
Thrombin (Fx II)
In addition to Fx XII activating clotting, what does Fx XIIa activate?
So what are the 3 mediators of increased vascular permeability?
What is the chemotaxis mediator?
What does Fx XIIa initiate?
-Kinin system
-Clotting system
-Fibrinolytic system
-Complement system
What are 2 sources of arachidonic acid?
-linoleic acid conversion
What enzymes synthesize AA metabolites?
-Cyclooxygenases (COX)
What are the AA metabolites called?
What can eicosanoids do?
Mediate virtually every step of inflammation
What 2 mediators are generated by the cyclooxygenase pathway?
-Thromboxane (TxA2)
What are prostaglandins involved in?
Pain and fever
What is the function of 5-Hete?
What is the function of LTB4?
What do Leukotrienes C4, D4, and E4 do?
-Increased permeability
What does Prostacyclin PGI2 cause?
-Inhibits platelet aggregation
What does Thromboxane TxA2 cause?
-Promotes platelet aggregation
What do the prostaglandins do?
-Potentiate edema
What do the lipoxins do?
Vasodilate and stimulate monocyte adhesion