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88 Cards in this Set
- Front
- Back
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What is acute inflammation?
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a RAPID response to injury
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What are the main players in acute inflammation?
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Leukocytes + Plasma proteins
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What are the 3 major components of acute inflammation?
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1. Vessel caliber alteration
2. Vessel structure changes 3. Chemotaxis of WBCs |
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What is an exudate?
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Fluid that has escaped from the vascular system as a result of significantly altered permeability of small blood vessels.
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3 characteristic findings that identify an exudate:
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-High protein
-Cell debris -Sp gravity >1.020 |
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What is a Transudate?
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An ultrafiltrate fluid that escaped from the vessel wall due to an osmotic or hydrostatic imbalance; not increased vascular permeability.
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What are the characteristic findings in a Transudate?
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-Low protein (mostly albumin)
-Low sp grav <1.012 |
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What are 6 stimuli for acute inflammation?
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ITPTFI
Infections Trauma Physical/chemical fx Tissue necrosis Foreign bodies Immune reactions |
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What are the 4 steps in changing the vascular in acute inflammation?
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1. Vasodilation
2. Increased permeability of microvasculature (outpouring) 3. Stasis 4. Leukocyte emigration |
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What 2 factors cause vasodilation of vessels?
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-Nitric oxide
-Histamine |
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What are two consequences of increased vascular permeability?
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-Edema (outflow of fluid)
-Lower colloid osmotic pressure in the capillary |
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Normally how does fluid change in capillary beds as it flows through?
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-Net flow out at afferent end
-Net flow in at efferent end due to increased colloid osmotic pressure |
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How does edema affect the fluid change as blood flows through capillary beds?
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Because protein is lost, the lower colloid osmotic pressure means fluid fails to be taken back up at the efferent end. EDEMA
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What is pus?
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A purulent exudate rich in leukocytes
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What is the first thing that causes increased microvascular permeability? How long does it last?
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Gaps in venular endothelium due to endothelial cell contractions; FAST and short-lived.
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What factors cause the fast and transient venular EC contraction?
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-Histamine
-Bradykinin -Leukotrienes -Substance P |
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What causes fast and LONG lived increased microvascular permeability?
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Direct injury
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What are 3 physical factors that can cause prolonged leakage?
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-Thermal injury
-UV light injury -Bacterial injury |
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What causes a late-response and long-lived increase in microvascular permeability?
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LEUKOCYTES injury to EC's
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What is the result of increased microvascular permeability again?
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Edema and increased transcytosis
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What other vessels are subject to leakiness?
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New vessels from angiogenesis
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What happens after microvascular permeability increases and stasis?
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Extravasation
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What are the 4 steps in extravasation?
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1. Margination
2. Rolling 3. Adhesion 4. Diapedesis |
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What is diapedesis?
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Transmigration across the endothelium
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What is the stimulus for leukocyte migration through interstitial tissue?
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A chemotactic trail of factors
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What molecules are responsible for leukocyte rolling?
-on ECs -on WBCs |
EC: P-selectin, E-selectin
WBC: Sialyl-lewis X, PSGL-1 |
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What molecules are responsible for leukocyte adhesion?
-on ECs -on WBCs |
ECs: ICAM-1, VCAM-1
WBC: LFA-1, VLA-4 (integrins) |
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What molecule is responsible for lymphocyte specific extravasation? Where does this occur?
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EC: GlyCam-1
Lymph: L-selectin (at peripheral lymphatic tissues) |
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What is the important molecule for leukocyte migration?
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EC: CD31 (PECAM)
WBC: CD31 |
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What two cytokines induce endothelial adhesion molecules?
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TNF
IL-1 |
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What is chemotaxis?
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The emigration of leukocytes toward an injury site
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What is one exogenous and three endogenous chemokines?
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-Bacterial products (exogenous)
-C5a, Leukotriene B4, Cytokines |
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What happens to leukocytes upon arrival at the injury site?
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Activation
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What allows for leukocyte activation?
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Surface receptors
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What are 4 classes of receptors on leukocytes that serve as activation signals?
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-TLRs
-7-transmemb GPC receptors -Cytokine receptors -Opsonin receptors |
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What is the cellular response of a WBC when a microbe's LPS binds to a TLR receptor?
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-Production of cytokines
-Respiratory burst, ROIs -Killing of microbes |
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What is the cellular response of a WBC when a microbe binds the MANNOSE receptor?
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Activation of the complement cascade, respiratory burst, and killing of the microbe
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What is the cellular response of a WBC when chemokines and other mediators bind 7-transmemb GPC receptors?
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-Increased integrin avidity
-Cytoskeletal changes -Chemotaxis and migration to tissues |
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There are 3 distinct steps in phagocytosis; what are they?
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1. Recognition/attachment of the particle to the cyte
2. Engulfment and vacuole formation 3. Killing/degradation |
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How do lysosomal enzymes get into the phagocytic vacuole?
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By fusion to form a phagolysosome
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What enzymes are required for generating NO, ROIs, and HOCl?
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-PHagocyte oxidase (NADPH)
-Nitric oxide synthase (inducible) -Myeloperoxidase |
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What does oxygen get converted to?
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Superoxide
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What does superoxide get converted to?
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Hydrogen peroxide
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What does H2O2 get converted to?
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Hypochlorite + Hydroxyl radical
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What happens AFTER normal phagocytosis to neutrophils?
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They undergo apoptotic cell death
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What disease is associated with defects in phagolysosome function?
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Chediak Higashi
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What disease is associated with defective microbicidal activity?
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Chronic granulomatous disease
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There are two sources of chemical mediators of inflammation; what are they?
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1. Cellular
2. Plasma |
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What are two forms of chemical mediators from cells?
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-Preformed in secretory granules
-Newly synthesized |
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What are 3 preformed mediators of inflammation in cells?
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1. Histamine
2. Serotonin 3. Lysosomal enzymes |
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Which cell type is serotonin specific to?
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Platelets
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What cells have Histamine?
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Mast cells
Basophils Platelets |
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What cellular mediators of inflammation are synthesized upon activation?
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-Prostaglandins/leukotrienes
-PAFs -ROI's, NO, cytokines |
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What cells produce nitric oxide?
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Macrophages
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What is the major source of plasma chemical mediators of inflammation?
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The liver
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What are the important chemical mediators of inflammation in the plasma? What 3 systems are involved?
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-Factor 12 (hageman) - Kinin system and Clotting system
-Complement System proteins |
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Which complement proteins are anaphylatoxins?
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C5a and C3a
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What are the Vasoactive amines?
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Histamine
Serotonin |
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What are the major effects of the vasoactive amines?
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-Arteriole dilation
-Venule permeability increase |
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How many proteins are in the complement system?
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20
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What are 3 effects that complement proteins have on inflammation?
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-Increased vascular permeability (C3a, C5a)
-Chemotaxis -Opsonization (C3b) |
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What triggers the kinin system?
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Hagemen factor 12
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What is the result of Kinin system activation?
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kallikreins generate kininogens
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What are Kallikreins?
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Specific proteases
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What are Kininogens?
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Vasoactive peptides
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What is the most important kininogen generated in the Kinin system?
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Bradykinin
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What are 4 effects of Bradykinin release?
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-Increased vascular permeability
-Smooth muscle contraction -Blood vessel dilation -Pain |
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What else does Hageman factor XII trigger?
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The clotting cascade
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What is the ultimate factor activated by the clotting cascade?
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Thrombin
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Thrombin causes what to form?
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Fibrin clots
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What factor provides the main link between coagulation and inflammation?
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Thrombin (Fx II)
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In addition to Fx XII activating clotting, what does Fx XIIa activate?
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Fibrinolysis
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So what are the 3 mediators of increased vascular permeability?
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-Bradykinin
-C3a -C5a |
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What is the chemotaxis mediator?
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C5a
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What does Fx XIIa initiate?
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-Kinin system
-Clotting system -Fibrinolytic system -Complement system |
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What are 2 sources of arachidonic acid?
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-Dietary
-linoleic acid conversion |
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What enzymes synthesize AA metabolites?
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-Cyclooxygenases (COX)
-Lipoxygenases |
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What are the AA metabolites called?
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Eicosanoids
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What can eicosanoids do?
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Mediate virtually every step of inflammation
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What 2 mediators are generated by the cyclooxygenase pathway?
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-Prostaglandins
-Thromboxane (TxA2) |
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What are prostaglandins involved in?
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Pain and fever
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What is the function of 5-Hete?
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Chemotaxis
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What is the function of LTB4?
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Chemotaxis
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What do Leukotrienes C4, D4, and E4 do?
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-Vasoconstriction
-Bronchospasms -Increased permeability |
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What does Prostacyclin PGI2 cause?
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-Vasodilation
-Inhibits platelet aggregation |
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What does Thromboxane TxA2 cause?
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-Vasoconstriction
-Promotes platelet aggregation |
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What do the prostaglandins do?
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-Vasodilate
-Potentiate edema |
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What do the lipoxins do?
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Vasodilate and stimulate monocyte adhesion
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