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26 Cards in this Set

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Endogenous and exogenous sources of chemical mediators
Exogenous sources

1. Cell derived mediators are produced de novo in response to inflammatory stimuli and is stored in intracellular granules

2. Plasma-derived mediators circulate in precursor form and require activation

Exogenous sources include bacterial endotoxin and cobra venom
How do chemical mediators control inflammatory and wound healing processes?
Chemical mediators...

1. are synthesized, released and activated in local area of injury

2. requires interaction w/ specific cell receptors

Durection and intensity regulated by...

1. Postive feedback loop
2. Generation of secondary chemical mediators
3. Rapid decay of meditiators due to short half-life and enzyme inactivators
Histamine
1. Stored in mast cells, blood basophils, and platelets

2. Involved in early phases of acute inflammation and inactivated by HISTIMINASE

3. Causes ↑ vasodilation and vasopermeabilty
Degranulation of mast cells is promoted by...
1. Physical agents (e.g. cold, trauma)

2. C3a and C3b

3. IgE mediated hypersensitivity reactions

4. IL-1
Platelet aggregation and degranulation promoted by...
1. Exposure to subendothelial collagen at the site of vascular injury

2. Exposure to platelet activating factors in IgE mediated reactions
Name the 4 systems of plasma proteases and the factor that links them
1. Kinin
2. Coagulation
3. Fibrinolytic
4. Complement

- Systems are linked by activation of inactive HAGEMAN FACTOR (FACTOR XII) to activated PREKALLIKREIN ACTIVATOR (FACTOR XIIa).

- Factor XII activated by exposure to subendothelial collagen or basement membrane as sites of vascular damage
The kinin system
1. Activation of factor XII ⇒ XIIa leads to BRADYKININ formation

2. Bradykinin similar to histamine (vasodilator + vasopermeabilty)

3. Bradykinin degraded by kininase

4. Kallikrein activates factor XII and amplifies effects of initial stimulus

5. Kallikrain converts C5 ⇒ C5a
The clotting system
1. Activated Hageman factor results in conversion of fibrinogen ⇒ fibrin by thrombin

2. Allows for STABLIZATION of wound

3. Serves as PROTECTION barrier to prevent spread of infection and entering new microbes

4. Creates ATTACHMENT SUBSTRATE for cells
The fibrinolytic system
1. Kallikrein converts plasminogen proactivator ⇒ plasminogen activator

2. Plasminogen activator converts plasminogen ⇒ plasmin

Plasmin (protease)

1. Lyses fibrin clots
2. Activates Hageman factors to factor XIIa ⇒ amplifying inflammatory response
3. Converts C3 ⇒ C3a
The complement system
1. Comprised of inactive C1-9 and its active cleavage products

2. Activated by classic or alternative pathways, but C3 activation step is critical

3. C5a ⇒ chemotaxis and regulates leokocyte adhesion molecules

4. C3a, C5a ⇒ bradykinin effects (vasodilation, vasopermeability)

5. C3b ⇒ opsonization
Arachadonic acid
1. Is a fatty acid that is membrane-bound in inactive esterified phopholipid form

2, Released during inflammation by phospholipase to generate leukotrienes, lipoxins, and prostaglandins in 2 ways:

- Cylcooxygenase pathway
- Lipooxygenase pathway
The complement system
1. Comprised of inactive C1-9 and its active cleavage products

2. Activated by classic or alternative pathways, but C3 activation step is critical

3. C5a ⇒ chemotaxis and regulates leokocyte adhesion molecules

4. C3a, C5a ⇒ bradykinin effects (vasodilation, vasopermeability)

5. C3b ⇒ opsonization
The fibrinolytic system
1. Kallikrein converts plasminogen proactivator ⇒ plasminogen activator

2. Plasminogen activator converts plasminogen ⇒ plasmin

Plasmin (protease)

1. Lyses fibrin clots
2. Activates Hageman factors to factor XIIa ⇒ amplifying inflammatory response
3. Converts C3 ⇒ C3a
Cylcooxygenase Pathway
1. PGI2 (prostacylin) ⇒ vasodilation & ↓ platelet aggregation

2. TXA2 (thromboxane) ⇒ vasoconstriction & ↑ platelet aggregation

3. PGD2, PGE2, PGF2 ⇒ vasodilation

4. PGE2 ⇒ fever, pain sensation, and illicitation
Aspirin and NSAIDS
Inhibits COX-1 and COX-2
Lipoxygenase Pathway
1. LTB4 ⇒ chemotaxis
2. LTD4, LTE4, LTC4 ⇒ ↑ vascular permeability and vasoconstriction
3. LXA4, LXB4 ⇒ negative regulation on leukotrienes
Vasoconstriction mediators
1. Thomboxane A2
2. LTD4, LTE4, LTC4
Vasodilation mediators
1. Prostaglandins I2, D2, E2, F2
2. NO
3. Platelet activating factor
4. Histamine (C3a, C5a)
5. Bradykinin
Vascular permeability mediators
1. Histamine (C3z, C5a)
2. Bradykinin
3. Platelet activating factor
4. Substance P
5. Leukotrienes D4, E4, C4
Pain mediators
1. Bradykinin
2. PGE2
Leukocyte recruitment/activation mediators
1. C5a
2. Leukotriene B4
3. Bacterial products
4. Chemokines
5. IL-1 and TNF
Tissue damaging elements
1. Macrophage and neutrophil lysosomal enzymes

2. ROS
Cytokines
1. Produced by lymphocytes (lymphokines) and monocyte-macrophages (monokines)
2. IL-1 and TNF produced by macrophages; effects fibroblasts, endothelium, and leukocytes and is important in FEVER production
3. TNF important in apoptosis
4. CHEMOKINES - family of cytokines important in chemotaxis
T/F: Platelet activating factor is more potent than histamine
TRUE: PAF is 100-10000x more potent than histmine in vasodilation and ↑ vascular permeability
T/F: Nitric oxide induces vasoconstriction
FALSE: Nitric oxide induces vasodilation
Neuropeptides
1. Example: calcitonin gene-related peptide and substance P

2. Maybe important in mediating vasodilation and ↑ vascular permeability