Flashcards in Chapter 13 - Inflammation and Cytokines Deck (56):
Injury to the epithelium causes:
exposure of collagen, platelet-activating factor release, tissue factor release from endothelium.
When platelets bind to exposed collagen matrix, they release________ which leads to _________ recruitment
platelet derived growth factor; PMN and Macrophage
______ are the dominant cells in wound healing. They release_________.
Macrophages. PDGF, IL-1 and TNF-alpha
Actions of PDGF:
-chemotactic and activates PMNs and Macros
-Chemotactic and activates fibroblasts
-Chemotactic for smooth muscle
Actions of EGF:
-chemotactic and activates fibroblasts
Actions of FGF (Fibroblastic growth factor):
-Chemotactic and activates fibroblasts
Platelet Activating factor generated where? does what?
Generated by phospholipase in endothelium
-Stimulates inflammatory cells, chemotactic, increases adhesion molecules
These cytokines are chemotactic for inflammatory cells:
-C5a and C3a
These cytokines are chemotactic for Fibroblasts:
These cytokines cause angiogenesis:
These cytokines cause epithelialization:
How long do PMN's last in tissue? in blood?
1-2 days in tissue, 7 days in blood
How long to Platelets last?
How are eosinophils involved in type I hypersensitivity reactions?
-Have IgE receptors for allergen
-Release major basic protein- stimulates basophils and mast cells to release histamine
How are Basophils involved in type I hypersensitivity reactions?
-Have IgE receptors
-Main source of histamine in blood
How are Mast cells involved in type I hypersensitivity reactions?
Primary cell in type I hypersensitivity reactions. Main source of histamine in tissues other than stomach.
What does Histamine do?
What does Bradykinin do?
-Contraction of Pulmonary Arterioles
The two main initial cytokines released in response to injury and infection are?
TNF alpha and IL-1
This cell type is the major producer of TNF
Cachexia is mediated by this cytokine
TNF's main functions are?
-Increases adhesion molecules
-Activates neutrophils and macrophages
-Fever, hypothermia, tachycardia, ^ Icardiac output, decrease SVRI
-(high doses cause circulatory collapse and multisystem organ failure)
This cell is the main source for IL-1
IL-1 causes fever through this mechanism
PGE-2 Mediated increased thermal set point (NSAIDS block PGE2)
How does fever occur in atelectasis?
Alveolar macrophages release IL-1
What does IL-1 do to IL-6 production?
What does IL-6 do?
-Increases Hepatic acute phase proteins (C-reactive protein, amyloid A)
What cells release interferons?
Lymphocytes in response to viral infections
What doe interferons do?
Activate macrophages, natural killer cells, cytotoxic T cells
-Inhibit viral replication
What is the most important stimulator for hepatic acute phase proteins?
These proteins are increased in Hepatic Acute Phase Response:
-C-reactive protein (opsonin, ^ complement)
-Amyloid A and P
-Alpha 1 antitrypsin
-alpha 1 chymotrypsin
These proteins are decreased in the hepatic acute phase response:
The first step in cell adhesion:
Rolling; L-selectins on leukocytes bind to E and P selectins
Second step in cell adhesion:
Anchoring; Beta 2 Integrans (CD11/18 molecules) in leukocytes bin ICAMs
Where are ICAM, VCAM, PECAM, FLAM located and what do they do?
Endothelial cells. Bind Beta 2 Integrins. Also help with transendothelial migration
The classic complement pathway is activated by what?
Antigen-Antibody Complex (IgG or IgM)
These factors are found only in the classic pathway:
C1, C2, C4
The alternative pathway is activated by what?
These factors are found only in the alternative pathway:
B, D, and P (Properdin)
This is factor is common to both and is the convergence point:
This electrolyte is needed for both pathways
These are the Anaphylatoxins of the complement, they do what?
C3a, C4a, C5a; increase vascular permeability, smooth muscle contraction, activate mast cells and basophils.
This is the membrane attack complex of complement
Complement Opsonization is caused by:
Complement Chemotaxis is caused by:
C3a and C5a
PGI2 and PGE2 cause what?
PGD2 causes what?
-Increased vascular permeability
NSAIDs do what?
Inhibit cyclooxygenase reversibly
Aspirin does what?
-Inhibits cyclooxygenase irreversibly
-Inhibits platelet adhesion by decreasing TXA2
Steroids do what to eicosanoid production?
Inhibit phospholipase which converts phospholipids to arachidonic acid.
What are LTC4, LTD4, LTE4?
Leukotrienes; slow reacting substances of anaphylaxix. Bronchoconstriction, vasoconstriction, increased permeability
What is LTB4
How long before catecholamines peak after injury?
Where is Norepinephrine released from?
Sympathetic postganglionic neurons and Adrenal Medulla
Where is Epinephrine released from?