Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
45 Cards in this Set
- Front
- Back
What are the Major Inflammatory products of the complement system?
|
C3a
C3b C5a |
|
What causes increased vascular permeability by way of HISTAMINE release?
|
C3a
C5a |
|
What activates WBC and increases avidity (affinity) of WBC INTEGRIN molecules
|
C5a
|
|
What upregulates LIPOXYGENASE PATHWAY of arachidonic acid metabolism?
|
C5a
|
|
What complement metabolite causes CHEMOTAXIS?
|
C5a
|
|
What complement metabolite causes OPONIZATION?
|
C3b
|
|
What are the actions of KALLIKREINS?
|
Activates
BRADYKININ FACTOR XII PLASMIN C5 to C5a |
|
What are the actions of BRADYKININ?
|
INCREASED vascular permeability
smooth muscle CONTRACTION produces PAIN |
|
The COAGULATION SYSTEM (intrinsic pathway) is activated by ?
--products active in mediating inflammation include |
Factor XII
|
|
What are the actions of THROMBIN?
|
Serotonin released from platelets
enhanced WBC adhesion FIBROBLAST proliferation |
|
Fibrinopeptides are created when ? changes FIBRINOGEN to FIBRIN
|
Thrombin
|
|
what are the actions of FIBRINOPEPTIDES
|
increase VASCULAR PERMEABILITY
chemotaxis |
|
What are the actions of Factor Xa
|
increase Vascular permeability
|
|
Fibrinolytic System is activated by ?
products active in mediating inflammation include ? and ? |
Kallikrein
--> PLASMIN --> Fibrin Split Products |
|
What is the actions of PLASMIN?
|
Cleaves C3 to C3a
cleaves FIBRIN to produce FIBRIN SPLIT PRODUCTS activate FACTOR XII activate TGF-B (wound healing) |
|
What are the actions of FIBRIN SPLIT PRODUCTS (from breakdown of fibrin during fibrinolysis) ?
|
Vascular Permeability
|
|
What causes FIBRIN to be broken down FIBRIN SPLIT PRODUCTS?
|
Plasmin
|
|
What pre-formed Vasoactive amines are stored in granules?
|
Histamine
Serotonin |
|
What are the actions of VASOACTIVE AMINES?
Histamine Serotonin |
Vasodilation of arterioles (constricts large arteries)
Increase vascular permeability of venules |
|
What cell has vasoactive amines --Histamine and Serotonin in pre-formed granules?
|
Platelets
|
|
Release of HISTAMINE from mast cells due to
--Immune Reactions --Complement Fragments --Cytokines |
immune reactions => IgE receptors
complement fragments => C3a and C5a cytokines => IL-1 and IL-8 |
|
Release of vasoactive amines from PLATELETS are stimulated by?
|
Throbin
contact with COLLAGEN PLATELET ACTIVATING FACTOR (mast cells) |
|
What prevents LYSOSOMAL PROTEASES from neutrophils and monocytes from staying active / keeps them in check ?
|
ALPHA - 1 - ANTI-TRYPSIN
plasma antiproteases |
|
PHOSPHOLIPASES are INHIBITIED from making Arachidonic Acid Metabolites by ?
what stimulates PHOSPHOLIPASES? |
Corticosteroids
Platelet Activating Factor |
|
What is the Arachidonic Acid Metabolite that causes--
Pain, Fever, and Vasodilation? Vascular permeability? Chemotaxis? |
Prostaglandin (pain, fever, and vasodilation)
Leukotrines (vascular permeability) Leukotrine B4 (chemotaxis) |
|
Which of the two pathways in arachidonic acid metabolites is involved with PROSTGLANDIN and THROMBOXANE synthesis?
|
Cyclooxygenase Pathway
|
|
Which of the two pathways in arachidonic acid metabolites is involved with LEUKOTRINE synthesis?
|
Lipoxygenase pathway
|
|
? inhibit the CYCLOOXYGENASE pathway and production of Prostaglandins
|
Non-Steroidal Anti- Inflammatory Drugs (NSAID)
|
|
What causes VASCULAR PERMEABILITY and VASODILATION and "PRIMES" WBCs?
|
Platelet Activating Factor
|
|
Which Nitric Oxide synthetase is induced when activated by cytokines such as TNF-α and TNF-γ
|
iNOS (macrophages)
|
|
What is the role of the neuropeptide SUBSTANCE P?
|
binds to receptor on target cell (especially lungs and GI tract)
activation of ARACHIDONIC ACID PATHWAY powerful mediator of INCREASED VASCULAR PERMEABILITY |
|
During leukocyte diapedisis
endothelial cells first produce ? which is considered to be "loose" (tethering / rolling) adhesion with WBCs |
Selectins
|
|
When WBCs and Endothelial cells have FIRM ADHESION (latching)
what proteins are involved? |
ICAMs
Integrins associated with LEUKOCYTE and ENDOTHELIAL activation |
|
Adhesion stimulation is mediated by ? for Leukocyte adhesion molecules
|
C5a
Chemotactic Complement Fragments |
|
Adhesion stimulation is mediated by ? for ENDOTHELIAL Cell adhesion molecules
|
IL - 1
|
|
Chemotactic agents bind to the leukocyte receptor site which triggers the ? in the cytoplasm (FILAMIN, GELSOLIN, PROFILIN, CALMODULIN)
motility is by action of a PSEUDOPOD (LAMELLIPOD) |
actin regulating elements
causes actin-myosin contraction |
|
What are the Chemotactic Agents?
|
N-formylated peptides (from bacteria)
C5a Leukotrine B4 (arachidonic acid metabolism in neutrophils and macrophages) IL-8 <<<< |
|
REMEMBER
IL-1 and TNF-alpha ARE NOT CHEMOKINES!! IL-8 IS A CHEMOKINE! |
REMEMBER
IL-1 and TNF-alpha ARE NOT CHEMOKINES!! IL-8 IS A CHEMOKINE! |
|
What are the 3 Leukocyte Activators?
|
TNF- Alpha
C5a Platelet Activating Factor 3 |
|
What are the 2 major Opsonins?
|
Fc Fragment of IgG
C3b, C3bi |
|
What are the primary cytokines involved with FEVER?
|
IL-1
TNF - alpha |
|
IL-1 stimulates ? synthesis in the HYPOTHALAMUS which alters the body temperature set-point.
TNF alpha? |
PROSTAGLANDIN
TNF acts by stimulating release of IL-1 and on the hypothalamus directly |
|
Acute Phase Protein production are produced by the ?
mediated by action of ? on ? |
Liver
IL-6 on hepatocytes acute phase proteins -c reactive protein (enhance opsonization) -Serum Amyloid A -Complement -Coagulation Factors (fibrinogen) |
|
How does one tell when there is an INCREASE of ACUTE PHASE PROTEINS?
|
results in increase in ERYTHROCYTE SEDIMENTATION RATE (ESR)
|
|
Pain is mediated by ? and ?
|
Prostaglandins
Bradykinin |