Ch 2 Pathoma Flashcards
Acute Inflammation characterized by
Presence of edema and neutrophils in tissue
Acute inflammation arises in response to
infection (to eliminate pathogen) or tissue necrosis (to clear necrotic debris) - it’s an immediate response with limited specificity
5 mediators of acute inflammation
TLRs, arachidonic acid metabolites, mast cells, complement, hageman factor (factor XII)
TLRs are present on
cells of innate immune system (macrophages, dendritic cells) - also present on cells of adaptive immunity (lymphocytes) so they play a role in acute and chronic inflammation
TLRs are activated by _______ and up regulate _______, a nuclear transcription factor that activates immune response genes
PAMPs (pathogen associated molecular patterns); NF-KB (acts as an on switch)
______ on macrophages recognizes LPS found on gram ______ bacteria
CD14 (a co-receptor for TLR4); negative (LPS acts as a PAMP)
Arachidonic acid is released by ________ and acted upon by ____ or _____ (2 possible pathways with distinct products)
phospholipase A2 (from phospholipid cell membrane); cyclooxyrgenase or 5-lipoxygenase
Cyclooxygenase produces ________ and 5-lipoxygenase produces ________.
prostaglandins; leukotrienes
Which three prostaglandins mediate vasodilation and increased vascular permeability and which one mediates pain and fever?
PGI2, PGD2, and PGE2; PGE2
4 key mediators that attract and activate neutrophils
LTB4 (leukotriene), C5a (complement), IL8 (cytokine), and bacterial products
LTC4, LTD4, and LTE4 (slow reacting substances of anaphylaxis) mediate these three things
vasoconstriction, bronchospasm, increased vascular permeability
Mast cells are activated by these three things
tissue trauma, complement proteins C3a and C5a, or cross linking of cell surface IgE by antigen
Immediate and delayed response of mast cells involve production of _______ and ______ respectively
histamine (which causes vasodilation and increased vascular perm); arachidonic acid metabolites particularly leukotrienes
Complement activations occurs via these three pathways
- classical - C1 binds IgG or IgM that is bound to antigen (GM makes classic cars); 2. alternative - microbe products directly activate complement; 3. MBL (mannose binding lectin) - MBL binds to mannose on microorganisms and activates complement
Complement activation pathways result in
production of C3 convertase (mediates C3 –> C3a and C3b), which in turn produces C5 convertase (mediates C5 –> C5a and C5b). C5b complexes with C6-C9 to form MAC (membrane attack complex - creates hole in microbe cell membrane)
This complement is chemotactic for neutrophils and this one is opsonin for phagocytosis
C5a; C3b
________ is an inactive pro inflammatory protein produced in the liver that is activated upon exposure to sub endothelial or tissue collagen
Hagemon factor (factor XII) (can lead to DIC)
Hagemon factor (factor XII) activates these three things
coagulation and fibrinolytic systems (can lead to DIC) - most impt; complement; kinin system (kinin cleaves high-molecular weight kininogen HMWK to bradykinin which mediates vasodilation and increased vascular perm and pain)
2 key mediators for pain
PGE2 and bradykinin
5 cardinal signs of inflammation
redness (rubor), warmth (calor), swelling (tumor), pain (dolor), and fever
The key mediators of redness and warmth are (3); the key mediators of swelling are (2); the key mediators of pain are (2)
histamine, prostaglandins, bradykinin; histamine, tissue damage; bradykinin and PGE2
Pathway of fever
pyrogens (like LPS from bacteria) cause macrophages to release IL1 + TNF –> increases COX activity in perivascular cells in hypothalamus –> increase PGE2
Leukocyte arrival in tissues (steps)
Margination, rolling, adhesion, and transmigration
Vasodilation slows blood flow in _________ which cause leukocytes to ________
postcapillary venules; marginate