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RESPONSE SYNDROME
BACTERIA
BURNS
INFEC
TION
sepsis
SIRS
ISCHEMIA
P
V
OTHERS
REGULATORS OF SIRS
CNS
HORMONAL
ACTH
Binds to receptors of Zona Fasciculata of adrenal
gland GLUCOCORTICOID
in states of stress
Hyperglycemia
Impaired wound healing
Immunosupressive
Anti inflammatory
Catecholamines
GH and IGF
Promote CHON synthesis, lopogenesis and
glycogenesis
enhance phagocytic activity of immunocytes
Insulin
Hyperglycemia and Insulin resistance
Hallmarks of critical illness due to catabolic
effects of circulating mediators
Promotes further immunosupressive effects , dec
phagocytosis and increased risk for infection
MEDIATORS of SIRS
CYTOKINES
Class of protein signaling compounds for innate
and adaptive immune responses
Mediate broad sequence of cellular responses
Mediate eradication of invading micro
organisms but exaggerated responses result in
hemodynamic instability (septic shock) and
metabolic derangements.
EICOSANOIDS
SEROTONIN
stimulates vasoconstriction,
bronchoconstriction, and platelet aggregation
blockade is associated with decreased
production of TNF and interleukin-1
HISTAMINE
H1 vasodilaton, bronchoconstriction,
H2 gastric parietal cell acid secretion
H3 auto receptor , downregulates H
H4 in eosinophils and mast cells
CELL Signaling
G- Protein- cAMP pathway and IP3 pathway
epinephrine , bradykinin, leukotriene
Ligand gated Ion Channels - Neurotransmitters,
amino acids, ach
Tyrosine Kinases signalling for several
growth and endothelial growth factor. IGF,EGF,
VEGF
Janus Kinase mediate signal transduction of
cytokines
Platelets
Activated platelets at the site of injury release
inflammatory mediators that serve as the
principal chemoattractant for neutrophils and
monocyte
Lymphocytes
B and T cells which are mediators of adaptive
immunity.
Secrete cyokines that promotes inflam cascades
Eosinophils
Activated by IL3 and 5. mainly antihelmintic
Mast Cells
Role in anaphylactic response to allergens
TNF released from Mast cells Neutrophil recruitment
Monocytes
Differentiates into macrophages, osteclasts and dendritic
cells.
Main effector cells of the immune response to infection
and injury
Neutrophils
First responders to sites of infection/injury
Potent mediators of acute inflammation.
ENDOTHELIUM-MEDIATED INJURY
VASCULAR ENDOTHELIUM
- overall anticoagulant properties
- BUT in Sepsis/injury becomes
procoagulant microthrombosis and organ
injury
Neutrophil-Endothelium Interaction
NO
Maintains smooth muscle relaxation
PROSTACYCLIN
PAF
Further activates Platelets and neutrophils and
increase vascular permeability
END