Endotoxin shock is initiated by aEUR'
Cytokines action Septic shock is caused by vasodilation and peripheral pooling of blood as a pa of systemic immune reaction to bacterial or fungal infection. Septic shock was earlier also known as endotoxic shock because it was believed to be most commonly associated with endotoxin secreted due to gram negative bacteria. Currently, septic shock is most .frequently triggered by grain positive bacterial infections followed by gram negative bacteria and fungi. Hence the older synonym of "endotoxic shock" is not appropriate. Septic shock may be caused by either gram positive or gram negative bacteria. The microbial triggers for septic shock are different in different bacterias :- - Grain negative bacteria --> * Lipopolysaccharide entotoxin - Gram positive bacteria * Lipoteichoic acid Cell wall murantyl peotide 'Superantigens Streptococcal pyrogenic exotoxin The primary initial event in endotoxic shock is release of cytokines irrespective of whether it is caused by gram positive or gram negative organism -The sequence of events leading to the production of primary cytokines is different in gram negative and grain positive bacterias but the result is the same i.e. both the gram (-ye) and gram (+ve) bacterias leads to production of same mediators of inflammation i.e. TNFa and IL-1. The sequence of events after the release of primary mediators of inflammation is same in both the types of bacteria. - Once the primary cytokines i.e. TNFa and IL-1 are released they activate endothelium and leucocytes to release secondary mediators. - The secondary mediators cause vasodilatation, vascular leak and endothelial damage. So two mechanisms are impoant in septic shock :- i) Release of primary mediators of inflammation TNFa and IL-1. ii) Activation and damage to endothelium Damage to endothelium leads to systemic inflammatory response which causes vasodilation and permeability leading to septic shock. But the initial primary event is the release of primary mediators of inflammation cytokines as a result of interaction between bacterial cell wall components and host cell. The endothelium is subsequently activated and damaged by these mediators (cytokines). Therefore cytokine release is the primary initiating factor in endotoxic shock.
Endothelial injury
Peripheral vasodilation
Increased vascular permeability
Cytokines action