endotoxic shock


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endotoxic shock

Septic shock due to release of endotoxins by gram-negative bacteria. Endotoxins are lipopolysaccharides in the cell walls that are released during both reproduction and destruction of the bacteria. They are potent stimulators of inflammation, activating macrophages, B lymphocytes, and cytokines and producing vasodilation, increased capillary permeability, and activation of the complement and coagulation cascades. See: endotoxin; septic shock
See also: shock

endotoxic

pertaining to or possessing endotoxin.

endotoxic shock
see toxemic shock.

shock

a condition of acute peripheral circulatory failure due to derangement of circulatory control or loss of circulating fluid. It is marked by hypotension, coldness of the skin and tachycardia.

allergic shock
see anaphylactic shock.
shock bodies
hyaline globules composed of fibrin degradation products which act as microthrombi and cause hemorrhage and necrosis.
burn shock
the loss and redistribution of fluid, electrolytes and plasma protein, increased blood viscosity and increased peripheral resistance that follow a severe burn contribute to shock.
cardiogenic shock
classically associated with acute myocardial infarction in humans; in animals may be caused by intrinsic congestive heart failure, cardiac depression caused by anesthetic overdosage or other drugs with negative inotropism, rarely, thromboembolism.
colloidoclastic shock
shock due to breakdown of the physical equilibrium of the body colloids. Thought to cause anaphylactic shock due to the absorption of the colloids into the bloodstream.
distributive shock
see vasogenic shock (below).
electric shock
see electrical injuries.
electroplectic shock
electric shock. See also electrical stunning.
endotoxic shock
caused by endotoxins, especially Escherichia coli. See also toxemic shock.
shock gut
animals in shock develop changes in the gut including congestion and hemorrhage into the lumen.
hypovolemic shock
shock due to reduced blood volume as a result of water deprivation, fluid loss due to diarrhea, vomiting, extensive burns, intestinal obstruction, whole blood loss.
insulin shock
a condition of circulatory insufficiency resulting from overdosage with insulin, which causes too sudden reduction of blood sugar. It is marked by tremor, weakness, convulsions and collapse.
irreversible shock
shock which has reached the stage where irreparable damage has been done to tissues, e.g. liver, kidneys and treatment will not salvage the patient although it might prolong life for a long time.
shock lung
animals in shock due to massive burns, septicemia, disseminated intravascular coagulation (DIC), acute viral or bacterial pneumonias or trauma develop an acute respiratory distress syndrome. The pulmonary lesion is a nonspecific acute or subacute interstitial pneumonia.
nervous shock
a temporary cessation of function in nervous tissue caused by an acute insult such as trauma without the part having been directly or detectably damaged. The loss of function is only temporary, usually for a few minutes but it may last for several hours. There may be residual signs due to direct damage when the shock passes. Stunning by a lightning stroke is an example.
shock organs
those organs, specific to each animal species, which respond to allergens circulating in the blood.
septic shock
see toxemic shock.
spinal shock
flaccid paralysis up and down the body from the site of the spinal cord lesion. Accompanied by a fall in skin temperature, vasodilatation and sweating. Signs disappear within an hour or two. There may be residual signs due to physical injury to tissue.
toxic shock
see toxemic shock.
vasogenic shock, vasculogenic shock
shock exists because of the severe reduction in effective circulating blood volume caused by sequestration of blood and other fluids in the vascular system and their withdrawal from the circulating blood. Is the classical shock of traumatic injury, burns, uterine prolapse, extensive surgery.
References in periodicals archive ?
Continuous venovenous hemofiltration improves cardiac performance by mechanisms other than tumor necrosis factor-alpha attenuation during endotoxic shock.
Oxidative stress and the glucocorticoid receptor (GR) expression decreasing have also been shown to play important roles in the occurrence of tissue injuries in endotoxic shock (Ho et al.
Silencing of caspase-8 and caspase-3 by RNA interference prevents vascular endothelial cell injury in mice with endotoxic shock.
The research team investigated the role of H2S in endotoxic shock, which causes a fatal loss of blood pressure and extensive tissue inflammation.