Shock

Explanation :
Causes of distributive shock -
Septic shock
Anaphylaxis 
Spinal cord injury

Anesthetic accident produces neurogenic shock

Explanation: LPS &teichoic acid are septic shock inducer.

Explanation -
In the early nonprogressive phase of shock, various neurohumoral mechanisms help maintain cardiac output and blood pressure. These mechanisms include baroreceptor reflexes, release of catecholamines and antidiuretic hormone, activation of the renin-angiotensin-aldosterone axis, and generalized sympathetic stimulation. The net effect is tachycardia, peripheral vasoconstriction, and renal fluid conservation; cutaneous vasoconstriction causes the characteristic “shocky” skin coolness and pallor (notably, septic shock can initially cause cutaneous vasodilation, so the patient may present with warm, flushed skin). Coronary and cerebral vessels are less sensitive to sympathetic signals and maintain relatively normal caliber, blood flow, and oxygen delivery. Thus, blood is shunted away from the skin to the vital organs such as the heart and the brain.

In case of Distributive shock there is peripheral vasodilation & pooling of blood in periphery.

Explanation :
In progressive phase of shock -
Persistent oxygen deficit leads to intracellular aerobic respiration is replaced by anaerobic glycolysis with excessive production of lactic acid. The resultant metabolic lactic acidosis lowers the tissue pH, which blunts the vasomotor response; arterioles dilate, and blood begins to pool in the microcirculation.
Peripheral pooling not only worsens the cardiac output but also puts endothelial cells at risk for the development of anoxic injury with subsequent DIC.
With widespread tissue hypoxia, vital organs are affected and begin to fail.