In hemorrhage, larger arterioles vasoconstrict in response to the sympathetic nervous system. Which categories of shock are associated with vasodilation oflarger arterioles?
The microvascular circulation plays an integral role in regulating cellular perfusion and is significantly influenced in response to shock. The microvascular bed is innervated by the sympathetic nervous system and has a profound effect on the larger arterioles. Following hemorrhage, larger arterioles vasoconstrict; however, in the setting of sepsis or neurogenic shock, these vessels vasodilate. Additionally, a host of other vasoactive proteins, including vasopressin, angiotensin II, and endothelin-1, also lead to vasoconstriction to limit organ perfusion to organs such as skin, skeletal muscle, kidneys, and the gastrointestinal (GI) tract to preserve perfusion of the myocardium and central nervous system (CNS).
Which of the following is true about antidiuretic hormone (ADH) production in injured patients?
The pituitary also releases vasopressin or antidiuretic hormone (ADH) in response to hypovolemia, changes in circulating blood volume sensed by baroreceptors and left atrial stretch receptors, and increased plasma osmolality detected by hypothalamic osmoreceptors. Epinephrine, angiotensin II, pain, and hyperglycemia increase production of ADH. ADH levels remain elevated for about 1 week after the initial insult, depending on the severity and persistence of the hemodynamic abnormalities. ADH acts on the distal tubule and collecting duct of the nephron to increase water permeability, decrease water and sodium losses, and preserve intravascular volume. Also known as arginine vasopressin, ADH acts as a potent mesenteric vasoconstrictor, shunting circulating blood away from the splanchnic organs during hypovolemia. This may contribute to intestinal ischemia and predispose to intestinal mucosal barrier dysfunction in shock states. Vasopressin also increases hepatic gluconeogenesis and increases hepatic glycolysis.
Which of following occur as a result of epinephrine and norepinephrine?
Epinephrine and norepinephrine have a profound impact on cellular metabolism. Hepatic glycogenolysis, gluconeogenesis, ketogenesis, skeletal muscle protein breakdown, and adipose tissue lipolysis are increased by catecholamines. Cortisol, glucagon, and ADH also contribute to the catabolism during shock. Epinephrine induces further release of glucagon, while inhibiting the pancreatic P-cell release of insulin. The result is a catabolic state with glucose mobilization, hyperglycemia, protein breakdown, negative nitrogen balance, lipolysis, and insulin resistance during shock and injury. The relative underuse of glucose by peripheral tissues preserves it for the glucose-dependent organs such as the heart and brain.
A patient has a blood pressure of 70/50 mm Hg and a serum lactate level of 30 mg/100 mL (normal: 6-16). His cardiac output is 1.9 L/min, and his central venous pressure is 2 em H2O. The most likely diagnosis is:
The findings given in the question are characteristic of hypovolemic shock, which can be defined as inadequate tissue perfusion secondary to an extracellular fluid loss. The high lactate level is a result of anaerobic metabolism due to decreased blood flow to tissues. The hemodynamic measurements indicate both low blood flow and low venous return. The total combination is most consistent with a diagnosis of hypovolemic shock. Pulmonary embolus, congestive heart failure, and cardiac tamponade are all associated with a high central venous pressure. Septic shock, particularly in its early phases, is usually hyperdynamic, and affected patients have a greater-than-normal cardiac output. Complete hemodynamic monitoring is vital in hypovolemic shock so that prompt diagnosis and rational therapy can be expeditiously carried out.
Which cytokine is anti-inflammatory and increases after shock and trauma?
Interleukin (IL)-10 is considered an anti-inflammatory cytokine that may have immunosuppressive properties. Its production is increased after shock and trauma, and it has been associated with depressed immune function clinically, as well as an increased susceptibility to infection. IL-10 is secreted by T cells, monocytes, and macrophages, and inhibits proinflammatory cytokine secretion, 02 radical production by phagocytes, adhesion molecule expression, and lymphocyte activation. Administration of IL-10 depresses cytokine production and improves some aspects of immune function in experimental models of shock and sepsis.
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