Metabolic Response to Trauma/Critical Illness Flashcards
causes of hypermetabolic responses
sepsis, trauma, burns, major surgery, stress, fractures
neurohormones released as a response to stress
catecholamines, glucocorticoids, glucagon, ADH, aldosterone
inflammatory hormones released at site of injury
cytokines, eicosanoids
causes renal sodium retention
Aldosterone
stimulates renal tubular water absorption
antidiuretic hormone (ADH)
acts on adrenal cortex to release cortisol hence stimulating lipolysis, mobilizing amino acids from skeletal muscles, and stimulates gluconeogenesis
ACTH
from adrenal medulla and stimulate glycogenolysis, fat mobilization, gluconeogenesis
epinephrine and norepinephrine (Catecholamines)
types of cytokines
interleukins, tumor necrosis factor (TNF), and eicosanoids
local (paracrine) effects of cytokines
wound healing, angiogenesis, white cell migration, localize the wound
generalized effects of cytokines
mobilize AA and stimulate acute phase protein synthesis by liver
responsible for fever/ increase metabolic rate
eicosanoids
mediators of inflammation
PGE2 and PGF2alpha
phases following trauma
phase I: Ebb/unresuscitated phase
phase II: flow phase (adrenergic - corticoid)
phase III: recovery/convalescent/anabolic phase
why is there lactic acidosis in ebb phase and flow phase
impaired tissue oxygenation –> anaerobic glycolysis –> impaired blood flow –> impairment of cori cycle –> lactic acid build up
characteristics of ebb phase
most impo: low insulin, decreased metabolic rate
hypovolemia, shock, tissue hypoxia, lactic acidosis, insulin level drop, glucagon and epinephrine high, low body temp, decreased metabolic rate