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
how long does ebb phase last
few hours
most time is spent in what phase
flow phase
characteristic of flow phase
everything is increased - increased cardiac output, body temp, energy expenditure, insulin, glucagon, cortisol, catecholamines, inflammatory cytokines
what phase - increased glucose production hence hyperglycemia, protein catabolism, free FA, increased lipolysis
flow phase - extra energy is diverted towards the wound
difference in metabolic rate in starvation and following injurty
metabolic rate is decreased in starvation and increased following injury
major difference in ebb phase and flow phase
ebb phase has low insulin while flow phase has increased insulin
signs of insulin resistance
increased hepatic gluconeogenesis and decreased uptake of glucose by adipose tissue and muscle (GLUT 4 less active)
what happens to type I diabetic patients already on insulin following an injury/infection
they experience ketoacidosis because they are not responding to normal doses of insulin because of insulin resistance so insulin does must be increased!
state of insulin resistance
greater than 200 units/day of insulin, increased cytokines, cortisol, epinephrine
blood glucose and insulin level in flow phase and prolonged starvation
glucose and insulin level increased due to insulin resistance in flow phase
glucose level and insulin level decreased in starvation
energy for brain in flow phase vs. prolonged starvation
in flow phase - glucose
prolonged starvation - glucose and ketone bodies
glucose uptake by adipose tissue and muscle in flow phase vs. prolonged starvation
flow phase - low because of insulin resistance
prolonged starvation - low because of low insulin
gluconeogenesis in flow phase vs. prolonged starvation
flow phase - high to maintain high glucose levels
prolonged starvation - high to maintain normal glucose levels
why is there lower levels of ketone bodies in trauma/injury despite TAGs being broken down
maybe high levels of insulin or because of high metabolic rate peripheral tissues are utilizing them
protein metabolism in flow phase
increased proteolysis, increased ubiquitin-proteasome action, reduced synthesis of protein, increased urea nitrogen excretion (hence neg N balance)
how are AA used in proteolysis
to maintain immune system, gluconeogenesis, acute phase protein synthesis in liver
what can be used to monitor patient in the ICU to see if their condition is worsening or getting better
the level of C-reactive protein (getting lower = getting better)
nitrogen balance when patient is out of flow phase and into anabolic/recovery phase
positive nitrogen phase
what can result if patient depletes too much protein in flow phase
impaired wound healing, decreased immune response, hypermetabolism, breakdown of gut mucosal barrier, decreased respiratory effort
treats poor wound healing following surgery or trauma
vitamin C, zinc, copper
prereq for enteral nutrition
functional GI tract
why is enteral nutritional support better than parenteral ?
decreases mortality and bacterial translocation
also decreases sepsis
in critical injury, does ketone bodies correspond to increase in free FA
nah
