MNT for Metabolic Stress, Sepsis, Trauma, Burns, and Surgery Flashcards
Metabolic Stress
- Sepsis
- Trauma
- Surgery: systemic response is activated, physiologic and metabolic changes follow and may lead to shock and/or other negative outcomes
Metabolic Response to Stress
Involves most metabolic pathways. Rapid loss of LBM results in:
- negative nitrogen balance
- muscle wasting
Ebb Phase
- Immediate- hypovolemia, shock, tissue hypoxia
- Decreased cardiac output
- Decreased oxygen consumption
- Lowered body temperature
- Insulin levels drop because glucagon is elevated
Flow Phase
- Follows fluid resuscitation and O2 transport
- Increased cardiac output begins
- Increased body temperature
- Increased energy expenditure
- Total body protein catabolism begins
- Marked increase in glucose productions, FFAs, circulating insulin, glucagon, and cortisol
Hormonal and Cell-Mediated Response
There is a marked increase in glucose production and uptake secondary to gluconeogenesis, and:
- elevated hormonal levels
- marked increase in hepatic amino acid uptake
- protein synthesis
- accelerated muscle breakdown
Starvation vs Stress
Metabolic response to stress differs from the responses to starvation.
Starvation
Decreased energy expenditure, use of alternative fuels, decreased protein wasting, stored glycogen used in 24 hours.
Late Starvation
Fatty acids, ketones, and glycerol provide energy for all tissues except brain, nervous system, and RBCs.
Hormonal Stress Response
- Aldosterone
- Antidiuretic Hormone (ADH)
- ACTH
- Catecholamines
Aldosterone
Corticosteroid that causes renal sodium retention.
Antidiuretic Hormone (ADH)
Stimulates renal tubular water absorption. These conserve water and salt to support circulating blood volume.
ACTH
Acts on adrenal cortex to release cortisol (mobilizes amino acids from skeletal muscles).
Catecholamines
Epinephrine and norepinephrine from renal medulla to stimulate hepatic glycogenolysis, fat mobilization, and gluconeogenesis.
Cytokines
-Interleukin 1
-Interleukin 6
-Tumor necrosis factor (TNF)
Released by phagocytes in response to tissue damage, infection inflammation, and some drugs and chemicals.
Interleukin 1
Metabolic effect that increases body temperature.