Metabolic Response to Trauma/Critical Illness

Question 1

causes of hypermetabolic responses

Answer 1

sepsis, trauma, burns, major surgery, stress, fractures

Question 2

neurohormones released as a response to stress

Answer 2

catecholamines, glucocorticoids, glucagon, ADH, aldosterone

Question 3

inflammatory hormones released at site of injury

Answer 3

cytokines, eicosanoids

Question 4

causes renal sodium retention

Answer 4

Aldosterone

Question 5

stimulates renal tubular water absorption

Answer 5

antidiuretic hormone (ADH)

Question 6

acts on adrenal cortex to release cortisol hence stimulating lipolysis, mobilizing amino acids from skeletal muscles, and stimulates gluconeogenesis

Answer 6

ACTH

Question 7

from adrenal medulla and stimulate glycogenolysis, fat mobilization, gluconeogenesis

Answer 7

epinephrine and norepinephrine (Catecholamines)

Question 8

types of cytokines

Answer 8

interleukins, tumor necrosis factor (TNF), and eicosanoids

Question 9

local (paracrine) effects of cytokines

Answer 9

wound healing, angiogenesis, white cell migration, localize the wound

Question 10

generalized effects of cytokines

Answer 10

mobilize AA and stimulate acute phase protein synthesis by liver

Question 11

responsible for fever/ increase metabolic rate

Answer 11

eicosanoids

Question 12

mediators of inflammation

Answer 12

PGE2 and PGF2alpha

Question 13

phases following trauma

Answer 13

phase I: Ebb/unresuscitated phase
phase II: flow phase (adrenergic - corticoid)
phase III: recovery/convalescent/anabolic phase

Question 14

why is there lactic acidosis in ebb phase and flow phase

Answer 14

impaired tissue oxygenation –> anaerobic glycolysis –> impaired blood flow –> impairment of cori cycle –> lactic acid build up

Question 15

characteristics of ebb phase

Answer 15

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

Question 16

how long does ebb phase last

Answer 16

few hours

Question 17

most time is spent in what phase

Answer 17

flow phase

Question 18

characteristic of flow phase

Answer 18

everything is increased - increased cardiac output, body temp, energy expenditure, insulin, glucagon, cortisol, catecholamines, inflammatory cytokines

Question 19

what phase - increased glucose production hence hyperglycemia, protein catabolism, free FA, increased lipolysis

Answer 19

flow phase - extra energy is diverted towards the wound

Question 20

difference in metabolic rate in starvation and following injurty

Answer 20

metabolic rate is decreased in starvation and increased following injury

Question 21

major difference in ebb phase and flow phase

Answer 21

ebb phase has low insulin while flow phase has increased insulin

Question 22

signs of insulin resistance

Answer 22

increased hepatic gluconeogenesis and decreased uptake of glucose by adipose tissue and muscle (GLUT 4 less active)

Question 23

what happens to type I diabetic patients already on insulin following an injury/infection

Answer 23

they experience ketoacidosis because they are not responding to normal doses of insulin because of insulin resistance so insulin does must be increased!

Question 24

state of insulin resistance

Answer 24

greater than 200 units/day of insulin, increased cytokines, cortisol, epinephrine

Question 25

blood glucose and insulin level in flow phase and prolonged starvation

Answer 25

glucose and insulin level increased due to insulin resistance in flow phase glucose level and insulin level decreased in starvation

Question 26

energy for brain in flow phase vs. prolonged starvation

Answer 26

in flow phase - glucose | prolonged starvation - glucose and ketone bodies

Question 27

glucose uptake by adipose tissue and muscle in flow phase vs. prolonged starvation

Answer 27

flow phase - low because of insulin resistance prolonged starvation - low because of low insulin

Question 28

gluconeogenesis in flow phase vs. prolonged starvation

Answer 28

flow phase - high to maintain high glucose levels prolonged starvation - high to maintain normal glucose levels

Question 29

why is there lower levels of ketone bodies in trauma/injury despite TAGs being broken down

Answer 29

maybe high levels of insulin or because of high metabolic rate peripheral tissues are utilizing them

Question 30

protein metabolism in flow phase

Answer 30

increased proteolysis, increased ubiquitin-proteasome action, reduced synthesis of protein, increased urea nitrogen excretion (hence neg N balance)

Question 31

how are AA used in proteolysis

Answer 31

to maintain immune system, gluconeogenesis, acute phase protein synthesis in liver

Question 32

what can be used to monitor patient in the ICU to see if their condition is worsening or getting better

Answer 32

the level of C-reactive protein (getting lower = getting better)

Question 33

nitrogen balance when patient is out of flow phase and into anabolic/recovery phase

Answer 33

positive nitrogen phase

Question 34

what can result if patient depletes too much protein in flow phase

Answer 34

impaired wound healing, decreased immune response, hypermetabolism, breakdown of gut mucosal barrier, decreased respiratory effort

Question 35

treats poor wound healing following surgery or trauma

Answer 35

vitamin C, zinc, copper

Question 36

prereq for enteral nutrition

Answer 36

functional GI tract

Question 37

why is enteral nutritional support better than parenteral ?

Answer 37

decreases mortality and bacterial translocation also decreases sepsis

Question 38

in critical injury, does ketone bodies correspond to increase in free FA

Answer 38

nah