Metabolic Response to Trauma/Critical Illness Flashcards

1
Q

causes of hypermetabolic responses

A

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

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2
Q

neurohormones released as a response to stress

A

catecholamines, glucocorticoids, glucagon, ADH, aldosterone

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3
Q

inflammatory hormones released at site of injury

A

cytokines, eicosanoids

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4
Q

causes renal sodium retention

A

Aldosterone

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5
Q

stimulates renal tubular water absorption

A

antidiuretic hormone (ADH)

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6
Q

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

A

ACTH

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7
Q

from adrenal medulla and stimulate glycogenolysis, fat mobilization, gluconeogenesis

A

epinephrine and norepinephrine (Catecholamines)

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8
Q

types of cytokines

A

interleukins, tumor necrosis factor (TNF), and eicosanoids

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9
Q

local (paracrine) effects of cytokines

A

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

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10
Q

generalized effects of cytokines

A

mobilize AA and stimulate acute phase protein synthesis by liver

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11
Q

responsible for fever/ increase metabolic rate

A

eicosanoids

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12
Q

mediators of inflammation

A

PGE2 and PGF2alpha

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13
Q

phases following trauma

A

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

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14
Q

why is there lactic acidosis in ebb phase and flow phase

A

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

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15
Q

characteristics of ebb phase

A

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

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16
Q

how long does ebb phase last

A

few hours

17
Q

most time is spent in what phase

A

flow phase

18
Q

characteristic of flow phase

A

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

19
Q

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

A

flow phase - extra energy is diverted towards the wound

20
Q

difference in metabolic rate in starvation and following injurty

A

metabolic rate is decreased in starvation and increased following injury

21
Q

major difference in ebb phase and flow phase

A

ebb phase has low insulin while flow phase has increased insulin

22
Q

signs of insulin resistance

A

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

23
Q

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

A

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

24
Q

state of insulin resistance

A

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

25
Q

blood glucose and insulin level in flow phase and prolonged starvation

A

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

glucose level and insulin level decreased in starvation

26
Q

energy for brain in flow phase vs. prolonged starvation

A

in flow phase - glucose

prolonged starvation - glucose and ketone bodies

27
Q

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

A

flow phase - low because of insulin resistance

prolonged starvation - low because of low insulin

28
Q

gluconeogenesis in flow phase vs. prolonged starvation

A

flow phase - high to maintain high glucose levels

prolonged starvation - high to maintain normal glucose levels

29
Q

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

A

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

30
Q

protein metabolism in flow phase

A

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

31
Q

how are AA used in proteolysis

A

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

32
Q

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

A

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

33
Q

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

A

positive nitrogen phase

34
Q

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

A

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

35
Q

treats poor wound healing following surgery or trauma

A

vitamin C, zinc, copper

36
Q

prereq for enteral nutrition

A

functional GI tract

37
Q

why is enteral nutritional support better than parenteral ?

A

decreases mortality and bacterial translocation

also decreases sepsis

38
Q

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

A

nah