Nutrition and Intensive Care Flashcards

1
Q

explain the role of cytokines

A
  • cytokines: interleukins, tumor necrosis factor (TNF), eicosanoids (PGE2) are released by phagocytes in response to tissue damage, infxn, inflammation
    • have a local (paracrine) effect as well as systemic
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2
Q

describe local effects of cytokines

A
  • promote wound healing by ingrowth of fibroblasts
  • stimulate angiogenesis
  • increase white cell counts and facilitate white cell migration
  • localize the wound
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3
Q

describe system effects of cytokines

A
  • mobilization of amino acids, stimulation of acute phase protein synthesis by liver
  • fever (increase metabolic rate)
  • pain
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4
Q

name the most important mediator of inflammation

A

phospholipid -> arachidonic acid -> PGE2 (prostaglandin)

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5
Q

contrast the ebb phase and the flow phase

A
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6
Q

describe the ebb phase

A
  • immediate response following an injury: hypovolemia, shock, tissue hypoxia
  • decreased cardiac output
  • decreased O2 consumption (decreased metabolic rate)
  • lowered body temp.
  • insulin levels drop and glucagon and epi. are elevated
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7
Q

describe the changes in carbohydrate metabolism during the ebb phase

A
  • elevated blood glucose level (hyperglycemia is proportional to the severity of the injury/stress)
    • hyperglycemia is due to the presence of epi and glucocorticoids that stimulates liver glycogenolysis and gluconeogenesis
  • low insulin levels w/ slightly increased glucose production
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8
Q

describe the flow phase (aka adrenergic/cortisol)

A
  • typically lasts up to 2 weeks following initial injury
  • increased cardiac output begins
  • increased body temp. (fever)
  • increased energy expenditure (increased metabolic rate - hypermetabolic state)
  • increase in circulating catecholamines, glucagon, cortisol, inflammatory cytokines
    • increase in the counter regulatory hormones results in insulin resistance
  • insulin secretion is elevated
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9
Q

describe metabolism during the flow phase (aka adrenergic/corticoid)

A
  • increase in glucose production and hyperglycemia
  • total body protein catabolism begins
  • increase in circulating free FAs due to increased adipose tissue lipolysis
  • mobilization of energy stores to facilitate wound healing
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10
Q

describe the metabolic rate following critical illness

A

the metabolic rate (REE) is proportional to the severity of the illness

in prolonged starvation, there is an adaptive decrease in metabolic rate (adaptation to increase survival)

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11
Q

describe the caloric requirements for an adult during the flow phase

A
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12
Q

describe the glucose levels and insulin levels during the flow phase

A
  • hyperglycemia
  • increased insulin levels, but there is insulin resistance caused by the increased counter-regulatory hormones (epi and glucocorticoids)
    • increased hepatic gluconeogenesis from amino acids derived from muscle proteolysis (due to epi and glucocorticoids)
    • reduced uptake of glucose by muscle and adipose tissue (GLUT-4 is less active due to insulin resistance)
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13
Q

describe lactic acidosis in critically injured patients

A
  • impaired tissue oxygenation resulting in anaerobic glycolysis (if associated with a low blood flow)
  • impaired blood flow also results in impairment of the Cori cycle (glucose-lactate cycle)
  • lactic acidosis indicates poor prognosis
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14
Q

describe carb metabolism in diabetic patients during the flow phase

A
  • regulation of blood glucose level in diabetics important during hypermetabolic state but difficult to achieve due to additional insulin resistance
    • many pts with T2D present with hyperosmolar hyperglycemia state
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15
Q

contrast carb metabolism during the flow phase of critical illness and prolonged starvation

A
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16
Q

describe ketogenesis during the flow phase

A
  • ketosis is not observed in patients with trauma
    • may be due to high levels of insulin; insulin inhibits ketogenesis
    • peripheral tissues are rapidly using ketone bodies (due to higher metabolic rate)
    • ketogenesis is inversely proportional to severity of injury
17
Q

contrast lipid metabolism in flow phase vs prolonged starvation

A
18
Q

describe protein catabolism during the flow phase

A
  • protein catabolism is proportional to the severity of the illness
  • in prolonged starvation there is an adaptive decrease in protein catabolism
    • protein sparing adaptation to increase survival
  • both critical illness and starvation are states of negative nitrogen balance, but protein depletion is more severe in critical illness
19
Q

describe the mechanism of protein metabolism and excretion during the flow phase

A
  • the ubiquitin-proteasome system for proteolysis in skeletal muscle cells is activated by stress/illness
  • there is reduced protein synthesis and amino acid uptake by muscle
  • muscle proteolysis releases aminos acids into circulation
  • amino acid catabolism in liver forms ammonia which is converted to urea
  • urine urea nitrogen (UNN) excretion in grams/day may be used to evaluate degree of muscle proteolysis
20
Q

there is a ____ nitrogen balance in patients during the flow phase

A

there is a negative nitrogen balance in patients during the flow phase

  • intake of nitrogen <<<< output of nitrogen
  • patients lose significant amounts of body tissue/muscle protein following illness
21
Q

what is the purpose of increased muscle protein catabolism?

A
  • skeletal muscle is the major source of nitrogen (amino acids) following extensive injury
    • glutamine and alanine: majority of the released amino acids
    • amino acids are used for hepatic gluconeogenesis (C-skeleton) and the amino group is used for the formation of urea
    • amino acids are also used for maintenance of the immune system (synthesis of immunoglobulins)
    • amino acids are used for acute-phase protein synthesis by the liver
22
Q

describe acute phase response by the liver

A
  • cytokines released during inflammatory process stimulate the liver to synthesize a group of proteins called acute phase proteins
    • synthesized in increased amount during inflammation; not specific for the inflammatory response
    • includes C-reactive protein, a1-antitrypsin, ceruloplasmin, haptoglobin
23
Q

describe how serum C-reactive protein correlates with prognosis

A
  • the degree of rise of the acute phase proteins is proportional to the severity of injury
  • normalization of CRP levels indicate good response to therapy and good prognosis
24
Q

contrast protein metabolism during the flow phase vs prolonged starvation

A
25
Q

describe immune modulating nutrients

A
  • includes supplemental glutamine, arginine and branched chain amino acids for enhancement of immune function
    • glutamine is used for nucleotide synthesis in rapidly diving cells (like lymphocytes)
  • inclusion of antioxidants
  • omega-3 fatty acids modulate immune response
26
Q

name vitamins and minerals given during nutritional support

A
  • vitamin C
    • facilitates wound healing (prolyl hydroxylase)
  • thiamine, niacin
    • due to increased hypermetabolism
  • zinc
    • maintain immune function and improve appetite
  • copper
    • cofactor for lysyl oxidase that is required to form crosslinks in collagen and improves wound healing
27
Q

contrast ketone body synthesis in T1D vs T2D in the flow phase

A
  • T1D = high ketone bodies
  • T2D = not high ketone bodies but hyperosmolarity is seen
28
Q

describe the anabolic phase of recovery

A
  • in the anabolic/recovery phase, there is positive nitrogen balance and build-up of tissue proteins
    • important to increase protein intake to allow for anabolism
  • rebuilding of adipose tissue stores during this phase
  • normalization of plasma glucose levels, insulin levels and tissues are sensitive to insulin