Metabolic response to injury and infection Flashcards

1
Q

Explain what happens to energy metabolism in burns (being burnt):

A
  • EE is raised quite dramatically
  • increased utilisation and oxidation of fatty acids
  • increase in REE/oxygen usage
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2
Q

What drives hypermetabolism and hypercatabolism?

A
hormonal activation (heightened catabolic hormones and cytokines)
- catecholamines
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3
Q

What happens as a result of hypermetabolism and hypercatabolism?

A
  • lypolysis
  • glycogenolysis
  • cortisol and inflammatory - - cytokines cause muscle protein breakdown
  • raised gluconeogenesis
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4
Q

What happens as a consequence of anabolic resistance?

A
  • during stress response, androgens and other anabolic mediators are suppressed (reduction in LH production)
  • insulin resistance (a major anabolic hormone)
  • GH raised, but IGF-1 from liver is reduced
  • binding proteins are altered
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5
Q

What is the purpose of a stress response?

A

Reprioritisation of activities towards immune activity/function and hepatic synthesis of acute phase proteins, APPs (and gluconeogenesis)

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6
Q

What is the inflammatory cytokines role in the stress response?

A

orchestrates the response

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7
Q

What happens as a result of inflammatory cytokines orchestrating stress response?

A
  • Reduced muscle protein synthesis
  • increased breakdown
  • net release of amino acids
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8
Q

What are one of the side effects of illness/injury?

A

muscle wasting

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9
Q

What are the effects of protein metabolism in combination with bed rest/reduced physical activity/anorexia?

A
  • loss of lean tissue from muscles (depends on severity/duration)
  • increases morbidity and mortality
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10
Q

What is common in sepsis?

A

mitochondrial dysfunction

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11
Q

What happens as a result of mitochondrial dysfunction in sepsis?

A
  • lead to organ failure

- associated with risk of death

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12
Q

What are the effects of systemic inflammation in sepsis?

A
  • heightened inflammatory cytokine release
  • ROS production
  • Catabolic hormone mediators
  • impaired perfusion early in shock, reduced O2
  • ROS effects on complex activity in mitochondria
  • Effects on gene transcription of mito. biogenesis markers
  • Low T3
  • Damaged mito. undergo mitophagy
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13
Q

What are some examples of ROS?

A
  • Nitric oxide
  • Hydrogen sulphide
  • carbon monoxide
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14
Q

What are some examples of mitochondria biogenesis markers?

A
  • PGC-1a

- NRFs

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15
Q

What is T3’s role on mitochondria?

A

Has potent effect on mito. function and biogenesis

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16
Q

What are some therapeutic nutrients for treatment of injury, illness related metabolic problems?

A
  • glutamine
  • lipid (N-3, N-6)
  • anti-oxidants (NAC, vit. C)
  • amino acids
  • fish oils
17
Q

What are the effects from lipid treatment?

A
  • changes in membrane phospholipids

- changes in cytokine and lipid-derived mediator production

18
Q

What are the effects from antioxidant treatment?

A
  • suppression of oxidant effects, NFkB effects

- altered cytokine production

19
Q

What are the effects from “protein and amino acid deficiency” treatment?

A
  • influence on acute-phase proteins and endogenous antioxidants
  • altered cytokine production