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Yr 2 - Clinical Pathology > Nutritional Support in Trauma > Flashcards

Nutritional Support in Trauma Flashcards

1
Q

Definition of trauma?

A

An injury or wound to living tissue caused by an extrinsic agent.

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2
Q

Immediate potential causes of mortality following physical trauma?

A
  • Intravascular fluid loss
  • Extravascular volume increase
  • Tissue destruction
  • Obstructed/Impaired breathing
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3
Q

Later potential causes of mortality following physical trauma?

A
  • Starvation
  • Infection
  • Inflammation
  • Psychological
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4
Q

What year was penicillin discovered?

A

1928

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5
Q

Major causes of mortality following trauma;

A
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6
Q

Clinical Case:

Joe suffered multiple fractures and severe internal injuries in a motorcycle accident.

  • As he could not eat or drink he was given iv fluids (3L 5% dextrose / day)
  • He lost weight rapidly and died 15 days later
  • The death certificate cited “Pneumonia” as the cause of death

What happened to Joe’s energy metabolism? What was the cause of death?

A
  • Haemorrhage
  • Brain injury
  • Muscle wasting –> respiratory –> pneumonia
  • Infection
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7
Q

Phases of trauma;

  • Phase 1 –> clinical shock
  • Phase 2 –> hypercatabolic state
  • Phase 3 –> recovery (anabolic state)
A
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8
Q

What is a hypercatabolic state?

A

A biochemical state characterised by;

  1. increased circulating catabolic hormones (eg, cortisol, catecholamines)
  2. Increased inflammatory cytokines (eg, tumor necrosis factors, interleukin-1beta)
  3. Decreased anabolic insulin effects** with consequent **insulin resistance
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9
Q

During phase 1 (clinical shock) describe the;

  1. Circulating volume
  2. RBCs
  3. WBCs
  4. Cardiac output
  5. Organ perfusion
  6. Energy substrate delivery
A

ALL DECREASED –> can lead to major organ dysfunction AND infection barrier penetration leading to sepsis

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10
Q

Signs and symptoms of shock?

A
  • Tachycardia
  • Tachypnoea
  • Peripheral vasoconstriction (cold, pale): selective peripheral shut-down to preserve vital organs
  • Hypovolaemia
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11
Q

What can a decrease in RBCs in shock lead to?

A
  • Cellular hypoxia
  • Anaerobic metabolism
  • Lactate accumulation
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12
Q

What are your primary aims in phase 1 (clinical shock)?

A
  1. Stop haemorrhage
  2. Prevent infection
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13
Q

Why are patients in shock following trauma susceptible to infection?

A
  1. Decreased WBCs
  2. Infection barrier penetration from trauma
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14
Q

There is an increased secretion of catecholamines in phase 2 (catabolic state). What is the purpose of this?

A

Body is in catabolic state –> trying to release energy!

  1. Catecholamines activate glucagon secretion
  2. There is also activated ACTH secretion which increases cortisol secretion

These both have insulin resistant effects.

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15
Q

How does this increase in catecholamines/cortisol/glucagon increase glucose levels?

A
  • Increased oxygen consumption
  • Increased metabolic rate
  • Increased negative nitrogen balance
  • Increase glycolysis –> glucose
  • Increased lipolysis –> free fatty acids
  • Increased proteolysis –> amino acids
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16
Q

What triggers this catabolic state?

A
  • Stress/pain (adrenaline)
  • Inflammatory cascade activated
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17
Q

What are your primary aims in phase 2 (catabolic)?

A
  • Avoid sepsis
  • Provide adequate nutrition
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18
Q

When does the anabolic state/recovery state occur?

A
  • Occurs approx 3-8 days after uncomplicated surgery
  • May not occur for several weeks after severe trauma and sepsis
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19
Q

What does the anabolic state typically coincide with?

A

Beginning of diuresis and request for oral intake

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20
Q

The anabolic state invovles the gradual restoration of what?

A
  • body protein synthesis
  • Normal nitrogen balance
  • Fat stores
  • Muscle strength
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21
Q

What is there a risk of during the anabolic state?

A

Refeeding syndrome risk

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22
Q

What is the obesity paradox during the anabolic state?

A

Those who are a little overweight tend to recover better

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23
Q

Describe the inflammatory response at a trauma site

A
  1. Bacteria and pathogens enter wound
  2. Platelets release clotting factors
  3. Mast cells secrete factors that mediate vasodilation to increase blood delivery to the injured area
  4. Neutrophils + macrophages recruited to phagocytose pathogens
  5. Macrophages secrete cytokines to attract immune cells + proliferate the inflammatory response
  6. Inflammatory response continues until wound is healed
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24
Q

What are the major proinflammatory cytokines?

A

IL-1, TNF-a

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25
Q

What is IL-1 and TNF-a produced mainly by?

A

Activated macrophages

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26
Q

Effect of IL-1 and TNF-a on;

a) catabolic hormones
b) anabolic hormones
c) appetite
d) acute phase proteins

A

a) increases catabolic hormomones (ACTH –> cortisol, catecholamines –> glucagon)
b) decreases anabolic hormones (GH, insulin)
c) decreased appetite
d) increased acute phase proteins

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27
Q

what are the catabolic hormones?

A

Adrenaline, cortisol, and glucagon are catabolic hormones

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28
Q

What is the catabolic state?

A

A breakdown state where stored nutrients are put to use;

  • Glycogen [via Adrenaline (muscle) / Glucagon (liver)] –> glucose
  • Fat –> free fatty acids
  • Protein –> amino acids
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29
Q

Catabolism is necessary for survival but if persists / is severe can cause mortality. How?

A

Decreased appetite and increased inflammation

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30
Q

What are the 3 phases of the catabolic response to trauma?

A
  1. Phase 1. Glycogenolysis (24 hours max)
  2. Phase 2. Gluconeogenesis
  3. Phase 3. Lipolysis + Ketogenesis
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31
Q

What is occurring during the glycogenolsysis phase of the catabolic response?

A
  • Glucagon triggers glycogen –> glucose
  • Adrenaline triggers glycogen –> glucose
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32
Q

What drives the breakdown of glycogen in muscle?

A

Adrenaline

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33
Q

What drives the breakdown of glycogen in liver?

A

Glucagon

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34
Q

Can adrenaline directly stimulate glycogen breakdown?

A

Yes; markedly stimulates glycogen breakdown in muscle and, to a lesser extent, in the liver.

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35
Q

What occurs during the gluconeogenesis phase of catabolism?

A

Run out of glycogen, body switches to breaking down protein (skeletal musle and secreted protein breakdown)

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36
Q

Is the gluconeogenesis phase of catabolism effective?

A

Not really;

  • 1Kg muscle = 200g protein = 120g glucose
  • Amino-acids → Glucose + Lactate production (lactate poisonous if builds up)
  • Nitrogen loss ~ 60-70 g/day but may be up to 300 g (body enters negative nitrogen balance)
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37
Q

What occurs during phase 3 (lipolysis and ketogenesis) of catabolism?

A
  1. Lipids broken down –> free fatty acids
  2. FFAs metabolised –> acetyl CoA
  3. Acetyl CoA causes release of –> acetoacetate and hydroxybutyrate (ketones that can be used energy substrate)
38
Q

Glucose pathway;

A
39
Q

Catabolic response to trauma - Glycogenolysis;

A
40
Q

In health, glycogen stores can maintain [Glucose] for how long?

A

Up to 24 hours

41
Q

Does the brain have a glycogen store?

A

No

42
Q

What are the O2 and glucose requirements of the brain?

A
  • Requirement of 120g / day
  • WILL NOT SURVIVE MORE THAN 2 MINUTES OF CIRCULATORY FAILURE
  • Adapts to using ketones as an energy substrate (when glucose runs out)
43
Q

Are the kidneys and liver capable of gluconeogenesis?

A

Yes - can survive hours of interruption of blood supply

44
Q

Different tissues use different substrates to make glucose.

a) what can the liver/kidney use?
b) what can skeletal muscle use?

A

a) fatty acids / amino acids
b) glycogen stores / fatty acids

45
Q

Catabolic response to trauma - Lipolysis

A
46
Q

Catabolic response to trauma - Proteolysis

A
47
Q

Describe the protein turnover during catabolic state

A
  1. Amount of new protein synthesised reduces and profile of proteins synthesised changes
  2. Skeletal muscle proteolysis increases
48
Q

What is the purpose of skeletal muscle proteolysis increasing following trauma?

A

Amino acids transported to liver for gluconeogenesis + protein synthesis.

49
Q

How are albumin levels affected during protein turnover in trauma?

A

Decreased albumin

50
Q

How are inflammatory modulators and scavengers (CRP, haptoglobin, clotting factors, modulators of clotting e.g. protease inhibitors) affected during protein turnover in trauma?

A

Increased

51
Q

What is the primary stimulation for protein breakdown in trauma/sepsis?

A

Cytokine secretion from activated macrophages

52
Q

How can prolonged proteolysis dring trauma be life threatening?

A

Further proteolysis results in life-threatening damage to essential structural and secreted protein;

  • Stuctural; Respiratory muscle weakness results in poor cough, retention of secretions –> pneumonia
53
Q

Which of the following are features of a hypercatabolic state that follows traumatic shock?

  1. Negative nitrogen balance
  2. Insulin resistance
  3. Fluid retention
  4. Increased energy requirements
A

ALL OF THEM

54
Q

When is lactate produced?

A

Anaerobic metabolism and hypoxia

55
Q

How does anaerobic metabolism lead to lactate production? How can lactate affect tissues?

A
  1. Pyruvate does not undergo oxidative phosphorylation via the TCA cycle but is reduced to lactate
  2. Anaerobic metabolism can only continue until [Lactate] becomes toxic (H+ inhibits enzymes)
  3. Increased lactate = tissue hypoxia
56
Q

What does the failure of blood lactate to return to normal following trauma resuscitation indicate?

A

Poor prognosis

57
Q

Blood lactate prognostic values;

A
58
Q

How can anaerobic respiration lead to a viscious cycle?

A
  1. Mitochondrial failure due to hypoxia
  2. Decreased Oxidative Phosphorylation
  3. NADH accumulates instead of NAD+ (so no energy drive in cell)
  4. Anaerobic glycolysis continues
59
Q

What is a good prognostic marker following trauma?

A

Lactate levels

60
Q

Can adequate nutrition reverse a hypercatabolic state?

A

No - but can help prognosis

61
Q

What is primary malnutrition?

A
  • Protein/calorie undernutrition (starvation)
  • Dietary deficiency of specific nutrients (e.g. trace elements, water soluble vitamins / fat soluble vitamins)
62
Q

What is secondary malnutrition?

A

Secondary malnutrition arises when an individual’s dietary intake is sufficient, but energy is not adequately absorbed by the body;

  • Appetite is suppressed
  • Absorption and utilisation are inadequate

OR increased demand for specific nutrients to meet physiological needs

63
Q

When dealing with nutrition during trauma, what needs to be considered?

A
  • demands of hypermetabolic phase
  • pre-trauma nutritional state
64
Q

Why does trauma lead to nitrogen loss?

A
  • Stress produces nitrogen losses, driven by the catabolic actions of cortisol and adrenaline
  • Skeletal muscle breakdown provides substrate for gluconeogenesis and also releases nonessential amino acids that are excreted in the urine as urea.
65
Q

Immobilisation increases the loss of which electrolytes?

A

Calcium, Phosphate, Magnesium etc

66
Q

How can trauma affect the protective cell barriers in the gut?

A

Trauma-induced breakdown of protective cell barriers in the gut

67
Q

What are the consequences of malnutrition?

A
  • Negative Nitrogen balance
  • Muscle wasting
  • Widespread cellular dysfunction
    • infection
    • poor wound healing
    • changes in drug metabolism
    • prolonged hospitalisation
    • increased mortality
68
Q

What is the overall incidence of malnutrition in hospitalised patients?

A

Approx 50%

69
Q

How should nutrition be delivered in a trauma patient?

A
  • Use the gut if possible (nasogastric tubes)
  • If gut not working, need TPN (total parenteral nutrition)
70
Q

What is refeeding syndrome?

A

Refeeding syndrome involves metabolic abnormalities when a malnourished person begins feeding, after a period of starvation or limited intake.

71
Q

Pathogenesis of refeeding syndrome?

A
  • Refeeding causes insulin release
  • Insulin causes;
    • rapid uptake of glucose, phosphorus, magneium and potasssium (cause hypo- of these)
    • increased thiamine use –> thiamine deficiency
72
Q

What are the consequences of refeeding syndrome?

A
  • Cardiovascular arrhythmias – cardiogenic shock
  • Gastrointestinal disturbance – D+V, maldigestion
  • Musculoskeletal – weakness, rhabdomyolysis
  • Respiratory – respiratory failure
  • Neurologic – Wernicke encephalopathy, tetany
  • Renal – acute tubular nephrosis
  • Hepatological – acute liver failure
  • Increased mortality
73
Q

CF involves a mutation in the CFTR protein (a cAMP dependent chloride channel). Where is this located?

A

Localises to the apical membrane of secretory and absorptive epithelial cells within;

  • airways,
  • pancreas,
  • liver,
  • intestine,
  • sweat glands,
  • vas deferens
74
Q

What does the CFTR protein facilitate?

A
  • CFTR facilitates production of thin, watery, free-flowing mucus
    • Lubricating airways and secretory ducts
    • Protecting the lining of the airways, digestive system, reproductive system
  • So that macromolecules (e.g. digestive enzymes) can be secreted smoothly out of secretory ducts
75
Q

The failure to maintain hydration of macromolecules in the lumen of the ducts of the pancreas and intestine in CF leads to what?

A
  • Secretions precipitate –> obstruction
  • Digestive enzyme deficiencies –> malnutrition
76
Q

How can CF lead to

a) structural lung damage?
b) infection in lung?

A

a) ↑ bacterial colonisation –> neutrophils accumulate + secrete elastase —> structural lung damage
b) Dead neutrophils release DNA ↑ viscocity of sputum –> Infection + Persistent inflammatory state

77
Q

What can babies with CF present with at birth?

A

Meconium ileus (around 15%) –> may require surgical resection (risk of intestinal failure)

78
Q

How can CF lead to nutrional deficiencies?

A
  1. Surgical resection of bowel at birth if born with meconium ileus
  2. Pancreatic damage –> exocrine insufficieny
79
Q

What exocrine insufficiencies are often present in CF? What can each lead to?

A
  • Decreased insulin –> diabetes
  • Decreased lipase –> lipid malabsorption, steatorrhoea, fat soluble vitamin deficiency
  • Decreased protease –> protein malnutrition
80
Q

How can nutritional deficiencies present in infants with CF?

A

Poor appetite, failure to thrive, low weight

81
Q

Treatment for respiratory disease in CF?

A

To decrease infection and inflammation:

  • Physiotherapy
  • Exercise
  • Bronchodilators
  • Antibiotics (oral / nebuliser / iv)
  • Steroids
  • Mucolytics (DNase)
82
Q

Treatment for GI disease in CF?

A

To maintain body weight and avoid catabolic state;

  • Pancreatic enzyme replacement (Creon)
  • Nutritional supplements
  • Fat-soluble vitamins
  • High calorie diet
  • Ursodeoxycholic acid
83
Q

What are creon delayed release capsules? Used to treat?

A

Capsules containing lipases, proteases, and amylases for the treatment of exocrine pancreatic insufficiency (EPI) due to cystic fibrosis, chronic pancreatitis, pancreatectomy, or other conditions.

84
Q

CF treatment?

A
  • Prompt use of appropriate Antibiotics
  • Lifelong nutritional supplements
  • Early use of nutritional support in acute illness
  • CFTR modulators – Ivakaftor, Tezacaftor, Elaxacaftor
85
Q

What is Wernicke-Korsakoff Syndrome?

A

A type of brain disorder caused by a vitamin B-1/thiamine deficiency

86
Q

What is thiamine a cofactor for?

A

Several enzymes; transketolase, PDH, α-KGDH

These are important enzymes for;

  • Glycolysis
  • Citric acid cycle (TCA)
  • Synthesis of Nucleic acid, neurotransmitter, glutathione, steroids
87
Q

What can thiamine deficiency lead to?

A

Mitochondrial damage, cellular necrosis, oxidative stress, Purkinje cells in cerebellum.

88
Q

Clinical presentation of Wernicke Encephalopathy?

A
  • Confusion
  • Ataxia (unsteady gait)
  • Neural Oculomotor disturbances
  • Korsakoff psychosis
89
Q

What is Korsakoff psychosis?

A

Korsakoff psychosis is a late complication of persistent Wernicke encephalopathy and results in memory deficits, confusion, and behavioral changes.

90
Q

What is the major risk factor for B1/thiamine deficiency?

A

Alcohol dependency;

  • decreased thiamine absorption
  • decreased thiamine stores in liver
  • poor diet
  • ?Genetic predisposition
91
Q

What are other risk factors for B1/thiamine deficiency?

A
  • Cancer chemo; decreased appetite, increased demand for nucleic acid synthesis
  • Anorexia nervosa
  • Refeeding syndrome
92
Q
A

Yr 2 - Clinical Pathology (80 decks)

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