Trauma & Nutrition Flashcards

1
Q

What are consequences of fractures & internal injuries?

A
  • Blood loss, impaired breathing, infection barrier penetration
  • Dec circulating volume
  • Dec red cells (Dec O2)
  • Dec white cells (dec immune response)
  • Dec cardiac output/BP
  • Dec organ perfusion
  • Dec energy substrate delivery to cells & tissues
  • Major organ dysfunction
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2
Q

What are the 3 phases after a severe trauma

A
  • Phase 1: clinical shock
  • Phase 2: Hypercatabolic state
  • Phase 3: Recovery-anabolic state
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3
Q

Describe what happens in phase 1 of a trauma?

A
  • Develops within 2-6hrs after injury
  • Lasts 24-48hrs
  • Cytokines, Catecholamines & cortisol secreted
  • Inc HR (tachycardia), RR
  • Peripheral VasoC (preserve vital organs)
  • Hypovolaemia
  • Primary aims= stop bleeding, prevent infection
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4
Q

Describe what happens in phase 2 of a trauma?

A
  • Develops approx 2 days after injury
  • Necessary for survival but if persists inc mortality
  • Catecholamines, glucagon, ACTH–>cortisol
  • Inc O2 consumption, metabolic rate
  • Inc negative N2 balance (skeletal muscle breakdown to release aa)
  • Inc glycolysis (skeletal energy reserve depleted)
  • Inc lipolysis (adipose tissue breakdown to release fatty acids)
  • Primary aims= avoid sepsis, provide adequate nutrition
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5
Q

Describe what happens in phase 3 after a trauma?

A
  • 3-8days after injury/ uncomplicated surgery
  • Coincides with beginning of diuresis & request for oral intake
  • Gradual restoration of body protein synthesis, normal N2 balance, fat stores, muscle strength
  • Aims= adequate nutrition, avoid refeeding syndrome, obesity paradox
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6
Q

What is the mechanism of action when a wound in incured?

A

1) Bacteria & pathogens enter wound
2) Platelets releasec clotting factors
3) Mast cells secrete factors mediating VasoD to inc blood delivery to area
4) Neutrophils & macrophages recruited for phagocytosis
5) Macrophages secrete cytokines to attract immune cells & proliferate inflammatory response
6) Inflammatory response continues until wound is healed

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7
Q

What is lost from capillaries when inflammatory mediators are released in an injury?

A
  • Systemic capillary leak of substances into surrounding tissue
  • H2O
  • Albumin
  • NaCl
  • Energy substrates
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8
Q

What do cytokines/TNF/IL induce? (clinically and at a cellular level)

A
  • Fever
  • Fibroblast proliferation (repair)
  • Anorexia
  • T cell activation & B cell proliferation
  • Endocrine effects (catabolic & anabolic)
  • Acute phase proteins
  • Metabolic effects (catabolic)
  • Local effects (chemotaxis, VasoD, cell adhesion proteins)
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9
Q

What are the endocrine effects of cytokines (IL-1 & TNFa)?

A
  • Inc ATCH converted to cortisol
  • Inc glucagon
  • Inc catecholamines
  • Cytokine mediated inhibition of anabolic hormones: dec insulin, dec growth hormone
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10
Q

What happens in terms of energy delivery after trauma compared to normal?

A

Normal met= Oxidation of dietary carbs, lipids & proteins. Glycogen stores maintain glucose for unto 24hrs
Trauma met= brain has no glycogen store so adapts to ketones as energy substrate (won’t survive >2mins of failed blood supply), kidneys/liver capable of gluconeogenesis (can survive hours of interrupted blood supply)

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11
Q

How do different tissues use different substrates?

A
  • Liver & kidneys= fatty acids/aa

- Skeletal muscle= glycogen stores/fatty acids

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12
Q

What happens when the supply of glucose & O2 is interrupted?

A
  • Glycogenolysis: Glycogen–> glucose
  • Gluconeogenesis: Skeletal & secreted protein breakdown. AA become glucose & lactate
  • Lipolysis & ketogenesis: FFA–> acetyl CoA–> acetoacetate & hydroxybutyrate (ketones) gradual change to ketone metabolism by CNS which spares protein stores & muscles
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13
Q

What are ketones and what do they cause?

A
  • Acids

- Diuresis with loss of H2O & electrolytes

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14
Q

What are negative implications of hypoxia?

A
  • Anaerobic metabolism
  • 1mole glucose–> 2 mole ATP
  • Loss of ATP= loss of membrane Na/K pump= cellular swelling
  • Loss of membrane integrity= lysosomal enzyme release
  • Lactic acid production= metabolic acidosis= cell death
  • Inadequate energy production=metabolic failure= cell death
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15
Q

What is the difference between normal protein turnover and that in trauma?

A
  • Normal= balance between synthesis of new protein & skeletal muscle proteolysis. Maintenance of muscle mass & plasma protein
  • Trauma= Inc skeletal muscle proteolysis (inc in FAA transported to liver for gluconeogenesis & protein synthesis, inc plasma ammonia, inc N2 loss) & dec synthesis of new protein (dec albumin, inc inflame modulators & scavengers)
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16
Q

What will stop/not stop muscle wasting?

A
  • In starvation administration of calories as lipids, carbs
  • In trauma/sepsis primary stimulation for protein breakdown is cytokine secretion from activated macrophages. Further proteolysis= life-threatening damage to essential structural & secreted proteins
17
Q

How can lactate produce hypoxia?

A

1) Pyruvate not undergo oxidative phosphorylation via TCA cycle so reduced to lactate
2) Anaerobic metabolism continues until lactate becomes toxic- H+ inhibits enzymes
3) inc lactate= tissue hypoxia
4) mitochondrial failure due to hypoxia
5) even further dec oxidative phosphorylation
6) NADH–> NAD+
7) more anaerobic glycolysis

18
Q

In nutritional support what needs to be considered?

A
  • Demands of hyper metabolic phase

- Pre-trauma nutritional state

19
Q

How much N2 can be lost in trauma?

A
  • Fractured long bones= 60-70g muscle protein

- Severe burns= 300g muscle protein

20
Q

What does immobilisation increase the loss of?

A
  • Calcium
  • Magnesium
  • Phosphate
21
Q

What is primary malnutrition?

A
  • Protein-calorie undernutrition (starvation)

- Dietary deficiency of specific nutrients (trace elements, water/fat soluble vitamins)

22
Q

What is secondary malnutrition?

A
  • Nutrients present in adequate amounts but appetite suppressed
  • Absorption & utilisation are inadequate
  • Inc demand for specific nutrients to meet physiological needs
23
Q

What are consequences and associations of malnutrition?

A
  • Negative N2 balance
  • Muscle wasting
  • Widespread cellular dysfunction
  • Associated with: infection, poor wound healing, changes in drug metabolism, prolonged hospitalisation, inc mortality
24
Q

What is the mechanism of refeeding syndrome? What are the consequences)

A

1) Starvation/malnutrition
2) Protein catabolism
3) Protein, fat, mineral, electrolyte depletion, salt/water intolerance
4) Refeeding (switch to anabolism)
5) Fluid, salt, nutrients cause insulin secretion
6) inc protein & glycogen synthesis
7) inc glucose uptake, utilisation of thyamine, uptake of K, P, Mg
8) leads to hypokalaemia, hypomagnesaemia, salt & water retention-oedema, thiamine deficiency, hypophosphataemia

25
Q

What cells does CF affect?

A
  • cAMP dependent chloride channels on apical membrane of secretory & absorptive epithelial cells
  • Airways, pancreas, liver, intestines, sweat glands, vas deferens
26
Q

What are problems caused by pancreatic cysts in CF?

A
  • Dec insulin= diabetes
  • Dec lipase= lipid malabsorption, steatorrhoea, fat soluble vitamin deficiency
  • Dec proteases= protein malnutrition