Trauma & Nutrition Flashcards
What are consequences of fractures & internal injuries?
- 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
What are the 3 phases after a severe trauma
- Phase 1: clinical shock
- Phase 2: Hypercatabolic state
- Phase 3: Recovery-anabolic state
Describe what happens in phase 1 of a trauma?
- 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
Describe what happens in phase 2 of a trauma?
- 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
Describe what happens in phase 3 after a trauma?
- 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
What is the mechanism of action when a wound in incured?
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
What is lost from capillaries when inflammatory mediators are released in an injury?
- Systemic capillary leak of substances into surrounding tissue
- H2O
- Albumin
- NaCl
- Energy substrates
What do cytokines/TNF/IL induce? (clinically and at a cellular level)
- 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)
What are the endocrine effects of cytokines (IL-1 & TNFa)?
- Inc ATCH converted to cortisol
- Inc glucagon
- Inc catecholamines
- Cytokine mediated inhibition of anabolic hormones: dec insulin, dec growth hormone
What happens in terms of energy delivery after trauma compared to normal?
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)
How do different tissues use different substrates?
- Liver & kidneys= fatty acids/aa
- Skeletal muscle= glycogen stores/fatty acids
What happens when the supply of glucose & O2 is interrupted?
- 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
What are ketones and what do they cause?
- Acids
- Diuresis with loss of H2O & electrolytes
What are negative implications of hypoxia?
- 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
What is the difference between normal protein turnover and that in trauma?
- 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)
What will stop/not stop muscle wasting?
- 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
How can lactate produce hypoxia?
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
In nutritional support what needs to be considered?
- Demands of hyper metabolic phase
- Pre-trauma nutritional state
How much N2 can be lost in trauma?
- Fractured long bones= 60-70g muscle protein
- Severe burns= 300g muscle protein
What does immobilisation increase the loss of?
- Calcium
- Magnesium
- Phosphate
What is primary malnutrition?
- Protein-calorie undernutrition (starvation)
- Dietary deficiency of specific nutrients (trace elements, water/fat soluble vitamins)
What is secondary malnutrition?
- Nutrients present in adequate amounts but appetite suppressed
- Absorption & utilisation are inadequate
- Inc demand for specific nutrients to meet physiological needs
What are consequences and associations of malnutrition?
- Negative N2 balance
- Muscle wasting
- Widespread cellular dysfunction
- Associated with: infection, poor wound healing, changes in drug metabolism, prolonged hospitalisation, inc mortality
What is the mechanism of refeeding syndrome? What are the consequences)
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
What cells does CF affect?
- cAMP dependent chloride channels on apical membrane of secretory & absorptive epithelial cells
- Airways, pancreas, liver, intestines, sweat glands, vas deferens
What are problems caused by pancreatic cysts in CF?
- Dec insulin= diabetes
- Dec lipase= lipid malabsorption, steatorrhoea, fat soluble vitamin deficiency
- Dec proteases= protein malnutrition
