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Flashcards in Trauma and nutrition Deck (42):

What are possible clinical features of physical trauma?

- Intravascular fluid loss
- Extravascular volume
- Tissue destruction
- Obstructed/Impaired breathing


What are the consequences of trauma to energy substrate delivery to cells?

- Blood loss + impaired breathing + infection barrier penetration
= reduced circulating volume
= reduced RBCs (= reduced O2)
= reduced white cells (=reduced immune response)
= reduced cardiac output/BP
= reduced organ perfusion
= reduced energy substrate delivery to cells and tissues


What is shock?

Interruption to the supply of substrates to the cell
-Oxygen, glucose, water, lipids, amino acids, micronutrients

Interruption to the removal of metabolites from the cell
-CO2 , water, free radicals, toxic metabolites


What are the features of Phase 1 (shock) following trauma?

- Develops within 2-6 hours after injury
- Lasts 24 – 48h
- Cytokines, Catecholamines and cortisol secreted
- Tachycardia
- Increased RR
- Peripheral vasoconstriction (selective peripheral shut-down to preserve vital organs)
- Hypovolaemia


What are the primary treatment aims during phase 1?

1. Stop bleeding
2. Prevent infection


What are the features of Phase 2 (catabolic state) following trauma?

- Develops approx 2 days after injury
- Neccesary for survival but if persists / is severe, increases risk of mortality
- Catecholamines
- Glucagon
- ACTH -> Cortisol
- Increased O2 consumption
- Increased metabolic rate
- -ve nitrogen balance (skeletal muscle breakdown to release AAs)
- Gycolysis (skeletal energy reserve depleted)
- Lipolysis (adipose tissue breakdown to release to release fatty acids)


What are the primary treatment aims during phase 2?

1. Avoid sepsis
2. Provide adequate nutrition


What are the features of Phase 3 (anabolic state) following trauma?

- Occurs approx 3-8 days after uncomplicated surgery
- May not occur for weeks after severe trauma and sepsis
- Coincides with beginning of diuresis and request for oral intake

Gradual restoration of
- body protein synthesis
- Normal nitrogen balance
- Fat stores
- Muscle strength


What are the treatment aims during Phase 3?

- Adequate nutrition supply is critical in this phase
- Refeeding syndrome risk
- May last a few weeks / a few months
- Obesity paradox


What is the inflammatory response at a trauma site?

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


Which cytokines are involved in the inflammatory response?

- IL-1
- IL-6


What are the catabolic effects of cytokines?

Cytokine mediated secretion of catabolic hormones (e.g. IL-1 and TNF-alpha):
- increased ACTH (-> cortisol)
- increased Glucagon
- increased Catecholamines

Cytokine mediated inhibition of anabolic hormones:
- Growth hormone
- Insulin


What is normal metabolism?

Oxidation of dietary Carbohydrate, lipid and protein


In health, how long can glycogen stores maintain the glucose supply for?

24 hrs


What are the energy requirements of the brain?

- Brain has no glycogen store.
- Obligate substrate = Glucose
- Requires continuous supply of glucose and O2
(requirement =120g / day =1Kg muscle)


For how long will the brain survive during circulatory failure?

>2 mins


How does the brain adapt to a shortage in glucose?

Adapts to using ketones as an energy substrate


How are the kidneys and liver capable of surviving hours of interruption of blood supply?

Capable of gluconeogenesis.


What energy substrates are used by the liver are kidney?

Fatty acids and amino acids


What energy substrates are used by skeletal muscle?

Glycogen stores and fatty acids


For how long can glycogenolysis provide glucose from glycogen stores when the glucose supply have been interrupted?

24 hrs


How much glucose can be harvested from 1kg of muscle via gluconeogenesis?

1kg muscle = 200g protein = 120g glucose (+ lactate)


What is the nitrogen loss from gluconeogenesis?

60-70 g/day but may be up to 300g


What is lipolysis?

Free fatty acids -> acetyl CoA -> acetoacetate & hydroxybutyrate


How does the CNS adapt to spare protein stores and muscle.

Gradual change to ketone metabolism


What is a problematic side-effect of the CNS changing to ketone metabolism?

Ketones cause a diuresis with loss of H2O + electrolytes


How do tissues adapt to hypoxia?

Anaerobic metabolism


How many moles of ATP are produced by aerobic metabolism vs anaerobic metabolism?

36:2 aerobic:anaerobic


What are the consequences of the ATP deficit caused by the switch to anaerobic metabolism?

Loss of ATP = loss of membrane Na/K pump = cellular swelling +
Loss of membrane integrity = lysosomal enzyme release


What is lactic acidosis?

- [Lactate] >5.0 mmol/L


Why will the administration of adequate calories as carbohydrate/lipid not stop muscle wasting in a patient with sepsis?

The primary stimulation for protein breakdown is cytokine secretion from activated macrophages?


What are the pathological consequences of proteolysis in sepsis?

- Life-threatening damage to essential structural and secreted protein.
- Respiratory muscle weakness results in poor cough retention of secretions and pneumonia


How is lactate used as a prognostic marker in trauma?

- Failure of blood lactate to return to normal following trauma resuscitation carries a poor prognosis

- Blood lactate (mmol/L)
5 = ~100% mortality


Why might lactate be such a good prognostic marker?

Vicious cycle :
- Mitochondrial failure due to hypoxia
- Reduced Oxidative Phosphorylation
- Anaerobic glycolysis continues


What will be the nitrogen loss per day following the fracture of a long bone?



What will be the nitrogen loss per day following severe burns?

300g per day


Immobilisation increases losses of what substances?

Calcium, Phosphate, Magnesium etc


What is primary malnutrition?

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


What is secondary malnutrition?

- Nutrients present in adequate amounts but appetite is suppressed
- Nutrients present in adequate amounts but absorption and utilization are inadequate
- Increased demand for specific nutrients to meet physiological needs


What are the consequences of malnutrition?

- Negative Nitrogen balance
- Muscle wasting
- Widespread cellular dysfunction
- Associated with (infection, poor wound healing, changes in drug metabolism, prolonged hospitalisation, increased mortality)


What is refeeding syndrome?

- During refeeding, insulin secretion resumes in response to increased blood sugar; resulting in increased glycogen, fat and protein synthesis.
- This process requires phosphates, magnesium and potassium which are already depleted and the stores rapidly become used up.
- Formation of phosphorylated carbohydrate compounds in the liver and skeletal muscle depletes intracellular ATP and 2,3-diphosphoglycerate in red blood cells, leading to cellular dysfunction and inadequate oxygen delivery to the body's organs.
- Refeeding increases the basal metabolic rate.
- Intracellular movement of electrolytes occurs along with a fall in the serum electrolytes, including calcium and magnesium.
- Levels of serum glucose may rise and the B1 vitamin thiamine may fall.
- Cardiac arrhythmias are the most common cause of death from refeeding syndrome, with other significant risks including confusion, coma and convulsions and cardiac failure.


Why do people with cystic fibrosis suffer malnutrition?

Pancreatic insufficiency

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