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Flashcards in 22 Nutrition and trauma Deck (20)

What are the immediate features of physical trauma?

Intravascular fluid loss.
Extravascular volume.
Tissue destruction.
Obstructed/impaired breathing.


What are the causes of mortality after major trauma? (3)

0-5 days: haematological shock and head injury.
5-15 days: Acute Respiratory Distress Syndrome.
10-35 days: Multi organ failure.


What is shock?

Interruption to the supply of substrates to the cell and removal of metabolites.


What are the three physiological phases after trauma?

1. Clinical shock.
2. Hypercatabolic state.
3. Recovery (anabolic state).


Describe phase 1 (SHOCK) after trauma.
Chemicals released? (3)
Effects (4)
What do doctor aim to do then?

2-6hrs later, lasts 24-48hrs.
Cytokines, catecholamines + cortisol release.
High hr + rr. Peripheral vasoconstriction. Hypovolaemia.
Stop bleeding + prevent infection.


Describe phase 2 (catabolism) after trauma.
Chemicals released? (3) Effects (5).
What do doctor aim to do then?

2 days after.
Catecholamines, glucagon + ACTH release.
Increase O2 + metabolic rate. -ve N balance. Increased glycolysis + lipolysis.
Avoid sepsis, provide nutrition.


Describe phase 3 (anabolism) after trauma.
Features (5)
What do doctor aim to do then?

3-8 days after, weeks if severe.
Restoration of N balance, protein synthesis, fat stores + muscle strength. Coincides with diuresis.
Nutrition, refeeding syndrome risk.


What mediates the inflammatory response after trauma? (3)
What are the endocrine effects of these cytokines?

IL-1, IL-6, TNF.
Increased catabolic hormone secretion: ACTH, glucagon, catecholamines.
Inhibition of anabolic hormones: growth hormone, insulin.


In health, how long can glycogen stores maintain blood glucose?

24 hours.


What is the metabolic response to trauma? (3)

1. 24hrs glycogenolysis.
2. Skeletal + secreted protein breakdown. N loss 60-300g/day. Lactate produced.
3. Lipolysis + ketogenesis. Causes diuresis. Acetoacetate + hydroxybutyrate produced.


How does anaerobic metabolism lead to cell death?

Inadequate energy produced (1mol glucose-2mol ATP) -> metabolic failure.
Lactic acid production -> metabolic acidosis.


How does protein turnover change after trauma?

Decreased albumin synthesis. Increased inflammatory modulator and clotting factor synthesis
Increased skeletal muscle proteolysis - increase free AA (for gluconeogenesis), increased plasma [ammonia], increased N2 loss.


Do adequate calories prevent muscle wasting after trauma?

Breakdown mediated by cytokine secretion from activated macrophages.


How is lactate used as a prognostic marker in trauma?

Failure to return to normal = poor prognostic marker. >5mml/l = 100% mortality.


What is the vicious cycle of lactate production after trauma?

Hypoxic mitochondrial failure. Oxidative phosphorylation decreases. NADH > NAD+. Anaerobic glycolysis continues.


When does nitrogen loss peak after trauma?
What amounts are lost following fracture of long bone vs sever burns.

Bone: 60-70g.
Sever burns: 300g.


Distinguish between primary and secondary malnutrition.

1: protein/calorie/nutrient undernutrition.
2: suppressed appetite, absorption + utilisation inadequate, increased demand.


How does referring syndrome occur?

Refeeding switches body to anabolism. CHO is energy source, insulin section.
Increase in protein/glycogen synthesis, increase in glucose/ thiamine/ K+/ Mg2+/ PO4- uptake.
Results in blood deficiency of these.
Leads to cardiac arrhythmia and failure


What does the exocrine insufficiency in cystic fibrosis cause? (3 enzymes + effects)

Low insulin - diabetes.
Low lipase - lipid malabsorption, steatorrhoea, fat soluble vitamin deficiency.
Low proteases - protein malnutrition.


How are the GI components of cystic fibrosis treated? (4)

Creon (enzyme replacement - lipase, protease, amylase).
Nutritional supplement.
High calorie diet.
Ursodeoxycholic acid.

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