22 Nutrition and trauma Flashcards Preview

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Flashcards in 22 Nutrition and trauma Deck (20):
1

What are the immediate features of physical trauma?

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

2

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.

3

What is shock?

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

4

What are the three physiological phases after trauma?

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

5

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.

6

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.

7

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.

8

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.

9

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

24 hours.

10

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.

11

How does anaerobic metabolism lead to cell death?

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

12

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.

13

Do adequate calories prevent muscle wasting after trauma?
Why?

No.
Breakdown mediated by cytokine secretion from activated macrophages.

14

How is lactate used as a prognostic marker in trauma?

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

15

What is the vicious cycle of lactate production after trauma?

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

16

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

4-8days.
Bone: 60-70g.
Sever burns: 300g.

17

Distinguish between primary and secondary malnutrition.

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

18

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

19

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.

20

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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