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Flashcards in Nutritional Support in Trauma Deck (53)
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1

What are the 3 phases of trauma

1. Clinical Shock
2.Hypercatabolic state
3.Recovery- anabolic state

2

When does phase 1: shock occur and how long does it last for?

2-6 hrs after injury. Lasts 24-48hrs

3

What chemical modulators are released into the blood in phase 1: shock

Cytokines, catecholamines, cortisol

4

4 clinical effects of phase 1: shock

Tachycardia
Increased resp. rate
Peripheral vasoconstriction
Hypovolaemia

5

Aims during phase 1

Stop bleeding
Prevent infection

6

When does phase 2 present

2 days after injury

7

What chemical modulators are released into the blood during phase 2

Catecholamines, glucagon, ACTH

8

4 clinical effects of phase 2

Increase in O2 consumption
Increase in metabolic rate
Increase in glycolysis
Increase in lipolysis

9

When does phase 3 present

Coincides with beginning of diuresis and requenst for oral intake. May not occur for weeks after severe trauma and sepsis

10

What is the obestiy paradox

Obesity is survival advantage in the recovery of trauma

11

What are the 3 cytokines that play the biggest roles after trauma

IL-1, IL-6 and TNF

12

What endocrine effects to cytokines have, after trauma

Cytokine mediated secretion of catabolic hormones (increase in ACTH, glucagon, catecholamines)
Cytokine mediated inhibition of anabolic hormones (less growth hormone, less insulin)

13

How many grams of glucose/day/kg does the brain require?

120g

14

What does the brain use as an energy substrate when glucose is not available?

Ketones

15

How do the kidneys and liver adapt to less glucose availibility?

Gluconeognesis

16

What substrates does the liver and kidney use for gluconeogenesis?

Fatty acids/amino acids

17

What substrates does skeletal muscle use for gluconeogenesis?

Glycogen stores/amino acids

18

What are the 3 main metabolic responses to trauma, i.e. what happens when the supply of glucose and oxygen is interrupted?

Glycogenolysis
Gluconeogeneis
Lipolysis and ketogenesis

19

How are lipids used to make ketones simultaneously?

FFA>Acetyl CoA>Acetoacetate+Hydroxybutyrate

20

What are the cellular effects of anaerobic respiration

Loss of membrane Na/K pump>cellular swelling and loss of membrane integrity>lysosomal enzyme release

21

What pH, H+conc. and lactate conc. is considered lactic acidosis

60mmol/L
>5.0mmol/L

22

What are the 2 main metabolic effects of anaerobic respiration, and how do they come about?

Metabolic failure (inadequate energy production)
Metabolic acidosis (lactic acid production)

23

What are the effects of trauma on levels of:
inflammatory modulators
albumin
free amino acids
ammonia conc. in plasma
N2 loss

Inflammatory modulators increase
Albumin decreases
free amino acids increase
Ammonia concentration in plasma increases
Nitrogen loss increases

24

What is the difference in administering adequate calories in patients who are starving and in trauma/sepsis patients?

In starvation, this will reverse muscle wasting. This is not true for trauma/sepsis patients

25

Why does providing calories not reverse muscle wasting in trauma/septic patients?

Because primary stimulation for protein breakdown is cytokine secretion from activated macrophages

26

What concentration of lactate in the blood has a 100% mortality?

>5mmol/L

27

At what time after trauma does N2 losses peak?

4-8 days

28

Protein calorie undernutrition (starvation)

Primary malnutrition

29

Nutrients present in adequate amounts by appetite is suppressed, or absorption and utilization are inadequate or increased demand for specific nutrients to meet physiological needs

Secondary malnutrition

30

Describe refeeding syndrome

Triggers insulin release, which results in cellular uptake of potassium, phosphate and magnesium- lowers the concentrations of these in the blood as well as thiamine deficiency and salt and water retention (oedema)

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