Nutritional Support in Trauma

Question 1

What are the 3 phases of trauma

Answer 1

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

Question 2

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

Answer 2

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

Question 3

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

Answer 3

Cytokines, catecholamines, cortisol

Question 4

4 clinical effects of phase 1: shock

Answer 4

Tachycardia
Increased resp. rate
Peripheral vasoconstriction
Hypovolaemia

Question 5

Aims during phase 1

Answer 5

Stop bleeding

Prevent infection

Question 6

When does phase 2 present

Answer 6

2 days after injury

Question 7

What chemical modulators are released into the blood during phase 2

Answer 7

Catecholamines, glucagon, ACTH

Question 8

4 clinical effects of phase 2

Answer 8

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

Question 9

When does phase 3 present

Answer 9

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

Question 10

What is the obestiy paradox

Answer 10

Obesity is survival advantage in the recovery of trauma

Question 11

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

Answer 11

IL-1, IL-6 and TNF

Question 12

What endocrine effects to cytokines have, after trauma

Answer 12

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

Question 13

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

Answer 13

120g

Question 14

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

Answer 14

Ketones

Question 15

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

Answer 15

Gluconeognesis

Question 16

What substrates does the liver and kidney use for gluconeogenesis?

Answer 16

Fatty acids/amino acids

Question 17

What substrates does skeletal muscle use for gluconeogenesis?

Answer 17

Glycogen stores/amino acids

Question 18

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

Answer 18

Glycogenolysis
Gluconeogeneis
Lipolysis and ketogenesis

Question 19

How are lipids used to make ketones simultaneously?

Answer 19

FFA>Acetyl CoA>Acetoacetate+Hydroxybutyrate

Question 20

What are the cellular effects of anaerobic respiration

Answer 20

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

Question 21

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

Answer 21

60mmol/L

>5.0mmol/L

Question 22

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

Answer 22

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

Question 23

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

Answer 23

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

Question 24

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

Answer 24

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

Question 25

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

Answer 25

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

Question 26

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

Answer 26

>5mmol/L

Question 27

At what time after trauma does N2 losses peak?

Answer 27

4-8 days

Question 28

Protein calorie undernutrition (starvation)

Answer 28

Primary malnutrition

Question 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

Answer 29

Secondary malnutrition

Question 30

Describe refeeding syndrome

Answer 30

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)

Question 31

How common is CF?

Answer 31

1 in 2500 newborns

Question 32

Describe the cystic fibrosis transmembrane regulator (CFTR) protein

Answer 32

cAMP dependent chloride channel that facilitates the production of mucus

Question 33

4 main effects of CF

Answer 33

Malnutrition-digestive enzyme deficiencies Infection and persistent inflammatory state Meconium ileus at birth Severe hepatobiliary disease Pancreatic cysts, decreased exocrine insufficiency

Question 34

How common is meconium ileus?

Answer 34

15%

Question 35

What are the results of exocrine insufficiency in CF?

Answer 35

less insulin- diabetes less lipase-lipid malabsorption, steatorrhoea, fat soluble vit.deficiency less proteases

Question 36

Pancreatic enzyme replacement

Answer 36

Creon

Question 37

Name 4 commensal flora of gut

Answer 37

Bacteroides Clostridium perfringens Escherichia coli Enterococcus faecalis

Question 38

Anaerobic gram -ve bacilli -commensal flora of the gut

Answer 38

Bacteroides

Question 39

Anaerobic gram +ve bacilli

Answer 39

Clostridium perfringens

Question 40

Faculative gram -ve bacilli

Answer 40

Escherichia coli

Question 41

faculative gram +ve cocci

Answer 41

Enteroccocus faecalis

Question 42

Common bacterial causes of diarrhoea

Answer 42

``` Salmonella Shigella E.coli Campylobacter Vibrio cholerae C.diff Staph A Bacillus cereus ```

Question 43

Common parasitic causes of diarhhoea

Answer 43

Entamoeba hist. giardia lamblia cryptosporidium

Question 44

Common viral causes of diarrhoea

Answer 44

norovirus | rotavirus

Question 45

Complications of diarrhoea

Answer 45

Dehydration renal failure Haemolytic urinary sundrome (HUS) Toxic megacolon Guillian barre syndrome- associated with campylobacter

Question 46

Which 4 bacteria act by adhering to the gut wall and cause gastroenteritis this way, rather than by producing enterotoxins?

Answer 46

Shigella E.coli (enteroadherent forms) Campylobacter Salmonellae

Question 47

Which bacteria can cause gastroenteritis and grows on undercooked meat?

Answer 47

Campylobacter

Question 48

How does E.Coli 0157 cause gastroenteritis

Answer 48

Enterotoxin production. 10-15% patients develop haemolytic uraemic syndrome

Question 49

Toxin mechanism of action for E.coli 0157

Answer 49

Activates G protein, increases cAMP, activates ion channels which over-excrete Cl- and water follows by osmosis (opposite of CF)

Question 50

What is the danger of killing E.coli bacteria

Answer 50

Release more of the toxin and can make the disease worse

Question 51

In what circumstances would you give antibiotics with someone with gastroenteritis

Answer 51

Very young and v.cold Camplylbacter-prolonged or severe symptoms Invasion e.g positive blood cultures

Question 52

What bacteria accounts for 99% pseudomembranous colitis?

Answer 52

C.Diff

Question 53

Current C.Diff infection therapy

Answer 53

Oral metronidazole/oral vancomycin