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Clinical Pathology > Nutritional Support in Trauma > Flashcards

Nutritional Support in Trauma Flashcards

1
Q

What are the 3 phases of trauma

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

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

A

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

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3
Q

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

A

Cytokines, catecholamines, cortisol

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4
Q

4 clinical effects of phase 1: shock

A

Tachycardia
Increased resp. rate
Peripheral vasoconstriction
Hypovolaemia

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5
Q

Aims during phase 1

A

Stop bleeding

Prevent infection

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6
Q

When does phase 2 present

A

2 days after injury

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7
Q

What chemical modulators are released into the blood during phase 2

A

Catecholamines, glucagon, ACTH

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8
Q

4 clinical effects of phase 2

A

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

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9
Q

When does phase 3 present

A

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

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10
Q

What is the obestiy paradox

A

Obesity is survival advantage in the recovery of trauma

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11
Q

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

A

IL-1, IL-6 and TNF

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12
Q

What endocrine effects to cytokines have, after trauma

A

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

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13
Q

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

A

120g

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14
Q

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

A

Ketones

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15
Q

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

A

Gluconeognesis

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16
Q

What substrates does the liver and kidney use for gluconeogenesis?

A

Fatty acids/amino acids

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17
Q

What substrates does skeletal muscle use for gluconeogenesis?

A

Glycogen stores/amino acids

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18
Q

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

A

Glycogenolysis
Gluconeogeneis
Lipolysis and ketogenesis

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19
Q

How are lipids used to make ketones simultaneously?

A

FFA>Acetyl CoA>Acetoacetate+Hydroxybutyrate

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20
Q

What are the cellular effects of anaerobic respiration

A

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

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21
Q

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

A

60mmol/L

>5.0mmol/L

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22
Q

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

A 
Metabolic failure (inadequate energy production)
Metabolic acidosis (lactic acid production)
23
Q 
What are the effects of trauma on levels of:
inflammatory modulators
albumin
free amino acids
ammonia conc. in plasma
N2 loss
A 
Inflammatory modulators increase
Albumin decreases
free amino acids increase
Ammonia concentration in plasma increases
Nitrogen loss increases
24
Q

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

A

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

25
Q

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

A

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

26
Q

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

A

> 5mmol/L

27
Q

At what time after trauma does N2 losses peak?

A

4-8 days

28
Q

Protein calorie undernutrition (starvation)

A

Primary malnutrition

29
Q

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

A

Secondary malnutrition

30
Q

Describe refeeding syndrome

A

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)

31
Q

How common is CF?

A

1 in 2500 newborns

32
Q

Describe the cystic fibrosis transmembrane regulator (CFTR) protein

A

cAMP dependent chloride channel that facilitates the production of mucus

33
Q

4 main effects of CF

A

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

34
Q

How common is meconium ileus?

A

15%

35
Q

What are the results of exocrine insufficiency in CF?

A

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

36
Q

Pancreatic enzyme replacement

A

Creon

37
Q

Name 4 commensal flora of gut

A

Bacteroides
Clostridium perfringens
Escherichia coli
Enterococcus faecalis

38
Q

Anaerobic gram -ve bacilli -commensal flora of the gut

A

Bacteroides

39
Q

Anaerobic gram +ve bacilli

A

Clostridium perfringens

40
Q

Faculative gram -ve bacilli

A

Escherichia coli

41
Q

faculative gram +ve cocci

A

Enteroccocus faecalis

42
Q

Common bacterial causes of diarrhoea

A 
Salmonella
Shigella
E.coli
Campylobacter
Vibrio cholerae
C.diff
Staph A
Bacillus cereus
43
Q

Common parasitic causes of diarhhoea

A

Entamoeba hist.
giardia lamblia
cryptosporidium

44
Q

Common viral causes of diarrhoea

A

norovirus

rotavirus

45
Q

Complications of diarrhoea

A

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

46
Q

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

A

Shigella
E.coli (enteroadherent forms)
Campylobacter
Salmonellae

47
Q

Which bacteria can cause gastroenteritis and grows on undercooked meat?

A

Campylobacter

48
Q

How does E.Coli 0157 cause gastroenteritis

A

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

49
Q

Toxin mechanism of action for E.coli 0157

A

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

50
Q

What is the danger of killing E.coli bacteria

A

Release more of the toxin and can make the disease worse

51
Q

In what circumstances would you give antibiotics with someone with gastroenteritis

A

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

52
Q

What bacteria accounts for 99% pseudomembranous colitis?

A

C.Diff

53
Q

Current C.Diff infection therapy

A

Oral metronidazole/oral vancomycin

Clinical Pathology (53 decks)

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