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Biochemistry > Trauma > Flashcards

Trauma Flashcards

1
Q

Definiton of trauma

A

Life or limb threatening injury
Includes surgery and burns
W.H.O have a scoring system to define level of trauma

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2
Q

How many deaths per year due to trauma and what age is it the main cause of death for?

A

15,000 deaths per year

Under 35’s (main cause of death)

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3
Q

How much does trauma cost the NHS a year

A

£7.5billion

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4
Q

How many seriously injured in road traffic accidents and how many deaths?

A

22,807 seriously injured

1775 deaths

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5
Q

Why has there been a large fall since 1979?

A

Due to improvements in vehicle design e.g. airbags and seatbelts.

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6
Q

What does an ‘immediate death’ from trauma mean?

A

Death from non-survivable injuries

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7
Q

What does ‘early death’ from trauma mean?

A

Death in the first few hours after trauma, due to significant haemorrhage or major organ damage.

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8
Q

What does ‘late death’ from trauma mean?

A

Death in the next days/weeks from progressive deterioration/complications.

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9
Q

What would happen to a 70kg person who suffered a massive head injury and lost 50% of circulating blood volume?

A

Death.

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10
Q

What is the metabolic response to trauma? (Bi-phasic response and recovery)

A

Initial compromise

1) Ebb
2) Flow
3) Recovery

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11
Q

Summarise ‘ebb’

A

Initial homeostatic response –> hypometabolism

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12
Q

Summarise ‘flow’

A

Continuing homeostatic response; hyper metabolism/catabolism

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13
Q

What phase does recovery undergo?

A

Anabolic phase

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14
Q

Why may there not be enough circulating blood volume?

A

Maybe due to significant bleeding from wounds.

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15
Q

Why may it be difficult to distinguish the start and end of ebb and flow from each other?

A

The phases transition smoothly.

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16
Q

Describe the 4 main stages of ‘ebb’

A

1) Initial compromise
2) Inadequate circulating blood volume
3) Reduced O2 supply, increased anaerobic respiration
4) Lactic acid levels increase (due to anaerobic response) and pH begins to fall

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17
Q

What is the equation of the dissociation of lactic acid?

A

Lactic acid –> Lactate + Proton

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18
Q

Where and what is lactate converted too and what does it produce as a result of being oxidised by the heart?

A

Converted by the liver back into glucose. Produces ATP when oxidised by the heart.

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19
Q

What buffers the pH when it falls due to XS lactic acid?

A

Carbonic acid system and breathed out as water/CO2.

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20
Q

What happens to homeostatic response following large blood loss?

A

Blood flow to liver reduces, which reduces ability of liver to produce ATP from lactate (excaberating the problem).

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21
Q

When is the Cori Cycle prompted?

A

By increased levels of lactate in blood tissues.

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22
Q

If circulation is inadequate during Cori Cycle, then what continues to rise?

A

Lactate levels.

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23
Q

Where are 4 places the lactate-converted-glucose go to, from the liver?

A

1) Erythrocytes
2) Muscle
3) Bone Marrow
4) Lymph Nodes
And any excess lactate in any of these places goes back to the liver to be converted back into glucose.

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24
Q

What does poor perfusion of tissues in ‘ebb’ phase mean for lactate levels?

A

Increase, as less lactate can be converted back into glucose.

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25
Q

What can happen in stage 1 of ‘ebb’ phase with adequate treatment?

A

Compensatory response stage. Move to ‘flow’ phase.

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26
Q

What happens to organs and homeostasis in stage 2 of ‘ebb’ phase?

A

Organs: inadequate vital organ perfusion, Insult to homeostasis progresses, Possible progress to ‘flow’ phase

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27
Q

What happens to organs in stage 3 of ‘ebb’ phase and what occurs as a result? How long does this occur after initial compromise?

A

Irreversible damage to major organs –> death. May occur hours/weeks after initial compromise.

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28
Q

What happens if the trauma is a minor compromise (ebb)?

A

The compensatory homeostatic response (stage 1) may be sufficient to promote recovery without further treatment.

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29
Q

During trauma, what happens to blood volume and blood pH?

A

Falls.

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30
Q

What two pathways mediate the initial homeostatic response?

A

HPA (hypothalamic pituitary) Axis, Sympathetic nervous system

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31
Q

Which hormone is directly released and increased by the anterior pituitary?

A

Growth hormone

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32
Q

Which hormone is released and increased from the adrenal context, by stimulation of ACTH?

A

Cortisol

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33
Q

Which nerve causes vasoconstriction when the body undergoes trauma?

A

Sympathetic nerves

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34
Q

Which hormone increases and what hormone decreases when the pancreas is stimulated by the sympathetic nerve?

A

Glucagon increases, insulin decreases

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35
Q

Which hormone is released and increased by the adrenal medulla (when stimulated by the sympathetic nerve)?

A

Adrenaline

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36
Q

What 4 hormones do we not know the role off during trauma?

A

TSH, T4, Oestrogen, Testosterone

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37
Q

What cytokines are released due to an immune response during an initial compromise?

A

TNF-a, IL-1, IL-6

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38
Q

How long does the ebb stage last for post injury?

A

12-24 hours

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39
Q

During an immune response to trauma, what impact do the cytokines have?

A
  • causes local and systemic inflammation
  • activates leucocytes
  • contributes to metabolic changes
  • down-regulates protein-C activity
  • triggers release of ‘acute-phase’ proteins, including fibrinogen
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40
Q

What does fibrinogen do?

A

Clot blood

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41
Q

What is protein-C’s activity?

A

It plays an important role in regulating anti-coagulation, which will decrease risk of thrombosis.

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42
Q

Why may major trauma also lead to coagulopathy?

A

Due to fibrinolysis and activation of Protein-C, which contrasts with hypercoagulation caused by immune response activation, and this results in a dangerously dynamic situation.

43
Q

What was hypercoagulation originally thought to be due from? (Post trauma)

A

Fluids administered during treatment.

44
Q

What is hypercoagulation post trauma actually due too?

A

Dilution of clotting factors in the blood caused by fluid shifting from cells and extracellular fluid into the intravascular compartment.

45
Q

What is generalised coagulopathy (clotting disorder) due from?

A

Intrinsic to trauma response.

46
Q

If immune response triggers hyper-coagulation, what may this result in?

A

Disseminated intravascular coagulation (DIC), which is frequently fatal.

47
Q

When are clotting factors given?

A

Now given with blood units.

48
Q

What is given to reduce small-vessel bleeding?

A

Tranexamic acid (TXA) - prevents excessive blood loss from trauma.

49
Q

What is CRASH-2 trial 2010 and what was found?

A

Clinical randomisation of an anti-fibrinolytic in significant haemorrhage. Early administration of TXA safely reduced the risk of death in bleeding trauma patients and is highly cost-effective. Treatment beyond 3 hours of injury is unlikely to be effective.

50
Q

What happens to glucagon levels and insulin levels in ‘ebb’ phase and why (glycogenolysis)?

A

Glucagon increases (to enable stored glycogen in the liver to be converted to glucose and released into bloodstream), insulin decreases (to prevent glucose in the bloodstream from being resorbed).

51
Q

What increases in the blood due to liver glycogenolysis during ‘ebb’ phase?

A

Blood glucose levels, and blood lactate levels.

52
Q

What process in the muscle occurs due to blood lactate levels increasing, and what increases (and decreases) as a result?

A

Muscle glycogenolysis, adrenaline increases, O2 decreases.

53
Q

What would an increase in glucagon, decrease in insulin and an increase in cortisol lead too during ebb phase?

A

Adipocyte lysis.

54
Q

What 3 molecules increase in the blood as a result of adipocyte lysis?

A

Free fatty acids, glycerol and lactate.

55
Q

Why does lipolysis occur during ?

A

So the free fatty acids that are released can be used by most organs in the body (because they promote gluconeogenesis), leaving glucose for the brain to use.

56
Q

Why are lactic acid and glycerol levels elevated during ebb phase?

A

Muscle uses up local glycogen stores, and through anaerobic glycolysis, lactic acid increases.

57
Q

What requires glucose during trauma?

A
  • brain and erythrocyte for function
  • damaged tissue
  • immune cells
  • muscle (locally derived from muscle glycogen stores and metabolised anaerobically)
58
Q

Where does glucose go from the liver? Where does glucose go from muscle?

A

Liver releases glucose into circulation to maintain elevated blood glucose levels. Muscle uses it for muscle only (local use).

59
Q

What happens if free fatty acid concentration increases?

A

Rate of oxidation of FFA’s by tissues (used for fuel) increases.

60
Q

What are FFA’s converted too, for what process, and by what organ?

A

Converted into glycerol, for use in gluconeogenesis, by the liver.

61
Q

What is lipolysis?

A

Fatty acid metabolism.

62
Q

What happens to levels of: glucagon, insulin, adrenaline and GH during the fasting state?

A

Everything increases except insulin, which decreases. The effects of these hormones are key as they have effects on FFA and glycerol in lipolysis.

63
Q

What 2 hormones stimulate fatty acid release from triglycerides? And where are the fatty acids stored?

A

Adrenaline and glucagon. Stored in adipocyte fat droplets as triacylglycerol (TAG) (3x fatty acids and glycerol).

64
Q

What is insulins role in lipolysis?

A

Counter the responses to adrenaline and glucagon to induce fat storage, hence why insulin decreases so the mechanism of fatty acid release can occur.

65
Q

What physiological changes occur in ‘flow phase’ if circulating blood volume is restored?

A

Vasodilation, increased cardiac output, increased tissue perfusion, increased oxygen consumption, increased metabolic activity, increased body temperature.

66
Q

What is the state of the immune system during flow phase?

A

Fully activated - continuing effects of cytokines.

67
Q

What happens to blood levels and pressure during flow phase?

A

Both are restored.

68
Q

Why are fuel sources still required for proliferating cells during flow phase?

A

For immune system and body repair.

69
Q

What are glycogen stores like during flow phase and what happens to endocrine effects?

A

Glycogen stores are already depleted from ebb phase. Endocrine effects still present.

70
Q

What is the total glycogen store of the body?

A

400-500g

71
Q

How much glycogen does the liver provide?

A

100-150g

72
Q

What is the normal glucose usage (g/min g/h) and how many hours does it supply the body with?

A

0.10 g/min (6g/h). Supplies for around 16-24hr.

73
Q

What is the glucose usage during trauma (g/min g/h) and how long will it supply the body for?

A

0.15g/min (9g/h). Supplies for around 10-15hr.

74
Q

What is gluconeogenesis?

A

Formation of glucose from non-carbohydrate substrates to supply essential needs.

75
Q

What molecules can be used in gluconeogenesis?

A

Amino acids, lactate/lactic acid, glycerol

76
Q

What hormones can stimulate the process of gluconeogenesis?

A

Glucagon, cortisol, adrenaline

77
Q

During fatty acid metabolism, what happens to free fatty acids and what happens to glycerol when both are released from TAG?

A

FFA go into tissues, and glycerol goes into the liver.

78
Q

Which hormone promotes the release of amino acids from skeletal muscle protein?

A

Cortisol.

79
Q

What 2 routes can amino acids undergo after being released from skeletal muscle protein?

A

Can be oxidised directly as fuel in tissues or it can be used by the liver for gluconeogenesis.

80
Q

What promotes the use of amino acids to be used as fuel during flow phase?

A

Increased plasma amino acid levels in the blood.

81
Q

What is amino acid metabolism used to produce?

A

Immune system proteins and proliferating cells.

82
Q

What is glutamine, where is it synthesis and stored?

A

Glutamine is considered an essential amino acid during stress and critical illness, used by immune and other proliferating cells. Synthesised and stored in muscles.

83
Q

Glutamine is promising for use as a ‘nutraceutical’ to aid recovery. What is a nutraceutical?

A

A nutraceutical is a pharmaceutical-grade and standardized nutrient. Regulated as dietary supplements in the US as they don’t have ‘nutraceuticals’.

84
Q

What are insulin levels like during ‘flow phase’? And what are FFA and glucose levels like?(Consider what they’re like during ebb phase.)

A

Insulin levels begin to revise back to normal levels. But cells display a level of ‘insulin resistance’, so glucose and FFA levels remain raised.

85
Q

What are some complications of trauma? (6 to mention)

A

Infection/sepsis (now thought to be a form of SIRS in response to an infection) and complications of multiple injury. Multiple organ failure (MOF). Reperfusion damage. SIRS. Disseminated intravascular coagulation (DIC). Muscle wasting due to loss of protein.

86
Q

Explain MOF.

A

Damage to organs away from the site of injury caused by pro-inflammatory cytokines.

87
Q

Explain reperfusion damage to vascular endothelium.

A

Free radical formation when perfusion improves after a period of ischemia, it leads to damage to capillaries/ small vessels and can lead to MOF

88
Q

Explain SIRS and what hormones/cytokines are thought to play a role in the control of the immune response?

A

Systemic inflammatory response syndrome - uncontrolled immune response leading to widespread inflammation. Cortisol, IL-4, IL-10 thought to play a role in the control of the immune response.

89
Q

Explain DIC and when is it detected?

A

Cause by damage to the endothelial cells and leads to platelet adhesion followed by local thrombosis. Can trigger further damage and disseminated clotting. Frequently fatal. Detected by low platelet levels and clotting factors.

90
Q

Explain muscle wasting and what can it lead too if it gets highly severe.

A

Due to protein breakdown for use in gluconeogenesis but also to synthesis proteins for cell proliferation (wound repair/immune system). Can be so severe, particularly in sepsis patients that it leads to death. Total parenteral nutrition (TPN) support (supplies all daily nutritional requirements).

91
Q

What is the recovery phase and what happens to the metabolic rate during this phase?

A

Anabolic phase. Metabolic rate reduces to ‘normal’. Tissues repair completes and ‘convalescence’ occurs.

92
Q

Summarise what homeostatic mechanisms and the responses of the endocrine and immune system do during trauma?

A

HM’s act to preserve life. E&IS responses cause biochemical changes at metabolic level.

93
Q

What 4* parameters are the same during ebb and flow?

A

Blood glucose, plasma FA’s, blood catecholamines (all increase), and plasma insulin* (both decrease - during flow it gradually increases but due to insulin resistance of the cells, glucose and FA remain high, meaning insulin remains low).

94
Q

What 3 parameters differ during ebb and flow and how?

A

Cardiac output, O2 consumption and body temp. All 3 are low during ebb and high during flow.

95
Q

Even though heart rate increases during trauma, why is cardiac output reduced during ebb phase?

A

Due to reduced circulating blood volume - heart rate increases significantly as the heart attempts to compensate for this.

96
Q

Which cytokine increases glycogenolysis and gluconeogenesis?

A

TNF

97
Q

Which 3 cytokines stimulate muscle protein breakdown and gluconeogenesis?

A

IL-1, TNF, IL-6.

98
Q

Which cytokines increase FA mobilisation?

A

IL-2 and TNF.

99
Q

Which cytokine has emerged as one of the potential mediators that link obesity-derived chronic inflammation with insulin resistance?

A

IL-6.

100
Q

In response to trauma, what does the cytokine IL-1 cause and what cells produce it?

A

Causes fever, hypotension, increases ACTH, insulin and glucagon secretion. Produced by endothelial cells.

101
Q

In response to trauma, what does the cytokine IFN cause and what cells produce it?

A

Fever, myalgia and increase in macrophage activity. Produced by kupffer cells.

102
Q

In response to trauma, what does the cytokine IL-6 cause and what cells produce it?

A

Increase in B-cell proliferation, increase in B-cell antibody synthesis and increase in acute phase protein synthesis.

103
Q

In response to trauma, what does the cytokine

TNF cause and what cells produce it?

A

Fever, increase in vascular permeability and increase in acute phase protein synthesis.

104
Q

Why is the flow phase known as the ‘catabolic’ phase?

A

The metabolic response to stress is mediated by catabolic hormones such as glucagon, catecholamines and corticosteroids and by insulin resistance.

Biochemistry (7 decks)

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