Diseases of GI Tract - Trauma and Nutrition (23) Flashcards Preview

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Flashcards in Diseases of GI Tract - Trauma and Nutrition (23) Deck (146):
1

Trauma

An injury/wound to living tissue caused by an extrinsic agent

2

Trauma

An injury/wound to living tissue caused by an extrinsic agent

3

Examples of trauma

RTA, stabbing, gunshot wound, burns, tumour excision, caesarean section, amputation of diabetic foot

4

Immediate features of physical trauma

Intravascular fluid loss, extravascular volume, tissue destruction, obstructed/impaired breathing

5

Later feature of physical trauma

Starvation, infection, inflammation

6

Consequences of fractures and internal injuries

Blood loss, impaired breathing and infection penetration (decrease circulating vol, RBC, WBC, CO/BP, organ perfusion, energy substrate delivery to cells/tissues), major organ dysfunction

7

What is shock?

Interruption to the supply of substrates to cells (O2, glucose, water, lipids, aa, micronutrients) and removal (CO2, water, free radicals, toxic metabolites)

8

Phase 1 of shock

Clinical shock

9

Phase 2 of shock

Hyper catabolic state

10

Phase 3 of shock

Recovery - anabolic state

11

Causes of shock

Injury, surgery, burns, infection

12

Phase 1 (shock) develops how soon after injury?

2-6 hours

13

How long does phase 1 shock last

24-48 hours

14

What is secreted in phase 1 shock?

Cytokines, catecholamines and cortisol

15

What happens in Phase 1 shock?

Tachycardia, high RR, peripheral vasoconstriction, hypovolemia

16

Primary aims in Phase 1 shock

Stop bleeding and prevent infection

17

Phase 2 (catabolic) develops how soon after injury?

2 days

18

Phase 2 (catabolic) how long does it last?

Necessary for survival but if persists/severe > increase mortality

19

Phase 2 (catabolic) what is secreted?

Catecholamines, glucagon, ACTH > cortisol

20

What happens in Phase 2 (catabolic)?

Increased O2 consumption, metabolic rate, negative nitrogen balance (breakdown aa), glycolysis, lipolysis

21

Primary aims in Phase 2 (catabolic)

Avoid sepsis and provide adequate nutrition

22

When does phase 3 (anabolic) occur?

3-8 days after uncomplicated surgery, coincides with beginning of diuresis and request for oral intake

23

What is diuresis?

Increased urine output, lots of waste removed by kidneys

24

What happens in phase 3 (anabolic)?

Gradual restoration of protein synthesis, N2 balance, fat stores, muscle strength

25

Primary aims of phase 3 (anabolic)

Adequate nutrition (refeeding syndrome risk), obesity paradox

26

What is obesity paradox?

Recover better if obese

27

How long does phase 3 (anabolic) last?

A few weeks/months

28

Inflammatory response at a trauma site

1. Bacteria and pathogens enter wound
2. Platelets release clotting factors
3. Mast cells secrete factors that mediate vasodilation to increase blood delivery to injured area
4. Neutrophils and macrophages recruited to phagocytose pathogens
5. Macrophages secrete cytokines to attract immune cells and proliferate inflammatory response
6. Continues until wound is healed

29

When capillaries leak what do they release?

H2O, NaCl, Albumin and energy substrates

30

Which cytokines are involved in inflammation?

IL-1, IL-6, TNF

31

What does cytokine release cause?

- Chemotaxis, vasoldilation, cell adhesion proteins
- Catabolic and anabolic effects
- Anorexia
- T cell activation and B cell proliferation
- Activation of acute phase proteins
- Fever
- Fibroblast proliferation (repair)

32

5 cardinal signs of inflammation

1. Heat
2. Redness
3. Swelling
4. Pain
5. Loss of function

33

Cytokines and catabolic hormones

(IL-1 and TNF-a), Increase ACTH (cortisol), glucagon and catecholamines

34

Cytokines and anabolic hormones

Decrease GH and insulin

35

How long can glycogen stores maintain conc of glucose for?

Up to 24hrs

36

How long will brain survive in circulatory failure?

No more than 2 minutes

37

What does normal metabolism involve?

Oxidation of dietary carbohydrate, lipid and proteins

38

How long can kidney and liver survive, and why?

Hours due to being capable of gluconeogenesis

39

What substrates can liver and kidney use for energy?

Fatty acids or aa

40

What substrates can skeletal muscle use for energy?

Glycogen stores or fatty acids

41

Metabolic response to trauma - glucose

1. Glycogenolysis
2. Gluconeogenesis
3. Lipolysis and ketogenesis

42

Glycogenolysis

(24 hours max) Glycogen > glucose

43

Gluconeogenesis

- Break down of skeletal muscle (1kg muscle = 120g glucose)
- aa > glucose and lactate production
- Nitrogen loss 60-300g/day

44

Lipolysis and ketogenesis

- FFA > acetyl CoA > acetoacetate and hydroxybutyrate
- Change to ketone metabolism (sparing protein stores and muscles)

45

Problems with ketones

Acids and cause a diuresis (loss of H20 and electrolytes)

46

Aerobic metabolism

Glycolysis, tricarboxylic aid cycle, oxidative phosphorylation

1 mole of glucose > 36 ATP

47

Anaerobic metabolism

1 mole of glucose > 2 ATP

48

Loss of ATP leads to

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

49

Lactic acidosis pH

50

Lactic acidosis [H+]

> 60 nmol/L

51

Lactic acidosis [lactate]

> 5.0 nmol/L

52

Increase skeletal muscle proteolysis due to

- Increase free amino acids > liver > gluconeogenesis and protein synthesis
- Increase plasma [NH4+]
- Increase N2 loss (urinary excretion of urea)

53

Decrease synthesis of new protein

- Increase inflammatory modulators and scavengers (CRP, haptoglobin, clotting factors, protease inhibitors)
- Decrease albumin

54

Starvation and lack of protein

Increase calories to prevent muscle wasting

55

Sepsis/trauma and lack of protein

Increasing calories won't help as protein breakdown is caused by cytokine release from activated macrophages

56

Lactate production

- Pyruvate doesn't undergo oxidative phosphorylation via TCA cycle > reduced to lactate
- anaerobic metabolism can only continue until becomes toxic [lactate]
- [H+] inhibits enzymes and > tissue hypoxia

57

what amount of Blood lactate mmol/L post trauma leads to 100% mortality?

>5 mmol/L

58

Lactate vicious cycle

Mitochondrial failure (hypoxia) > decrease in oxidative phosphorylation > NADH > NAD+ > anaerobic glycolysis

59

When does nitrogen loss peak?

4-8 days

60

What does immobilisation increase the loss of?

Ca, Ph, Mg

61

Primary malnutrition

Protein-calorie (starvation) and nutrient deficiencies

62

Secondary malnutrition

Nutrients present but appetite suppressed/absorption, increased demand for specific nutrients

63

Consequences of malnutrition

- Neg N2 balance
- Muscle wasting
- Widespread cellular dysfunction

64

What is malnutrition associated with?

Infection, poor wound healing, changes in drug metabolism, prolonged hospitalisation, increased mortality

65

Refeeding syndrome

Metabolism catabolic > anabolic, cellular uptake of K, Ph and Mg and salt and water retention (oedema)

66

How many newborn infants does CF affect in UK?

1/2,500

67

CFTR protein

cAMP dependent Cl- channel, localises to the apical membrane of secretory and absorptive epithelial cells with airways, pancreas, liver, intestine, sweat glands and vas deferens

68

CFTR protein function

Facilitates production of thin, watery, free-flowing mucus (lubricates airways and secretory ducts and protects airways, digestive and reproductive system)

69

Lung disease and CFTR

Increase bacterial colonisation and neutrophils, elastase secreted which digests lung proteins, dead neutrophils released DNA > increase viscosity of CF sputum > mucous plugging

70

GI disease in CF

- Meconium ileus at birth
- Hepatobiliary disease (hepatic metabolism of lipids, steroids, drugs and toxins compromised)
- Pancreatic cysts, exocrine insufficiency (decrease insulin, lipase and proteases)

71

Symptoms of GI disease in CF

Poor appetite, failure to thrive and low weight

72

CF respiratory disease treatment

Physio, exercise, bronchodilators, antibiotics, steroids, mucloytics (DNase)

73

GI disease

Pancreatic enzyme replacement (Creon), nutritional supplements, high calorie diet, Ursodeoxycholic acid

74

Ursodeoxycholic acid

Maintain body weight, avoid catabolic state, introduce artificial feed early if sick

75

Examples of trauma

RTA, stabbing, gunshot wound, burns, tumour excision, caesarean section, amputation of diabetic foot

76

Immediate features of physical trauma

Intravascular fluid loss, extravascular volume, tissue destruction, obstructed/impaired breathing

77

Later feature of physical trauma

Starvation, infection, inflammation

78

Consequences of fractures and internal injuries

Blood loss, impaired breathing and infection penetration (decrease circulating vol, RBC, WBC, CO/BP, organ perfusion, energy substrate delivery to cells/tissues), major organ dysfunction

79

What is shock?

Interruption to the supply of substrates to cells (O2, glucose, water, lipids, aa, micronutrients) and removal (CO2, water, free radicals, toxic metabolites)

80

Phase 1 of shock

Clinical shock

81

Phase 2 of shock

Hyper catabolic state

82

Phase 3 of shock

Recovery - anabolic state

83

Causes of shock

Injury, surgery, burns, infection

84

Phase 1 (shock) develops how soon after injury?

2-6 hours

85

How long does phase 1 shock last

24-48 hours

86

What is secreted in phase 1 shock?

Cytokines, catecholamines and cortisol

87

What happens in Phase 1 shock?

Tachycardia, high RR, peripheral vasoconstriction, hypovolemia

88

Primary aims in Phase 1 shock

Stop bleeding and prevent infection

89

Phase 2 (catabolic) develops how soon after injury?

2 days

90

Phase 2 (catabolic) how long does it last?

Necessary for survival but if persists/severe > increase mortality

91

Phase 2 (catabolic) what is secreted?

Catecholamines, glucagon, ACTH > cortisol

92

What happens in Phase 2 (catabolic)?

Increased O2 consumption, metabolic rate, negative nitrogen balance (breakdown aa), glycolysis, lipolysis

93

Primary aims in Phase 2 (catabolic)

Avoid sepsis and provide adequate nutrition

94

When does phase 3 (anabolic) occur?

3-8 days after uncomplicated surgery, coincides with beginning of diuresis and request for oral intake

95

What is diuresis?

Increased urine output, lots of waste removed by kidneys

96

What happens in phase 3 (anabolic)?

Gradual restoration of protein synthesis, N2 balance, fat stores, muscle strength

97

Primary aims of phase 3 (anabolic)

Adequate nutrition (refeeding syndrome risk), obesity paradox

98

What is obesity paradox?

Recover better if obese

99

How long does phase 3 (anabolic) last?

A few weeks/months

100

Inflammatory response at a trauma site

1. Bacteria and pathogens enter wound
2. Platelets release clotting factors
3. Mast cells secrete factors that mediate vasodilation to increase blood delivery to injured area
4. Neutrophils and macrophages recruited to phagocytose pathogens
5. Macrophages secrete cytokines to attract immune cells and proliferate inflammatory response
6. Continues until wound is healed

101

When capillaries leak what do they release?

H2O, NaCl, Albumin and energy substrates

102

Which cytokines are involved in inflammation?

IL-1, IL-6, TNF

103

What does cytokine release cause?

- Chemotaxis, vasoldilation, cell adhesion proteins
- Catabolic and anabolic effects
- Anorexia
- T cell activation and B cell proliferation
- Activation of acute phase proteins
- Fever
- Fibroblast proliferation (repair)

104

5 cardinal signs of inflammation

1. Heat
2. Redness
3. Swelling
4. Pain
5. Loss of function

105

Cytokines and catabolic hormones

(IL-1 and TNF-a), Increase ACTH (cortisol), glucagon and catecholamines

106

Cytokines and anabolic hormones

Decrease GH and insulin

107

How long can glycogen stores maintain conc of glucose for?

Up to 24hrs

108

How long will brain survive in circulatory failure?

No more than 2 minutes

109

What does normal metabolism involve?

Oxidation of dietary carbohydrate, lipid and proteins

110

How long can kidney and liver survive, and why?

Hours due to being capable of gluconeogenesis

111

What substrates can liver and kidney use for energy?

Fatty acids or aa

112

What substrates can skeletal muscle use for energy?

Glycogen stores or fatty acids

113

Metabolic response to trauma - glucose

1. Glycogenolysis
2. Gluconeogenesis
3. Lipolysis and ketogenesis

114

Glycogenolysis

(24 hours max) Glycogen > glucose

115

Gluconeogenesis

- Break down of skeletal muscle (1kg muscle = 120g glucose)
- aa > glucose and lactate production
- Nitrogen loss 60-300g/day

116

Lipolysis and ketogenesis

- FFA > acetyl CoA > acetoacetate and hydroxybutyrate
- Change to ketone metabolism (sparing protein stores and muscles)

117

Problems with ketones

Acids and cause a diuresis (loss of H20 and electrolytes)

118

Aerobic metabolism

Glycolysis, tricarboxylic aid cycle, oxidative phosphorylation

1 mole of glucose > 36 ATP

119

Anaerobic metabolism

1 mole of glucose > 2 ATP

120

Loss of ATP leads to

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

121

Lactic acidosis pH

122

Lactic acidosis [H+]

> 60 nmol/L

123

Lactic acidosis [lactate]

> 5.0 nmol/L

124

Increase skeletal muscle proteolysis due to

- Increase free amino acids > liver > gluconeogenesis and protein synthesis
- Increase plasma [NH4+]
- Increase N2 loss (urinary excretion of urea)

125

Decrease synthesis of new protein

- Increase inflammatory modulators and scavengers (CRP, haptoglobin, clotting factors, protease inhibitors)
- Decrease albumin

126

Starvation and lack of protein

Increase calories to prevent muscle wasting

127

Sepsis/trauma and lack of protein

Increasing calories won't help as protein breakdown is caused by cytokine release from activated macrophages

128

Lactate production

- Pyruvate doesn't undergo oxidative phosphorylation via TCA cycle > reduced to lactate
- anaerobic metabolism can only continue until becomes toxic [lactate]
- [H+] inhibits enzymes and > tissue hypoxia

129

what amount of Blood lactate mmol/L post trauma leads to 100% mortality?

>5 mmol/L

130

Lactate vicious cycle

Mitochondrial failure (hypoxia) > decrease in oxidative phosphorylation > NADH > NAD+ > anaerobic glycolysis

131

When does nitrogen loss peak?

4-8 days

132

What does immobilisation increase the loss of?

Ca, Ph, Mg

133

Primary malnutrition

Protein-calorie (starvation) and nutrient deficiencies

134

Secondary malnutrition

Nutrients present but appetite suppressed/absorption, increased demand for specific nutrients

135

Consequences of malnutrition

- Neg N2 balance
- Muscle wasting
- Widespread cellular dysfunction

136

What is malnutrition associated with?

Infection, poor wound healing, changes in drug metabolism, prolonged hospitalisation, increased mortality

137

Refeeding syndrome

Metabolism catabolic > anabolic, cellular uptake of K, Ph and Mg and salt and water retention (oedema)

138

How many newborn infants does CF affect in UK?

1/2,500

139

CFTR protein

cAMP dependent Cl- channel, localises to the apical membrane of secretory and absorptive epithelial cells with airways, pancreas, liver, intestine, sweat glands and vas deferens

140

CFTR protein function

Facilitates production of thin, watery, free-flowing mucus (lubricates airways and secretory ducts and protects airways, digestive and reproductive system)

141

Lung disease and CFTR

Increase bacterial colonisation and neutrophils, elastase secreted which digests lung proteins, dead neutrophils released DNA > increase viscosity of CF sputum > mucous plugging

142

GI disease in CF

- Meconium ileus at birth
- Hepatobiliary disease (hepatic metabolism of lipids, steroids, drugs and toxins compromised)
- Pancreatic cysts, exocrine insufficiency (decrease insulin, lipase and proteases)

143

Symptoms of GI disease in CF

Poor appetite, failure to thrive and low weight

144

CF respiratory disease treatment

Physio, exercise, bronchodilators, antibiotics, steroids, mucloytics (DNase)

145

GI disease

Pancreatic enzyme replacement (Creon), nutritional supplements, high calorie diet, Ursodeoxycholic acid

146

Ursodeoxycholic acid

Maintain body weight, avoid catabolic state, introduce artificial feed early if sick

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