Diseases of GI Tract - Trauma and Nutrition (23) Flashcards
(146 cards)
1
Q
Trauma
A
An injury/wound to living tissue caused by an extrinsic agent
2
Q
Trauma
A
An injury/wound to living tissue caused by an extrinsic agent
3
Q
Examples of trauma
A
RTA, stabbing, gunshot wound, burns, tumour excision, caesarean section, amputation of diabetic foot
4
Q
Immediate features of physical trauma
A
Intravascular fluid loss, extravascular volume, tissue destruction, obstructed/impaired breathing
5
Q
Later feature of physical trauma
A
Starvation, infection, inflammation
6
Q
Consequences of fractures and internal injuries
A
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
Q
What is shock?
A
Interruption to the supply of substrates to cells (O2, glucose, water, lipids, aa, micronutrients) and removal (CO2, water, free radicals, toxic metabolites)
8
Q
Phase 1 of shock
A
Clinical shock
9
Q
Phase 2 of shock
A
Hyper catabolic state
10
Q
Phase 3 of shock
A
Recovery - anabolic state
11
Q
Causes of shock
A
Injury, surgery, burns, infection
12
Q
Phase 1 (shock) develops how soon after injury?
A
2-6 hours
13
Q
How long does phase 1 shock last
A
24-48 hours
14
Q
What is secreted in phase 1 shock?
A
Cytokines, catecholamines and cortisol
15
Q
What happens in Phase 1 shock?
A
Tachycardia, high RR, peripheral vasoconstriction, hypovolemia
16
Q
Primary aims in Phase 1 shock
A
Stop bleeding and prevent infection
17
Q
Phase 2 (catabolic) develops how soon after injury?
A
2 days
18
Q
Phase 2 (catabolic) how long does it last?
A
Necessary for survival but if persists/severe > increase mortality
19
Q
Phase 2 (catabolic) what is secreted?
A
Catecholamines, glucagon, ACTH > cortisol
20
Q
What happens in Phase 2 (catabolic)?
A
Increased O2 consumption, metabolic rate, negative nitrogen balance (breakdown aa), glycolysis, lipolysis
21
Q
Primary aims in Phase 2 (catabolic)
A
Avoid sepsis and provide adequate nutrition
22
Q
When does phase 3 (anabolic) occur?
A
3-8 days after uncomplicated surgery, coincides with beginning of diuresis and request for oral intake
23
Q
What is diuresis?
A
Increased urine output, lots of waste removed by kidneys
24
Q
What happens in phase 3 (anabolic)?
A
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
