Chapter 10: Nutrition Flashcards

1
Q

Caloric need

A

Approximately 20-25 cal/kg/d

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2
Q

Calories/gram: fat

A

9 Calories/gram

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3
Q

Calories/gram: protein

A

4 calories / gram

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4
Q

Calories/gram: oral carbohydrates

A

4 calories / gram

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5
Q

Calories/gram: dextrose

A

3.4 calories / gram

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6
Q

Nutritional requirements for average healthy male

A
  • 20% protein calories (1g protein/kg/d; 20% should be essential amino acids)
  • 30% fat calories - important for essential fatty acids
  • 50% carbohydrate calories
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7
Q

% kcal requirement increase: trauma, surgery, or sepsis

A

20% - 40%

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8
Q

kcal/day requirement: pregnancy

A

300 kcal / day

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9
Q

kcal/day requirement: lactation

A

500 kcal / day

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10
Q

Calculation: calorie requirement in burns

A

25 kcal/kg/d + (30 kcal/d x % burn)

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11
Q

Calculation: protein requirement in burns

A

1-1.5 g/kg/d + (3g x %burn)

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12
Q

What is much of energy expenditure used for?

A

Heat production

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13
Q

How does fever affect basal metabolic rate?

A

Fever increased BMR 10% for each degree above 38.0 degrees Celsius

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14
Q

Calculation: caloric need in obesity

A

Weight = [(actual weight - ideal body weight) x 0.25] + IBW

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15
Q

Calculates basal energy expenditure based on weight, height, age, and gender

A

Harris-Benedict Equation

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16
Q

Glucose goals central line TPN

A

Glucose based

- Maximum glucose administration -> 3 g/kg/h

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17
Q

Fat based central nutrition

A

Peripheral line parenteral nutrition (PPN) - fat based

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18
Q

Fuel for colonocytes

A

Short-chain fatty acids (e.g., butyric acid)

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19
Q

Fuel for small bowel enterocytes

A

Glutamine

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20
Q
  • MC amino acid in bloodstream and tissue
  • Releases NH4 in kidney, thus helping with nitrogen excretion
  • Can be used for gluconeogenesis
A

Glutamine

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21
Q

Primary fuel for most neoplastic cells

A

Glutamine

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22
Q

Half-life: albumin

A

18 days

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23
Q

Half-life transferrin

A

10 days

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24
Q

Half-life prealbumin

A

2 days

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25
Q

Normal protein level

A

6.0 - 8.5

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26
Q

Normal albumin level

A

3.5 - 5.5

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27
Q

Acute indicators of nutritional status

A

Retinal binding protein.
Prealbumin.
Transferrin.

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28
Q

Ideal body weight:

  • Men
  • Women
A
  • Men = 106lb + 6lb for each inch over 5ft

- Women = 100lb + 5lb for each inch over 5 ft

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29
Q

Preoperative signs of poor nutritional status

A
  • Acute weight loss > 10% in 6 months

- Weight

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30
Q

Strong risk factor for morbidity and mortality after surgery

A

Low albumin (

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31
Q

Ratio of CO2 produced to O2 consumed

A

Respiratory quotient - measurement of energy expenditure

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32
Q

Def: RQ > 1

A

Lipogenesis (overfeeding)
Tx: decreased carbohydrates and caloric intake.
- High carbohydrate intake can lead to CO2 buildup and ventilator problems

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33
Q

Def: RQ

A

Ketosis and fat oxidation (starving)

- Tx: increased carbohydrates and caloric intake

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34
Q

RQ: pure fat utilization

A

RQ = 0.7

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35
Q

RQ: pure protein utilization

A

RQ = 0.8

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36
Q

RQ: pure carbohydrate utilization

A

RQ = 1.0

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37
Q

Post op: diuresis phase

A

Post op days 2-5

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38
Q

Post op: catabolic phase

A

Post op days 0 -3

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39
Q

RQ: pure carbohydrate utilization

A

RQ = 1.0

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40
Q

What is the degree of injury proportional to?

A

The magnitude of metabolic response

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41
Q

When does glycogen deplete?

A

Depleted after 24-36 hours of starvation on (2/3 in skeletal muscle, 1/3 in liver) -> body then switches to fat.

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42
Q

Where is glucose-6-phosphatase found?

A

Only in the liver.

None in skeletal muscle: G6P stays in muscle after breakdown from glycogen and is utilized.

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43
Q

Gluconeogenesis precursors (x4)

A

Amino acids (esp alanine).
Lactate.
Pyruvate.
Glycerol.

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44
Q

Simplest amino acid precursor for gluconeogenesis.

- Primary substrate for gluconeogenesis

A

Alanine

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45
Q

Only amino acids to increase during times of stress

A

Alanine and phenylalanine

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46
Q

Where does gluconeogenesis occur in late starvation?

A

Kidney

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47
Q

Why do protein-conserving mechanisms not happen after trauma?

A

Secondary to catecholamines and cortisol.

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48
Q

Main source of energy in starvation and in trauma

A

Fat (ketones)

- In trauma, energy is more mixed (fat and protein)

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49
Q

% weight loss: pt can tolerate without complications

A

15%

50
Q

When do you consider Dobhoff tube or TPN?

A

After about 7 days without eating.

51
Q

Why do you want to feed gut?

A

To avoid bacterial translocation (bacterial overgrowth, increased permeability due to starved enterocytes, bacteremia) and TPN complications

52
Q

Consider when regular feeding not possible (e.g., CVA) or predicted to not occur for > 4 weeks

A

PEG tube

53
Q

Utilizes ketones with progressive starvation (normally uses glucose)

A

Brain

54
Q

Obligate glucose users

A

Peripheral nerves.
Adrenal medulla.
Red blood cells.
White blood cells.

55
Q
  • Occurs when feeding after prolonged starvation / maturation.
  • Results in decreased K, Mg, PO4-.
  • Causes cardiac dysfunction, profound weakness, encephalopathy.
A

Refeeding syndrome

56
Q

How do you prevent referring syndrome?

A

10 - 15 kcal/kg/d

57
Q
  • Anorexia, weight loss, wasting
  • Thought to be mediated by TNF-alpha
  • Glycogen breakdown, lipolysis, protein catabolism
A

Cachexia

58
Q

Kawshiorkor

A

Protein deficiency

59
Q

Marasmus

A

Starvation

60
Q

gram protein = gram nitrogen

A

6.25g protein = 1g nitrogen

61
Q

Calculate nitrogen balacne

A

Nin-Nout =

[protein/6.25] - [24hr urine N + 4g]

62
Q

More protein ingested than excreted (anabolism)

A

Positive N balance

63
Q

More protein excreted than taken in (catabolism)

A

Negative N balance

64
Q

g/d: total protein synthesis for a healthy, normal 70kg male

A

250 g/d

65
Q
  • Responsible for amino acid production and breakdown

- Urea production is used to get rid of ammonia from amino acid breakdown

A

Liver

66
Q

Amino acids: majority of protein breakdown from skeletal muscle

A

Glutamine and alanine

67
Q

Broken down by pancreatic lipase, cholesterol esterase, and phospholipase to micelles and free fatty acids

A

Triacylglycerides (TAGs), cholesterol, and lipids

68
Q

Aggregates of bile salts, long-chain free fatty acids, and monoacylglycerides
- Enter enterocyte by fusing with membrane

A

Micelles

69
Q

Increase absorption area for fats, helping form micelles

A

Bile salts

70
Q

Used to synthesize bile salts

A

Cholesterol

71
Q

Fat soluble vitamins, absorbed in micelles

A

A, D, E, K

72
Q

Enter enterocyte by simple diffuse

A

Medium and short chain fatty acids

73
Q

Composition of chylomicrons

A

90% TAGS

10% phospholipids / proteins / cholesterol

74
Q

Where do chylomicrons go after they are formed (form micelles and other fatty acids when they enter the enterocytes)?

A

Lymphatics by way of the thoracic duct

75
Q

Enter lymphatics along with chylomicrons

A

Long-chain fatty acids

76
Q

Fatty acids: enter the portal system (same as amino acids and carbohydrates)

A

Medium- and short-chain fatty acids

77
Q

On endothelium in liver and adipose tissue; clears chylomicrons and TAGs from the blood, breaking them down to fatty acids and glycerol

A

Lipoprotein lipase

78
Q

On endothelium in the liver and adipose tissue; binds short and medium-chain fatty acids

A

Free fatty acid-binding protein

79
Q

Used for fuel by cardiac and skeletal muscles

A

Saturated fatty acids

80
Q

Preferred source of energy for colonocytes, liver, heart, and skeletal muscle

A

Fatty acids (ketones - acetoacetate, beta-hyroxybutyrate)

81
Q

Used as structural components for cells

A

Unsaturated fatty acids

82
Q

In fat cells; breaks down TAGS (storage form of fat) to fatty acids and glycol, which are released into the bloodstream; sensitive to growth hormone, catecholamines, glucocorticoids

A

Hormone-sensitive lipase (HSL)

83
Q

Essential fatty acids

A

Linolenic, linoleic

84
Q
  • Needed for prostaglandin synthesis (long-chain fatty acids)
  • Important for immune cells
A

Essential fatty acids (linolenic, linoleum)

85
Q

What does carbohydrate digestion start with?

A

Begins with salivary amylase, then pancreatic amylase and disaccharidases

86
Q

Carbs: absorbed by secondary active transport; released into portal vein

A

Glucose and galactose

87
Q

Carbs: facilitated diffusion, released into portal vein

A

Fructose

88
Q

Fructose + glucose

A

Sucrose

89
Q

Galactose + Glucose

A

Lactose

90
Q

Glucose + Glucose

A

Maltose

91
Q

What does protein digestion begin with?

A

Stomach pepsin, then trypsin, chymotrypsin, and carboxypeptidase

92
Q

Released from pancreas and activated by enterokinase, which is release from the duodenum

A

Trypsinogen

93
Q

What releases enterokinase?

A

Duodenum

94
Q

Activates trypsinogen

A

Enterokinase

95
Q
  • Activates pancreatic protein enzymes

- Can auto activate other trypsinogen molecules

A

Trypsin

96
Q

Broken down to amino acids, dipeptides, and tripeptides by proteases

A

Protein

97
Q

How is protein absorbed?

A

Secondary active transport

98
Q

Where are free amino acids released after protein digestion?

A

Into portal vein

99
Q

Why limit protein intake in liver and renal failure?

A

To avoid ammonia buildup and possible worsening encephalopathy

100
Q

Branched chain amino acids

A

Leucine, isoleucine, valine (“LIV”)

101
Q
  • Metabolized in muscle
  • Possibly important in patients with liver failure
  • Are essential amino acids
A

Branched-chain amino acids (LIV: leucine, isoleucine, valine)

102
Q

Essential amino acids

A

Leucine, isoleucine, valine, arginine, histidine, lysine, methionin, phenylalanine, threonine, and tryptophan

103
Q

General composition TPN

A
  • 10% amino acid
  • 50% dextrose
  • Electrolyes (Na, Cl, K, Ca, -Mg, PO4, Acetate)
  • Mineral and vitamine
  • Lipids (given separately from TPN)
104
Q

Deficiency: Chromium

A

Hyperglycemia, encephalopathy, neuropathy

105
Q

Deficiency: Selenium

A

Cardiomyopathy, weakness

106
Q

Deficiency: Copper

A

Pancytopenia

107
Q

Deficiency: Zinc

A

Poor wound healing

108
Q

Deficiency: Phosphate

A

Weakness (failure to wean off ventilator), encephalopathy, decreased phagocytosis

109
Q

Deficiency: Thiamine (B1)

A

Wernicke’s encephalaopthy, cardiomyopathy

110
Q

Deficiency: Pyridoxine (B6)

A

Sideroblastic anemia, glossitis, peripheral neuropathy

111
Q

Deficiency: Cobalamin (B12)

A

Megaloblastic anemia, peripheral neuropathy, beefy tongue

112
Q

Deficiency: Folate

A

Megaloblastic anemia, glossitis

113
Q

Deficiency: Niacin

A

Pellagra (diarrhea, dermatitis, dementia)

114
Q

Deficiency: Essential fatty acids

A

Dermatitis, hair loss, thrombocytopenia

115
Q

Deficiency: Vitamin A

A

Night blindness

116
Q

Deficiency: Vitamin K

A

Coagulopathy

117
Q

Deficiency: Vitamin D

A

Rickets, osteomalacia, osteoporosis

118
Q

Deficiency: Vitamin E

A

Neuropathy

119
Q

Glucose is utilized and converted to lactate in muscle

A

Cori Cycle

120
Q

Goes to liver and is converted back to pyruvate and eventually glucose via gluconeogenesis

A

Lactate