Right 2 Flashcards

1
Q

The average energy intake is

A

~2600 kcal/d for American
men and ~1800 kcal/d for American women, though these estimates
vary with body size and activity level.

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2
Q

Formulas for roughly estimating
REE are useful in assessing the energy needs of an individual whose
weight is stable. Thus,

A

for males, REE = 900 + 10m, and for females,

REE = 700 + 7m, where is m mass in kilograms

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3
Q

The calculated REE

is then adjusted for physical activity level by multiplying by

A

1.2 for

sedentary, 1.4 for moderately active, or 1.8 for very active individuals.

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4
Q

The nine essential

amino acids are

A

histidine, isoleucine, leucine, lysine, methionine/

cystine, phenylalanine/tyrosine, threonine, tryptophan, and valine

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5
Q

For adults, the recommended dietary allowance (RDA) for protein

A

is ~0.6 g/kg desirable body mass per day, assuming that energy needs
are met and that the protein is of relatively high biologic value. Current
recommendations for a healthy diet call for at least 10–14% of calories
from protein

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6
Q

Fats are a concentrated source of energy and
constitute, on average, 34% of calories in U.S. diets. However, for
optimal health, fat intake should total

A

no more than 30% of calories.
Saturated fat and trans fat should be limited to <10% of calories and
polyunsaturated fats to <10% of calories, with monounsaturated fats
accounting for the remainder of fat intake

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7
Q

least 45–55% of total

calories should be derived from carbohydrates. The brain requires

A

~100 g of glucose per day for fuel; other tissues use about 50 g/d. Some
tissues (e.g., brain and red blood cells) rely on glucose supplied either
exogenously or from muscle proteolysis. Over time, adaptations in
carbohydrate needs are possible during hypocaloric states. Like fat
(9 kcal/g), carbohydrate (4 kcal/g), and protein (4 kcal/g), alcohol
(ethanol) provides energy (7 kcal/g)

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8
Q

For adults, 1–1.5 mL of water per kilocalorie of energy expenditure
is sufficient under usual conditions to allow for normal variations
in physical activity, sweating, and solute load of the diet.

A

Water
losses include 50–100 mL/d in the feces; 500–1000 mL/d by evaporation
or exhalation; and, depending on the renal solute load, ≥1000
mL/d in the urine. I

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9
Q

Fever increases water losses by

~200 mL/d per °C; diarrheal losses vary but may be as great as

A

5 L/d

in severe diarrhea.

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10
Q

When renal function is normal and solute
intakes are adequate, the kidneys can adjust to increased water intake
by excreting up to

A

18 L of excess water per day

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11
Q

Increased water needs during pregnancy are ~30 mL/d.

A

During lactation, milk production increases daily water requirements
so that ~1000 mL of additional water is needed, or 1 mL for each milliliter
of milk produced

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12
Q

benchmark recommendations regarding

nutrient intakes have been developed to guide clinical practice.

A

These
quantitative estimates of nutrient intakes are collectively referred to
as the dietary reference intakes (DRIs

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13
Q

Thiamine deficiency is therefore

more common in cultures that rely heavily on a

A

rice-based diet.
Tea, coffee (regular and decaffeinated), raw fish, and shellfish contain
thiaminases, which can destroy the vitamin

drinking large
amounts of tea or coffee can theoretically lower thiamine body stores.

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14
Q

In Western countries, the primary causes of

thiamine deficiency are alcoholism and chronic illnesses such as cancer.

A

Alcohol interferes directly with the absorption of thiamine and
with the synthesis of thiamine pyrophosphate, and it increases urinary
excretion. Thiamine should always be replenished when a patient with
alcoholism is being refed, as carbohydrate repletion without adequate
thiamine can precipitate acute thiamine deficiency with lactic acidosis

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15
Q

Wet beriberi presents primarily
with cardiovascular symptoms that are due to impaired myocardial
energy metabolism and dysautonomia

A

; it can occur after 3 months
of a thiamine-deficient diet. Patients present with an enlarged heart,
tachycardia, high-output congestive heart failure, peripheral edema

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16
Q

dry beriberi present with a symmetric
peripheral neuropathy of the motor and sensory systems, with
diminished reflexes.

A

The neuropathy affects the legs most markedly,

and patients have difficulty rising from a squatting position

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17
Q

Alcoholic patients with chronic thiamine deficiency also may have
central nervous system (CNS) manifestations known as

A

Wernicke’s
encephalopathy, which consists of horizontal nystagmus, ophthalmoplegia
(due to weakness of one or more extraocular muscles),
cerebellar ataxia, and mental impairment (Chap. 467). When there
is an additional loss of memory and a confabulatory psychosis, the
syndrome is known as Wernicke-Korsakoff syndrome. Despite the
typical clinical picture and history, Wernicke-Korsakoff syndrome is
underdiagnosed.

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18
Q

The laboratory diagnosis of thiamine deficiency usually is made by
a functional enzymatic assay of transketolase activity measured before
and after the addition of thiamine pyrophosphate.

A

A >25% stimulation
in response to the addition of thiamine pyrophosphate (i.e., an activity
coefficient of 1.25) is interpreted as abnormal.

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19
Q

In acute thiamine deficiency with either cardiovascular or neurologic signs,

A

200 mg of thiamine three times daily should be given intravenously
until there is no further improvement in acute symptoms;
oral thiamine (10 mg/d) should subsequently be given until recovery
is complete.

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20
Q

niacin refers to nicotinic acid and nicotinamide and their
biologically active derivatives. Nicotinic acid and nicotinamide serve
as precursors of two coenzymes,

A

nicotinamide adenine dinucleotide
(NAD) and NAD phosphate (NADP), which are important in numerous
oxidation and reduction reactions in the body.

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21
Q

Niacin deficiency causes

A

pellagra, which is found
mostly among people eating corn-based diets in parts of China,
Africa, and India.

Pellagra in North America is found mainly
among alcoholics; among patients with congenital defects of intestinal
and kidney absorption of tryptophan (Hartnup disease

Bright red glossitis then ensues and is
followed by a characteristic skin rash that is pigmented and scaling,
particularly in skin areas exposed to sunlight. This rash is known as
Casal’s necklace because it forms a ring around the neck

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22
Q

The primary
manifestations of this syndrome are sometimes referred to as “the
four D’s”:

A

dermatitis, diarrhea, and dementia leading to death.

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23
Q

Treatment of pellagra consists of oral supplementation with

A

100– 200 mg of nicotinamide or nicotinic acid three times daily for 5 days.
High doses of nicotinic acid (2 g/d in a time-release form) are used
for the treatment of elevated cholesterol and triglyceride levels and/
or low high-density lipoprotein cholesterol levels

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24
Q

is also important for connective tissue
metabolism and cross-linking (proline hydroxylation), and it is a component
of many drug-metabolizing enzyme systems, particularly the
mixed-function oxidase systems.

A

Vitamin C

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25
Q

Administration of vitamin C (200 mg/d) improves the symptoms

of scurvy within several days.

A

High-dose vitamin C supplementation
(e.g., 1–2 g/d) may slightly decrease the symptoms and duration of
upper respiratory tract infections.

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26
Q

Vitamin C supplementation has also

been reported to be useful in

A

Chédiak-Higashi syndrome (Chap. 80)

and osteogenesis imperfecta

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27
Q

Taking g of vitamin C in a single dose may result in
abdominal pain, diarrhea, and nausea. Since vitamin C may be
metabolized to oxalate, it is feared that chronic high-dose vitamin C
supplementation could result in an increased prevalence of kidney
stones. However, except in patients with preexisting renal disease, this
association has not been borne out in several trials

A

> 2

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28
Q

is a water-soluble vitamin that plays a role in gene expression,
gluconeogenesis, and fatty acid synthesis and serves as a CO2 carrier on
the surface of both cytosolic and mitochondrial carboxylase enzymes.

A

Biotin

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29
Q

is believed to have caused
the “burning feet syndrome” seen in prisoners of war during World
War II.

A

Pantothenic acid deficiency

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30
Q

is a precursor for acetylcholine, phospholipids, and betaine.

Choline is necessary for the structural integrity of cell membranes, cholinergic neurotransmission, lipid and cholesterol metabolism, methyl-group metabolism, and transmembrane signaling

A

Choline

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31
Q

Retinaldehyde
(11-cis) is the essential form of vitamin A that is required for normal
vision, whereas

A

retinoic acid is necessary for normal morphogenesis,

growth, and cell differentiation.

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32
Q

is the most prevalent carotenoid

with provitamin A activity in the food supply

A

β-Carotene

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33
Q

VIt A deficiency

This condition
includes milder stages of night blindness and conjunctival xerosis (dryness)
with Bitot’s spots (white patches of keratinized epithelium
appearing on the sclera) as well as rare, potentially blinding corneal
ulceration and necrosis.

A

Keratomalacia (softening of the cornea) leads

to corneal scarring

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34
Q

Any stage of xerophthalmia should be treated with

A

60 mg (or RAE) of vitamin A in oily solution, usually contained in a soft-gel capsule.
The same dose is repeated 1 and 14 days later. Doses should be
reduced by half for patients 6–11 months of age. Mothers with night
blindness or Bitot’s spots should be given vitamin A orally–either 3
mg daily or 7.5 mg twice a week for 3 months

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35
Q

Infants 6–11 months of age should

receive 30 mg vitamin A;

A

children 12–59 months of age, 60 mg.
For reasons that are not clear, vitamin A supplementation has not
proven useful in high-risk settings for preventing morbidity or death
among infants 1–5 months of age.

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36
Q

vit a toxicity

A
Acute toxicity
is manifested by increased intracranial pressure, vertigo, diplopia,
bulging fontanels (in children), seizures, and exfoliative dermatitis
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37
Q

represents the classic disease of
vitamin D deficiency. Signs of deficiency are muscle soreness, weakness,
and bone pain. Some of these effects are independent of calcium
intake.

A

Rickets

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38
Q

There are two natural forms of vitamin K:

A

vitamin K1, also known as
phylloquinone, from vegetable and animal sources, and vitamin K2,
or menaquinone, which is synthesized by bacterial flora and found in
hepatic tissue. Phylloquinone can be converted to menaquinone in
some organs.

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39
Q

Vitamin K is required for the posttranslational carboxylation of glutamic
acid,

A

which is necessary for calcium binding to γ-carboxylated
proteins such as prothrombin (factor II); factors VII, IX, and X;
protein C; protein S; and proteins found in bone (osteocalcin) and vascular
smooth muscle (e.g., matrix Gla protein).

40
Q

Vitamin K is found in

A

green leafy vegetables such as
kale and spinach, and appreciable amounts are also present in margarine
and liver. Vitamin K is present in vegetable oils; olive, canola, and
soybean oils are particularly rich sources

41
Q

The symptoms of vitamin K deficiency are due to hemorrhage;

A

newborns are particularly susceptible because of low fat stores,
low breast milk levels of vitamin K, relative sterility of the infantile
intestinal tract, liver immaturity, and poor placental transport.
Intracranial bleeding as well as gastrointestinal and skin bleeding can
occur in vitamin K–deficient infants 1–7 days after birth. Thus, vitamin
K (0.5–1 mg IM) is given prophylactically at delivery.

42
Q

Vitamin K deficiency

A

is treated with a parenteral dose of 10 mg. For patients with chronic
malabsorption, 1–2 mg/d should be given orally or 1–2 mg per week
can be taken parenterally

43
Q

is an integral component of many metalloenzymes in the body;
it is involved in the synthesis and stabilization of proteins, DNA, and
RNA and plays a structural role in ribosomes and membranes

A

Zinc

44
Q

mild chronic zinc
deficiency can cause stunted growth in children, decreased taste sensation
(hypogeusia), and impaired immune function. Severe chronic zinc
deficiency has been described as a cause of hypogonadism and dwarfism
in several Middle Eastern countries. In these children, hypopigmented
hair is also part of the syndrome.

A

Acrodermatitis enteropathica
is a rare autosomal recessive disorder characterized by abnormalities in
zinc absorption.

45
Q

Zinc (20 mg/d until recovery) may be an effective adjunctive

A

therapeutic strategy for diarrheal disease and pneumonia in children
≥ 6 months of age.

46
Q

is
an X-linked metabolic disturbance of copper metabolism characterized
by mental retardation, hypocupremia, and decreased circulating
ceruloplasmin

A

Menkes kinky hair syndrome

47
Q

The diagnosis of is usually based on low serum
levels of copper (<65 μg/dL) and low ceruloplasmin levels (<20 mg/
dL).

A

copper deficiency

48
Q

Serum levels of copper may be elevated

A

in pregnancy or stress
conditions since ceruloplasmin is an acute-phase reactant and 90% of
circulating copper is bound to ceruloplasmin.

49
Q

is an endemic
cardiomyopathy found in children and young women residing in
regions of China where dietary intake of selenium is low (<20 μg/d).

A

Keshan disease

50
Q

Malnutrition can arise from primary or secondary causes, resulting
in the former case from inadequate or poor-quality food intake
and in the latter case from

A

diseases that alter food intake or nutrient

requirements, metabolism, or absorption.

51
Q

Primary malnutrition
occurs mainly in developing countries and under conditions of political
unrest, war, or famine.

A

Secondary malnutrition, the main form
encountered in industrialized countries, was largely unrecognized
until the early 1970s, when it was appreciated that persons with adequate
food supplies can become malnourished as a result of acute or
chronic diseases that alter nutrient intake or metabolism, particularly
diseases that cause acute or chronic inflammation

52
Q

Marasmus is the end result of

a long-term deficit of dietary energy, whereas kwashiorkor

A

has been

understood to result from a protein-poor diet

53
Q

is a state in which virtually
all available body fat stores have been exhausted due to starvation
without systemic inflammation

A

Marasmus (starvation–related malnutrition)

54
Q

is a state that involves substantial loss of lean body mass

in the presence of chronic systemic inflammation

A

Cachexia (chronic disease–related

malnutrition)

55
Q

Acute ↓ energy and protein
intake with substantial
systemic inflammation

A

Kwashiorkor (Acute
Disease– or Injury–
Related Malnutrition)

56
Q

kwashiorkor

A

The major sine qua non is
severe reduction of levels of serum proteins such as albumin (<2.8 g/dL)
and transferrin (<150 mg/dL) or of iron-binding capacity (<200 μg/dL).
Cellular immune function is depressed, as reflected by lymphopenia
(<1500 lymphocytes/μL in adults and older children) and lack of
response to skin test antigens (anergy

57
Q

After ~10 days of total starvation, an unstressed
individual loses about 12–18 g of protein per day (equivalent to ~60 g
of muscle tissue or ~2–3 g of nitrogen). I

A

In contrast, in injury and sepsis,
protein breakdown accelerates in proportion to the degree of stress,
reaching 30–60 g/d after elective surgery, 60–90 g/d with infection,
100–130 g/d with severe sepsis or skeletal trauma, and >175 g/d with
major burns or head injuries

58
Q

is
the only fuel that can be utilized by hypoxemic tissues (anaerobic glycolysis),
white blood cells, and newly generated fibroblasts.

A

Glucose

59
Q

remains prevalent, causing

goiter, hypothyroidism, and cretinism.

A

Iodine deficiency

60
Q

is endemic in
many populations, producing growth retardation, hypogonadism, and
dermatoses and impairing wound healing

A

Zinc deficiency

61
Q

Nutritional Deficiency: The High-Risk Patient

A

Underweight (body mass index <18.5) and/or recent loss of ≥10% of usual
body mass
Poor intake: anorexia, food avoidance (e.g., psychiatric condition), or NPOa
status for more than ~5 days
Protracted nutrient losses: malabsorption, enteric fistulas, draining abscesses
or wounds, renal dialysis
Hypermetabolic states: sepsis, protracted fever, extensive trauma or burns
Alcohol abuse or use of drugs with antinutrient or catabolic properties:
glucocorticoids, antimetabolites (e.g., methotrexate), immunosuppressants,
antitumor agents
Impoverishment, isolation, advanced age

62
Q

BMI values <18.5 are

considered underweight;

A

<17, significantly underweight; and <16,
severely wasted. Values of 18.5–24.9 are normal; 25–29.9, overweight;
and ≥30, obese.

63
Q

The triceps is a convenient site that is generally

representative of the body’s overall fat level.

A

A thickness <3 mm

suggests virtually complete exhaustion of fat stores

64
Q

(the half-life of serum albumin is

A

~21 days,

whereas those of prealbumin and retinol-binding protein are ~2 days and ~12 h, respectively), some of these proteins

65
Q

Multiplying by 1.1–1.4 yields a range
10–40% above basal that estimates the 24-h energy expenditure of the
majority of patients.

A

The lower value (1.1) is used for patients without

evidence of significant physiologic stress; the higher value (1.4) is

66
Q

can also be useful in patients who have
difficulty weaning from a ventilator and whose energy needs therefore
should not be exceeded to avoid excessive CO2 production. Patients at
the extremes of weight (e.g., obese persons) and/or age are good candidates
as well, because the Harris-Benedict equations were developed
from measurements in adults with roughly normal body weights

A

Indirect calorimetry

67
Q

2.8–3.5 g/dL: Protein depletion or systemic inflammation

A

<2.8 g/dL: Possible acute malnutrition or severe

inflammation

68
Q

Body Mass Index (BMI), Muscle Mass, and Protein Energy Malnutrition (PEM)

A
>30 Normal Obese
25–29.9 Normal Overweight
20–24.9 Normal Normal
>18.5 Decreased PEM despite adequate or
excessive adipose tissue store
>18.5 Decreased Moderate PEM
<16 Decreased Severe PEM
<13 Decreased Lethal in men
<11 Decreased Lethal in women
69
Q

is the provision of liquid formula meals through a tube

placed into the gut.

A

Enteral SNS

70
Q

is the direct infusion of complete
mixtures of crystalline amino acids, dextrose, triglyceride emulsions,
and micronutrients into the bloodstream through a central venous
catheter or (rarely in adults) via a peripheral vein.

A

Parenteral SNS

71
Q

The chief disadvantage of tube feeding in acute illness is

intolerance due to gastric retention, risk of vomiting, or diarrhea.

A

The presence of severe coagulopathy is a relative contraindication to the
insertion of a feeding tube. In adults, parenteral nutrition (PN) almost
always requires aseptic insertion of a central venous catheter with a
dedicated port.

72
Q

A previously well-nourished
person can tolerate
whereas the degree of tolerance to prolonged starvation is much less
in patients whose skeletal muscle mass is already reduced, whether
from PEM, from the muscle atrophy of old age (sarcopenia), or
from muscle atrophy due to neuromuscular disease.

A

~7 days of starvation without harm, even in the

presence of a moderate systemic response to inflammation (SRI),

73
Q

In general, unintentional weight loss of
>10% during the previous 6 months or a weight-to-height ratio that is <90% of standard, when associated with physiologic impairment, crudely predicts that the patient has moderate PEM.

A

Weight loss

>20% of usual or <80% of standard makes severe PEM more likely

74
Q

is a negative acute-phase protein and hence a

marker of the SRI.

A

Serum albumin

75
Q

A major disadvantage of enteral SNS is that the amounts of protein and calories provided to critically ill patients commonly fail to reach target goals within the first

A

7–14 days after SNS is initiated.
This problem is compounded by the lack of enteral products that allow the provision of the recommended protein target of 1.5–2.0 g/kg without simultaneously inducing potentially harmful caloric overfeeding.

76
Q

The bowel and its associated
digestive organs derivesecretion of gastrointestinal
hormones that stimulate gut trophic activity

A

70% of their required nutrients directly from
nutritional substrates absorbed from the intestinal lumen. Enteral
feeding also supports gut function by stimulating splanchnic blood
flow, neuronal activity, IgA antibody release, and

77
Q

In renal disease, except
for brief periods, protein intakes should approach the required
level for normal adults of at least

A

0.8 g/kg and should aim for
1.2 g/kg as long as severe azotemia does not occur
Patients with
severe renal failure who require SNS need concurrent renal replacement
therapy.

78
Q

In hepatic failure, protein intakes of

A

1.2–1.4 g/kg (up to 1.5 g/kg) should be provided as long as encephalopathy due to protein
intolerance does not occur. In the presence of protein intolerance,
formulas containing 33–50% branched-chain amino acids are
available and can be provided at the 1.2- to 1.4-g/kg level

79
Q

Cardiac patients and many other severely stressed patients often benefit from fluid and sodium restriction

A

to 1000 mL of PN formula and

5–20 meq of sodium per day.

80
Q

Normal adults require

A

~30 mL of fluid/kg of body weight from all
sources each day as well as the replacement of abnormal losses such
as those caused by diuretic therapy, nasogastric tube drainage, wound
output, high rates of perspiration (which can be several liters per
day during periods of extreme heat), and diarrhea/ostomy losses.

81
Q

Fluid restriction may be necessary in

patients with fluid overload.

A

Total fluid input can usually be limited to 1200 mL/d as long as urine is the only significant source of fluid
output. In severe fluid overload, a 1-L central vein PN solution of 7%
crystalline amino acids (70 g) and 21% dextrose (210 g) can temporarily
provide an acceptable amount of glucose and protein substrate in
the absence of significant catabolic stress

82
Q

For normally nourished,

healthy individuals, the total energy expenditure is

A

~30–35 kcal/kg.

83
Q

Critical illness increases resting energy expenditure, but this increase is significant only in initially well-nourished individuals with a robust SRI who experience, for example, severe multiple trauma, extensive burns, sepsis, sustained high fever, or closed head injury. In these situations, total energy expenditure can reach

A

40–45 kcal/kg

84
Q

The chronically starved patient with adapted PEM has a reduced energy expenditure and is inactive, with a usual total energy expenditure of

A

~20–25 kcal/kg.

85
Q

SNS is at least as effective as 100% for the first

A

10 days of critical illness, actual measurement of energy expenditure generally
is not necessary in the early period of SNS

86
Q

Insulin resistance due to the SRI is associated with

A

increased gluconeogenesis and reduced peripheral glucose utilization, with resulting hyperglycemia. Hyperglycemia is aggravated by excessive exogenous carbohydrate administration from SNS.

87
Q

Hypocaloric nutrition, with provision of

A

~1000 kcal and 70 g protein per day for up to 10 days, requires less fluid and reduces
the likelihood of poor glycemic control, although a higher protein intake would be optimal. During the second week of SNS, energy and protein provision can be advanced to 20–25 kcal/kg and 1.5 g/kg
per day, respectively, as metabolic conditions permit

88
Q

The daily protein recommendation for healthy adults is

A

0.8 g/kg, but body proteins are replenished faster with 1.5 g/kg in patients with PEM, and net protein catabolism is reduced in critically ill patients when 1.5–2.0 g/kg is provided.

89
Q

In patients who are not critically ill but who require SNS in the acute-care setting, at least

A

1 g of protein/ kg is recommended, and larger amounts up to 1.5 g/kg are appropriate
when volume, renal, and hepatic tolerances allow.

90
Q

Iron is a highly reactive catalyst of oxidative reactions and thus is not included in PN mixtures. The parenteral iron requirement is normally

A

only ~1 mg/d.

91
Q

Peripheral PN may be enhanced by

A

small amounts of heparin (1000 U/L) and co-infusion with parenteral
fat to reduce osmolarity, but volume constraints still limit the value of
this therapy, especially in critical illness

92
Q

The subclavian approach is best tolerated by the patient and is the
easiest to dress.

A

The jugular approach is less likely to cause a pneumothorax.
Femoral vein catheterization is strongly discouraged because of
the risk of catheter infection

93
Q

to the daily parenteral formula for hospitalized
patients with temporary catheters reduces the risk of fibrin sheath
formation and catheter infection.

A

The addition of 6000 U of heparin

94
Q

The most common problems caused by parenteral SNS

are fluid overload and hyperglycemia (Table 98e-7).

A

Hypertonic
dextrose stimulates a much higher insulin level than meal feeding.
Because insulin is a potent antinatriuretic and antidiuretic hormone hyperinsulinemia leads to sodium and fluid retention

95
Q

Infections of the central access catheter rarely occur in the

A

first 72 h. Fever during this period is usually attributable to infection
elsewhere or another cause. Fever that develops during parenteral SNS
can be addressed by checking the catheter site and, if the site looks
clean, exchanging the catheter over a wire, with cultures taken through
the catheter and at the catheter tip

96
Q

If cultures are positive for more pathogenic bacteria or
for fungi like Candida albicans, it is generally best to replace the catheter
at a new site.

A

Whether antibiotic treatment is required is a clinical
decision, but C. albicans grown from the blood culture in a patient
receiving PN should always be treated with an antifungal drug because
the consequences of failure to treat can be dire.