Nutrition and Specific Disease States Flashcards

1
Q

role of fiber in diabetes

A

slows down gastric emptying to reduce spike in blood sugar, reduces LDL and increases satiety

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2
Q

Is fiber recommended in gastroparesis

A

No

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3
Q

Probiotics mechanism of action

A

when probiotics reach the ileum/colon, endogenous bacteria consume and ferment pre biotics and produce short chain fatty acids which increases bacterial mass and enzyme activity

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4
Q

Uses for probiotics

A

help reduce flatulence, bloating, abdominal pain

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5
Q

What is the recommended fiber intake daily

A

20-35/day

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6
Q

detriments of too much protein

A

pre-renal azotemia, kidney stones, increased risk of osteoporosis

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7
Q

______ based sterols lower cholesterol absorption and are recommended as cholesterol lowering agents

A

soy based

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8
Q

Are immune modulating enteral formulas with omega 3 fatty acids and antioxidants recommended for Acute Respiratory Distress Syndrome or Severe Acute Lung Injury?

A

No

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9
Q

Which EN formulas should be considered for patients with traumatic brain injury

A

Formulas containing fish oil, arginine, omega 3 fatty acids with DHA (immune modulating)

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10
Q

What causes high creatinine loss

A

diarrhea, high output fistula or ostomy losses

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11
Q

Which populations are immune modulating EN formulas appropriate for per ASPEN

A

SICU

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12
Q

an amino acid which functions in immune function, wound healing, synthesis of nitrous oxide and plays roles in respiratory and cardiac function

A

arginine

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13
Q

hydroxy beta methylbutyrate (HMB) protein is shown to

A

increase lean muscle mass

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14
Q

HMB protein has been studied in which populations

A

AIDS, ALS and muscular dystrophy

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15
Q

symptoms of fatty acid deficiency

A

scaly rash, color spots, alopeica, dull/easily plucked hair, xerosis, follicular hyperkeratosis

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16
Q

Patients with liver cirrhosis are at risk for what deficiencies

A

fat soluble vitamins (ADEK) and thiamine

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17
Q

what is the recommended modality of artificial nutrition for an open abdomen

A

EN, when the peritoneum is left open and the viscera are protected with a temporary dressing

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18
Q

what type of EN feeding tube is recommended for gastroparesis in the setting of postprandial nausea and vomiting

A

jejunostomy

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19
Q

what mode of artificial nutrition is recommended in hyperemesis gravidarum

A

EN in conjunction with anti-emetic therapy

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20
Q

what are 3 parameters for assessing EN efficacy in pregnancy

A

maternal dry weight gain, fetal growth, nitrogen balance

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21
Q

what items should be labeled on an enteral product

A
Patient Name
Product Name
Strength
Additives
Volume
Expiration Date and Time
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22
Q

advantages of a ready to hang enteral formula

A

decreases risk of infection (less to handle)
longer hanging time
decreased RN time

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23
Q

disadvantages of ready to hang EN formula

A

decreased individualization

could be accidentally be administered into IV tubing (sentinel event)

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24
Q

what is the most likely source of EN formula contamination

A

organisms on the hands of healthcare workers

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25
Q

what are 2 potential points of contamination of EN formulas

A

preparing and dispensing

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26
Q

in order to ensure feeding tube patency flush the tube how often for continuous/intermittent feedings

A

every 4-6 hours

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27
Q

in order to ensure feeding tube patency when giving medications flush ___ to ___mL of formula before/after each med using a ____ to ___mL syringe

A

15-30mL of water with a 50-60mL syringe

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28
Q

why shouldn’t small syringes be used to flush tubes

A

may cause rupture from too much pressure

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29
Q

if a fiber rich formula is being used, what is the recommended French size range

A

10-12 French

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30
Q

advantages of an open enteral feeding system

A

can be more individualized with the volume

reduces waste

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31
Q

what is the hang time for an open enteral feeding system

A

8-12 hours

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32
Q

what are the disadvantages of an open enteral feeding system

A

uses bags
only 8-12 hour hang time
higher risk of contamination than RTH
requires additional RN time

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33
Q

to minimize infections, enterally fed patients (open system) should have bags and tubing changed

A

every 24 hours

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34
Q

in a closed system enteral feeding what is the hang time/how long can it last after being opened

A

48 hours

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35
Q

what is the optimal storage temperature for EN formulas to prevent microbial growth and contamination

A

39 degrees F, 4 degrees C

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36
Q

the most likely formula to become contaminate is

A

blenderized

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37
Q

SIBO can cause

A

enteritis, marked diarrhea, abdominal cramps, hypoalbuminemia, protein catabolism, cachexia, fever, sepsis

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38
Q

what are potential causes of SIBO

A

altered GI anatomy, Roux-en-Y bypass, ileal resection

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39
Q

is PN in patients for chemo/radiation recommended for routine use per ASPEN

A

no, can cause infectious complications and no clinical improvement

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40
Q

ASPEN recommends thorough assessment of a cancer patients _________ and only use PN when ___ and ____ for __ to __ days

A

nutrition status

malnourished AND unlikely to use gut in 7-14 days

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41
Q

what is the preferred nutrition method for patients with cancer and a functional GI tract

A

enteral nutrition

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42
Q

PN as a primary treatment for ulcerative colitis has shown _____ benefit

A

NO

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43
Q

a patient with a high output ostomy of 3 liters, with an elevated BUN/Cr should have a treatment plan of while on PN

A

increased sodium fluids

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44
Q

sodium loss from a high output fistula can be up to

A

100 mEq/L

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45
Q

a high BUN:Cr ratio indicates

A

volume depletion

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46
Q

patients with ____ and ____ disease are more prone altered protein metabolism due to decreased excretion of urea

A

hepatic/renal disease

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47
Q

In a patient with elevated ammonia what is used for treatment and prevention

A

reduce total amino acids

restrict protein in refractory encephalopathy

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48
Q

(TRUE/FALSE) Nutrition support is understood to be a therapy to attenuate the metabolic response to stress, prevent metabolic oxidative stress, and modulate the immune response.

A

TRUE.

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49
Q

**What are the nutrition requirements for TBI?

A
  • ENERGY: IC, if unable use 140% x the Harris-Benedict equation.
  • PROTEIN: 1.3 to 1.5 g/kg/d
  • Early nutrition is key, start EN ASAP
  • Supplementation with zinc and IGF-1 has been shown to improve outcomes after TBI.
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50
Q

Define hyponatremia. What can it contribute to?

A
  • Serum sodium less than 135 mg/dL.
  • Contributes to worsening cerebral edema, intracranial pressure elevations and death from herniation
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51
Q

Define SIAD. How does it relate to TBI? What is the primary treatment?

A
  • SIAD = Syndrome of Inappropriate Anti-Diuresis
  • TBI is a common cause of SIAD, which results in euvolemic hyponatremia
  • FR is primary treatment
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52
Q

Define CSW (Cerebral Salt Wasting). How does it relate to TBI? What is the treatment/management?

A
  • A rare hypovolemic hyponatremia characterized by increased natriuresis (excretion of sodium in the urine).
  • Like SAID, CSW is usually transient after TBI
  • CSW is a diagnosis of exclusion
  • Managed with IV Sodium supplemention
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53
Q

Define diabetes insipidus.

A
  • A hypernatremic state characterized by a deficiency in vasopressin (neurogenic- most common type), lack of response to vasopressin (nephrogenic), OR accelerated degradation of vasopressin (gestational).
  • BASICALLY: DAMAGE TO THE HYPOTHALAMUS OR POSTERIOR PITUITARY, usually as a result of rotational forces sustained in MVC, reduces central vasopressin production leading to neurogenic diabetes insipidius after TBI.
  • Supplementation of salt-free water and replacement of vasopressin can reduce serum sodium to normal levels
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54
Q

(FILL IN THE BLANKS)

As with hyponatremia, hypernatremia should be corrected NO FASTER than X to X mEq/L/d to avoid worsening of cerebral edema.

A
  • 10 to 12 mEq/L/day
  • (relates to previous 3 conditions: SIAD, CSW, Diabetes insipidus).
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55
Q

What medications (4) used in TBI treatment have been shown to reduce measured energy expenditure?

A
  • Proproanolol
    • Reduced by 5 to 18%
  • Morphine
    • Reduced up to 8%
  • Pentobarbital (used to reduce intracranial pressure)
    • Reduced up to 32%
  • NMBAS (also used to reduce intracranial pressure)
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56
Q

At present, which pharmaconutrients lack the available information to recommend specific dosing strategies for patients with TBI?

A
  • L-arginine
    • Clinical research has not found that arginine supp in trauma and TBI improves outcomes
  • Glutamine
    • Low plasma glutamine concentration at ICU admission is an independent risk factor for post-ICU morality in critically ill patients; but early provision of glutamine did not improve outcomes in large-scale study
  • Omega-3 FA
    • No clinical data available
  • Antioxidants
    • Ascorbic acid and alpha-tocopheral levels; not enough information
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57
Q

**What are the nutrition recommendations for energy and protein for patients with SCI (spinal cord injury?)

A
  • ** ENERGY: IC first, or 15% less than Harris-Benedict equation (no validated predictive equation best determines the SCI energy expenditure)
  • PROTEIN: 1.5 to 2.0 g/kg/d (immediately following a SCI)
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58
Q

**What are the general energy recommendations for weight maintenance for quadriplegic patients?

A

** 20 to 22 kcal/kg/d OR 55 to 90% of the Harris-Benedict equation.

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59
Q

**What are the general energy recommendations for weight maintenance for paraplegic patients?

A

** Energy recommendations are increased slightly to 22 to 24 kcal/kg/d OR 80 to 90% of the Harris-Benedict equation)

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60
Q

**What is the protein intake for patients in long-term care after a SCI?

A

**Healthy patients; 0.8 to 1.0 g/kg/d

If pressure injuries: 1.25 to 1.5 g/kg/d with energy (30 to 35 kcal/kg/d), sufficient daily fluid, and vitamin/mineral supplementation if intake is poor or deficiencies are suspected.

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61
Q

**Healthy patients; 0.8 to 1.0 g/kg/d

If pressure injuries: 1.25 to 1.5 g/kg/d with energy (30 to 35 kcal/kg/d), sufficient daily fluid, and vitamin/mineral supplementation if intake is poor or deficiencies are suspected.

A

**

EN start within 24 to 48 hours of admission.

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62
Q

**What are the energy requirements for patients with acute stroke?

A
  • **IC is the gold standard; no equation has been validated to precisely determine the energy expenditure for the stroke population.
  • Based on available data, the energy requirements following an ischemic stroke are likely close to estimated BMR via Harris-Benedict equation or Penn-State equation.
  • Patients with hemorrhagic stroke, especially SAH, have elevated energy needs as compared with estimates of BMR.
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63
Q

**What are the protein requirements for patients following an acute stroke?

A

** Recommended protein goals range from 1.0 to 1.5 g/kg/d

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64
Q

If hypernatremia protocols aim for serum sodium ranges of 140 to 150 mg/dL to minimize cerebral edema, what should you recommend?

A

A concentrated enteral formula with 1.5 to 2.0 kcal/mL may be appropriate to provide less water. Then advancing to a standard formula as the patient progresses.

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65
Q

Explain the level 1 dysphagia diet.

A

PUREED (homogenous, very cohesive, and pudding-like in texture, requiring very little chewing ability.

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66
Q

Explain the level II dysphagia diet.

A

MECHANICALLY ALTERED

  • Cohesive, moist, semisolid foods, requiring some chewing
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67
Q

Explain the level III dysphagia diet.

A

SOFT FOODS that requiring more chewing; most advanced dysphagia diet.

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68
Q

(TRUE/FALSE)

Although overeating creates risks for SCI patients, poor intake may increase the risk of pressure ulcers. When pressure ulcer incidence was examined in SCI patients, a higher percentage of underweight patients developed pressure ulcers compared to healthy weight, overweight or obese patients with SCI.

A

TRUE.

Monitoring weekly weight changes throughout the rehab program is useful in guiding adjustments in energy requirements.

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69
Q

Explain implication of nutrition status in patients with ALS.

A
  • ALS = Lou Gehrig’s disease; a rapidly progressing, degenerative motor neuron disease that results in significant muscle weakness and atrophy
  • 75% of ALS patients will experience bulbar involvement (includes muscles that control speech, swallowing, and chewing, that can lead to substantial weight loss)
  • Malnutrition is an independent prognostic factor of ALS survival; 8-fold increase in poor nutrition status
  • Early nutrition interventions has been shown to maintain good nutrition status for a longer period of time.
  • PEG placement earlier in the disease process is more effective at preserving nutrition status for a longer period of time.
    • ***It is recommended that PEG is placed whle forced vital capacity is more than 50% of predicted value or when patients has dysphagia or a BMI less than 20 or loses 5 to 10% of UBW.
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70
Q

**What are the energy requirements for patients with ALS?

A
  • **Mifflin St. Jeor and Harris-Benedict equations have been shown to be the most accurate methods, with HB being the most practical
  • Some research supports increasing the calculated resting energy expenditure by 10%
    • Others: recommend energy needs to be 120% greater than BMR by IC and 130% x HB equation.
  • As the ratio of organ mass to muscle mass increases, patients may require 34 to 35 kcal/kg/d
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71
Q

**What are the protein requirements for patients with ALS?

A

** Ranges from 0.8 to 1.2 g/kg/day

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72
Q

Explain the ketogenic diet.

A
  • Well documented use for therapy in controlling seizures in the pediatric population
  • To decrease seizures, a 4:1 ratio of fat to CHO and protein is recommended; which can be titrated down as the disease state stabilizes.
  • Note many medications contain CHOs and must be taken into account when calculating diet.
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73
Q

Explain the modified Atkins diet.

A
  • A 1:1 ratio fat to protein and CHO can be used once a patient’s seizure frequency is more stable.
  • Shown to reduce seizures in adults and adolescents with drug-resistant epilepsy.
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74
Q

Limited information is known about nutrition and Parkinson’s disease. What is the overall pattern with body weight patterns in Parkinsons?

A
  • In the beginning stages of the disease, body weight increases, likely due to a decrease in motor function.
  • As the disease progresses, weight loss occurs. It is theorized that the metabolic rate increases because of worsening rigidity and dyskinesia.
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75
Q

Explain the relationship between carbidopa/levodopa drug therapy and protein intake.

A
  • The medication and protein compete for transport in the SI and blood-brain barrier.
  • Fluctuations in absorption in leveodopa can affect motor function, and this drug therapy. has been associated with decreased intake of protein.
  • Higher levodopa requirements have been associated with increased constipation, and diet mgmt is recommended.
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76
Q

Define sepsis.

A
  • Life-threatening organ dysfunction caused by a dysregulated host response to infection.
  • The systemic response to infection
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77
Q

Define septic shock.

A
  • Refers to a subset of sepsis in which profound circulatory, cellular, and metabolic abnormalities are associated with a greater risk of mortality than with sepsis alone
  • Associated with hemodynamic instability, which is primarily refractory hypotension with systolic peak pressure less than 90 mmHg, mean arterial pressures less than 65 mmHG or a drop of greater than 40 mmHg from baseline.
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78
Q

The metabolic response to sepsis is in many ways similar to the response that follows major surgery or trauma. What are both responses characterized by?

A
  • Increases in energy expenditure
  • Protein catabolism
  • Oxidation of stored lipids alson with significant alterations in the body’s ability to metabolize CHOs
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79
Q

In what ways is appropriate nutrition therapy during sepsis and severe infections essential?

A
  • Plays a key role in modulating the inflammatory response
  • Maintaining immune function
  • Abrogating skeletal muscle catabolism
  • Improving wound healing
  • Maintaining GI and pulmonary mucosal barrier function
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80
Q

What is the glucose target for patients with sepsis?

A

No greater than 180 mg/dL.

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81
Q

(TRUE/FALSE)

Following the onset of sepsis, glycogen stores are depleted within hours and endogenous lipid and protein become the major source of oxidative energy substrate.

A

TRUE.

Related to catabolic hormones stimulating glycogenolysis and gluconeogenesis.

However, oxidation of lipid from endogenous adipose stores is impaired during sepsis.

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82
Q

Why does sepsis result in hyperglycemia?

A

Sepsis results in hyperglycemia secondaryto alterations in:

  • Endogenous glucose production
  • Decreased glucose uptake
  • Insulin resistance

Gluconeogenesis increases with progressive organ failure

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83
Q

(TRUE/FALSE)

Although protein breakdown and synthesis both continue to occur at acclerated rates during sepsis, patients remain in generalized net-negative N balance for variable periods even after the inciting insult has been resolved.

A

TRUE.

The acceleration of peripheral muscle protein breakdown noted in sepsis is accompanied by diminished AA uptake by muscle. Excreted in increased amounts in the urine during sepsis.

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84
Q

(TRUE/FALSE)

Mammalian species have no “storage” of protein and that any protein utilized during catabolic stress of any kind comes at the expense of other tissues that are more labile.

A

TRUE.

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85
Q

Explain hepatic reprioritization.

A
  • During sepsis, hepatic uptake of AAs and hepatic protein synthesis are increased, which allows a substrate for gluconeogenesis and production of acute-phase protein.
  • However, the increase in hepatic protein synthesis is NOT uniform
  • Although serum concentrations of positive acute-phase proteins (such as haptoglobin and CRP), increase in response to stress, synthesis of negative acute-phase proteins, such as albumin and prealbumin, falls.
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86
Q

(FILL IN THE BLANK)

As the systemic response to sepsis progresses, protein catabolism XXXX, and the failure of synthetic processes to keep up with the breakdown rate results in XXXX of skeletal protein.

A
  • INCREASES
  • SEVERE LOSSES
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87
Q

What does prolonged catabolism of skeletal protein result in?

A
  • Compromises respiratory function
  • Impaires wound healing
  • Exacerbates immunosuppression
  • Accelerates the loss of strength and endurance necessary for recovery
  • Increases ventilator-dependent time and ICU stay
  • Increases thromboembolic disease
  • Increase recovery time
  • Increases mortality incidence.
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88
Q

(TRUE/FALSE)

**SCCM/ASPEN recommend that clinicians evaluate weight loss and nutrition history prior to admission, level of disease severity and GI function.

A

**TRUE

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89
Q

(TRUE/FALSE)

Practitioners are often concerned that EN may increase ischemic injury during states of decreased perfusion of the splanchnic organs in septic patients, especially if the patient is receiving vasoactive medications.

A

TRUE.

Lab evidence provides support for the OPPOSING VIEW: namely that EN provides protection and even enhances perfusion during septic states.

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90
Q

What are some approaches to maintaining visceral perfusion?

A
  • Adequate resuscitation
  • Glycemic control
  • Correction of acidosis
  • Correction of electrolyte abnormalities
  • Minimizing the use of anticholinergic medications, narcotics and other medications that decrease intestinal motility
  • Instituting EN, even at low rates, within the first 24 to 48 hours of the onset of SIRS or sepsis
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91
Q

**What are SCCM/ASPEN recommendations related to nutrition support in a critically ill septic patient?

A

**ASPEN/SCCM guidelines recommend trophic feeding (10 to 20 kcal/hr or 500 kcal/d) for the initial phase of sepsis, advancing as tolerated after 24 to 48 hours to greater than 80% of target energy goal over the first week.

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92
Q

**What are the SCCM/ASPEN recommendations related to PN in a critically ill septic patient?

A

**When a patient is in the acute phase of severe sepsis, the ASPEN/SCCM guidelines suggest NOT using exclusive PN or supplemental PN in conjunction with EN regardless of patient’s degree of nutrition risk.

Obviously, if the gut is deemed unreliable, PN may be selected.

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93
Q

What is the 3-armed approach to management of sepsis?

A
  1. Source control
  2. Early antibiotic administeration
  3. Resuscitation
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94
Q

Define hypotensive.

A

Mean arterial pressure less than 65 mmHg

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95
Q

(TRUE/FALSE)

There is a single laboratory/hemodynamic parameter signaling the successful resuscitation of the critically ill patient in shock.

A

FALSE.

There is NOT; Generally, clinicians use the trends in hemodynamic parameters, including mean arterial pressures, central venous pressures, and vasopressor requirements, in conjunction with urine output, arterial base deficit, serum lactate and venous oxygen saturations, to determine the relative success of resuscitation.

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96
Q

Define NMI (nonocclusive mesenteric ischemia.

A
  • A uncommon compklication following the early initiation of enteral feeding in the underresuscitated patient
  • It is a low flow state that most commonly affects the distribution of the superior mescenteric artery, which can result in irreversible ischemia and necrosis of the associated small and large bowel.
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97
Q

**When does SCCM/ASPEN recommend initiation of enteral support in critically ill septic patients?

A

**SCCM/ASPEN guidelines recommend that critically ill patients receive EN therapy within 24 to 48 hours of making the diagnosis of severe sepsis/septic shock, as soon as resuscitation is complete and the patient is hemodynamically stable.

Feeding immediately after the initial dx of sepsis yields a distinct set of problems.

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98
Q

How should GI intolerance be continually reassessed?

A
  • Abdominal distention
  • Increased gastric residual volumes
  • Increased NG output
  • Abdominal pain
  • Diarrhea
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99
Q

(TRUE/FALSE)

Impaired gastric and proximal GI motility can be addressed efficiently through the placement of postpyloric feeding tubes.

A

TRUE.

They can be done successfully at bedside in more than 80% of patients.

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100
Q

What are two prokinetic agents?

A
  1. Erythromycin: acts on motilin receptors, resulting in increased motility, although its use may be limited by tachyphylaxis (short/rapid drug intolerance)
  2. Metoclopramide: a 5-HT(4) receptor agonist, works via cholinergic stimulation and is most effiacious in the proximal gut

No single prokinetic agent will have uniform success in the ICU, and the factors contributing to GI dysmotility in each patient must be considered.

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101
Q

**What are the energy requirements for patients with sepsis/septic shock?

A
  • **Increases of 20 to 60% over basal expenditure
  • Range of 20 to 30 kcal/kg/d is considered safe for critically ill patients (excluding the morbidly obese)
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102
Q

**What are the CHO recommendations related to energy expenditure in critically ill septic patients?

A
  • **CHO administeration should supply 50 to 60% of the total energy prescription to avoid exceeding the maximum contribution of glucose oxidation and contributing to excess lipogenesis.
  • Glucose admin. rates greater than 4 to 6 mg/kg/min result in excess lipogensis and lead to hyperglycemia.
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103
Q

**In critical care and sepsis patients, the amount of ILES should not exceed XXXXX, if XXXX.

A
  • **1.0 g/kg/d
  • if soybean oil is the source of lipid.

Guidelines for enteral lipid delivery are similar to those for parenteral lipid provision. The usual lipid goal of 1.0 g/kg/d can be liberalized when enteral lipids include lipid substrates containing omega-3 FAs, MCTs, and SCFA. And a mixture of lipid fuels should be delivered whenever possible.

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104
Q

(TRUE/FALSE)

**Conflicting data prevented the ASPEN/SCCM guidelines from making a recommendation for use of anti-inflammatory lipid formulas at this time.

A

TRUE.

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105
Q

**What are the SCCM/ASPEN guidelines for protein in sepsis?

A

** 1.5 to 2.0 g/kg/d (possibly even up to 2.5 g/kg/d in selected cases).

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106
Q

(TRUE/FALSE)

**ASPEN/SCCM guidelines recommend use of an arginine/fish oil formula only in surgical ICU patients and do NOT recommend their routine use in patients with sepsis alone.

A

**TRUE.

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107
Q

(TRUE/FALSE)

**SCCM/ASPEN guidelines recommend that clinicians supplement severely ill ICU patients with enteral or parenteral glutamine.

A

FALSE.

It is NOT recommended.

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108
Q

**Does SCCM/ASPEN have specific guidelines for supplementing zinc, selenium, or antioxidants in sepsis?

A

**NO

There is not a definitive recommendation.

The literature suggests clinicians provide at least the RDA of antioxidants vitamins and trace elements to critically ill patients throughout hospitalization.

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109
Q

Define SIRS.

A

Systemic Inflammatory Response Syndrome (SIRS)

  • Entails the presence of 2 out of 4 abnormal systems
    • Heart Rate
    • Respiratory Rate
    • Temperature
    • WBC count
  • When 2 of these are met, the local injury of trauma or burn is producing a systemic reaction.
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110
Q

Name some counter-regulatory hormones.

A
  • Epinephrine
  • Norepi
  • Glucagon
  • Cortisol

Named as such because they oppose the effects of insuling and other anabolic hormones. The responsiveness of tissues, especially skeletal muscle, to insulin is severly blunted.

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111
Q

Name the 3 effective treatment strategies of SIRS.

A
  1. Delivery of oxygen to vital tissues
  2. Source control (control of bleeding, necrotic, and infected tissues)
  3. Provision of nutrition support.
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112
Q

Define mucosal acidosis.

A

A measure of reduced intraoperative splanchnic perfusion, is associated with:

  • Exaggerated local and systemic immune responses
  • Increased intestinal permeability
  • Increase in septic complications
  • A trend toward increased multiorgan dysfunction syndrome
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113
Q

Define postprandial hyperemia.

A

The presence of luminal nutrients increases GI blood flow.

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114
Q

(TRUE/FALSE)

Clinical and laboratory evidence suggests that EN is contraindicated with the use of vasopressive agents.

A

FALSE.

IT IS NOT contraindicated. Use of EN in such patients should be conservative, with the EN advanced only when the patient demonstrates tolerance. Following adequate resuscitation, EN may protect the GI tract, especially the mucosa, from relatively low levels of ischemia.

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115
Q

(TRUE/FALSE)

Malnutrition related to stress or trauma differs from starvation-related malnutrition in that the former stems from increased resting energy expenditure and tremendous mobiliation of protein deposits.

A

TRUE.

It is driven by systemic inflammation. This systemic inflammation can drive catabolism to the severity of affecting cardiac mass and function. Which can continue for weeks to months after the patient is discharged from the ICU.

Noted as “acute-disease” or “injury-related malnutrition” to acknowledge this phenomenon.

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116
Q

**ASPEN/SCCM guidelines recommend assessment using XXXXX or XXXXX to identify patients who would benefit from nutrition therapy.

A
  • NRS-2002 (Nutrition Risk Screening)
    • Attempts to account for both preexisting malnutrition (ie: weight loss, decreased food intake) AND severity of illness (ie: type of injury, APACHE II score)
  • NUTRIC (Nutrition Risk in Critically Ill)
    • Focus on severity of illness.
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117
Q

What are the 3 main categories for surgical ICU patients?

A
  1. Postoperative major elective surgery
  2. Major injury (ie: burns and trauma)
  3. Serious sepsis
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118
Q

(TRUE/FALSE)

Body weight measured in the ICU is not a valid indicator of body cell mass.

A

TRUE.

Ideally, weight changes should be monitored weekly. Acute weight changes are most likely due to fluid shifts, as 1 L of fluid equals 1 kg body weight.

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119
Q

(TRUE/FALSE)

Fluid shifts and increased permeability change the proportion of fluid to protein, effectively altering the measured concentration of serum proteins. Therefore, in patients with acute illness, inflammation, or injury (such as in the early postoperative period and in trauma and burn patients), transport proteins cannot reliably be regarded as a marker of nutrition status, but can only be interpreted as a marker of severity of illness and inflammation.

A

TRUE.

Albumin, prealbumin, transferrin, and retinol-binding protein, are negative acute phase response proteins.

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120
Q

**How should energy needs be calculated in trauma patients?

A

**ASPEN/SCCM guidelines recommend using IC to measure resting energy expenditure in the critically ill, surgical, injured and burn patients, when it is available.

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121
Q

Describe the “PEPuP protocol.”

A
  • Driven by the bedside nurse
  • Uses daily volume based goals, liberalizes the GRV threshold, and initiates protein supplementation with motility agents on Day 1 of a patient’s ICU stay.
  • Increased protein delivery by 14% and energy by 12% in trial.
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122
Q

Once a PEG tube is placed, how long do you have to wait until TF is initiated?

A

May be used for feeding within 2 hours; instead of the routine 24-hour delay.

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123
Q

**What is the current recommendation for stressed patients (including those with burns), for protein?

A
  • **20 to 25% of total nutrient intake by provided by protein
  • Equates to ~ 1.5 to 2.0 g/kg/d, with the higher range to promote N equilibrium
  • 2.0 g/kg/d IBW has been suggested for obese patients (BMI equal or greater than 30)
  • In patients with large surface area burns, 3 to 4 g/kg/d may be required.
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124
Q

(TRUE/FALSE)

It has been suggested that ICU patients receiving continuous renal replacement therapy (CRRT) should receive 2.0 to 2.5 g/kg/d to overcoe protein losses in the dialysate.

A

TRUE.

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125
Q

What is the minimum amount of dextrose necessary to maintain CNS function?

A

120 g/day

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126
Q

What are isomotic fluids (such as NS and lR) used for?

A
  • Isomotic fluids or balanced electrolyte solutions are typically used for fluid and electrolyte replacement
  • When these are used as maintenance, 5% dextrose will be added as an energy source (for protein sparing, prevention of ketosis and maintanence of stable glucose levels).
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127
Q

What is the Parkland formula?

A
  • Most commonly used method to determine adult fluid resuscitation requirements
  • Used for patients with greater than 15% TBSA second- and third-degree burns.
    • (4 mL LR for X body weight (kg)) X (TBSA)
  • One half of this total amount is administered in the first 8 hours after the burn
  • The remaining amount is given over the next 16 hours, followed by maintenance fluids.
  • Inhalation injury results in additional fluid needs and is often estimated as another 10% of TBSA.
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128
Q

(FILL IN THE BLANK)

Monitoring urine output is an essential part of providing fluid to thermal injury patients, as adequate hydration should result in a minimum of XXXX.

A
  • 0.3 to 0.5 mL/kg/hour
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129
Q

What are the vitamin/mineral recommendations for burn patients with less than 20% TBSA and burn patients undergoing delayed reconstructive patients?

A

A daily MVI

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130
Q

What are the vitamin and mineral recommendations for burn patients with greater than 20% TBSA?

A
  • Daily MVI
  • 20,000 IU Vitamin A
  • 220 mg zinc
  • 500 mg ascorbic acid BID

Selenium, copper and vitamin D may be considered if levels are low.

131
Q

**In previously well-nourished patients, when should PN be initiated, according to ASPEN/SCCM guidelines?

A

**Only after efforts to provide nutrition via the enteral route have failed to advance EN to meet 60% of target goal energy for 7 to 10 days.

EXCEPTIONS:

  • Preexisting malnutrition
  • Cannot receive EN
  • Are expected to undergo major upper GI surgery
132
Q

**For patients that are in the ‘PN exception group,’ when should PN be initiated, according to ASPEN/SCCM guidelines?

A

**Patients include:

  • Preexisting malnutrition
  • Cannot receive EN
  • Are expected to undergo elective major upper GI surgery

ASPEN/SCCM recommend that 5 to 7 days of preoperative PN be provided with continued PN postoperatively.

If EN was contraindicated and the malnourished GI surgery patient did not receive preoperative PN, ASPEN/SCCM recommend (based on limited data), that initiation of PN be delayed postoperatively for 5 to 7 days if EN continues to be contraindicated. PN provided for fewer than 5 days has not shown benefit.

133
Q

(TRUE/FALSE)

Some authors advocate small bowel feeding in critically ill patients because it is associated with decreased gastroesophageal reflux, reduced aspiration, and increase in nutrient delivery, and a shorter time to achieve desired nutrient delivery.

A

TRUE.

134
Q

In what situations as a clinician, should you recommend a small bore feeding tube?

A

Patients who are high risk for aspiration and gut dysmotility.

  • Undergone major intra-abdominal surgery
  • Prior episode of aspiration or emesis
  • Persistent high GRVs (greater than 500 mL)
  • Unable protect the airway
  • Require prolonged supine or prone positioning.
135
Q

At what point, is it appropriate to switch to nighttime cycling EN?

A

May be considered when patients are meeting more than 60% of their energy goal by the oral route prior to discontinuing EN. To maximize intake, oral dietary restrictions are discouraged.

136
Q

What are the objectives of the ERAS protocol?

A

The objectives are to avoid starvation, decrease the physiological stress of surgery (which induces IR), and limit postoperative IV fluids, while optimizing pain control, GI function, and mobilization.

137
Q

What is the ERAS protocol?

A
  • Avoid preoperative fasting:
    • Solid meals are provided up until 6 hours before surgery.
    • 800 mL (~ 100 g and 400 kcal) of a CHO-rich, CL is given at midnight and 400 mL of the same formula is given again 2 hours before the surgical intervention
  • Patients receive a smaller volume of IV fluids
138
Q

**What are the ASPEN/SCCM guidelines for PN.

A

**PN should be reserved and initiated only after the first 7 days of hospitalization in patients WITHOUT malnutrition.

139
Q

(TRUE/FALSE)**

ASPEN/SCCM guidelines recommend that use of continuously administered enteral immunonutrition formulations with supplemental omega-3 FAs and arginine in postoperative and trauma ICU patients.

A

TRUE.**

140
Q

(TRUE/FALSE)**

ASPEN/SCCM guidelines recommend adding glutamine to EN for any critically ill.

A

FALSE**

NOT recommended adding until additional evidence is available.

141
Q

Define inhalation.

A

An active process driven by a set of muscles that work in concert to bring air into the lungs

142
Q

Define expiration.

A
  • Under normal circumstances, it is a passive process inw hich the diaphragm and intercostal muscles relax allowing the thoractic cavity to return to its normal resting state.
  • In times of distress, primary and accessory muscles can aid in forced exhalation.
143
Q

Define hypercapnia.

A

CO2 retention

  • Can result from hypoventilation
  • This situation, the patient may require noninvasive ventilator support, which involves positive airway pressure ventilation via an airtight mask (like CPAP), as well as, supplemental O2.
  • Common causes:
    • Obstructive pulmonary disease
    • Sleep apnea
    • Obesity leading to a collape of the upper airways (aka obesity hypoventilation syndrome)
144
Q

Explain Type 1 hypoxemic respiratory failure.

A
  • Occurs when the partial pressure of oxygen (PaO2) in arterial blood flow is less than 60 mmHg.
  • AKA: This type is secondary to a failure of oxygen exchange and typically occurs at the level of the alveoli
  • Mechanisms:
    • Diffusion defect (ie: underlying lung disease)
    • Ventilation-perfusion mismatch (ie: PNA)
    • Hypoventilation when it leads to low oxygen levels (ie: opiate intoxication)
    • Shunt physiology (ie: Severe ARDS)
  • No matter the mechanism: Insufficient alveoli oxygen levels leads to reduced arterial hemoglobin oxygen saturation (SaO2) and therefore reduced tissue oxygenation (HYPOXIA).
145
Q

Explain Type II hypercapnic respiratory failure.

A
  • High body CO2 levels, which occurs when the partial pressure of arterial carbon dioxide (PaCO2) is elevated and causes blood pH to be less than 7.37.
  • Hypercapnia occurs from either”
    • Too much CO2 production through increased cellular respiration secondary to increased overall metabolic function OR,
    • Decreased alveolar ventilation causing decreased CO2 gas exchanges
  • Common causes:
    • Exacerbations of COPD
    • Opiate overdose
    • Chest wall defects
    • Decreased respiratory muscle function (r/t ALS or muscular dystrophy)
146
Q

Explain Type III Mixed Hypoxemic-Hypercapnic respiratory failure.

A
  • Commonly encountered in the perioperative setting due to anesthesia.
  • This form is always acute and frequently secondary to atelectasis (a complete or partial collapse of lung segments)
147
Q

Explain Type IV Shock-Related respiratory failure.

A
  • Can be caused by:
    • Sepsis
    • Hypovolemia
    • Cardiogenic shock
  • The presence of shock puts increased strain on the respiratory system and often subsequently leads to respiratory failure.
148
Q

What is the Berlin criteria/definition for ARDS?

A
  • Acute Respiratory Distress Syndrome
  • It is a potentially severe form of type I respiratory failure
  • (1) Respiratory symptoms within 7 days of a known clinical insult (ie: PNA or sepsis), leads to
  • (2) Bilateral lung opacities on chest radiograph or CT scan,
  • (3) The respiratory failure and lung opacities are not explained by HF or fluid overload; AND
  • (4) An oxygenation impairment is present, as defined by the ratio of PaO2 to FiO2, aka the P:F ratio
149
Q

What is the clinical criteria for mild ARDS?

A
  • A P:F ratio (PaO2 to FiO2) is between greater to 200 mmHg and less than or equal to 300 mm
150
Q

What is the clinical criteria for moderate ARDS?

A

A P:F ratio (PaO2 to FiO2) is between greater to 100 mmHg and less than or equal to 200 mm

151
Q

What is the clinical criteria for severe ARDS?

A

A P:F ratio (PaO2 to FiO2) of less than or equal to 100 mmHg.

152
Q

What are common causes of ARDS?

A
  • Direct Causes:
    • Gastric aspiration leading to PNA
  • Indirect causes, include:
    • Sepsis, Trauma, and Acute pancreatitis
153
Q

Why is the exudative phase (0 to 7 days) so important when discussing ARDS?

A
  • Associated with widespread lung inflammation and injury, which causes proteinaceous fluid to leak into the alveolar spaces, contributing to hypoxemia.
  • Inflammatory mediators also induce a catabolic response culminating in protein breakdown.
  • Consequatial diaphragmatic weakness places the patient at risk for PMV.
154
Q

**(TRUE/FALSE)

Based on high quality evidence, the SCCM/ASPEN 2016 nutrition therapy guidelines did make a recommendation regarding the routine use of an enteral formulation characterized by the anti-inflammatory lipid profile in patients with ARDS.

A

FALSE***

There is only low quality evidence, therefore SCCM/ASPEN did NOT make this recommendation.

155
Q

Define RR.

A
  • Respiratory rate
  • Frequency of respiration; the number of breaths delivered per minute
156
Q

Define TV

A
  • Tidal Volume
  • The volume of gas delivered during a breath
157
Q

Define minute ventilation.

A

The TV multiplied by the RR

158
Q

Define vital capacity.

A

The volume of change of the lung between full inspiration and maximal expiration

159
Q

Define lung compliance.

A
  • The relationship of volume of gas and pressure of the lung (V/P)
  • The lung’s ability to stretch and expand
  • Diseased lungs frequently have poor compliance, which may increase the work of breathing.
160
Q

Define breath type (r/t MV modes)

A

Two types of breath are possible on MV

  1. Mandatory breath: an assisted breath delivered by the mechanical ventilator based on the set RR
  2. Spontaneous breath: may be assisted or unassisted and is a breath initially generated (triggered) by the patient.
161
Q

Define PEEP

A
  • A positive pressure applied at the end of expiration during mechanical ventilation to prevent alveolar collapse and subsequent barotrauma
162
Q

Define volume control (in reference to MV)

A

The delivery of a predetermined inspiratory volume despite changing lung compliance or respiratory muscle activity

163
Q

Define pressure control (r/t MV modes)

A
  • The delivery of a predetermined inspiratory pressure throughout inspiration despite changing respiratory muscle activity.
  • The volume of gas delivered (TV) with this type of breath varies depending on the lung compliance.
164
Q

Define asthma.

A

A chronic inflammatory disorder of the airways, which leads to recurrent but reversible episodes of airway obstruction and is manifested clinically by chest tightness, coughing, wheezing and SOB

165
Q

Define COPD

A
  • A common, preventable, and treatable disease, characterized by persistent airways limitation that is usually progressive and associated with an enhanced chronic inflammatory response in the airways and the lungs to noxious particles or gas
  • 3rd leading cause of death in the US
166
Q

What is the BODE index used for? Explain what it is.

A
  • Scale used to stage COPD according to degree of airflow limitation
    • B: BMI
    • O: Obstruction as assessed by FEV
    • D: Dyspnea as assessed by modified Medical Research Council score
    • E: Exercise capacity as measured by 6-minute walk distance.
167
Q

Define pulmonary cachexia syndrome.

A
  • Malnutrition associated with advanced lung disease (such as COPD)
  • Defined as a lean BMI of less than 17 in men and less than 14 in women
168
Q

Define interstitial lung disease (ILDs)

A
  • A heterogeneous group of disorders that are classifed together because of similar radiographic, clinical and pathological manifestations
  • ILDs cause lung restriction
  • Numerous causes:
    • Occupational and environmental agents
    • Drug-induced etiologies
    • Radiation-induced etiologies
    • Connective Tissue disorders
    • Idiopathic causes
  • ILDs commonly cause: Chronic Hypoxemix Respiratory Failure.
169
Q

Why can malnutrition be present with patients with CF?

A

Malnutrition from either pancreatic insufficiency or steatorrhea can be caused by malabsorption leading to nutrition deficiencies.

170
Q

(TRUE/FALSE)

BMI is an accurate measurement of nutritional status is patients with CF.

A

FALSE

Many patients do no reach their full growth potential, which means that BMI may not be as accurate

171
Q

How does the CMS define PMV?

A

Ventilator dependence for more than 21 days for at least 6 hours per day.

172
Q

Define chronic critical illness.

A

Defined as an ICU stay longer than 14 days with continued low-grade organ dysfunction.

173
Q

Define persistent inflammatory and immunocompromised catabolic syndrome (PICS).

A

Occurs in patients who survive acute critical illness and multiple organ failure, only to enter a state of chronic critical illness (after 14 days) characterized by low-grade organ dysfunction plus immune suppression with malnutrition, muscle weakness, recurrent infections, and poor wound healing.

174
Q

(FILL IN THE BLANK)

In patients with low nutrition risk, exclusive PN should be withheld during the first X days following ICU admission if the patient cannot maintain volitional intake and if early EN is not feasible.

A
  • 7 days
175
Q

(FILL IN THE BLANK)

When EN is not feasible in patients determined to be high nutrition risk or severly malnourished, consider initiating exclusive PN XXXX days following ICU admission.

A
  • As soon as possible
176
Q

(FILL IN THE BLANK)

In patients at either low or high nutrition risk, consider use of supplemental PN after X to X days if the patient is unable to meet >60% of energy and protein requirements by the enteral route alone.

A
  • 7 to 10 days
177
Q

(FILL IN THE BLANK)

In appropriate patients requiring PN, consider hypocaloric pN dosing (which is?) with adequate protein (which is?) initially over the XXX of hospitalization in the ICU.

A
  • < equal 20 kcal/kg/day or 80% estimated energy needs
  • Adequate protein: >equal 1.2 g/kg/d
  • First week
178
Q

If IC is not available, what equation should be used to estimate energy requirements for obese critically ill patients?

OR

For hypocaloric, high-protein regimen, what should you recommend?****

A
  • Penn State University 2010 equation
  • Less than 14 kcal/kg ABW with 1.2 to 1.5 g/kg ABW***
179
Q

Describe the pathogenesis of VAP.

A
  • Ventilator-Associated PNA
  • Difficult to determine, but it is thought to involve colonization of the oral pharynx, larynx, and upper esophagus with bacteria as well as microaspiration of secretions with bacteria.
  • The placement of the endotracheal tube causes the trachea to be stented open and provides passage for secretions and bacteria into the lower respiratory tract.
180
Q

List some prevention strategies for VAP.

A
  • If possible, avoid intubation by using noninvasive means of respiratory support
  • Minimize sedation and analgesia as tolerated and needed for effective patient care, and if possible, provide a daily sedation vacation
  • Maintain the patients physical conditioning through early mobilization and in-bed exercise
  • Use continous subglottic suctioning to decrease pooling of oral secretions
  • Elevate the head of the patient’s bed by more than 45 degree when possible
  • Maintain the ventilator circuit by mniminizing changes to the circuit unless it is soiled or malfunctioning
  • Decrease the patient’s time on mechnical vent if possible
  • Provide oral care with chlorhexidine
  • Consider probiotic use in select patient populations
  • Limit broad spectrum abx
181
Q

(TRUE/FALSE)

Patients with ARDS are, however, frequently placed in the prone position because recent evidence suggests this position improves the outcomes for these patients. Enteral feeding is generally considered safe in the prone positition, but patients should be monitored closely for intolerance and aspiration.

A

TRUE.

182
Q

What are the medical managements of Gastroparesis?

A

Antiemetics and prokinetic agents may reduce symptoms with significant N & V (scheduled dosing is best)

  • Metoclopramide (prokinetic): most commonly used bc of its rapid onset of action and efficacy; take NO longer than 12 weeks d/t risk of irreversible tardive dyskinesia
  • IV Erythromycin (prokinetic)
  • Domperidone: Not commercially available in the US
  • Cisapride: Withdrawn from US market d/t associated cardiac arrhythmia
183
Q

What are other oral nutrition interventions with Gastroparesis?

A
  • SFM
  • Use liquid calories
  • Maximize glucose control
  • Medications
  • Fat in liquids should be tolerated before restricting them
  • Treat SIBO
  • Monitor & Replace: Iron, Vitamin B12, Calcium, Vitamin D
184
Q

what is the inpatient glycemic target for critically ill patients

A

140-180 mg/dL

185
Q

Under conditions of sepsis and stress, glucose production will ____ and glucose uptake will ____

A

increased blood glucose production & decreased glucose uptake

186
Q

during sepsis and stress hormones induce ____ resistance and ____

A

insulin resistance

hyperglycemia

187
Q

what immunomodulating nutrients may be harmful in patients with sepsis/septic shock

A

arginine

188
Q

Arginine is considered beneficial for immune function because

A

it increases tissue oxygenation

189
Q

what is a benefit of enteral glutamine supplementation in the critically ill patient with multi organ failure

A

decreases nosocomial infections

190
Q

what are the counter regulatory hormones responsible for hypercatabolism in critically ill trauma patients?

A

Glucagon
Epinephrine
Cortisol

191
Q

Glucagon, epinephrine and cortisol are hormones released during _____ and lead to these four metabolic processes

A
traumatic injury
glycogenolysis
gluconeogenesis
proteolysis
free fatty acid release
192
Q

What is the goal of releasing hormones such as epinephrine, cortisol, and glucagon during trauma

A

maintain survival and homeostasis and promote recovery

193
Q

In a trauma patient, after timely resuscitation, restoration of perfusion, oxygenation and hemodynamic stability, what is the next important component of supportive therapy

A

early initiation of nutrition

194
Q

In patients with burns, providing caloric support above energy expenditure has been found to have ____ effect on preservation of lean body mass

A

have no effect

195
Q

although patients with burns have increased caloric needs, feeding in excess is still not recommended because it may cause

A

hyperglycemia, hepatic steatosis, or prolonged ventilatory dependence

196
Q

In pulmonary insufficiency, excessive calorie administration may cause increased blood pCO2 resulting in

A

respiratory acidosis

197
Q

respiratory acidosis results from disorders producing alterations in ventilatory control due to the increased production of

A

CO2 and respiratory muscle weakness

198
Q

Essential fatty acid deficiency in patients with cystic fibrosis is rare after _____ because EFA profiles have been shown to improve after it

A

lung transplantation

199
Q

In cystic fibrosis, disruption of the exocrine function of the pancreas contributes to malabsorption of

A

fat, protein and fat soluble vitamins

200
Q

EFAD status is usually evaluated by measuring

A

triene: tetraene ratio

201
Q

clinical trials have ____ results in using omega 3 fatty acids in routine supplementation in the management of CF

A

mixed

202
Q

what is the best choice for feeding a pancreatic insufficient infant with CF and why

A

Human Milk with enzymes because it has good immunologic properties, growth factors, pre and probiotics

203
Q

Protein hydrolysate or free amino acid formulas with MCT are not indicated in infants with CF unless

A

there is another medical reason such as bowel resection leading to malabsorption or liver abnormalities

204
Q

What is the glomerular filtration rate (GFR) for a patient with ESRD?

A

<15mL/min/1.73m2

205
Q

a GFR indicating stage 1 kidney damage equates to

A

> 90mL/min/1.73m2

206
Q

what is a GFR of Stage 2 Kidney damange

A

60-89mL/min/1.73m2

207
Q

what is a GFR of Stage 3 Kidney Damage

A

30-59 mL/min/1.73m2

208
Q

what is a GFR of Stage 4 kidney disease

A

15-29mL/min/1.73m2

209
Q

Increased mortality in maintenance of HD patients has been associated with

A

low baseline body fat percentage and low muscle mass

210
Q

low muscle mass reflects poor ____ status and ______

A

nutrition status

inflammation

211
Q

low fat mass reflects low body stores of _____

A

energy

212
Q

Elevated CRP levels in HD can cause

A

weight loss
decreased albumin
decreased appetite

213
Q

which BMI is considered protective in HD patients

A

30-34.9

214
Q

A BMI less than ____ and hypoalbuminemia are strong indicators of mortality in HD patients

A

< 23

215
Q

What has been shown to delay weaning from mechanical ventilation in patients with chronic obstructive pulmonary disease who are receiving enteral nutrition

A

refeeding syndrome
underfeeding
overfeeding

216
Q

Hypophosphatemia can delay weaning from mechanical ventilation because

A

hypophosphatemia exacerbates respiratory dysfunction, diaphragmatic weakness and decreased cellular energy production

217
Q

_____ feeds are defined as feeding in an amount of substrate enough to provide gut stimulation and are typically at a rate of 10-20mL/hr of EN

A

trophic feeds

218
Q

What is the maximum dietary protein intake in critically ill adult patients getting continuous renal replacement therapy (CRRT)

A

2.5 g/kg/day

219
Q

high protein needs of 2.5g/kg/day in the critically ill adult on CRRT is due to

A

hyper-catabolism, obligatory use of protein as preferred fuel source during the stress response and the likelihood of significant protein losses in CRRT effluent

220
Q

Typical protein losses in CRRT equate to

A

10-17%

221
Q

what are some disadvantages of going over 2.5g/kg/day of protein in CRRT

A

uremia
increased hepatic and renal demand
increased costs

222
Q

what are the protein requirements for a stable patient getting peritoneal dialysis

A

1.2-1.3 g/kg/day (when clinically stable)

223
Q

what are some causes of protein energy malnutrition in liver disease

A
malabsorption
decreased kcal intake
abnormal fuel metabolism
early satiety
fat malabsorption from altered bile acid circulation
increased protein and fat oxidation
224
Q

Energy expenditure is ___ in patients with infections and ascites with liver disease

A

increased

225
Q

Protein energy malnutrition is most common in which of the following types of liver disease

A

Cirrhosis

226
Q

patients with viral disease such as hepatitis B and C are not susually

A

severely malnourished

227
Q

Patients with chronic heart failure are typically on a loop diuretic. These patients are at risk for

A

azotemia

228
Q

Loop diuretics cause electrolyte imbalances as a result of decreased urine output, so azotemia is caused by

A

volume depletion

229
Q

hypoglycemia requiring dextrose infusions to maintain euglycemia, is most likely to occur in which type of liver disease

A

Fulminant Hepatic Failure from impaired glycogenolysis, gluconeogenesis, and hyperinsulinemia requiring aggressive glucose administration

230
Q

which metabolic derangements are common in fulminant hepatic failure

A

impaired glycogenolysis
hypoglycemia
impaired gluconeogenesis
hyperinsulinemia

231
Q

patients with fulminant hepatic failure are in a ____ state with increased energy ____ and can rapidly become ____

A

hypercatabolic
expenditure
malnourished

232
Q

In cirrhotic patients, which of the following should be implemented to assist in avoiding fasting association starvation during the night

A

late evening snack

233
Q

Cirrhotic patients have ____ glycogen stores and utilize more ____ as fuel during periods of prolonged starvation (usually seen in an overnight fast of 12-18 hours)

A

depleted glycogen stores

fat as fuel

234
Q

what is an important indicator of protein energy malnutrition in chronic liver disease

A

muscle wasting & subcutaneous fat

235
Q

in patients with chronic liver disease, using triceps skin fold and mid arm circumference can possibly be skewed by

A

fluid retention

236
Q

Treatment for patients with overt hepatic encephalopathy who have impairments in cognitive and neuromuscular function include

A

supplementing zinc, thiamine, b6 and b12, use lactulose, provide a meal pattern of 3 meals and 3 snacks

237
Q

______ is no longer restricted in patients with advanced liver disease

A

protein restriction

238
Q

what micronutrients are common deficiencies in chronic liver disease due to poor intake and decreased absorption

A
thiamine
vitamin B6
B12
Folate
zinc
239
Q

which types of cancer have the highest prevalence & severity of weight loss

A

pancreatic and gastric cancer

240
Q

what types of cancer have the lowest prevalence of weight loss

A

sarcomas, breast cancer, hematological cancers

241
Q

that is the benefit of megesterol acetate in patients with cancer associated cachexia?

A

improves appetite and ameliorates weight loss

242
Q

______ is a synthetic progestational agent that promotes weight gain and helps to stimulate the appetite

A

megace

243
Q

In the first 1-3 months after a bone marrow transplant the nutritional needs of a patient are best met with

A

30-35 kcal/kg body weight

>/= 1.5 g protein/kg body wt

244
Q

Which nutrient should NOT be supplemented routinely in the early stages following hematopoietic stem cell transplantation (HSCT)

A

Iron

245
Q

in Hematopoietic Stem Cell Transplantation, blood products and transfusions are required before, after, and during HSCT and can cause an overabundance of which nutrient

A

iron

246
Q

Iron overload in HSCT patients can increase the chance of

A

acute graft vs host disease
blood/fungal infection
sinusoidal obstruction of liver

247
Q

What acute changes in serum chemistry profile would be expected in a patient who is experiencing tumor lysis syndrome?

A

hyperkalemia

hyperphosphatemia

248
Q

_____ is caused by massive tumor cell lysis with the release of large amounts of potassium, phosphate and nucleic acids into systemic circulation

A

Tumor Lysis Syndrome

249
Q

Tumor Lysis Syndrome is common after

A

initiation of cytotoxic therapy

250
Q

What is the best treatment of diarrhea in inflammatory bowel disease

A

Start anti-diarrheal agents once infectious etiology is ruled out

251
Q

Anti-diarrheal medication should not be given to patients with IBD until what has been ruled out. Why?

A

infectious diarrhea such as CDiff. If to they can develop toxic megacolon

252
Q

In patients with extensive bowel resection ______ can be given in conjunction with anti diarrhea medications

A

Cholestyramine to help with bile salt malabsorption

253
Q

how much stool output is concerning for possible electrolyte deficiencies and volume depletion

A

> 500mL for 2 consecutive days

254
Q

there are currently no evidenced based recommendations for using ___ or ____ as standard therapy with diarrhea

A

prebiotics & probiotics

255
Q

A patient with Chron’s Disease that involves the distal ileum should be closely monitored for malabsorption of which micronutrient

A

vitamin B12

256
Q

what is a major contributing factor in the development of metabolic bone disease in patients with IBD?

A

corticosteroid use

257
Q

complications of metabolic bone disease is associated with IBD are

A

osteopenia and osteoporosis

258
Q

when patients are on long term steroids, what should be supplemented to reduce osteopenia

A

calcium & vitamin D

259
Q

what is commonly found in patients with IBD?

A
malnutrition
vitamin D deficiency
corticosteroid therapy
magnesium deficiency
chronic inflammation
260
Q

____, ____ and _____ may be associated with PN associated MBD

A

aluminum toxicity, hypercalciuria, magnesium deficiency

261
Q

In patients with severe acute pancreatitis, the use of enteral nutrition via naso-jejunal feeding tube rather than PN is associated with

A

a lower risk of developing infectious complications, maintained equal nitrogen balance and reduced incidence of hyperglycemia than those with PN

262
Q

when is PN recommended in severe acute pancreatitis

A

when EN is not available, tolerated or patient is not meeting nutritional requirements via EN alone

263
Q

A patient with chronic heart failure on high dose furosemide is started on EN for an inability to consume adequate oral nutrition. Despite a slow advancement to goal feeding rate, he suffers from electrolyte imbalance and peripheral neuritis. Deficiency of which vitamin should be suspected in the cause of his symptoms

A

Thiamine

264
Q

which two medications are known for decreasing thiamine by uptake of cardiac cells in heart failure patients

A

furosemide and digoxin

265
Q

Thiamine deficiency is a form of _____ which is characterized by an enlarged heart, electrolyte alterations, vasodilation and peripheral neuritis

A

Wet BeriBeri

266
Q

gastric hypersecretions following significant small bowel resection can become problematic. Which of the following medications have shown to be the most successful in suppressing gastric hypersecretion

A

Proton Pump Inbitors

267
Q

What metabolic complication may occur in patients with short bowel syndrome and small bowel intestinal bacterial overgrowth

A

metabolic acidosis

268
Q

intestinal resection involving removal of the terminal ileum and or the ileocecal valve with the colon in continuity predisposes patients to

A

small intestinal bacterial overgrowth

269
Q

in rare instances patients with short bowel syndrome can develop ____and encephalopathy. D lactate producing bacteria thrive in an acidic environment which is common in SBS as a result of metabolism of unabsorbed carbs leading to the production of lactate and decreases the pH

A

metabolic acidosis

270
Q

patients with short bowel syndrome would benefit most from octreotide injections in the presence of

A

refractory diarrhea not controlled with diet and medication

271
Q

what medication reduces the production of a variety of GI secretions and slows jejunal transit

A

octreotide

272
Q

why should Octreotide by reserved only for patients with large volume stool loss whose fluid & electrolyte management is problematic

A

increases the risk for cholelithiasis
expensive
can inhibit bowel adaptation
has not been shown to improve absorption or eliminate the need for PN

273
Q

what diet should be recommended to patients with short bowel syndrome (ileal resection) and colon in continuity

A

high complex carbohydrates 50-60% of total calories, low fat (20-30%) to increase energy absorption, optimize SCFA production & reduce instance of steatorrhea

274
Q

a high complex carb diet low in fat helps reduce

A

magnesium & calcium losses, decreases oxalate absorption

275
Q

oxalates bind to ____ and are excreted in the stool

A

calcium

276
Q

patients with SBS who have a colon in continuity should restrict dietary oxalate intake & consume high calcium food or calcium citrate supplements to avoid

A

oxalate nephrolithiasis

277
Q

A patient with SBS (regardless of bowel anatomy) complex carbs are important in the diet becuase

A

they reduce the osmotic load & may help with intestinal adaptation

278
Q

Why are complex carbs recommended in SBS verses simple sugars

A

they take longer to break down than simple sugars which improves tolerance

279
Q

why should concentrated sugars be avoided in short bowel syndrome

A

they can generate a high osmotic load and increase or promote stool output

280
Q

calcium oxalate nephrolithiasis can occur in patients with short bowel syndrome with an intact colon who

A

don’t maintain adequate hydration

281
Q

patients with short bowel syndrome are at a high risk for oxalate stones because

A

there is increased availability of oxalate absorption in the colon as patients with SBS usually have steatorrhea

282
Q

normally, oxalates bind to ____ and are excreted through the stool

A

calcium & magnesium

283
Q

in patients with SBS and steatorrhea, why are oxalates absorbed at an increased rate?

A

calcium binds to fatty acids, allowing excess and unbound oxalate to be absorbed from the colon & be filtered through the kidneys leading to stone formation also exacerbated by dehydration

284
Q

to avoid calcium oxalate nephrolithiasis, maintaining hydration with a goal urine output of _____ is important, with oral calcium supplements between ___ and ___ mg/day not exceeding ___ mg a a time is recommended

A

> 1200mL a day

800-1200mg/calcium a day at does of no more than 500mg at one time

285
Q

low dietary fat intake of 20-30% of total kcals is important in SBS in order to

A

minimize steatorrhea
minimize oxalate absorption
minimize loss of calcium & magnesium

286
Q

SBS patients with less than ____ cm of terminal ileum resected are at lower risk of bile salt malabsorption & steatorrhea

A

100

287
Q

what types of fistulas will result in the greatest degree of nutritional loss

A

proximal high output

288
Q

the higher a fistula occurs in the GI tract, the ____ the output and risk of metabolic derangements

A

higher (more proximal)

289
Q

patients with proximal high output fistulas in their GI tract will reuqire

A

increased protein/calorie needs

close monitoring of fluids & electrolytes

290
Q

patients with low output fistulas less than ____mL/day of stool loss will decrease the possibility of enteral nutrition

A

500mL/day

291
Q

to minimize fistula output in distal ileal or colonic fistulas, what type of enteral nutrition formula should be used as high up as possible to increase surface area for absorption

A

fiber free or low fiber

292
Q

A 24 year old, 10 week pregnant woman presents with persistent nausea & vomiting for the past 6 weeks associated with a 10% wt loss. Her symptoms were refractory to a 48 hour trials of anti-emetics & IVF. Given mother’s nutritional status, decision was made to initiate nutrition support. What vitamin should be supplemented in this patient before providing nutrition support

A

thiamine

293
Q

A 24 year old, 10 week pregnant woman presents with persistent nausea & vomiting for the past 6 weeks associated with a 10% wt loss. Her symptoms were refractory to a 48 hour trials of anti-emetics & IVF. Given mother’s nutritional status, decision was made to initiate nutrition support to minimize further deterioration of the mother’s nutritional status & possible negative side effects on the fetus. What is the most appropriate initial nutrition therapy to implement

A

EN with polymeric formula via NG tube

294
Q

severe, intractable nausea and vomiting complicated by dehydration, electrolyte imbalance, nutrition deficiencies and weight loss in pregnant women is called

A

hyperemesis gravidarum

295
Q

because constipation is often a problem in pregnancy, what type of formula should be considered in EN

A

fiber

296
Q

A 14 year old with a 4 month history of intentional weight loss of 15% of her usual weight & a BMI < the 5th percentile is diagnosed with anorexia nervosa. She is admitted to the hospital for medical stabilization and is unwilling to consume enough food to meet her nutritional needs. A 24 hour calorie count reveals that the patient is consuming a very restricted diet averaging 850 calories a day. Which is the most appropriate nutrition intervention at this time

A

structured meal plan with supplemental enteral feedings

297
Q

what is the preferred modality for nutrition rehabilitation

A

oral refeeding

298
Q

a critically ill hyperglycemic patient receiving continuous enteral nutrition with a history of insulin dependent diabetes should ideally be placed on

A

continuous IV infusion

299
Q

in the critical care setting, _______ has been shown to be the best method for achieving glycemic targets and allows for off cycles during the 24 hr period when EN is held or discontinued

A

continuous IV insulin infusion

300
Q

Human Immunodeficiency Virus (HIV) associated lipodystrophy syndrome is most commonly associated with which class agent to treat HIV infection

A

nucleoside reverse transcriptase inhibitors (NRTI’s)

301
Q

_____ is manifested by subcutaneous adipose tissue loss with visceral adipose tissue sparing or accumulation

A

HIV associated lipodystrophy syndrome

302
Q

where is subcutaneous tissue loss often seen in HIV

A

face, buttocks, lower extremities

303
Q

Patients with lipodystrophy are at increased risk of being

A

insulin resistant

304
Q

what is the most appropriate feeding strategy for a morbidly obese trauma patient

A

hypocaloric high protein

305
Q

zinc supplementation should be considered for patients with

A

unexplained skin rashes & alopecia

306
Q

Zinc is an essential trace element for ____ and ___

A

cell replication & growth

307
Q

Zinc is a cofactor for ____ & ____ synthesis and proliferation of inflammatory cells/epithelial cells

A

collagen & protein synthesis

308
Q

zinc deficiencies usually occur from

A

GI surgery
diseases that impair intestinal absorption
diseases that increase zinc loss es
Celiac, CF, IBD, Chron’s

309
Q

Chronic diarrhea &exudate from large wounds cause ___ deficiency

A

zinc

310
Q

why are zinc levels not always reflective of zinc status?

A

the presence of inflammation and are dependent on albumin for transport, so interpret cautiously in presence of hypoalbuminemia & inflammation

311
Q

what are the symptoms of zinc deficiency

A

rash, alopecia, impaired night vision, alterations in taste & smell, impaired immune function, anorexia, and diarrhea

312
Q

Nutrition support for solid-organ transplant patients receiving cyclosporine may need to be modified due to the presence of

A

hyperkalemia

313
Q

Cyclosporines, medications used after solid organ transplantation for immune suppression can cause electrolyte imbalances including

A

hyperkalemia, hypomagnesemia
hyperglycemia
hypercholesterolemia as it effects the renin angiotensin aldosterone system altering potassium homeostasis as well as decreased renal excretion of potassium

314
Q

A patient with AKI who requires PN would most likely benefit from a solution containing

A

essential and non essential amino acids

315
Q

A 51 year old F who is 10 years post gastric bypass surgery presents w/ numbness & tingling in her distal lower extremities that had progressively worsened. She had been on an oral MVI supplement. She was significantly anemic & neutropenic. Her vit B12 level was normal as were her serum iron, ferritin and transferrin levels. What nutritional deficiency is the most likely cause of all of these symptoms

A

Copper deficiency

316
Q

Vitamin B12 deficiency in gastric bypass can cause

A

anemia & peripheral neuropathy (numbness & tingling in lower extremities)

317
Q

Iron & Folate deficiencies cause ____ in gastric bypass patients

A

anemia

318
Q

Thiamin deficiency can cause peripheral neuropathy but not _____ in gastric bypass patients

A

not anemia

319
Q

what are the symptoms of copper deficiency

A

anemia
leukopenia
neutropenia
peripheral neuropathy

320
Q

ERAS (Enhanced Recovery After Surgery) is a care program that has been shown to improve outcome after major surgery. The key mechanisms behind the ERAS effectiveness is

A

decrease the stress of surgery and support recovery

321
Q

what are the objectives of ERAS

A

avoid starvation before surgery

limit post op IVF

optimize GI function & mobilization

322
Q

What is done as part of ERAS protocol

A

avoid preop fasting by providing CHO nutrition/fluid and withholding routine bowel prep

323
Q

ERAS was originally designed for which types of surgeries

A

colon resection