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Clinical Nutrition 2 > Pancreatitis > Flashcards

Pancreatitis Flashcards

1
Q

When does the incidence of pancreatitis peak?

A

Between 40-70 years old

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2
Q

Mortality for acute, necrotizing and severe?

A

5%, 17% and 30%

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3
Q

What are the costs of pancreatitis?

A
  • Nearly $9,000 fo a 8-10 day hospital stay

- However, after hospital many cannot work (cost to individual)

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4
Q

Acute mortality due to gallstones or idiopathic?

A

10-25%

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5
Q

Chronic mortality due to alcoholism?

A

5%

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6
Q

What is the key concept to understand w/ pancreatitis?

A

The pancreas is an endocrine and an exocrine gland. When a blockage of the ducts leads to the build-up and subsequent digestion of the pancreas, this can also affect the exocrine function where insulin and glucagon are altered.

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7
Q

Which cells secrete NaHCO3, K+, Na+ and Cl- in the pancreas?

A

-Duct cells

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8
Q

Which cells secrete digestive enzymes in the pancreas?

A

Acinar cells

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9
Q

Provide 8 major digestive enzymes secreted from the acinar cells

A
  • Trypsin
  • Chymotrypsin
  • Carboxypolypeptidase
  • Deoxy/Ribonuclease
  • Eleastrase
  • Lipase
  • Cholesterol esterase
  • Alpha-Amylase
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10
Q

What normally activates trypsin?

A

Brush border enzymes, such as enterokinase

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11
Q

In the fasted state, is there secretions from the pancreas?

A

Yes, basal flow of secretion

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12
Q

What stimulates the pancreas in the cephalic/anticipatory state?

A

-Vagal nerve stimulation

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13
Q

What stimulates the pancreas in the fed state?

A

-Distention will stimulate the pancreas via vagal nerve

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14
Q

What stimulated the intestinal production of secretin and CCK?

A

Chyme

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15
Q

What does secretin stimulate?

A
  • Release and contraction of pancreas in a negative-feedback loop fashion
  • Allows for the neutralization of contents in the SI
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16
Q

What prevents further CCK production?

A

Active proteases which are released from the pancreas upon stimulation

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17
Q

What are other inhibitory factors in the intestinal phase?

A
  • PPY

- Somatostatin

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18
Q

What is pancreatitis?

A

The inflammation of the pancreas and the ducts

-There are acute and chronic forms

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19
Q

What is pancreatitis characterized by?

A
  • Edema, cellular exudate, fat necrosis

- Autodigestion, necrosis hemorrhage of pancreatic tissue

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20
Q

Signs/symptoms of pancreatitis?

A
  • Nausea, vomiting, abdo distention, steatorrhea

- Hypotension and dehydration

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21
Q

What are common causes of acute pancreatitis?

A
  • Biliary tract disease/cholelithiasis
  • Alcoholism
  • Idiopathic
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22
Q

Other causes of acute pancreatitis?

A
  • Infection, drugs, surgery, cancer
  • Obesity, hyperlipidemia
  • Hyperparathyroidism, hypercalcemia
  • Exposure to toxins
  • Trauma, ERCP
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23
Q

Theories of acute pancreatitis?

A
  • Autocatalytic digestion

- Rate formation of trypsin > inhibitors

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24
Q

___ with uncomplicated, mild to moderate pancreatitis will advance to oral diet within a week of admission

A

80%

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25
Q

___ of acute pancreatitis patients require nutrition support

A

20%

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26
Q

Why may alcohol cause pancreatitis?

A

May cause random spasms over the years which can cause idiopathic digestion

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27
Q

Which stress factor should be used with HB in acute pancreatitis?

A

As they are in catabolic state, try 1.39 x HB

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28
Q

Clinical symptoms/presentations of acute pancreatitis?

A
  • Abdominal pain, nausea and vomiting
  • SIRS/shock, fever, edema
  • Exudate in peritoneal and pleural spaces
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29
Q

Biochemical presentations of acute pancreatitis?

A
  • Elevated levels of pancreatic enzyme, amylase, lipase
  • Elevated liver enzymes in biliary causes
  • Low blood calcium
  • Elevated serum TG
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30
Q

There is often elevated TGs, and fat necrosis around the pancreas during acute pancreatitis, what would we estimate their maximal fat clearance to be?

A

1 mg/kg/day

Recall lipid clearance in the critically ill patient

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31
Q

What is exudate?

A

Any fluid that has exuded from a tissue/capillary due to injury/inflammation

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32
Q

What is the pathogenesis of chronic pancreatitis linked to?

A
  • Alcoholsim
  • Cystic fibrosis
  • Chemical exposures
  • Recurrent acute
  • –> Insult w/o symptoms
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33
Q

What is chronic pancreatitis exacerbated in? What does this cause?

A
  • Alcohol intake

- Presents with acute like symptoms

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34
Q

How does alcohol elicit both acute/chronic pancreatitis?

A

-Damages the acinar cells, and will stimulate secretin with the induction of spasms within the ducts –> And cause a precipitation of protein within the ducts

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35
Q

How does cystic fibrosis lead to chronic pancreatitis?

A

-Mucus secretions and flow of enzymes is impaired, therefore enzymes collect and are activated in ducts –> Infections and digestion

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36
Q

What do the symptoms of chronic pancreatitis depend on?

A

Stage of disease and alcohol intake

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37
Q

Symptom of chronic pancreatitis?

A
  • Abdominal pain, vomiting
  • Malabsorption, steatorrhea
  • Weight loss
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38
Q

Biochemical presentations in chronic pancreatitis?

A

High amylase and lipase followed by low concentrations as acinar cells atrophy

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39
Q

Other symptoms of acute pancreatitis?

A

-Pericardial effusions, ascites, psychosis, necrosis of bone, decreased insulin and glucagon

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40
Q

Chronic pancreatitis may have _____

A

recurrent acute episodes

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41
Q

What is nutrition support based on?

A

-Severity of scores and likelihood of not achieving oral intake within 7-days

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42
Q

Typical nutritional managements in more severe cases of acute pancreatitis?

A

-NPO, TPN or EN

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43
Q

Typical nutritional management for mild & moderate cases of acute pancreatitis?

A
  • Oral feeds
  • Low fat high CHO and PRO for some
  • Clear fluids to begin, transition to full fluid diets (consider fat)
  • No alcohol
  • Frequent, small meals
44
Q

Typical nutritional management for chronic pancreatitis?

A
  • Replacement enzymes w/ meals
  • Antacids
  • Low fat/high-pro diet
  • CHO depends on islet function
  • MCT oil an EN
  • No alcohol
  • Vitamin supplement (fat soluble and B12)
45
Q

Why are antacids key if we provide enzyme supplementation?

A

Too acidic of a PH will simply digest the enzymes.

46
Q

Why is MCT oil desirable?

A

-Less reliant on bile, and may result in less of a stimulation of CCK

47
Q

How is Ransons criteria determined?

A
  • 5 observations on bloods are checked at admission or diagnosis
  • 6 observations on bloods are re-checked during the initial 48 hrs
48
Q

What happens when >/= 3 of ransons criteria are present?

A

> 60% of patients die in hosptialization

49
Q

What is checked for increases in Ransons criteria?

A

-WBC
-Blood glucose
-Lactic dehydrogenase
-Aspartate transaminase
BUN
-Acid/Base deficit
-Fluid sequestration

50
Q

What is checked for decreases in Ransons criteria?

A
  • Hematocrit
  • Arterial PO2
  • Calcium
51
Q

What does APACHE stand for?

A

Acute Physiology and Chronic Health Evaluation

52
Q

What is inculded in the APACHE score?

A
  • Age
  • Rectal temo
  • MAP
  • HR
  • PaO2
  • Artetial pH
  • Serum K, Na, Cr, Hct, WBC
  • Glasgow comma Scale Score
  • Chronic health status
53
Q

What is the APACHE and RANSON which indicates mild/moderate pancreatitis?

A

APACHE II <9

Ransons <2

54
Q

What will a CT scan indicate for mild/moderate pancreatitis? What is the mortality rate? How many will reach PO diet in 7 days?

A
  • No necrosis
  • 0%
  • 81%
  • -> Focus on supportive management
55
Q

What is the APACHE and RANSON which indicates severe pancreatitis?

A

APACHE II >10

Ransons >3

56
Q

What will a CT scan indicate for severe pancreatitis? What is the mortality rate? How many will reach PO diet in 7 days?

A
  • Necrosis
  • 19%
  • 0%
  • -> Focus on EN and PN Managements
57
Q

In the case of a mild pancreatitis, and the oral diet is not tolerates, when should we progress to EN?

A

Only use EN if the oral diet fails over 4 days

58
Q

What needs to be evaluated to establish disease severity?

A

-SIRS,APACHE, RANSONS and CT necrosis

59
Q

Where are mild cases admitted? Moderate/severe? How are they fed?

A
  • Admit to ICU

- Place NG tube and initiate standard EN

60
Q

What happens if NG EN is not tolerated?

A
  • Switch to N feeds

- Start PN if intolerant >5days.

61
Q

Why should we use gastric feeds?

A
  • Gastric as better stimulation which is not observed in the jejunum
  • Gastric access is much easier to obtain
62
Q

If a severe or moderate pancreatitis patient tolerates NG EN, how can we progress?

A

If appropriate, we may advance to oral diet per patient wishes

63
Q

What are the nutritional goals in the mild and moderate case?

A
  • Maintain or achieve optimal nutrition status
  • Reduce steatorrhea
  • Minimize pain
  • Avoid alcohol
64
Q

What does ASPEN recommend about low fat diet in mild states?

A

No evidece

  • Use self-selection in context of standard nutrition therapy
  • However, not for ICU patients
  • If oral intake fails, initiate EN after 4 days
65
Q

What are some important considerations in nutrition support regarding the acute, severe, pancreatic patient?

A
  • Hyperglycemia and insulin resistance is common (40-90%)
  • Hypertriglyceridemia in 12-15% of cases
  • Electrolyte and micronutrient deficiencies
66
Q

Why hyperglycemia?

A

-Critical illness and residual islet cell function

67
Q

Why typerTG?

A
  • Low LPL (cannot clear lipids)

- Hyperglycemia induced

68
Q

Which electrolyte/micronutrient imbalance is present in 25% of cases

A

Hypocalcemia

69
Q

Energy in AP nutrition support?

A

25 kcal/kg/day

-Avoid overfeeding

70
Q

Why is HB x 1.39 (high) and 25 kcal/kg/day (low) recommended for NS?

A
  • What someone NEEDS is not necessarily wha they should be fed
  • We are often aiming for 80% of the target
  • 25 kcal/kg/day likely more appropriate, but try both and use clinical judgement
71
Q

Protein in AP?

A

1.5 g/kg/day

72
Q

What should be used in terms of energy for a septic, AP patient?

A

HB x (1.39 + 1.15)

73
Q

Goals in providing adequate kcal and protein in AP patient?

A
  • Support acute phase protein
  • Minimize nitrogen losses
  • Manage imbalances
74
Q

Why is enteral nutrition the preferred method in AP?

A
  • Maintain gut integrity, decrease septic and metabolic complications, decrease cost
  • Reduced stress response compared to PN
  • Reduced infection
  • Reduced LOS by 4 days
  • Reduced surgical intervention
  • Reduced organ failure
75
Q

Which organs are likely to fail in pancreatitis?

A
  • Respiratory system (PENN state, may be sedated, propofol)

- Kidney (Higher protein, CRRT, hypotension)

76
Q

Which mode of feeding will provide pancreatic rest while using the GIT?

A

Enteral support below the ligament of Treitz (LOT) via nasojejunal tube

77
Q

If there is pain, where should we feed?

A

Below LOT

78
Q

How should EN be administered?

A
  • Initiate within 48-72 hours of admission
  • Continuous infusion over 24 hours a day
  • Initiate feeding 25 ml/hour and advance to reach 25 kcal/kg over 24-48 hours
79
Q

EER in pancreatitis?

A

25 kcal/kg/day or indirect calorimetry

80
Q

Estimated protein in pancreatitis?

A
  1. 5 k/kg/day

- Up to 2g/kg/day (MUHC)

81
Q

Formulation of EN in pancreatitis?

A

-Standard polymeric formula, mixed protein, fat CHO

82
Q

What kind of formula should we use if intolerance in expected?

A
  • Semi-elemental or elemental or very low-fat formulas

- R/o C.Diff and sorbitol containing meds first

83
Q

What type of formula should we use if steatorrhea?

A

Semi-elemental with mCT

84
Q

CHO limit in pancreatitis on EN? Why?

A

5 mg/kg/min

  • Due to hyperglycemia and hyperTG
  • -> On exam, use both 5 and 3 then rationalize whether it is a severe or mild case
85
Q

When can we advance EN feeds to oral diet? When do we switch to PN?

A
  • Advance to oral diet when no pain for 24 hours

- Switch to PN if there is intolerance

86
Q

When is PN only considered?

A

In patients for whom enteral access is not possible or not tolerate or the most SEVERE cases

87
Q

What are the severe cases where PN is warranted?

A
  • Persistent ileus

- Small intestinal obstruction

88
Q

When can we initiate PN?

A

5 days after admission, even if high risk (already at high risk for infection, risk outweighs benefit)

89
Q

Type of PN?

A

Mixed fuel

90
Q

PN energy?

A

Increase slowly to reach 25-35 kcal/kg

91
Q

CHO limit in PN?

A

-5 mg/kg/min or 3 mg/kg/min

92
Q

Protein in PN?

A

1.2-1.5 g/kg/day

93
Q

Intralipid in PN?When?

A

Less than 15-30% of kcal

-When TG <400 mg/dL or 4.52 mmol/L

94
Q

Lipid of _____ does not cause hyperTG

A

1 mg/kg/day

95
Q

When is pancreatitis chronic?

A

When there is pancreatitis insufficiency

96
Q

Overarching goal in nutrition support of chronic pancreatitis?

A

Restore and maintain weight

97
Q

Meals in chronic pancreatitis?

A
  • Frequent, small meals moderate to low in fat
  • However, low fat ay exacerbate malnutrition, and tolerance is the goal
  • MCT may be used
98
Q

What must be taken in chronic pancreatitis?

A

Pancreatic enzymes taken with food (no more than 30 mins prior, or smaller amounts during meals)

99
Q

What should be avoided in diet in chronic pancreatitis?

A

-Alcohol, coffee, tea, spices, irritant condiments

100
Q

What should be monitored in chronic pancreatitis?

A
  • Monitor fat, water-soluble vitamins
  • Medical management of pH
  • Treat with insulin if hyperglycemia or diabetes
101
Q

Lipase dosages per meal?

A

500-2500 U lipase/kg/meal

102
Q

Lipase dosages per day?

A

<10000 U lipase/kg/day

103
Q

Lipase per g of dietary fat per day at meals and snacks?

A

1000-4000 U lipase/1 g dietary fat per day

104
Q

Guidelines for pancreatic enyzmes?

A
  • Swallow without crushing
  • The enteric coating will become activated at > pH 5, therefore consider adding something to increase/neutralize the pH, such as antacids
105
Q

When will the pH in the SI be <5?

A

When bile acid not active, in pancreatitis

106
Q

What are the two functions of antacids?

A
  • Enteric coat activation of pancreatic enzyme replacements

- Aid in fat malabsorption

107
Q

In failure of oral diet, what is preferred in terms of NS in chronic pancreatitis?

A
  • EN preferred

- Semi-elemental and elemental best given pancreatic insufficiency (enzymes do not lend to tube feeding)

Clinical Nutrition 2 (21 decks)

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