Clinical Nutrition

Front 1

Pancreatitis

Back 1

Intrapancreatic activation and release of enzymes (amylase, lypase), causing auto-digestion of the pancreas and surrounding areas

Front 2

Common cause of pancreatitis

Back 2

Alcoholism

Front 3

Twp enzymes secreted by the pancreas and their function

Back 3

Lipase for fat
Amylase for starches

Front 4

Clinical presentation of pancreatitis

Back 4

- abdominal pain, nausia, vomiting, anorexia
- ileus of the stomach and/or intestine
- increased serum amylase + lypase
- pain can be sudden onset

Front 5

Potential complications of acute pancreatitis

Back 5

- necrotizing pancreatitis
- pseudocyst
- abscess
- fistulas
- acute respiratory distress sydrome
- diabetes
- malabsorption

Front 6

Treatment of Pancreatitis

Back 6

1. Remove cause if possible - i.e. gall stone or alcohol
2. Supportive treatment

Front 7

Supportive treatment of pancreatitis

Back 7

- electrolyte replacement and balance
- fluid replacement, blood pressure mgmt
- pain mgmt
- intensive care mgmt if severe
i.e. respiratory care or surgery

Front 8

Nutritional Considerations for pancreatitis

Back 8

- if mild - NPO for up to a week, then slow intro of clear fluids to solid diet (+/- low fat)
- if severe - consider nutrition support right away (very catabolic, very long course)

Front 9

What is another main function of the GI tract other than absorption?

Back 9

Immune function

Front 10

Why is EN preferred over TPN now in pancreatitis?

Back 10

- use to think TPN allowed for "pancreatic rest"
- decr. complications using EN
- maintain gut barrier
- maintain immune function of gut
- decr. costs

Front 11

Objectives of the Cochrane Review: Enteral vs Parenteral Nutrition for Acute Pancreatitis

Back 11

To campare TPN vs EN lookig at specific outcomes such as mortality, infection, length of stay etc.

Front 12

Results of the Cochrane Review: Enteral vs Parenteral Nutrition for Acute Pancreatitis

Back 12

- Significant benefits favoring EN over TPN by decreasing mortality, multiple organ failure, systemic infection, and operative interventions
- studies were of "moderate" quality
- best evidence to date favours the se of EN over TPN**

Front 13

What is the largest immunological component of the body?

Back 13

The intestine

Front 14

GALT

Back 14

Gut Associated Lymphoid Tissue

Front 15

Function of GALT

Back 15

Stimulates protective immunity without an excessive inflammatory response

Front 16

Innate Defenses of the intestine - Luminal factors

Back 16

- digestive secretions and enzymes
- gastric acid
- secretary IgA

Front 17

Innate defenses of the intestine - physical barriers

Back 17

- mucus layer
- intestinal epithelial cells

Front 18

Innate defenses of the intestine - mechanical factors

Back 18

- peristalsis
- digestive secretions
- desquamation

Front 19

Adaptive immunity of the intestine

Back 19

- T-cells and B-cells: make antibodies to invading pathogens such as viruses. they form memory cells that remember the same pathogen for faster antibody production in future infections

Front 20

Four segments of GALT - described

Back 20

1. Intestinal Epithelial cells
2. Lamina propria - connective tissue beneath the epithelium with activated lymphocytes
3. peyer's patches - lymphoid tissue in the mucosa and submucosa layers of the intestine
4. mesentaric lymph nodes - encapsulated lymph tissue with B and T cells and macrophages

Front 21

Four segments of GALT

Back 21

1. Intestinal epithelial cells
2. Lamina propria
3. Peyer's patches
4. Mesentaric lymph nodes

Front 22

Some highlights of GALT

Back 22

- largest lymphoid organ in the body
- produces 70-80% of body's IgA
- MLNs trap microorganisms and present antigens to lymphocytes
- overall effect if to prevent infectious and immunogenic agents into the systemic circulation (blood is sterile)

Front 23

EN may be used in presence of pancreatic complications such as...

Back 23

fistulas, ascites and pseudocysts

Front 24

Is nutrition therapy generally needed for mild to moderate pancreatitis?

Back 24

When pt has been NPO for 5-7 days, yes

Front 25

Is nutrition therapy generally needed for severe pancreatitis?

Back 25

Yes

Front 26

Is continuous or cyclical or bolus EN infusion preferred in severe pancreatitis?

Back 26

Continuous

Front 27

In severe pancreatitis is using PN (when EN is not tolerated).. IV _______ are generally safe and well tolerated as long as baseline _____ are below _____ and there is no previous history of _____

Back 27

fat emulsions, triglycerides, 4.4 mmol/L, hyperlipidemia

Front 28

Energy requirements in pancreatitis

Back 28

BMR + 20-40%
- goal is to match current requirement, not repletion

Front 29

Protein requirements in pacreatitis

Back 29

1.2-1.5 g/kg, depending on severity of disease

Front 30

Micronutrient requirements in pancreatitis

Back 30

- if alcoholic, give specific choices for alcoholism
- otherwise give multivitamin

Front 31

patient may need ____ with EN or TPN to avoid hyperglycemia

Back 31

Insulin

Front 32

Once the pt is pain free and the disease is resolving - consider ____

Back 32

Oral fluids

Front 33

Name some ongoing problems with chronic pancreatitis

Back 33

- glucose control
- maldigestion and steatorrhea (lipase <10% normal)
- need for enzyme supplements with all meals (lipase, protease, amylase)
- chronic anorexia, pain, nausea

Front 34

More ongoing problems with chronic pancreatitis

Back 34

- may become addicted to narcotics for chronic pain
- poor fat-soluble vitamin status
- lack of other micronutrients due to poor general intake (or if alcoholic)
- may tolerate a low fat diet if malabsorption occurs (50 g fat diet)

Front 35

How do you know if you are malabsorbing fat?

Back 35

Quantitative Fecal Fat Test
- 72 hours of stool collection and calorie count and high fat diet of 100g/day

Front 36

Normal fecal fat =

Back 36

< 7% of intake

Front 37

Quantitative Fecal Fat Test Calculation

Back 37

[(g dietary fat intake - g fecal fat excreted)/(g dietary fat intake)] * 100