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Gastrointestinal 2 > Nutrition and Diseases of GI > Flashcards

Nutrition and Diseases of GI Flashcards

1
Q

What are the two parts to dysphagia?

A
  1. oropharyngeal dysphagia= transfer dysphagia (initiating a swallow).
  2. esophageal dysphagia= after swallowing, food getting stuck (intrinsic; webs…, or extrinsic; mediastinal mass).
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2
Q

Why is dysphagia important?

A
  • weight loss (an energy INTAKE problem).
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3
Q

What important questions should you ask in regard to dysphagia?

A
  • Do you have problems swallowing liquids, solids, or both?

- Do you have loss of appetite, weight loss, nausea, vomiting, or heartburn

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4
Q

What are some examples of esophageal dysphagia motility disorders?

A
  • achalasia
  • scerloderma (systemic sclerosis)
  • sjogren’s syndrome
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5
Q

What are some stomach disorders that can cause gastric outlet obstruction?

A
  • malignancy (adenocarcinoma, lymphoma, stromal tumors).
  • infections (TB)
  • infiltartive (amyloidosis, sceroderma)
  • stricture (peptic, post-radiation, pancreatic pseudocyst)
  • pyloric stenosis
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6
Q

What is atrophic gastritis?

A
  • chronic inflammation of the stomach mucosa, leading to loss of gastric glandular cells (impairing secretion of HCl, pepsin, and intrinsic factor).
  • B12 deficiency occurs leading to megaloblastic anemia.
  • may also see iron deficiency anemia (microcytic)
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7
Q

What is gastroparesis?

A

delayed gastric emptying, usually associated with T2DM, but can be due to Parkinson’s, MS, brainstem tumor, chemo, or paraneoplastic syndromes. Signs and symptoms:
- nausea, vomiting, abdominal pain, a feeling of fullness after eating just a few bites.

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8
Q

What nutritional interventions do we do for gastroparesis?

A

stage approach:

  • stage 1= introduce liquid
  • stage 2= low residue/low fat
  • stage 3= maintenance
  • if that fails we go to enteral or parenteral nutrition.
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9
Q

How does enteral vs parenteral nutrition differ?

A
  • enteral= provision of protein, calories, electrolytes, trace elements, and fluids via INTESTINAL ROUTE (tube through nose into stomach or small bowel).
  • parenteral= an INTRAVENOUS solution that contains dextrose, lipids, amino acids, vitamins, and trace elements.
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10
Q

Is enteral nutrition preferred?

A

YES via temporary nasojejunal tube or permanent surgically placed jejunal feeding tube.

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11
Q

When do we use parenteral nutrition?

A

reserved for those who are enterally intolerant (malignancy or diabetic gastroparesis).

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12
Q

What nutritional implications will we see with Roux-en-Y gastric bypass?

A

malabsorption of Vitamin B12, B1 (thiamin), D, K, folate, iron, and calcium

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13
Q

What nutritional implications will we see with laproscopic adjustable gastric banding?

A

folic acid deficiency

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14
Q

What nutritional implications will we see with BPD and BPD/DS?

A
  • vitamin A, D, E, and K deficiency, protein-calorie malnutrition, malabsorption of calcium, zinc, selenium, potassium, chloride, phosphorus, and magnesium.
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15
Q

What are general recommended supplements for pts with bariatric surgery?

A
  • multivitamin with iron
  • calcium with vitamin D
  • oral vitamin B12
  • iron with vitamin C (to increase absorption of iron)
  • thiamin
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16
Q

What is the nutritional problem with IBD?

A
  • malabsorption (iron, vitamin D, folate, vitamin A, and vitamin B12).
17
Q

What are the consequences of malnutrition?

A
  • growth failure (common in children with Crohn’s)
  • weight loss and reduced muscle mass
  • metabolic bone disease
  • anemia
18
Q

What percentage of lean body mass loss is the threshold for increased morbidity?

A

greater than 5 - 10%

19
Q

** What can cause metabolic bone disease?

A
  • glucocorticoid use
  • puberty delay
  • deficiencies of calcium, vit D, and vit K
20
Q

What is celiac disease?

A
  • autoimmune disorder of the small intestine with a reaction to gluten or various proteins found in wheat, barley, and rye.
21
Q

What is the human microbiome project?

A
  • NIH initiative to identify and characterize the microorganisms in health and disease. Goal is to develop a reference set of microbial genome sequences and to perform preliminary characterization of the human microbiome.
22
Q

By how much, does the total number of microbial cells in humans exceed the total number of human cells?

A
  • by a factor of 10!
23
Q

What is a nutritional problem in pts with cirrhosis?

A

they can take in nitrogen from proteins, but can’t synthesize ALBUMIN from it in the liver.

24
Q

How do we do a nutritional assessment?

A

History:

  • unintentional weight loss greater than 10% over 6 months.
  • GI symptoms
  • severity of liver disease (child-pugh score, MELD score).
  • micronutrient deficiency
25
Q

Is nutrition more relevant in acute or chronic pancreatitis?

A

CHRONIC

26
Q

How do you treat chronic pancreatitis from a nutritional standpoint?

A
  • alcohol cessation and low fat diet

* antioxidants seem to help

27
Q

*** Should we feed through the vein or the gut with acute pancreatitis?

A

enteral (through the gut)

28
Q

What is short bowel syndrome?

A
  • a malabsorptive state following massive resection of small intestine (less than 2 meters of bowel left). Usually results from resection for Crohn’s disease, radiation, or bowel infarction.
29
Q

Is malnutrition evident in up to 50% of hospitalized pts?

A

YES (hypermetabolism is the most common reason for admission to SICU)

30
Q

What do we need to distinguish in starvation?

A

stressed (hospitalized) from unstressed (healthy) models

31
Q

*** What happens to pts in an unstressed (healthy) starvation state?

A
  • conserve lean body mass (protein) and energy.
  • increased epinephrine and glucagon with lipolysis and glycogenolysis early.
  • next is acceleration of gluconeogenesis. If this continues, then 1/3 of body PROTEIN would lost in just a few weeks.
  • prolonged starvation= brain adapts to use ketone for energy so muscle protein losses are diminished (KETO-ADAPTATION).
32
Q

** Does keto-adaptation in STRESSED starvation occur? (TEST QUESTION)

A

NO!!

33
Q

What do we see in pts with stressed (hospitalized) pts?

A
  • increase in catabolic hormones (cortisol, glucagon, epinephrine).
  • increased cytokine response (IL-1, TNF)
  • most losses are NON-VISCERAL, rather they are lean tissue.
34
Q

Is hypercatabolism disconnected from hyper-metabolism?

A
  • YES catabolism is breakdown of lean tissue (proteins).

- Metabolism is calories and energy expenditure.

35
Q

Why is protein not viewed as an energy source?

A

bc it does not exist in storage form. It is either utilized or sacrificed. Protein takes energy to be used as energy.

36
Q

What are our body stores and how long do they last?

A
  • carbohydrate in the form of glycogen= lasts 36 hrs.

- fat= could last up to 60 days.

Gastrointestinal 2 (18 decks)

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