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Gastroenterology exam 2 > Small Bowel I > Flashcards

Small Bowel I Flashcards

1
Q

What are the 3 things that the colon absorbs?

A

Water
short chain fatty acids
Vitamin K

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2
Q

where does a majority of protein and fat digestion happen?

A

jejunum

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3
Q

Gastrin:

  1. location produced?
  2. release stimulant?
  3. Primary fx?
A
  1. G-cells, Antrum, duodenum
  2. dietary proteins, antral distention, vagal/adrenergic stimulation, Gastrin-releasing peptide (GRP)
  3. Stimulates acid + pepsinogen secretion, gastric mucosal growth
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4
Q

Cholecystokinin:

  1. location produced?
  2. release stimulant?
  3. Primary fx?
A
  1. I-cells, duodenum, jejunum
  2. fats, peptides/amino acids
  3. Simulates: pancreatic enzyme secretion, gallbladder contraction, relaxes sphincter of oddi, inhibits gastric emptying
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5
Q

Secretin:

  1. location produced?
  2. release stimulant?
  3. Primary fx?
A
  1. S-cells (Duodenum, jejunum)
  2. Fatty acids, luminal acidity, bile salts
  3. stimulates:
    - water + bicarb release from pancreas
    - flow and alkalinity of bile
    - Inhibits gastric acid secretion and motility and inhibits gastrin release
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6
Q

Somatostatin:

  1. location produced?
  2. release stimulant?
  3. Primary fx?
A
  1. D cells - Pancreatis islets, antrum, duodenum
  2. Gut: fat, protein, acid, gastrin, CCK
    Pancreas: glucose, amino acids, CCK
  3. Inhibits:
    -GI hormones
    -acid secretion
    -small bowel water and electrolyte secretion
    -secretion of pancreatic hormones
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7
Q

Gastrin-releasing peptide (GRP):

  1. location produced?
  2. release stimulant?
  3. Primary fx?
A
  1. small bowel
  2. vagal stimulation
  3. releases:
    - all GI hormones (except secretin)
    - GI secretion, motility
    - acid secretion, gastrin gastrin
    - growth of intestinal mucosa and pancreas
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8
Q

Gastric Inhibitory polypeptide:

  1. location produced?
  2. release stimulant?
  3. Primary fx?
A
  1. K cells - duodenum jejunum
  2. Glucose, fat, protein adrenergic stimulation
  3. Inhibits gastric acid and pepsin secretion
    Stimulates pancreatic insulin release in response to hyperglycemia
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9
Q

Motilin:

  1. location produced?
  2. release stimulant?
  3. Primary fx?
A
  1. Duodenum, jejunum
  2. Gastric distention, fat
  3. Stimulates upper gastrointestinal tract motility
    May initiate the migrating motor complex
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10
Q

Vasoactive intestinal peptide:

  1. location produced?
  2. release stimulant?
  3. Primary fx?
A
  1. Neurons throughout the gastrointestinal tract
  2. Vagal stimulation
  3. Primarily functions as a neuropeptide
    Potent vasodilator
    Stimulates pancreatic and intestinal secretion
    Inhibits gastric acid secretion
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11
Q

Neurotensin:

  1. location produced?
  2. release stimulant?
  3. Primary fx?
A
  1. N-cells: small bowel
  2. Fat
  3. Stimulates growth of small and large bowel mucosa
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12
Q

Enteroglucagon:

  1. location produced?
  2. release stimulant?
  3. Primary fx?
A
  1. I cells - Small bowel
  2. glucose, fat
  3. Glucagon-like peptide-1:
    Stimulates insulin release
    Inhibits pancreatic glucagon release
    Glucagon-like peptide 2:
    Potent enterotrophic factor
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13
Q

peptide YY:

  1. location produced?
  2. release stimulant?
  3. Primary fx?
A
  1. Distal small bowel, colon
  2. fatty acids, cholecystokinin
  3. Inhibits gastric, pancreatic secretion
    Inhibits gallbladder contraction
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14
Q

What are 3 areas that gut-associated lymphoid tissue is localized in?

A
  1. Peyer patches
  2. Lamina propria lymphoid cells
  3. Intraepithelial lymphocytes
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15
Q

What does IgA do? (3 things)

A
  1. inhibts the adherence of bacteria to epithelial cells
  2. neutralizes bacterial toxins + viral activity
  3. inhibits absorption of antigens from the gut
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16
Q

who should be tested for Celiac disease?

A 
chronic, recurrent diarrhea
malabsorption
weightloss
abdominal distention, bloating
Pts w T1DM, Downs, IgA deficiency, Turner, Williams, autoimmune thyroiditis
17
Q

How do you diagnose Celiac disease (for high risk and low risk)

A

high risk: duodenal biopsy then TTGA IgA

low risk: TTGA IgA then duodenal biopsy

18
Q

What are endoscopic features of Celiac Disease

A
  1. scalloping of the folds
  2. flattening of the folds
  3. nodularity
  4. multiple fissures = mosaic like appearance
19
Q

What are non GI presentation of Celiac Disease?

A
  1. Arthritis
  2. Iron deficiency
  3. Metabolic bone disease
  4. Hyposplenism
  5. Kidney disease
  6. Idiopathic pulmonary hemosiderosis
20
Q

What are two complicaions of Celiac Disease?

A
  1. Collagenous Sprue - collagen layer beneath basement membrane
  2. Cancer - Intestinal lymphoma
21
Q

What is the tx of Celiac (CELIAC)

A 
Consultation w dietician
Education about disease
Lifelong no gluten
Identify nutritional deficiencies
Access to an advocacy group
Continuous long-term followup by a multidisciplinary team
22
Q

What are usual deficiencies in Celiac disease?

A

Vit A, D, E, B12, copper, zinc, carotene, folic acid, ferritin, iron, thiamine, vitamin B6, magnesium, selenium

supplement w fiber too

23
Q

What is Protein-Losing Enteropathy? how does this happen? (2 ways)

A

excessive loss of serum proteins into the gastrointestinal tract = hypoalbuminemia, edema, effusions of the pleura and pericardium

mechanism:

  1. mucosal injury (IBD, Celiac disease)
  2. increased lymphatic pressure in gut
24
Q

In a patient with protein-losing enteropathy, what is the diagnosis if the patient has reduction of parietal cells and reduced acid secretion?

A

Menetrier’s disease

25
Q

In a patient with protein-losing enteropathy, what is the diagnosis if the patient has increased parietal cells and increased acid secretion?

A

exudative gastropathy

26
Q

In a patient with protein-losing enteropathy, what is the diagnosis if the patient has elevated gastrin levels/

A

gastrinoma

27
Q

When should you suspect protein losing enteropathy?

A 
edema
hypoproteinemia
hypoalbuminemia
diarrhea
alpha-1-antitrypsin in stool
28
Q

What is the nutritional maintenance of Protein-losing enteropathy?

A
  1. diet high in protein

2. diet low in long-chain fatty acids, instead: medium chain triglycerides + essential polyunsaturated fatty acids

29
Q

What are possible etiologies of Diabetic Enteropathy?

A
  1. vagal nerve/sympathetic nerve damage
  2. Abnormal motility = bacterial overgrowth = bile deconjugation/fat malabsorption
  3. artificial sweeteners (sorbitol) = diarrhea
30
Q

What is the treatment for Diabetic Enteropathy?

A
  1. Abx for bacterial overgrowth
  2. Antidiarrheals (loperamide, codeine, diphenoxylate)
  3. Clonidine - slows down accelerate GI transit
  4. Octreotide - increased mean gut motor migrating complex frequency
31
Q

What is the most sensitive diagnostic modality in patients suspected of having a small bowel neoplasm

A

Exploratory laparotomy

32
Q

What is the most common small bowel tumors?

A

Leimyoma (40%)

Adenocarcinoma (29-50%)!!

33
Q

What are the 3 histological classifications of polyps?

A
  1. tubular
  2. tubulovillous
  3. villous
34
Q

What size are adenomas considered worrisome?

A

> 2cm

Gastroenterology exam 2 (19 decks)

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