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GI > Stomach Lectures > Flashcards

Stomach Lectures Flashcards

1
Q

What is the proximal gastric motor function?

A

Initial receptive relaxation (storage, vagus nerve)

Followed by increase in tonic and phasic contractions (push into antrum)

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2
Q

What is the distal gastric motor function?

A

Baseline slow wave activity in muscle cell membrane potential – interstitial cells of Cajal
Sweep towards pylorus

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3
Q

How many distal gastric motor functions are there per minute?

A

about 3

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4
Q

How large of particles does the pyloric sphincter let through?

A

Liquids and 1-2 mm particles

Larger solids are retropelled back into antrum for more grinding (triturition)

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5
Q

What do receptors in the small intestine pay attention to?

A

The nutrient delivery – constant 1-4 kcal/minute delivery of energy to small intestine

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6
Q

When is secretin released?

A

When lipids, amino acids or HCl enters the duodenum – it relaxes gastric tone and inhibits contractions

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7
Q

When is somatostatin released?

A

In response to acids/peptides

It inhibits gastric emptying

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8
Q

When is Cholecystokinin released?

A

From the duodenum in response to fat – it inhibits gastric motility (increases small bowel motility)

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9
Q

What is the ileal brake?

A

The secretion of PYY in response to delivery of nutrients to distal small intestine

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10
Q

When are glucagon-like peptide-1 (GLP-1) and glucose-dependednt insulinotropic peptide (GIP) secreted?

A

Released into small intestine in response to glucose delivery
GLP-1 is also secreted in response to colonic fermentation of carbohydrates and intraduodenal glutamine, aa, fatty acids

*inhibits gastric motility

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11
Q

What does Ghrelin do?

A

Increases the rate of gastric emptying –induces migrating motor complex

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12
Q

Does a reduced caloric intake/weight loss cause delayed or sped-up gastric emptying?

A

Delayed

Also, faster gastric emptying in obese

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13
Q

What is scintigraphy?

A

Nuclear medicine test to assess emptying non-invasively

Uses a radiolabeled solid or liquid and detects the amount retained at set points in time

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14
Q

When does fasting motor activity occur after a meal?

A

Onset is delayed one hour for every 200 kcal ingested
Occurs every 90 minutes with fast
Allows for the clearance of large indigestible solids from gut

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15
Q

What is gastroparesis?

A

Delayed gastric emptying in the absence of mechanical obstruction
Symptoms = early satiety, postprandial fullness, nausea, vomiting, bloating, upper abdominal pain

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16
Q

What must you be sure to exclude with possible gastroparesis?

A

Exclude obstruction in the foregut

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17
Q

What are some medications that may induce gastric emptying delay?

A 
Anti-cholinergics
Opiates
NSAIDS
Pramlintide (amylin analog)
Exenatide (GLP-1 receptor agonist) 
Cyclosporine
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18
Q

What is the effect of vagal injury on gastric emptying?

A

Poor accommodation- liquids empty rapidly

Poor antral grinding- solids empty slowly

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19
Q

What is visceral hypersensitivity?

A

Postprandial pain but no ulcer
Lower threshold for pain (especially with stress)
Associated with anxiety and depression, aging, diabetes, analgesics
Mechanism unclear

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20
Q

What are some gastric dysfunctions seen in diabetes?

A

Long term Type I or Type II DM
Vagal dysfunction, loss of enteric neurons
Rapid or slow gastric emptying

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21
Q

What are some possible causes of elevated acid secretion?

A 
Elevated gastrin
Elevated vagal tone
Elevated histamine (mastocytosis, basophilic granulocytic leukemia) 
Elevated parietal cell mass/idiopathic
Paraneoplastic (non-gastrin: rare)
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22
Q

What do you need to interpret elevated gastrin levels?

A

pH

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23
Q

Hypersecretion of gastric acid due to a gastrin secreting neuroendocrine tumor

A

Zollinger-Ellison syndrome

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24
Q

What are the two types of ZE

A

Sporadic: Isolated gastrinoma, localize and remove for cure, usually in duodenum/pancreas
Component of Multiple Endocrine Neoplasia I (MEN I): multifocal, not curable, also associated with hyperparathyroidism, other islet cell tumors, pituitary tumors

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25
Q

What are some diagnostic features of ZE syndrome?

A

Elevated basal acid secretion (15mEq/hr)
Gastrin > 150 pg/mL (>1000 pg/ml diagnostic with low pH)
Secretin stimulation: gastrin increases > 120 pg/ml
PPI can cause a false negative test

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26
Q

Clinical manifestations of ZE syndrome

A

Severe ulcer disease – extends to distal duodenum/jejunum, relapsing ulcer, high PPI dose to cure
Diarrhea – large acidic fluid volume, inactivation of pancreatic enzymes, hypokalemia, steatorrhea, weight loss

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27
Q

What are some other causes of gastrin mediated high acid secretion?

A 
H. pylori (via reduced somatostatin) 
Antral G-cell hyperplasia
Gastric outlet obstruction
Retained antrum (gastric surgery) 
Cysteamine treatment 
Short bowel syndrome
Renal failure (rare)
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28
Q

Conditions that cause low acid secretion.

A 
Medications: PPI, H2RA, anticholinergic
Inflammatory destruction of parietal cells (gastritis) 
Acute H. pylori infection
Vagal injury/transection
VIP producing tumors
29
Q

How does low acid secretion commonly present?

A 
Overall well tolerated with modern diet, impaired protein digestion
Impaired absorption of Fe, Ca, B12 
Gastric bacterial overgrowth
Enteric infections/TB
Small bowel bacteria overgrowth
Impaired delivery of certain drugs
30
Q

Describe the Schilling Test for vitamin B12

A

4 steps:

  1. Replace B12 parenterally, do 24 hour collection of radiolabelled vitamin B12 orally – checks to see if you are absorbing it
  2. If low, repeat while giving IF – checks to see if you have IF deficiency
  3. If low, repeat after empiric antibiotic treatment for small bowel bacteria overgrowth – check to see if bacteria are not allowing you to create IF
  4. If still low, give pancreatic enzymes to test for pancreatic insufficiency or terminal ileal disease
31
Q

What is one main cause of decreased secretion of bicarb/mucous?

A

Overuse of NSAIDS

32
Q

Describe the bacteria H. pylori

A

Spiral shaped, microaerophilic, gram negative bacteria

Exclusively colonizes gastric type epithelium

33
Q

What is the hallmark of H. pylori infection?

A

Neutrophilic infiltration, along with lymphocytes, plasma cells, macrophages (chronic active gastritis)

34
Q

What is the virulence factor that is present in some strains of H. pylori and may cause more intense damage?

A

Cytotoxin-associated gene A [CagA]

35
Q

Describe the early stage of H. pylori.

A

Confined to the antrum
Inhibited D cell somatostatin secretion – increased gastrin secretion
Acid secretion increased
Duodenal ulcers

36
Q

Describe the late stage of H. pylori.

A

Colonization and inflammation expand to corpus/fundus
Destruction of parietal cells – acid decreased, gastrin increased
Gastric ulceration
If H. pylori eradication –> neutrophilic infiltration resolves, lymphocytic infiltration may persist

37
Q

Where is H. pylori infection most likely?

A

Developing countries
Crowding, poverty
Increased with age

38
Q

When do you acquire an H. pylori infection?

A

In infancy/childhood – fecal/oral, oral/oral transmission

39
Q

How do you diagnose an H. pylori infection?

A

Serology (persists even after eradication)
Endoscopic gastric mucosa biopsy
Urea breath testing
Stool antigen testing
False negative with recent antibiotics or PPI therapy

40
Q

What are some adverse effects of H. pylori infection?

A

Peptic ulcer
Enteric infections
Malnutrition/iron & B12deficiency
Gastric neoplasia –> Adenocarcinoma, MALToma, carcinoid

41
Q

What are some adverse effects of eliminating H. pylori?

A

GERD/adenocarinoma of esophagus
Weight gain
Atopic diseases

42
Q

Inherited form associated with immune response in the oxyntic mucosa against parietal cells and IF

A

Autoimmune gastritis

43
Q

What is associated with Autoimmune gastritis?

A

Lymphocytic inflammation with destruction of parietal cells
Associated with other autoimmune disease (thyroid, celiac, type I DM)
More common in women

44
Q

Inflammatory destruction of normal mucosa with replacement by metaplastic elements (commonly intestinal type with goblet cells)

A

Atrophic metaplastic gastritis

45
Q

Type A chronic gastritis

A

Autoimmune, first part of stomach, body and funds

46
Q

Type B chronic gastritis

A

H. pylori bacteria, second part of stomach, antrum

47
Q

What are some findings in atrophic metaplastic gastritis?

A

Achlorhydia–increased gastrin

Reduced/absent intrinsic factor

48
Q

What are some consequences of atrophic metaplastic gastritis?

A

Reduced acid secretion
Pernicious anemia
Gastric cancer
Gastric carcinoid

49
Q

What is the difference between gastritis and gastropathy?

A

Gastritis is an inflammation associated mucosal injury – infectious, autoimmune

Gastropathy is epithelial cell damage and regeneration with minimal or no associated inflammation (bile, alcohol, aspiring, NSAIDs, ischemia)

50
Q

What are some toxic gastric effects of NSAIDs?

A

Trapped in epithelial cells
Uncouple oxidative phosphorylation
Reduced energy production
Increased cell permeability
Rapid cell death and superficial mucosal injury
Inhibit COX-1 prostaglandin synthesis causing reduced blood flow and oxygen delivery, decreased mucin, bicarb and phospholipid secretion and decreased epithelial cell proliferation and migration

51
Q

What is the difference between an ulcer and an erosion?

A

Ulcer extends below muscularis mucosa

Erosion superficial to muscularis mucosa

52
Q

What are some risk factors for peptic ulcer disease?

A

Increasing age and smoking
H. pylori associated decreasing
NSAID/aspirin

53
Q

What is the breakdown of PUD in NSAID/aspirin users?

A

50% develop erosions
25% develop PUD
2-4% have complications resulting in hospitalizations

54
Q

90% of PUD is associated with what 3 things.

A
  1. Aspirin/NSAIDs
  2. Helicobacter pylori
  3. Surreptitious/unaware NSAID use
55
Q

What are some complications from PUD?

A 
Acute GI hemorrhage
Chronic GI blood loss/iron deficiency anemia 
Perforation/peritonitis/pancreatitis
Gastric outlet obstruction
GI fistula
Malabsorption/malnutrition/weight loss
Iatrogenic complications
56
Q

What are some symptoms of PUD?

A

Hematemesis (loss of 25% of total blood volume)
Melena, red blood per rectum (loss of 33% blood volume)
Recurrent post-prandial vomiting (obstruction)
Diarrhea (fistula)
May have no symptoms

57
Q

What do signet ring cells look like and what are they indicative of?

A

Munin-Filled vacuole with displaced nucleus

Diffuse type gastric adenocarcinoma

58
Q

How is the hereditary diffuse type of gastric adenocarcinoma inherited?

A

Autosomal dominant with high penetrance (80% of carriers will develop disease)
Associated with mutations in E-cadehere gene (CDH1)-tumor suppressor gene that affects cellular adhesion/motility

59
Q

What are the two types of gastric adenocarcinoma?

A 
Intestinal type (most common) - in distal stomach, H. pylori is the main risk factor, older men
Diffuse type -- younger age, associated with blood group A, signet ring cell histology, more aggressive
60
Q

What is the average age of onset of hereditary diffuse type gastric adenocarcinoma?

A

38 years

Increased risk of breast cancer

61
Q

What are some other heritable associations of gastric adenocarcinoma?

A

Familial adenomatous polyposis (FAP)
Lynch Syndrome
Peutz-Jeghers syndrome
Li-Fraumeni syndrome

62
Q

What is diffuse type EBV associated adenocarcinoma?

A

Male predominant
No age predilection
Higher proportion in developed countries
Less aggressive behavior

63
Q

What is adenocarcinoma of the cardia?

A

Incidence is rising

Risk factors = lack of H. pylori, male gender, obesity, smoking

64
Q

What are some common clinical presentations?

A 
Abdominal pain 
Early satiety and nausea (linitis plastica) 
Weight loss
Dysphagia
Vomiting
GI bleeding/perforation
65
Q

What are MALToma’s strongly associated with?

A

H. pylori – 80% regression with eradication

66
Q

What are some risk factors for gastric lymphoma?

A

Immunodeficiency/immunosuppresion
Celiac disease
Autoimmune disorders

67
Q

What is the common clinical presentation of gastric lymphoma?

A 
Epigastric pain
Anorexia
Weight loss
Nausea and/or vomiting
Occult GI bleeding
B symptoms
Rarely perforation
68
Q

What is the endoscopic appearance of gastric lymphoma?

A

Mucosal erythema

GI (34 decks)

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