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Gastrointestinal and Liver > Lectures 3,4: Stomach > Flashcards

Lectures 3,4: Stomach Flashcards

1
Q

What are the layers of the stomach?

A

Mucosa (epithelium, lamina propria, muscularis mucosae), submucosa (w/ plexus), muscularis externa (oblique, circular, longitudinal layer), serosa

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2
Q

Parietal cells make

A

Acid and intrinsic factor

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3
Q

ECL cells make

A

Histamine

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4
Q

Chief cells make

A

Pepsinogen

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5
Q

Where are the stem cells in the gastric fundic gland?

A

Mucous neck cells

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6
Q

Surface mucous cells make

A

Mucus, trefoil peptide, bicarbonate secretion

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7
Q

Functions of the stomach (3)

A

Mechanical churning of food; initiation of chemical digestion (acid, pepsin, lipase); produce intrinsic factor (B12 absorption)

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8
Q

Main function of fundus/body

A

Secretion reservoir

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9
Q

Main function of the antrum

A

Mixing, grinding

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10
Q

Inhibits gastric emptying…(what goes through intestine and product that does the inhibition; 3 for duodenum and 1 for ileum)

A

Duodenum: Secretin (via low pH), cholecystokinin (aa and fatty acids), vagal afferents (osmolarity); Ileum: PYY (carbohydrates)

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11
Q

Motilin: where it is made, what it does, action

A

Duodenum; binds to receptors on smooth muscle and causes motility by increase phase III contractions of migrating motor complex

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12
Q

Erythromycin is a _________ agonist

A

Motilin

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13
Q

What are the effects of gastric distention (2)? What nerve is involved?

A

Increased acid, pepsin release and increased gastrin release; vagal nerve also potentiates both of these actions

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14
Q

Three parietal cell receptors…what do they do?

A

CCK-B (gastrin), H2 (histamine), M3 (ACh) –> translocation of proton pump to cell surface

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15
Q

Describe parietal cell secretion pathways

A

Secretes H+ via H/K/ATPase and Cl- via chloride channel, also secretes HCO3- basolaterally

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16
Q

What is the effect of gastrin on the parietal cell? On the ECL cell?

A

Positive; positive

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17
Q

What does ECL do?

A

ECL produces histamine, which is a paracrine and positively effects the parietal cell

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18
Q

What is the effect of ACh on the parietal cell? On the ECL cell?

A

Positive; positive

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19
Q

How does the parietal system get turned off?

A

HCl positively effects the D cell, which releases SST –> inhibition of G, ECL, and parietal cells

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20
Q

What protects the stomach from developing ulcers?

A

Mucus-bicarbonate layer

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21
Q

Gastritis is defined by…

A

Superficial erosions

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22
Q

Why does an ulcer bleed?

A

Eaten into submucosa, which has blood vessels

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23
Q

Three consequences of ulcers

A

Bleeding, penetration (e.g. into pancreas –> pancreatitis, or colon), perforation

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24
Q

Duodenal ulcers are due to…

A

Hypersecretion of acid

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25
Q

Gastric ulcers are due to…

A

Disruption of mucus barriers (NSAIDs, aspirin)

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26
Q

Two most common causes of peptic ulcers…

A
  1. H pylori (interaction w/ cigarettes and alcohol); 2. NSAIDs, aspirin
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27
Q

Other causes of peptic ulcers…

A

Stress (burns, head trauma), gastrinoma (benign, gastrin-secreting tumor), rare causes due to overproduction of histamine (systemic mastocytosis = histamine production by mast cells and basophilic leukemia = histamine production by basophils)

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28
Q

H-pylori colonizes % of US population and what part of stomach?

A

50%; GASTRIC mucosa alone via burrowing through mucus gel above epithelium

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29
Q

What protective factor does H pylori produce?

A

Urease (produces ammonia from urea)

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30
Q

Mechanisms of injury via H pylori (4)

A
  1. Releasing cytotoxins on epithelium; 2. Disrupting mucous layer via proteases; 3. Stimulating host pro-inflammatory cytokines; 4. Inhibiting somatostatin by antral D cells –> acid hypersecretion
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31
Q

Another name for gastrinoma…treatment?

A

Zollinger-Ellison; surgery

32
Q

Presentation of peptic ulcer disease (5)

A
  1. Pain (epigastric, boring, relieved by food, may awaken patient in morning); 2. Bleeding (occult or overt); 3. Obstruction; 4. Perforation (free air under diaphragm); 5. Penetration (into adjacent organ)
33
Q

Peptic ulcer disease: treatment

A
  1. Remove inciting agent (treat H pylori; avoid NSAIDs, alcohol, surgical removal of gastrinoma); 2. Pharmacological (antacids, PPIs/H2 blockers, meds that enhance prostaglandin production); 3. Surgical therapy
34
Q

What are the three surgical treatments for peptic ulcer disease? When indicated?

A
  1. Highly selective vagotomy; 2. Antrectomy; 3. Subtotal gastrectomy; rare, only if complicated
35
Q

What is the Bilroth II procedure?

A

A form of antrectomy that plugs the stomach later into the SI than the duodenum to protect against bile refux

36
Q

Causes of hypergastrinemia (3)

A
  1. Insufficient amounts of luminal acid (because acid turns off gastrin via D cells, caused by PPIs/H2 blockers OR autoimmune gastritis w/ destruction of parietal cells = pernicious anemia); 2. Overproduction of gastrin (rare, due to antral G-cell hyperplasia OR retained antrum on duodenal stump after surgical antrectomy); 3. Ectopic production of gastrin (rare, gastrinoma)
37
Q

Describe acute erosive gastritis

A

Discrete foci of surface necrosis w/ potential for serious bleeding; etiology = NSAIDs or severe stress

38
Q

Burn-related ulcer

A

Curling ulcer

39
Q

Surgery-related or head trauma ulcer

A

Cushing ulcer

40
Q

Describe “chemical” gastropathy

A

Erythema on endoscopy +/- erosive gastritis mostly due to NSAIDs or bile reflux

41
Q

What does”chemical” gastropathy look like histologically? (3)

A

Loss of epithelial mucin, dilated capillaries, corkscrew gastric pits

42
Q

Describe chronic gastritis histologically

A

Mucosa infiltrated by mononuclear inflammatory cells (plasma cells and lymphocytes) and eosinophils

43
Q

Chronic gastritis can progress to…

A

Atrophic gastritis (loss of glands) with intestinal metaplasia (also a cancer risk)

44
Q

If the body of the stomach is involved, it is…

A

Autoimmune gastritis

45
Q

If the antrum of the stomach is involved, it is…

A

Antra-predominant (H pylori)

46
Q

If the whole stomach is involved (pangastritis), it is..

A

Multifocal atrophic gastritis (MAG, H pylori or other environmental factors)

47
Q

Chronic autoimmune gastritis: key features

A

LOSS OF PARIETAL CELL MASS –> hypochlorhydria (high pH), malabsorption of B12 (loss of intrinsic factor), G cell hyperplasia –> hypergastrinemia, ECL cell hyperplasia –> carcinoid tumors

48
Q

Chronic autoimmune gastritis is associated with what increase in gastric cancer?

A

3-fold

49
Q

Histological and gross appearance of chronic autoimmune gastritis

A

Reduced glands, loss of parietal/chief cells, replacement by antral/intestinal epithelium, chronic inflammation; gross = flat, loss of rugae

50
Q

Lab features of chronic autoimmune gastritis (5)

A

Anti-parietal cell/ anti-intrinsic factor Abs, elevated gastric pH, elevated serum gastrin, low B12, megaloblastic anemia

51
Q

Stain to detect G cell hyperplasia

A

Gastrin immunostain

52
Q

Stain to detect ECL cell hyperplasia

A

Chromogranin immunostain

53
Q

T/F: Carcinoids in the setting of chronic autoimmune gastritis are aggressive

A

False, they are generally indolent

54
Q

H. pylori gastritis is associated with what sequelae? Increased cancer risk?

A

Gastric and duodenum ulcers; 2-5 fold cancer risk

55
Q

How to test for H pylori?

A

Test for presence of urease by plating acid juice on urea, will alkalize very quickly

56
Q

H pylori: virulence factors (3)

A
  1. Proteolytic and glycolytic enzymes; 2. Cytotoxins; 3. Breakdown of acid-protective barriers
57
Q

Describe multifocal atrophic gastritis: define, etiology, and increased cancer risk

A

Pan-gastritis with large atrophy and reduced acid output; likely related to early H pylori infection and other env’t factrs; 10x increased cancer risk

58
Q

H. pylori tends to cause ulcers where? What percent of stomach ulcers are caused by H. pylori?

A

Duodenal bulb (80%); 70% of all ulcers in stomach caused by H. pylori

59
Q

MAG causes ulcers where?

A

Gastric only (not much acid produced, only degrades stomach due to weak barrier)

60
Q

Why does H. pylori cause duodenal ulcers?

A

In patients that over-secrete acid there is gastric metaplasia in duodenum (to protect against acid), which H pylori can colonize

61
Q

How long does a treated ulcer take to heal? What does delayed healing suggest?

A

About 6 weeks; occult gastric cancer

62
Q

Complications of H pylori (5)

A

Chronic gastritis, gastric peptic ulcer, duodenal peptic ulcer, gastric cancer, MALT (mucosa associated lymphoid tissue) lymphoma

63
Q

Gastric cancer risk factors (4)

A

Dietary (smoked/pickled/grilled), older age, genetic factors, chronic atrophic gastritis (H pylori, autoimmune, env’t)

64
Q

Two types of adencarcinoma gastric cancers

A

Intestinal (histologically looks like intestinal epithelium) and diffuse

65
Q

Intestinal: age/gender

A

55 yo, M>F

66
Q

Diffuse: age/gender

A

45 yo, F>M

67
Q

Intestinal: incidence/risk factors

A

Decreasing incidence, environmental, dietary, H pylori

68
Q

Diffuse: incidence/risk factors

A

Stable incidence, unknown risk (genetic?), maybe H pylori

69
Q

Intestinal: surrounding mucosa/gross/histological

A

Chronic gastritis, intestinal metaplasia, dysplasia w/ a discrete mass, malignant glands and tubules

70
Q

Diffuse: surrounding mucosa/gross/histologica

A

Often normal w/ ill-defined mass (hard to remove), poorly cohesive tumor cells

71
Q

Gross term related to diffuse gastric cancer

A

Linitis plastica: thick, rigid gastric wall

72
Q

What does a barium run look like if a patient has diffuse type?

A

Seriously shrunk, rigid, contracted stomach

73
Q

Histological cell term related to diffuse gastric cancer

A

Signet ring cells (look like a half moon)

74
Q

T/F: Gastric cancers are often fatal

A

True: very aggressive and metastatic

75
Q

Survival % for early (submucosal) gastric cancer; survival % for advanced (muscularis propria) gastric cancer

A

90%; 5%

76
Q

Krukenberg tumors

A

Bilateral metastatic disease causing ovarian enlargement

Gastrointestinal and Liver (19 decks)

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