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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
Gastric ulcers are due to...
Disruption of mucus barriers (NSAIDs, aspirin)
26
Two most common causes of peptic ulcers...
1. H pylori (interaction w/ cigarettes and alcohol); 2. NSAIDs, aspirin
27
Other causes of peptic ulcers...
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)
28
H-pylori colonizes % of US population and what part of stomach?
50%; GASTRIC mucosa alone via burrowing through mucus gel above epithelium
29
What protective factor does H pylori produce?
Urease (produces ammonia from urea)
30
Mechanisms of injury via H pylori (4)
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
31
Another name for gastrinoma...treatment?
Zollinger-Ellison; surgery
32
Presentation of peptic ulcer disease (5)
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
Peptic ulcer disease: treatment
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
What are the three surgical treatments for peptic ulcer disease? When indicated?
1. Highly selective vagotomy; 2. Antrectomy; 3. Subtotal gastrectomy; rare, only if complicated
35
What is the Bilroth II procedure?
A form of antrectomy that plugs the stomach later into the SI than the duodenum to protect against bile refux
36
Causes of hypergastrinemia (3)
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
Describe acute erosive gastritis
Discrete foci of surface necrosis w/ potential for serious bleeding; etiology = NSAIDs or severe stress
38
Burn-related ulcer
Curling ulcer
39
Surgery-related or head trauma ulcer
Cushing ulcer
40
Describe "chemical" gastropathy
Erythema on endoscopy +/- erosive gastritis mostly due to NSAIDs or bile reflux
41
What does"chemical" gastropathy look like histologically? (3)
Loss of epithelial mucin, dilated capillaries, corkscrew gastric pits
42
Describe chronic gastritis histologically
Mucosa infiltrated by mononuclear inflammatory cells (plasma cells and lymphocytes) and eosinophils
43
Chronic gastritis can progress to...
Atrophic gastritis (loss of glands) with intestinal metaplasia (also a cancer risk)
44
If the body of the stomach is involved, it is...
Autoimmune gastritis
45
If the antrum of the stomach is involved, it is...
Antra-predominant (H pylori)
46
If the whole stomach is involved (pangastritis), it is..
Multifocal atrophic gastritis (MAG, H pylori or other environmental factors)
47
Chronic autoimmune gastritis: key features
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
Chronic autoimmune gastritis is associated with what increase in gastric cancer?
3-fold
49
Histological and gross appearance of chronic autoimmune gastritis
Reduced glands, loss of parietal/chief cells, replacement by antral/intestinal epithelium, chronic inflammation; gross = flat, loss of rugae
50
Lab features of chronic autoimmune gastritis (5)
Anti-parietal cell/ anti-intrinsic factor Abs, elevated gastric pH, elevated serum gastrin, low B12, megaloblastic anemia
51
Stain to detect G cell hyperplasia
Gastrin immunostain
52
Stain to detect ECL cell hyperplasia
Chromogranin immunostain
53
T/F: Carcinoids in the setting of chronic autoimmune gastritis are aggressive
False, they are generally indolent
54
H. pylori gastritis is associated with what sequelae? Increased cancer risk?
Gastric and duodenum ulcers; 2-5 fold cancer risk
55
How to test for H pylori?
Test for presence of urease by plating acid juice on urea, will alkalize very quickly
56
H pylori: virulence factors (3)
1. Proteolytic and glycolytic enzymes; 2. Cytotoxins; 3. Breakdown of acid-protective barriers
57
Describe multifocal atrophic gastritis: define, etiology, and increased cancer risk
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
H. pylori tends to cause ulcers where? What percent of stomach ulcers are caused by H. pylori?
Duodenal bulb (80%); 70% of all ulcers in stomach caused by H. pylori
59
MAG causes ulcers where?
Gastric only (not much acid produced, only degrades stomach due to weak barrier)
60
Why does H. pylori cause duodenal ulcers?
In patients that over-secrete acid there is gastric metaplasia in duodenum (to protect against acid), which H pylori can colonize
61
How long does a treated ulcer take to heal? What does delayed healing suggest?
About 6 weeks; occult gastric cancer
62
Complications of H pylori (5)
Chronic gastritis, gastric peptic ulcer, duodenal peptic ulcer, gastric cancer, MALT (mucosa associated lymphoid tissue) lymphoma
63
Gastric cancer risk factors (4)
Dietary (smoked/pickled/grilled), older age, genetic factors, chronic atrophic gastritis (H pylori, autoimmune, env't)
64
Two types of adencarcinoma gastric cancers
Intestinal (histologically looks like intestinal epithelium) and diffuse
65
Intestinal: age/gender
55 yo, M>F
66
Diffuse: age/gender
45 yo, F>M
67
Intestinal: incidence/risk factors
Decreasing incidence, environmental, dietary, H pylori
68
Diffuse: incidence/risk factors
Stable incidence, unknown risk (genetic?), maybe H pylori
69
Intestinal: surrounding mucosa/gross/histological
Chronic gastritis, intestinal metaplasia, dysplasia w/ a discrete mass, malignant glands and tubules
70
Diffuse: surrounding mucosa/gross/histologica
Often normal w/ ill-defined mass (hard to remove), poorly cohesive tumor cells
71
Gross term related to diffuse gastric cancer
Linitis plastica: thick, rigid gastric wall
72
What does a barium run look like if a patient has diffuse type?
Seriously shrunk, rigid, contracted stomach
73
Histological cell term related to diffuse gastric cancer
Signet ring cells (look like a half moon)
74
T/F: Gastric cancers are often fatal
True: very aggressive and metastatic
75
Survival % for early (submucosal) gastric cancer; survival % for advanced (muscularis propria) gastric cancer
90%; 5%
76
Krukenberg tumors
Bilateral metastatic disease causing ovarian enlargement

Gastrointestinal and Liver (19 decks)

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