Lectures 3,4: Stomach Flashcards Preview

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

Flashcards in Lectures 3,4: Stomach Deck (76):
1

What are the layers of the stomach?

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

2

Parietal cells make

Acid and intrinsic factor

3

ECL cells make

Histamine

4

Chief cells make

Pepsinogen

5

Where are the stem cells in the gastric fundic gland?

Mucous neck cells

6

Surface mucous cells make

Mucus, trefoil peptide, bicarbonate secretion

7

Functions of the stomach (3)

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

8

Main function of fundus/body

Secretion reservoir

9

Main function of the antrum

Mixing, grinding

10

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

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

11

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

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

12

Erythromycin is a _________ agonist

Motilin

13

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

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

14

Three parietal cell receptors...what do they do?

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

15

Describe parietal cell secretion pathways

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

16

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

Positive; positive

17

What does ECL do?

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

18

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

Positive; positive

19

How does the parietal system get turned off?

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

20

What protects the stomach from developing ulcers?

Mucus-bicarbonate layer

21

Gastritis is defined by...

Superficial erosions

22

Why does an ulcer bleed?

Eaten into submucosa, which has blood vessels

23

Three consequences of ulcers

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

24

Duodenal ulcers are due to...

Hypersecretion of acid

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