Lec 3

Question 1

During what stages of digestion is acid secreted?

Answer 1

cephalic, gastric, and intestinal phases

Question 2

Where are chief and parietal cells located in gastric fundic gland?

Answer 2

• chief cells near base

- parietal cells in middle below mucous neck cells

Question 3

What substances are secreted by gastric fundic gland mucosa?

Answer 3

HCl
Pepsinogen
Intrinsic Factor

Question 4

What is the function of the stomach?

Answer 4

• mechanical churning
• initiate protein/fat digestion
• produce intrinsic factor for vit B12 absorption

Question 5

What does “the stomach as two organs” mean?

Answer 5

1st organ = secretes stuff = fundus and body + cardia

2nd organ = antrum = mixes and grinds

Question 6

What is motilin?

Answer 6

hormone made in duodenum
binds receptors on smooth muscle throughout gut and pro-motility

–> increases phase III contractions of migrating motor complex [MMC]

Question 7

What is effect of erythromycin on GI?

Answer 7

motilin agonist –> increase contraction of bowel

Question 8

What do stretch receptors on stomach act on?

Answer 8

• increase secretion of gastrin by G cells
• increase secretion of acid/pepsin
• activate vagus

Question 9

Where is histamine released from?

Answer 9

ECL cells in gastric fundus

Question 10

What is action of histamine in GI?

Answer 10

• binds H2 receptors on parietal cells

- stimulates parietal to secrete HCl

Question 11

What causes histamine to be released by ECL cells?

Answer 11

• ACh and gastrin

Question 12

What is gastrin?

Answer 12

a hormone released by G cells in the antrum –> goes through bloodstream to reach parietal cells in stomach fundus

Question 13

What is action of gastrin?

Answer 13

binds gastrin receptors [CCK-b} on parietal cells

stimulates parietal to secrete HCl

Question 14

Where is gastrin released from?

Answer 14

G cells in gastric antrum

Question 15

What is action of ACh in stomach?

Answer 15

released by vagus nerve and binds muscarinic M3 receptors on parietal cell

stimulates parietal cell to secrete acid
also stimulates ECL cell to release histamine

Question 16

What causes parietal cell to release HCl?

Answer 16

• ACh from vagus
• gastrin from G cells
• histamine from ECL cells
• stretch

Question 17

What are 2 effects of ACh on stomach?

Answer 17

• stimulates parietal cells to release acid

- stimulates ECL to release histamine

Question 18

What cells release somatostatin?

Answer 18

D cells in the antrum

Question 19

When is somatostatin released?

Answer 19

D cells sense low pH –> causes them to release somatostatin

Question 20

What is action of somatostatin?

Answer 20

• acts on G cells to inhibit gastrin release

- inhibits ECL cells and parietal cells directy

Question 21

Where is pepsinogen released from?

Answer 21

chief cells in the fundus

gets converted to pepsin in the acidic stomach

Question 22

How does acid get into the lumen of stomach?

Answer 22

in exchange for K through the H-K ATPase pump

Question 23

What makes up the mucus-bicarbonate barrier of stomach? What induces their secretion?

Answer 23

• mucus secreted by surface epithelium
• bicarbonate is within the mucus

their secretion is stimulated by prostaglandins

Question 24

What causes duodenal ulcers?

Answer 24

hypersecretion of acid

Question 25

What causes gastric ulcers?

Answer 25

disurption of mucus barriers [by NSAIDS, aspirin, etc]

Question 26

What are some things that cause peptic ulcer disease?

Answer 26

- H pylori - NSAIDS, aspirin - stress [due to ischemia] - gastrinoma cigarettes and alcohol may aggravate but are not independent risk factors

Question 27

Where does h pylori infect?

Answer 27

only colonizes gastric-type epithelium [not intestinal or squamous]

Question 28

WHat is use of h pylori urease?

Answer 28

protects the h pylori from the acid in gastric lumen

Question 29

What is the H pylori toxin that causes peptic ulcers?

Answer 29

CagA

Question 30

How are some common complications of h pylori?

Answer 30

- gastritis - peptic ulcer - associated w/ gastric adenocarcinoma and lymphoma

Question 31

What are x mech of action by which H pylori injures the mucosa?

Answer 31

- directly releases cytokines on epithelial cells - disrupts mucous layer by production of proteases - stimulates host pro-inflammatory cytokines - inhibits somatostatin by antral D cells --> thus more gastrin --> acid hypersecretion

Question 32

What is presentation of peptic ulcer disease?

Answer 32

- pain [may be relieve by food, may bore into back] - bleeding [melena, hematemesis] - gastric outlet obstruction - perforation - penetration

Question 33

What is most common cause of acute infectious gastritis?

Answer 33

h pylori

Question 34

What causes non-infectious acute gastritis?

Answer 34

aspirin, NSAIDS severe physical stress, radiation

Question 35

How do NSAIDS cause gastritis?

Answer 35

inhibit mucosal prostaglandin synthesis

Question 36

How does esophagus protect itself from acid?

Answer 36

LES excludes acid/pepsin from refluxing; esophageal motility keeps contents moving distally

Question 37

How does duodenum protect itself from acid?

Answer 37

neutralizes acid/pepsin with duodenal/pancreatic/biliary bicarbonate

Question 38

What are 3 basic types of treatment for peptic ulcer disease?

Answer 38

- remove inciting agent - medication - surgery

Question 39

What medications are used for peptic ulcer disease?

Answer 39

- antacids to neutralize acid - PPIs and H2 blcoekrs to block acid production - enhance prostaglandin production [sucralfate]

Question 40

How does a highly selective vagotomy work?

Answer 40

- eliminate cholinergic stimulus to parietal cells

Question 41

How does an antrectomy work?

Answer 41

remove gastrin-producing area and the are most susceptible to ulcer anatomosis either by Billroth I or Billroth II

Question 42

How does a subtotal gastrectomy work?

Answer 42

remove antrum and most of the body to the stomach; eliminates gastrin secretion and most of the parietal cells

Question 43

What is difference Billroth I and Billroth II?

Answer 43

Billroth I = hook up the duodenum to the fundus of the stomach; only works if top of duodenum is in good shape Billroth II = hook up the middle of the duodenum to the fundus of the stomach; leaves the top of the duodenum but its kind of off to the side

Question 44

What happens if you leave some of the antrum during billroth surgery?

Answer 44

you will have G cells there making gastrin but they are no longer in contact with the lumen so don't get turned off by low acid its like having a gastrinoma --> get hypersecretion of acid.

Question 45

What are major causes of hypergastrinemia?

Answer 45

- insufficient amount of luminal acid [due to destruction of parietal cells in pernicious anemia OR use of PPIs/H2 blockers] - overproduction of gastrin [antral G hyperplasia, retained antrum] - ectopic production of gastrin [gastrinoma]

Question 46

What is pernicious anemia?

Answer 46

autoimmune destruction of parietal cells leads to loss of acid secretion anti parietal cell and anti IF antibodies

Question 47

What is zollinger-ellison?

Answer 47

gastrin producing neuroendocrinetumor n pancrea or duodenal wall autonomously produces gastrin --> acid hypersecretion by parietal cells