Physiology of Acid Secretion

Question 0

Which gastric cells secrete somatostatin?

Answer 0

D cells.

Question 1

What is the function of enterochromaffin-like cells in the stomach?

Answer 1

Secretion of histamine.

Question 2

How is the function of D cells regulated?

Answer 2

Decreasing pH in the lumen of the stomach stimulates the secretion of somatostatin.

Question 3

How is the function of G cells regulated?

Answer 3

Somatostatin inhibits the secretion of gastrin.

Question 4

How is the function of ECL cells regulated?

Answer 4

(1) somatostatin inhibits the release of histamine.

(2) ACh from vagal nerve innervation and gastrin stimulate the release of histamine.

Question 5

How is the function of parietal cells regulated?

Answer 5

ACh from vagal nerve innervation, gastrin and histamine stimulate the secretion of HCl.

Question 6

What are the aggressive factors for acid peptic disease?

Answer 6

(1) acid
(2) NSAIDs
(3) H. pylori
(4) smoking, steroids, alcohol, caffeine, bile, pepsin

Question 7

What are defensive factors against acid peptic disease?

Answer 7

(1) mucus
(2) bicarbonate
(3) blood flow (delivery of O2 and mediators)
(4) cell regeneration
(5) prostaglandins

Question 8

How do the symptoms of duodenal and gastric ulcers differ?

Answer 8

D: burning, pinpoint epigastric pain

G: diffuse epigastric pain, nausea, vomiting, weight loss

Question 9

How do the onsets of duodenal and gastric ulcers differ?

Answer 9

D: 1-3 hrs after meals, empty stomach, relieved by food or antacids

G: immediately after meals, aggravated by food

Question 10

How do the gastric acid levels in duodenal and gastric ulcers differ?

Answer 10

D: normal to high

G: normal to low

Question 11

What is Zollinger-Ellison syndrome?

Answer 11

A fulminant peptic ulcer disease caused by a gastrinoma, a non-beta islet cell tumor that secretes gastrin. It is either sporadic or associated with MEN-1.

Question 12

What is the hallmark of ZES?

Answer 12

Inappropriate hypergastrinemia.

Question 13

What are causes of appropriate hypergastrinemia?

Answer 13

(1) PPIs and H2-receptor antagonists
(2) atrophic gastritis
(3) H. pylori pangastritis
(4) chronic renal failure
(5) vagotomy

Question 14

What are causes of inappropriate hypergastrinemia?

Answer 14

(1) ZES
(2) retained antrum syndrome
(3) antral H. pylori infection
(4) massive intestinal resection
(5) gastric outlet obstruction

Question 15

When should you consider ZES?

Answer 15

(1) severe peptic disease
(2) before anti-ulcer surgery
(3) Dx of MEN-1 syndrome
(4) non-NSAID, non-H. pylori ulcers

Question 16

How does the parietal cell mass differ in duodenal and gastric ulcers?

Answer 16

D: elevated
G: normal to low

Question 17

How is H. pylori adapted to infection and survival in the stomach?

Answer 17

(1) urease: creation of a non-acidic microenvironment by secreting ammonium.
(2) flagella and spiral morphology: penetration of mucus layer.
(3) proteases and phospholipase: disruption of mucosal barrier.
(4) adherence factors: exclusive attachment to mucus-secreting cells.
(5) non-invasion of mucosa: avoidance of immune response.

Question 18

What is the Gastrin Hypothesis for H. pylori duodenal ulcers?

Answer 18

(1) Antral infection inhibits somatostatin release, leading to unopposed gastrin secretion.
(2) Hypergastrinemia leads to elevated acid secretion.
(3) Duodenal gastric metaplasia permits colonization of duodenal bulb.
(4) Undermined local defenses and acid hypersecretion leads to ulcers.

Question 19

What are the spectrum of disorders following an H. pylori infection?

Answer 19

(1) chronic gastritis
(2) duodenal ulcers
(3) gastric ulcers
(4) gastric cancer
(5) maltoma

Question 20

What are some environmental factors for developing gastric cancer?

Answer 20

(1) nitroso compounds and salt
(2) smoking
(3) low vitamin C

Question 21

What is CagA?

Answer 21

It is a marker of virulence for H. pylori, though the role of the protein is unknown. It is associated with greater inflammation (elevated IL-1, IL-2, IL-8) and gastric cancer.

Question 22

J: This peptic ulcer is caused by ischemia and necrosis of the gastric mucosa after severe burns.

Answer 22

What is Curling’s ulcer.

Question 23

J: This peptic ulcer is caused by vagal stimulation from increased intracranial pressure after a head injury.

Answer 23

What is Cushing’s ulcer.

Question 24

What is in the ddx for ulcer-like pain and dyspepsia?

Answer 24

(1) peptic ulcer
(2) GERD
(3) gallstones
(4) pancreatitis
(5) pneumonia
(6) pulmonary embolus
(7) MI
(8) ruptured aortic aneurysm

Question 25

What functions are associated with COX1?

Answer 25

It is constitutively active and performs in some housekeeping activities:

(1) aggregation of platelets
(2) cytoprotection of the stomach (mucus, bicarbonate)
(3) blood flow to the kidney
(4) vessel dilatation

Question 26

What functions are associated with COX2?

Answer 26

It’s activity is inducible and it contributes to the inflammatory response.

Question 27

What are the cytoprotective effects of prostaglandins?

Answer 27

(1) increased mucus
(2) increased bicarbonate
(3) increased submucosal blood flow
(4) some direct action in reducing acid secretion

Question 28

Simply, how does the action of coxibs differ from NSAIDs?

Answer 28

Coxibs only inhibit COX2, sparing COX1.

Question 29

What is the MoA of NSAIDs?

Answer 29

They inhibit COX enzymes, lessening the inflammatory response. ( However it is the inhibition of COX1 specifically that leads to peptic ulcers.)