Acid-Peptic Disorders Flashcards Preview

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Flashcards in Acid-Peptic Disorders Deck (27)
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1
Q

Describe gastric mucosal cells and their products

A
Parietal cells: acid, intrinsic factor
G cells: gastrin
D cells: somatostatin
ECL cells: histamine
Chief cells: pepsinogen
Surface epithelial and mucus neck cells: Mucus/bicarbonate
2
Q

What stimulates parietal cell secretion? What inhibits it?

A

Stimulated by histamine, gastrin, vagal stimulation

Inhibition by PGE, PPI, antihistamine, atropine, SS

3
Q

Negative feedback on parietal cell acid secretion comes from what substance?

A

Somatostatin

4
Q

What is the role of normal mucus layer?

A

Mucus and bicarbonate prevent autodigestion from acid and pepsin in lumen

5
Q

What are prostaglandin-dependent protective factors (4)

A

Mucous layer thickness
Decreased pH gradient
Increased bicarbonate secretion
Increased mucosal blood flow

6
Q

What are aggressive factors in peptic ulcers? (4)

A

Acid
NSAIDs: local effect, COX inhibition
H. Pylori: decreased mucosal protection and increased acid output
Other: steroids, smoking, alf, bile, caffeine

7
Q

Gastric vs. Duodenal ulcers: Clinical presentation

A

Symptoms: Nausea/vomiting/diffuse pain vs. pinpoint burning pain
Onset: immediately after meals vs. 1-3hr after meals (empty stomach)
Acid: Normal-low vs. normal-high

8
Q

Trend in peptic ulcers in US

A

Uncomplicated ulcers declining: disappearance of H pylori

BUT complicated ulcer prevalence is unchanged (so increased proportion overall)

9
Q

What is Zollinger Ellison Syndrome?

A

A gastrin-secreting tumor that leads to fulminant peptic ulcer disease due to gastric acid hypersecretion

10
Q

What are other causes of hypergastrinemia? Appropriate vs. Inappropriate

A

Appropriate: Drugs (PPIs), atrophic gastritis, H pylori pangastritis, renal failure, vagotomy

Inappropriate: ZES, retained antrum syndrome, antral predominant H pylori (G-cell hyperplasia), intestinal resection, gastric outlet obstruction

11
Q

MEN-1 Syndrome

A

Autosomal dominant genetic disorder with MENIN mutation
3Ps+ATL
Can cause ZES

12
Q

When should you consider ZES?

A

Non-NSAID, non H pylori ulcer
Severe peptic disease (multiple recurrent non healing ulcers)
Diarrhea due to hypersecretion
MEN-1 syndrome

13
Q

Idiopathic peptic ulcer disease

A
Increased BAO (basal acid output), MAO
Not associated with hypergastrinemia
14
Q

Why is H pylori uniquely adapted for survival in stomach? (4)

A

Urease neutralizes local pH
Attaches directly to host epithelium
Modifies gastric acid secretion to permit maximal survival
Induces inflammation to permit nutrition

15
Q

What is global prevalence of h. pylori?

A

50%

16
Q

Pathophysiology of H Pylori Gastritis

A

Person to person transmission
Urease permits non-acidic microenvironment
Flagellae/spiral morphology enables penetration of mucus layer
Enzyme products permit disruption of mucosal barrier
Adherence factors: attachment to mucus cells
Immune response/inflammation causes gastritis
DOES NOT INVADE MUCOSA

17
Q

In what three ways can H pylori affect acid secretion?

A

Superficial gastritis=decrease in acid secretion from pangastritis (most common)
Antral predominant infection: Huge increase due to duodenal ulcer
Asymptomatic chronic infection: normal range of gastric output

18
Q

Gastrin Hypothesis of H Pylori Duodenal Ulcers

A

Antral H pylori inhibits somatostatin production: unopposed gastrin release–>gastric acid hyper secretion
Hypersecretion leads to duodenal gastric metaplasia (gastric cells in duodenal bulb) enables colonization in duodenal bulb
Local defenses undermined+hypersecretion=ulceration in duodenum

19
Q

What are sequelae of h. pylori infection?

A
Chronic gastritis
Duodenal ulcer (90%), gastric ulcer (70%)
Gastric cancer (.5%)
Maltoma (lymphocytic gastritis)
Non-ulcer dyspepsia
20
Q

What is the role of CagA in gastric cancer?

A

Present in 50-60% of H Pylori
Marker of virulence– associated with increased cytokine release and inflammation
Associated with gastric cancer

21
Q

IL-1B in Gastric Cancer

A

Polymorphism in IL-1B results in more inflammation–>more susceptible to gastric cancer (more gastritis)

22
Q

NSAIDs-induced mucosal injury

A

Inhibit both COX1 (constitutive) and COX2

No COX1==>lose prostaglandin-dependent processes: Acid inhibition, altered mucus, blood flow

23
Q

How do you avoid NSAID induced mucosal injury?

A

COXIBs (selective COXII inhibitors)

24
Q

What is affect of H Pylori on COX?

A

It induces COXII to reduce acid secretion

25
Q

Effect of H Pylori AND NSAID use?

A

Higher incidence of ulcers

26
Q

What are other causes of peptic ulcers? (4)

A

Stress: Curling’s ulcer (burns), Cushing’s ulcer (head trauma)
Chemo
Uremia
Cancer

27
Q

What are causes of non-ulcer dyspepsia?

GI (3) & Non-GO (4)

A

GI: GERD, gallstones, pancreatitis

Non-GI: Pneumonia, pulmonary embolus, MI, ruptured aortic aneurysm