4. Peptic Ulcer Disease

Question 1

Peptic Ulcer disease: clinical presntation?

(duodenal)

Answer 1

• epigastric “gnawing” pain
• often relieved by eating, drinking, antacids
• worse on empty stomach
• may awaken from sleep

Question 2

Peptic Ulcer disease: can we make a clinical diagnosis? why/not?

Answer 2

Ulcers may occur without symptoms

Ulcer-like suymptoms may occur without ulcers

Majority of patients with dyspepsia have non-ulcer dyspepsia

therefore have to do specific testing: UGI Barium study, upper endoscopy

Question 3

Benign/melig? how can we tell?

Answer 3

benign gastric ulcer.

This ulcer on the distal lesser curvature in the antrum is well circumscribed and lateral views demonstrate projection of the crater away from the lumen.

Question 4

What is this?

what would be different in a benign ulcer v a malignant ulcer?

Answer 4

duodenal ulcer

benign ulcers are smooth, regular. Symmetrically thickened (inflammatory) folds typically radiate to the ulcer base.

malignant: have irregular edges, and the surrounding, asymmetrical folds do not radiate to the base of the ulcer.

Question 5

what is the natural history of peptic ulcer disease?

Answer 5

• may be benign
• may be recurrent/intractable
• may have severe complications: hemorrhage, perforation, gastric outlet obstruction

Question 6

a “spurting” duodenal ulcer: how would it present?

Answer 6

• hematemesis (coffee grounds)
• hematochezia (fresh blood PR)
• melena

Question 7

ways to cure ulcers (via decr acid) surgically?

Answer 7

• want to remove parietal cells and their stimulus
• Selective vagatomy to decr neural stimulus
• Billroth I and II: vagotomy with antrectomy (removal of cholinergic and gastrin stimulus) to decr basal acid secretion. (resulted in decr acid by 80%)

Question 8

what does H Pylori do when it is in contact with gastric epithelium?

Answer 8

Attaches tightly to gastric epithelium/cell surface

May alter cell and activate bacterial functions, making them more toxic

Does not invade gastroduodenal tissue

Underlying mucosa now more vulnerable to peptic acid damage by disrupting overlying mucous, adhering epithelium, inciting inflammatory host response

Question 9

what 3 things can be caused by chronic H Pylori infection?

Answer 9

• Duodenal ulcer (10%)
• No significant disease (80%)
• Gastric cancer (10%) (due to atrophy –> metaplasia)

due to chronic superficial gastritis, may infect areas of gastric metaplasia in the duodenum.

Question 10

what else causes ulcers besides H Pylori?

Answer 10

• NSAIDs: via loss of mucosal defense.
• Zollinger Elison syndrome: gastrinoma. high rates of acid secretion. intractable PUD, complicated severe ulcer disease
• acute stress ulcerations of stomach and duodenum. due to shock, sepsis, trauma. lots of bleeding.

Question 11

What is the pathway for NSAIDs cuaseing GI toxicity?

Answer 11

Cyclooxygenase (COX) is the rate-limiting step in prostagandin synthesis.

NSAIDs are COX inhibitors (aspirin is irreversible; others are reversible)

NSAIDs therefore reduce gastro-duodenal prostaglandin mucosal concentrations,

–>resulitng in loss of mucus production, mucosal blood flow, and mucosal proliferation.