Peptic Ulcer Disease

Question 1

What is Peptic ulcer disease?

Incidence in general population

Answer 1

Ulceration disorder of stomach, esophagus or duodenum

~10% incidence

Question 2

What percentage are gastric ulcers?

Reasoning?

Answer 2

A gastric ulcer is in the stomach.

Stomach has strong mucous barrier (AKA resident protection)

Question 3

What percentage are duodenal?

Reasoning?

Answer 3

80%

Duodenum doesn’t have as strong a mucosa, it uses buffers to control acidic environment that must come in from elsewhere

Question 4

What layer is most often effected by PUD?

Answer 4

Mucosa

Question 5

What pattern is characteristic of it’s progression

Answer 5

remission and exacerbation

Question 6

The villain of the story?

Etiology

Answer 6

Helicobactor (H) Pylori Infection

Question 7

Where does H pylori hang out?

Normally and with PUD?

Answer 7

Normally- H pylori is a transient visitor in the stomach

During- Attaches to the mucosa and create a niche in a specific area

Question 8

How does H pylori deal with the acidic environment?

Chemistry

Answer 8

Neutralizes acid with Urease. Catalyzes NH3 + C02 + H20= H2c03 (which is carbonic acid and a volatile acid)

This breaks into Bicarbonate HC03- which provides a buffer against stomach acid

Question 9

What is the mechenism of damage to the mucosa?

Answer 9

Unclear

But there is inflm and the release of a hormone. (gastrin?) Hypergastrinemia stimulates the release of more HCL.

Question 10

What are the risk factors?

Answer 10

• HCL and biliary acid
• steroids and NSAIDS
• chronic gastritis
• smoking, alcohol and caffeine
• stress

Question 11

General Patho of PUD?

2 source of damage?

Answer 11

H. pylori infection -> Inflm -> tissue damage

AND

H pylori infection -> Inc gastrin -> gastric secretions -> tissue damage

NOTE - host cells are stimulated to release the gastrin

Question 12

What defensive factors will prevent H pylori’s evil PUD scheme?

Answer 12

• Regulation of secretion of acid (defensive mechanism)
• Intact perfusion (defensive mechanism)
• Regeneration of epithelial lining

When these fx properly offensive factors should not cause tissue damage

Question 13

What shuts down our defensive mechanism?

Answer 13

Risk factors

• HCL and biliary acid
• steroids and NSAIDS
• chronic gastritis
• smoking, alcohol and caffeine
• stress

Question 14

Main MNFTS

Answer 14

• ABD pain (burning, cramping)

* Nausea and vomiting (later stages)

Question 15

What are the main complications?

Answer 15

• Perforation (could end up with peritonitis)
• Hemorrhage (if blood vessels are damaged)

• Gastric obstruction
o D/t edema, spasm or Scar tissue contraction

Question 16

Dx

Answer 16

• Hx (reduce potential diagnosis that present with abd/chest pain)
• Serology (for antibodies to h pylori)
• Urea breath test UBT-
• Fecal Ag (proteins present on H pylori cells)
• Barium swallow ( show you location and number of ulcers)
• Endoscopy will allow for visualization of ulcer

Question 17

What is the UBT

Answer 17

• Urea breath test UBT- label urea with radioactive isotope, they drink it, h pylori turns to CO2 and NH2, look for label in breath

Question 18

Simple pharma Tx for PUD?

Answer 18

• Antacids (continue simply neutralizing of acids, dealing w/ MNFTS)

Question 19

What is the triple regiment tx for PUD?

What is strategy?

(The answer could use clarity)

Answer 19

PPI’s – (which block H+ secretion) + 2 abx (Amoxil, Biaxin) for 2 weeks
• NOTE - PPI’s (losec, nexum) - longer course of admin

o H2RA (block gastric acid secretion) + 2 abx
• Tagamet, Zantac
• Related to histamine reduction

STRATEGY- Stop infection then reduce acid to allow healing of ulcer. Goal= Cure

Question 20

With complication, what might be necessary?

Answer 20

Sx