Peptic Ulcer Disease

Question 1

How common is peptic ulcer disease?

Answer 1

~10% incidence

Question 2

What does the stomach secrete?

Answer 2

Mucous to protect the lining from the HCL secreted to chemically digest food

Question 3

Where is HCl secreted?

Answer 3

Parietal cells

Question 4

How does the duodenum protect itself against acid?

Answer 4

It does not have the same protection against acid as the stomach does, but pancreatic juice is released into the duodenum that buffers the low pH of gastric content, which neutralizes the acid (with bicarbonate)

Question 5

Where is the appearance of ulcers higher?

Answer 5

In the duodenum (bc it depends on the action of the pancreas. If acid enters the duodenum with no pancreatic juice present, this leads to damage)

Question 6

Peptic ulcer disease?

Answer 6

An ulcerative disorder of the upper GIT affecting mostly the duodenum (80%) and also the stomach (20%)

Question 7

Which tissue later does PUD affect?

Answer 7

Primarily the mucosa but can penetrate into deeper layers

Question 8

What does a pt with PUD experience?

Answer 8

Remissions and exacerbations

Question 9

Does HCl cause PUD?

Answer 9

NO, HCl does not cause PUD but rather an infection by the bacteria Helicobacter Pylori (H. Pylori)

Question 10

Is H. Pylori apart of the stomachs normal flora?

Answer 10

No, there is no flora in the stomach. When it invaded the body it secretes adhesion factors to attach itself to the wall of the stomach or duodenum

Question 11

Can HCl destroy bacteria? (more specifically H. Pylori)

Answer 11

Yes, however the microbe has a protective mechanism to survive.

Question 12

What is the bacterium’s protective mechanism to survive?

Answer 12

a. Bacteria produce urease which converts urea into carbon dioxide and NH2 in the stomach and duodenum.
b. Water present in the stomach combines with carbon dioxide to produce carbonic acid -> this is a volatile acid, meaning it dissociates rapidly into HCO3- and H+.
c. Bicarbonate is used to buffer the HCl to protect the bacteria from destruction
d. The bicarbonate does not buffer the acid in the entire stomach, but rather creates a micro-niche, an area immediately surrounding the bacteria that is neutralized

Question 13

H2CO3?

Answer 13

Carbonic acid

Question 14

HCO3-?

Answer 14

Bicarbonate

Question 15

Pathology of PUD?

Answer 15

Bacteria produce mediators that trigger inflammation, which consequently damages the area of the stomach/intestinal wall that the H. Pylori is attached. Bacteria also produce mediators that triggers hypergastrinemia

Question 16

Hypergastrinemia?

Answer 16

Excess production of gastrin in the blood

Question 17

Gastrin?

Answer 17

A hormone that increases HCl secretion.

Question 18

What occurs with increased HCl production?

Answer 18

Increased acid. The more acid that is produced, the more urease is produced by the bacteria to buffer the acid. Result: The acid erodes the already damaged stomach/intestinal wall (damaged by inflammation), while the bacteria remain unharmed in their micro-niche.

Question 19

What are protective factors used by the GIT?

Answer 19

1. Buffering in the duodenum with pancreatic juice
2. Regeneration of mucosal cells
3. Mucus protection in the stomach

Question 20

Offensive factors?

Answer 20

1. Increased acid

2. Bacteria

Question 21

Risk factors for PUD?

Answer 21

• NSAIDs
• irregular HCl & biliary acid
• Chronic gastritis
• Smoking
• Alcohol
• Caffeine
• along with an H. Pylori infection

Question 22

Give a summary of PUD.

Answer 22

H. pylori -> adheres to wall -> inflammation -> damage -> excess acid & further damage -> ulcer formation (offensive factors outweigh defense)

Question 23

In PUD, where does the most inflammation occur?

Answer 23

@ the site of the ulceration

Question 24

Where does the acid have the most impact?

Answer 24

@ the site of the ulceration

Question 25

Manifestations of PUD?

Answer 25

Heartburn, nausea + vomiting, and abdominal burning/cramping on an empty stomach

Question 26

Why does heartburn occur in PUD?

Answer 26

Acid affects the tissue causing a burning sensation

Question 27

Why does abdominal cramping/burning occur on an empty stomach?

Answer 27

there is no gastric content so the acid has nothing else to act on and is in contact with the stomach wall more readily.

Question 28

Why does N+V occur?

Answer 28

Not due to pain, it is a local manifestation

Question 29

Complications of PUD

Answer 29

• ulceration in the superficial layer impacts the blood vessels because the wall is very vascularized -> bleeding -> hemorrhage if a large vessel is impacted
• bleeding in the upper GIT -> dark occult blood in stools d/t oxidation
• Ulcer perforates through the entire wall (all layers) -> HCl spills out into the abdominal cavity -> chemical peritonitis
• Obstruction d/t edema, spasm or scar tissue contraction

Question 30

Diagnostics for PUD?

Answer 30

• Serology -> Ab formed against H. Pylori present
• Fecal antigens
• Urea Breath Test
• Endoscopy and biopsy
• Barium swallow test

Question 31

Why is an endoscopy typically done after a UBT indicated PUD?

Answer 31

To visualize the location of the ulcers and severity

Question 32

Treatment for PUD?

Answer 32

• TRIPLE REGIMEN = PPI + H2RA + 2 Abx

- may require surgery if there are complications

Question 33

What are the following drugs examples of?:

1. Zantac
2. Pariet
3. Mexium
4. Amoxicil
5. Losec
6. Flagyl
7. Biaxin
8. Tagemet

Answer 33

1. H2RA
2. PPI
3. PPI
4. Antibiotic
5. PPI
6. Antibiotic
7. Antibiotic
8. H2RA

Question 34

First line therapy?

Answer 34

PPI + amoxil + biaxin

Question 35

How long are antibiotics used for?

Answer 35

7-10 days to get rid of infection

Question 36

How long are PPIs and H2RAs used for?

Answer 36

Up to 6-8 weeks to allow the ulcers to heal