Peptic Ulcer Disease Flashcards
How common is peptic ulcer disease?
~10% incidence
What does the stomach secrete?
Mucous to protect the lining from the HCL secreted to chemically digest food
Where is HCl secreted?
Parietal cells
How does the duodenum protect itself against acid?
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)
Where is the appearance of ulcers higher?
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)
Peptic ulcer disease?
An ulcerative disorder of the upper GIT affecting mostly the duodenum (80%) and also the stomach (20%)
Which tissue later does PUD affect?
Primarily the mucosa but can penetrate into deeper layers
What does a pt with PUD experience?
Remissions and exacerbations
Does HCl cause PUD?
NO, HCl does not cause PUD but rather an infection by the bacteria Helicobacter Pylori (H. Pylori)
Is H. Pylori apart of the stomachs normal flora?
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
Can HCl destroy bacteria? (more specifically H. Pylori)
Yes, however the microbe has a protective mechanism to survive.
What is the bacterium’s protective mechanism to survive?
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
H2CO3?
Carbonic acid
HCO3-?
Bicarbonate
Pathology of PUD?
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
Hypergastrinemia?
Excess production of gastrin in the blood
Gastrin?
A hormone that increases HCl secretion.
What occurs with increased HCl production?
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.
What are protective factors used by the GIT?
- Buffering in the duodenum with pancreatic juice
- Regeneration of mucosal cells
- Mucus protection in the stomach
Offensive factors?
- Increased acid
2. Bacteria
Risk factors for PUD?
- NSAIDs
- irregular HCl & biliary acid
- Chronic gastritis
- Smoking
- Alcohol
- Caffeine
- along with an H. Pylori infection
Give a summary of PUD.
H. pylori -> adheres to wall -> inflammation -> damage -> excess acid & further damage -> ulcer formation (offensive factors outweigh defense)
In PUD, where does the most inflammation occur?
@ the site of the ulceration
Where does the acid have the most impact?
@ the site of the ulceration
