Flashcards in Peptic Ulcer Disease Deck (20):
1
What is Peptic ulcer disease?
Incidence in general population
Ulceration disorder of stomach, esophagus or duodenum
~10% incidence
2
What percentage are gastric ulcers?
Reasoning?
A gastric ulcer is in the stomach.
Stomach has strong mucous barrier (AKA resident protection)
3
What percentage are duodenal?
Reasoning?
80%
Duodenum doesn't have as strong a mucosa, it uses buffers to control acidic environment that must come in from elsewhere
4
What layer is most often effected by PUD?
Mucosa
5
What pattern is characteristic of it's progression
remission and exacerbation
6
The villain of the story?
(Etiology)
Helicobactor (H) Pylori Infection
7
Where does H pylori hang out?
Normally and with PUD?
Normally- H pylori is a transient visitor in the stomach
During- Attaches to the mucosa and create a niche in a specific area
8
How does H pylori deal with the acidic environment?
(Chemistry)
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
9
What is the mechenism of damage to the mucosa?
Unclear
But there is inflm and the release of a hormone. (gastrin?) Hypergastrinemia stimulates the release of more HCL.
10
What are the risk factors?
• HCL and biliary acid
• steroids and NSAIDS
• chronic gastritis
• smoking, alcohol and caffeine
• stress
11
General Patho of PUD?
2 source of damage?
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
12
What defensive factors will prevent H pylori's evil PUD scheme?
• 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
13
What shuts down our defensive mechanism?
Risk factors
• HCL and biliary acid
• steroids and NSAIDS
• chronic gastritis
• smoking, alcohol and caffeine
• stress
14
Main MNFTS
• ABD pain (burning, cramping)
• Nausea and vomiting (later stages)
15
What are the main complications?
• Perforation (could end up with peritonitis)
• Hemorrhage (if blood vessels are damaged)
• Gastric obstruction
o D/t edema, spasm or Scar tissue contraction
16
Dx
• 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
17
What is the UBT
• Urea breath test UBT- label urea with radioactive isotope, they drink it, h pylori turns to CO2 and NH2, look for label in breath
18
Simple pharma Tx for PUD?
• Antacids (continue simply neutralizing of acids, dealing w/ MNFTS)
19
What is the triple regiment tx for PUD?
What is strategy?
(The answer could use clarity)
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
20