Peptic Ulcer Disease Flashcards
(20 cards)
What is Peptic ulcer disease?
Incidence in general population
Ulceration disorder of stomach, esophagus or duodenum
~10% incidence
What percentage are gastric ulcers?
Reasoning?
A gastric ulcer is in the stomach.
Stomach has strong mucous barrier (AKA resident protection)
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
What layer is most often effected by PUD?
Mucosa
What pattern is characteristic of it’s progression
remission and exacerbation
The villain of the story?
Etiology
Helicobactor (H) Pylori Infection
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
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
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.
What are the risk factors?
- HCL and biliary acid
- steroids and NSAIDS
- chronic gastritis
- smoking, alcohol and caffeine
- stress
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
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
What shuts down our defensive mechanism?
Risk factors
- HCL and biliary acid
- steroids and NSAIDS
- chronic gastritis
- smoking, alcohol and caffeine
- stress
Main MNFTS
- ABD pain (burning, cramping)
* Nausea and vomiting (later stages)
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
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
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
Simple pharma Tx for PUD?
• Antacids (continue simply neutralizing of acids, dealing w/ MNFTS)
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
With complication, what might be necessary?
Sx
