Peptic Ulcer Disease Flashcards Preview

253-Green Patho > Peptic Ulcer Disease > Flashcards

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

With complication, what might be necessary?

Sx