Peptic Ulcer Disease & Hepatitis Flashcards
What is Peptic Ulcer disease?
Cause?
Where does it occur?
- Ulcerative disorder
- Helicobactor pylori infection
- Occurs in stomach (20%) or duodenum (80%)
- Primarily affects mucosa - Can affect deeper layers (if acid makes contact with them)
- Remission and exacerbations
Why is PUD most common in the duodenum?
stomach not common b/c built with protection; buffering occurs in duodenum normally, but if not intact will result in ulcer
WHy do you see remission and exacerbations in PUD?
- if thinking about food or eating, acid secreted
- Should be acute problem b/c is completely curable but if individual doesn’t seek medical attention see recurring remission and exacerbations
How is H Pylori able to infect the stomach?
- is transient visitor in the gut, not usually causing problems but can become problematic when produce niches for themselves (areas they colonize within stomach wall)
- Survive in harsh environment by secreting adhesion proteins that help to attach to epithelial tissue and urease (enzyme the breaks urea to ammonia NH3 & CO2) that creates formation of bicarbonate, which acts as buffer within these niches
General etiology of PUD
- How are the presence of bacteria contributing the the formation of the ulcer?
- Helicobactor pylori infection
- Exact mechanisms by which these bacteria cause the ulcer is unclear
o Inflm – when bacterial colonize, cause this
o Hypergastrinemia – gastrin hormone signals secretion of HCl; bacteria stimulates secretion of gastrin, and thus more HCl (inc HCl secretion) - Other factors play a role, but are not etiological…
Risk factors for PUD?
- HCl and biliary acid
- Steroids and NSAIDs –
- Chronic gastritis (d/t other bacterial infection or other – damages lining as well)
- Smoking, alcohol, caffeine (aggravate symptoms once disease is in place)
- Stress
Effect of steroids + NSAIDs as risk factors for PUD?
inc acid secretion and damages mucosal lining
How are HCL and biliary acid both considered etiological and risk factors in PUD?
etiology…have to have both the bacterial infection and the acid for the ulcer to form)
is risk factor in that it aggravates the ulcers once they exist
Risk factors AKA?
The opposite to this?
Offensive factors
Defensive factors
What defensive factors exist in r/t PUD?
o Regulation of acid secretion
o intact perfusion
o mucus
o regeneration of the mucosa (replenishment of cells, not speaking here of healing)
**these prevent the formation of peptic acid disease; normally these are able to outweight the action of the offensive factors…if then overcome by exceessive offensive factors, the disease will develop
Patho of PUD?
- H. pylori infection
- Inflm → tissue damage
- Inc gastrin prod (hypergastrinemia?) → inc acid secretion → tissue damage
- Defenses against gastric acid impeded by risk factors
- Penetrating ulcer forms
Mnfts of PUD?
- Abdominal pain: burning, cramping – often felt over the chest as well (and therefore cannot be defining feature of diagnosis)
- Nausea, vomiting (not very common presentation, is not d/t pain but rather GI symptom here)
Complications of PUD?
- Perforation of the ulcer
- Hemorrhage
- Gastric or duodenal obstruction – D/t edema, spasm (of muscle) or scar tissue contraction
Complication of perforation of the ulcer?
can end up with peritonitis as complication of this
Would you expect to see frank or occult blood in stool of individual with PUD?
high up in GI tract, would find OCCULT blood in stool (not frank) because of this location
Explain mechanism by which edema causes obstruction in PUD?
in lumen, not tissue edema, from exudate and mucus + air in the bowel….pressure increases in that area of the gut
Is scar tissue considered metaplasia?
No, because not considered normal tissue
Metaplasia = replacing normal tissue with normal tissue
Dx of PUD?
- Hx
- UBT (urea breath test), serology, fecal Ag
- Barium swallow →
- Endoscopy
How does a UBT work?
o Urea —–→ NH3 + CO2
o Trying to track the C molecule in urea –> person given solution with labeled carbon urea solution, which goes into stomach, if H. Pylori is present it will be producing urea -→ it will be converted to CO2 and ammonia, CO2 will also be labeled….this CO2 will be taken into blood and exhaled (person asked to exhale 2 hours after ingestion and exhales into 2 bags…then this air is checked for marked C in CO2.
o If person doesn’t have H. Pylori in gut and given urea solution, will only excrete
o ONLY time you’ll have urea is when H. Pylori is present! And urea is required for radioactive C to be seen.
What is serology?
looking for antibodies in the blood
How would you detect H. Pylori in the stool?
antigens (proteins) that are related to H. Pylori
Tx of PUD?
• Antacids? – will relieve pain temporarily by neutralizing acid
• Triple regimen: (to eradicate the bacteria and treat ulcers at the same time) – 2 possibilities
o H2RA (H2 receptor antagonist to block gastric secretion) + 2 Abx
o PPI (blocks H+ secretion) + 2 Abx
• Sx for complications (sometimes)
Why are H2RAs used in PUD?
Examples of H2RA?
o Histamine receptors blocked by H2RA b/c histamines facilitate acid secretion (histamine can’t bind so acid is not secreted)
o H2RA examples = zantac + tagamet